Classic Imaging Signs

A Guide to the Whole Body

Bo Gao
Alexander M. McKinney
Editors

123
Classic Imaging Signs
Bo Gao  •  Alexander M. McKinney
Editors

Shi Zhou  •  Shi Zuo

Associate Editors

Classic Imaging Signs

A Guide to the Whole Body
Editors
Bo Gao Alexander M. McKinney
Department of Radiology Department of Radiology
Affiliated Hospital University of Miami Miller
of Guizhou Medical University School of Medicine
Guiyang Miami, FL
China USA

ISBN 978-3-030-56347-9    ISBN 978-3-030-56348-6 (eBook)

https://doi.org/10.1007/978-3-030-56348-6

© Springer Nature Switzerland AG 2021

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Foreword: Imaging Signs

Radiologic and radiographic “imaging signs” are critical to our quick recog-
nition of disease states and instituting therapy. They are also perhaps even
more vital to the teaching element for trainees, since such prompt recognition
of an abnormal imaging pattern cements the appearance in the memory of the
learner for future recognition. The goal of proposing such “signs” is that
eventually a particular disease state’s radiologic appearance ultimately
becomes accepted as a classic “imaging sign,” and thus gains recognition
among radiologists and other subspecialists for general use. While it is
acknowledged that a disease state does not absolutely have to exhibit the clas-
sic imaging sign (e.g., the “Rigler sign” of pneumoperitoneum), it is quite
important to note such a sign, when present, as early as possible, in order to
alert the ordering provider to a preventable complications of the disease state.
The editors, Drs. Gao and McKinney et al., organized this text in a very
practical fashion that can serve as a quick reference to enhance the reader’s
understanding of each imaging sign, regardless of their level of training or
experience. While there are many other texts and websites that address imag-
ing signs by subspecialty (e.g., cardiothoracic or neuroradiology), body part
(e.g., lung or renal), or particular disease state (e.g., pneumoperitoneum or
meningioma), this text distinguishes itself as a compendium of each subspe-
cialty/organ system. The text is organized by each body part/organ system
(e.g., brain, spine, chest, etc.), with Individual topics for each sign. Another
distinguishing factor is that this text also provides the proven or presumed
pathophysiologic reasoning for that imaging appearance, as well as variants
or alternative names for each sign. Finally, I note that the editors incorporated
newer signs (e.g., the “swallowtail sign” on susceptibility-weighted MRI)
along with the classic imaging signs and attempted to provide the reliability
or sensitivity/specificity of these signs when such data were available.
Hence, this text on “Imaging Signs” will likely serve to augment both the
educational and clinical aspects for trainees and staff physicians, and enable
prompt recognition of particular disease states. This is becoming increasingly

v
vi Foreword: Imaging Signs

vital in this era of remote education, diagnosis, and therapy. Further editions
and versions will presumably expand upon this novel work and continue to
enlighten our trainees and provide a useful resource to practicing physicians.

Jafar Golzarian, MD
Professor of Radiology and Surgery
Vice Chair, Faculty Affairs Medical School
Director, Division of Interventional Radiology
University of Minnesota Medical Center
Minneapolis, MN, USA
Foreword: Classic Imaging Signs: A Guide
to the Whole Body

Medical imaging/radiology has developed tremendously in the last decades with

the emergence of novel imaging techniques, especially the flourishing of advanced
CT and MRI. In recent years, even with the rapid evolution of modern imaging
modalities, radiology still has an irreplaceable role in diagnosis within standard
clinical practice. The field of medical image analysis has grown exponentially,
with an increased number of pattern recognition tools and an increase in data set
sizes. Competent imaging acquisition often entails referring to other realms of
knowledge to acquire insights with the aid of metaphors. Problems with timing,
efficiency, and missed diagnoses may occur at all stages of the imaging chain.
This book Classic Imaging Signs: A Guide to the Whole Body is written by
leading experts with irrespective imaging specialty backgrounds. The editors,
Drs. Gao and McKinney et al., organized this text in a very practical fashion
that can serve as a quick reference to enhance the reader’s understanding of
each imaging sign. This book is intended to help radiologists and students
accomplish this task. It provides practicing radiologists and radiology resi-
dents or fellows with the level of knowledge necessary to avoid misinterpreta-
tion and help make precise diagnoses in the presence of certain classic
pathognomonic features. Judgment of image sign, as one of the core principles
of radiology, relies on the integration of multilayered data with distinctive
decision-making. If we are to use terms with full understanding, we should be
capable to visualize the object depicted by that term, imagine its radiologic
appearance, and transfer that picture to the radiologic image before us.
This book serves to augment both the educational and clinical aspects for
trainees and staff physicians, and enable prompt recognition of particular dis-
ease states. This is becoming increasingly vital in this era of remote educa-
tion, diagnosis, and therapy. The editors of this book have provided thorough
and illustrative reviews of these emerging and controversial topics. I con-
gratulate the editors on their accomplishment of this work, and I look forward
to future editions since we seemingly encounter new diseases and signs every
year. I am pretty glad to introduce this book to those who are addicted to the
clinical practice and research of clinical radiology.

Hai-yang Li, MD
Professor of Surgery
Chair, Clinical Medical School, Guizhou Medical University
President, The Affiliated Hospital of Guizhou Medical University
Guiyang, China

vii
Preface

Image signs refer to the normal structures of the human body or imaging
information or radiologic findings produced by pathology under any type of
imaging modalities. An “iconographic” glossary of terms used for imaging is
reproduced-placing side by side between radiological features and those may
be associated with signs, symbols, or naturalistic images. Specifically, image
signs refer to the metaphor of certain tissue, structure, or lesion. One way is
by linking anatomic structures and pathologic conditions with objects, places,
and concepts, and codifying these relationships as metaphoric signs. To
describe an unnoticed finding specific to a particular entity has always been a
challenge for the radiologists. Time will be needed on investigations before
we can add the specific finding to the legions of “signs” in radiology. The
“signs” may become part of our language of specialty after validating by dif-
ferent observers over time. The “classic signs” endorse us confidence in
determining the diagnosis. Some imaging signs have been acknowledged,
which are referred to as “Aunt Minnie.” When the sign is invoked, or an Aunt
Minnie is recognized, it often brings an impression of the image to mind, and
it may have specific diagnostic and pathologic significance. The advance of
radiology, evolving with such signs, renders an otherwise difficult diagnosis
easier, may help the radiologists appreciate the anatomy and pathology of an
underlying abnormality, and may quickly direct the physicians to the proper
diagnosis and timely intervention. This book systematically summarizes the
imaging characteristics and theory of modern imaging, primarily summarizes
the imaging signs characteristics and theory in the whole body, serving as a
clinical guidance and having a practical significance for the understanding,
prevention, and diagnosis of miscellaneous entities.
This book consists of 10 chapters and covers over 300 classic radiologic
signs with detailed discussion alongside illustrative photos for memory aids
and clarification. The book is featured as follows: (1) covers hot topics includ-
ing potential pitfalls of imaging and classic signs, (2) detailed discussions and
case show highlighting clues and misinterpretation, (3) succinct content
and bulleted text for quick and easy reference, and (4) detailed illustrations
and annotated images. The materials included in the book were collected
from various university hospitals and are well-organized, and all cases have
been reviewed by subspecialty experts. Photos illustrate the etymology of
each sign and enhance the learning experience. Accompanying text explains
the history and meaning of the descriptive or metaphoric sign. Uniquely writ-
ten from a practical point of view, each case leads you through a radiology

ix
x Preface

expert’s thought process in analyzing imaging pitfalls and classic signs of

different organs or systems. The cases highlight clinical presentation, rele-
vant pathology, anatomy, physiology, and pertinent imaging features of com-
mon disease processes. Key information is distilled into succinct, bulleted
with detailed illustrations and wonderful images. It is designed to enhance
recognition of specific imaging patterns, enabling the image interpreter to
confidently reach an accurate diagnosis. This book ought to be a valuable
review for trainees preparing for boards licensing examinations and can
become a trusted daily reference for practicing radiologists. We wish this
book to become an irreplaceable reference for readers confronted with the
challenges of imaging interpretation.
We sincerely appreciate all the experts and contributors who engaged in
this book.

Guiyang, China Bo Gao

Miami, FL, USA Alexander M. McKinney
Contents

1 Introduction��������������������������������������������������������������������������������������   1
Bo Gao, Cong-jie Long, Li Zhang, and Chi Shing Zee
2 Brain��������������������������������������������������������������������������������������������������   9
Alexander M. McKinney, Yang Wang, and Ze Zhang
3 Head and Neck ��������������������������������������������������������������������������������  85
Zhongxiang Ding, Guoyu Chen, and Alexander M. McKinney
4 Chest�������������������������������������������������������������������������������������������������� 103
Tao Jiang, Yanling Zhang, Shanshan Wu, and Jujiang Mao
5 Solid Organs of Upper Abdomen���������������������������������������������������� 177
Xin Li, Chengkai Zhou, and Jie Zhou
6 Gastrointestinal Tract���������������������������������������������������������������������� 239
Jiani Chen, Hengtian Xu, and Gui Quan Shen
7 Peritoneum and Pelvis �������������������������������������������������������������������� 273
Pinggui Lei, Bin Huang, and Hui Yu
8 Signs in Musculoskeletal Radiology ���������������������������������������������� 291
Haitao Yang, Lingling Song, and Zhaoshu Huang
9 Spine�������������������������������������������������������������������������������������������������� 327
Lingling Song, Wen Wang, Muxi Wu, and
Alexander M. McKinney
10 Vascular Imaging and Interventional Strategy ���������������������������� 349
Lei Xu, Xin Chen, and Shi Zhou
Index���������������������������������������������������������������������������������������������������������� 369

xi
Contributors

Associate Editors

Shi Zhou, MD  Department of Interventional Radiology, Affiliated Hospital

of Guizhou Medical University, Guiyang, Guizhou, China
Shi  Zuo, MD  Department of General Surgery, The Affiliated Hospital of
Guizhou Medical University, Guiyang, China

Contributors

Guoyu Chen, MD  Department of Radiology, Affiliated Hospital of Guizhou

Medical University, Guiyang, China
Cong-jie  Long, MD Department of Radiology, GuiQian International
General Hospital, Guiyang, China
Jiani Chen, MD  Department of Radiology, Affiliated Hospital of Guizhou
Medical University, Guiyang, China
Xin  Chen, MD  Department of Radiology, Affiliated Hospital of Guizhou
Medical University, Guiyang, China
Zhongxiang Ding, MD, PhD  Department of Radiology, Affiliated Hangzhou
First People’s Hospital, Zhejiang University School of Medicine, Hangzhou,
China
Bo Gao, MD, PhD  Department of Radiology, Affiliated Hospital of Guizhou
Medical University, Guiyang, China
Bin Huang, MD  Department of Radiology, Affiliated Hospital of Guizhou
Medical University, Guiyang, China
Zhaoshu  Huang, MD Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China
Tao  Jiang, MD Department of Radiology, Changhai Hospital, Shanghai,
China

xiii
xiv Contributors

Pinggui  Lei, MD, PhD Department of Radiology, Affiliated Hospital of

Guizhou Medical University, Guiyang, China
Xin Li, MD, PhD  Department of Radiology Union Hospital, Tongji Medical
College, Huazhong University of Science and Technology, Wuhan, China
Jujiang Mao, MD  Department of Radiology, Affiliated Hospital of Guizhou
Medical University, Guiyang, China
Alexander  M.  McKinney, MD Department of Radiology, University of
Miami Miller School of Medicine, Miami, FL, USA
Gui  Quan  Shen, MD Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China
Lingling Song, MD, PhD  Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China
Wen Wang, MD, PhD  Department of Radiology, Tangdu Hospital, Fourth
Military Medial University, Xi’an, China
Yang Wang, MD  Department of Radiology, Affiliated Hospital of Guizhou
Medical University, Guiyang, China
Muxi  Wu, MD  Department of Radiology, Affiliated Hospital of Guizhou
Medical University, Guiyang, China
Shanshan  Wu, MD Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China
Hengtian Xu, MD  Department of Radiology, Affiliated Hospital of Guizhou
Medical University, Guiyang, China
Lei  Xu, MD, PhD Department of Radiology, Beijing Anzhen Hospital,
Capital Medical University, Beijing, China
Haitao  Yang, MD, PhD Department of Radiology, The First Affiliated
Hospital of Chongqing Medical University, Chongqing, China
Hui Yu, MD, PhD  Department of Radiology, Affiliated Hospital of Guizhou
Medical University, Guiyang, China
Chi Shing Zee, MD  Department of Radiology, Keck School of Medicine,
University of Southern California, Los Angeles, CA, USA
Li  Zhang, MD  Department of Radiology, Affiliated Hospital of Guizhou
Medical University, Guiyang, China
Yanling  Zhang, MD Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China
Ze  Zhang, MD  Department of Radiology, Affiliated Hospital of Guizhou
Medical University, Guiyang, China
Contributors xv

Chengkai  Zhou, MD Department of Radiology Union Hospital, Tongji

Medical College, Huazhong University of Science and Technology, Wuhan,
China
Jie  Zhou, MD Department of Radiology, Affiliated Hospital of Guizhou
Medical University, Guiyang, China
Shi Zhou, MD  Department of Interventional Radiology, Affiliated Hospital
of Guizhou Medical University, Guiyang, China
 Introduction
1
Bo Gao, Cong-jie Long, Li Zhang,
and Chi Shing Zee

Contents
1.1 The Formation of Imaging Signs  2
1.2 The Features of Imaging Signs  2
1.3 Classification of Imaging Signs  3
1.4 The Role of Imaging Signs in Diagnosis  4
1.5 The Decision-Making of Imaging Signs  4
1.6 Radiomics and AI  6
References  6

Medical imaging/radiology has evolved tremen-
dously in the last decades with the emergence
of novel imaging techniques, especially the
flourishing of advanced CT and MRI. The field
of medical image analysis has grown exponen-
tially, with an increased number of pattern rec-
ognition tools and an increase in data set sizes
[1]. The competent imaging acquisitions often
entail referring to other realms of knowledge to
acquire insights with aids of metaphor [2]. The
B. Gao (*) · L. Zhang
Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China
C-J. Long
Department of Radiology, GuiQian International
General Hospital, Guiyang, China
C. S. Zee
Department of Radiology, Keck School of Medicine,
University of Southern California,
Los Angeles, CA, USA
problems with timing, efficiency, and missed
diagnoses may occur at all stages of imaging
chain. Judgment of imaging sign, as one of the
core principles of radiology, relies on the inte-
gration of multilayered data with distinctive
decision-­making [3].
Imaging signs refer to the normal structures
of the human body or imaging information
or radiological findings produced by pathol-
ogy under any type of imaging modalities [4].
An “iconographic” glossary of terms used for
imaging is reproduced by placing them side by
side between radiological features, and those
may be associated with signs, symbols, or
naturalistic images. Specifically, imaging signs
refer to the metaphor of a certain tissue, struc-
ture, or lesion. One way is by linking anatomic
structures and pathological conditions with
objects, places, and concepts and codifying
these relationships as metaphoric signs [5]. To
describe an unnoticed finding specific to a par-

© Springer Nature Switzerland AG 2021 1

B. Gao, A. M. McKinney (eds.), Classic Imaging Signs,
https://doi.org/10.1007/978-3-030-56348-6_1
2 B. Gao et al.
ticular entity has always been a challenge for
the radiologists. Time will be needed on inves-
tigations before we can add the specific find-
ing to the legions of “signs” in radiology. The
“signs” may become part of our language of
specialty after validating by different observers
over time. The “classic signs” endorse us con-
fidence in determining the diagnosis. Some of
imaging signs have been acknowledged, which
are referred to as “Aunt Minnie.” When the sign
is invoked, or an Aunt Minnie is recognized,
it often brings an impression of the image to
mind, and it may have specific diagnostic and
pathological significance [6]. The advance of
radiology evolves with such signs rendering an
otherwise difficult diagnosis easier, which may
help the radiologists appreciate the anatomy
and pathology of an underlying abnormality
and may quickly direct the physicians to the
proper diagnosis and timely intervention.
1.1  he Formation of Imaging
T signs [8]. This striking difference of percent-
Signs
The language of radiology is rich with descrip-
tions of imaging findings, often metaphorical,
which have been commonly used in the daily
radiology practice. The formulation of a medical
terminology generally follows the nomenclatural
rules such as customs, unity, science, and logis-
tics. The naming of imaging signs usually depends
on their cultural background or cognition of the
founder or the author, linguistic traditions, or con-
ventional principles as well [7]. For example, the
scholars are accustomed to using familiar persons’
names, Greek letters and myths, English letters,
foods, or animals and plants to name this meta-
phor. A collection of specialty-­specific signs can
be obtained from general medical dictionaries or
from encyclopedic texts in radiology and other
specialties [2].
The signs can be separated into two catego-
ries: metaphoric and eponymous. About 66% of
metaphoric signs (a total of 375) were collected
from citations in the researches, and texts were
radiological in reference [2]. The naming of
metaphoric sign was reported frequently in the
radiological literature collection in the second
half of last century, as a descriptive discipline
for growth of radiology [4]. The evolution of
radiology into a more analytic, data-driven
pattern has resulted in its decline since then
consequently. Eponyms usually recognize a
person’s discovery and help remind us that the
advancement of knowledge still depends on
people, and that is important when our lives
are so dominated by technology. However,
eponymous signs were relatively infrequently
seen in radiology specialty [2]. For example,
most radiologists are quite familiar with the
Rigler sign, which allows for the detection of
pneumoperitoneum on supine radiographs of
the abdomen [8]. The double-wall sign of free
intraperitoneal air remains an important obser-
vation. Unfortunately, only a few eponyms are
popularly used in radiological practice and
research, unlike in the specialty of medicine or
surgery. In every other specialty, the number of
eponymous signs exceeds that of metaphoric
ages highlights the significance of metaphors
for clinical diagnosis and educational instruc-
tion of radiology.
1.2  he Features of Imaging
T
Signs
Imaging signs are often associated or analogous
with certain objects or phenomena in nature,
which are used to name imaging signs and to
establish specific thinking connections with one
or more diseases. Thus, imaging signs may pres-
ent the following features:
1. Visualization: The inherent nature of radio-
logical images as simulacra of both normal
anatomy and disease entities makes imaging
findings well suited to explanation by means
of named patterns borrowed from other
realms of knowledge [2]. A specific image
sign is named after familiar things or phe-
nomena in nature or life. The visualized
composite is the common feature abstracted
from many kinds of specific images.
1 Introduction
Therefore, the scholars take this specific
metaphor as “Aunt Minnie.”
2. Characterization: The meaning of perceptual
input is often recognized through associa-
tions with pictures encountered previously
and understood both concretely and meta-
phorically in images interpretation [2]. A spe-
cific imaging sign often has its certain feature
in the diagnosis of a disease. Mastering the
main features of the metaphor may contribute
to making a final diagnosis or differential
diagnosis (DD). Pareidolias represent a quick
and easy way of enhancing perception,
improving the efficiency, and enhancing
accuracy of image analysis. Pareidolic asso-
ciations are commonly used in professional
education to enhance perception of radiologi-
cal abnormalities. For example, a couple of
animal-inspired neuroradiological pareido-
lias specific to movement disorder diagnoses
were defined [9].
3. Practicality: Imaging sign is vivid and conve-
nient to be recalled and is easy to be identi-
fied. The characterization also determines its
clinical practicability.
4. Periodicity: Different imaging signs have been
reported or found by radiologists at different
stages of imaging technologies. Additionally,
it should be a process to understand the dis-
eases, and the understanding of imaging signs
also has its period.
5. Hierarchy: Imaging signs are a combination
of image information representing in different
pathological stages of the disease, reflecting
the unity of structure, function, tissue mor-
phology, or biochemical changes.
1.3 Classification of Imaging
Signs
There are many methods to classify imaging
signs in clinical imaging interpretation: Based
on whether the signs are the reflections of lesion
itself, they can be divided into direct sign and
indirect sign; based on the importance of the
signs in imaging diagnosis and DD, they can be
divided into primary sign and secondary sign;
3
based on the specificity of the signs in imaging
diagnosis and DD, they can be divided into typi-
cal sign and atypical sign:
1. Direct sign vs. indirect sign: Direct sign is the
direct reflection of disease itself, is the main
imaging feature of the disease, and is the key
to imaging diagnosis. However, due to
“Different diseases share the same image” and
“One disease shows different images” or
direct signs are unremarkable early on, indi-
rect sign may sometimes become the main
basis for diagnosis. In different situations, the
status of direct and indirect signs can be
exchanged from one to another, and some-
times, both may be equally important.
2. Typical sign vs. atypical sign: Typical sign
refers to the standard morphology from com-
plex imaging of general situation, which usu-
ally reflects the essentials of the lesion.
Atypical sign is usually discrete and variant
and lacks characteristic signs of the disease.
Typical sign can only occur in some during
the course of the disease, or the disease pro-
gresses to a specific stage; in the early stages
of the disease, atypical sign prevails. The sig-
nificance of typical sign and atypical sign is
relative [10].
3. Primary sign vs. secondary sign: Primary
sign plays a major and decisive role in diag-
nosis of diseases among many of them;
secondary sign plays a non-primary or sub-
ordinate role. Direct sign is usually regarded
as primary sign, and indirect sign is regarded
as secondary sign. The secondary sign of
direct sign is predominant to indirect sign,
and primary sign of indirect sign is second-
ary to direct sign. Generally, as a direct sign
whether primary or secondary, it can clearly
render diagnosis.
4. Sufficient sign vs. necessary sign: Sufficient
sign means that once the sign appears, it must
be a certain disease. Necessary signs refer to
the percentage of the sign appearing in a dis-
ease that is 100%. Sufficient sign has strong
specificity and must be direct signs; necessary
sign has certain specificity and could be direct
sign or indirect sign. Sufficient sign and nec-
4 B. Gao et al.
essary sign are typical, primary, and essential
in imaging diagnosis.
5. Negative sign vs. possible sign: Negative sign
may implicate that the metaphor is unlikely to
occur in a disease; if it does, certain disease
could be excluded; possible sign imply it may
occur in a disease with low specificity, as an
indirect sign which may provide reference for
diagnosis.
1.4  he Role of Imaging Signs
T prior expertise [13]. Medical errors are a leading
in Diagnosis
Specific images realize the effective connec-
tion between metaphor and diagnosis of disease.
We should understand and master their features
and pathogenesis of the metaphor; otherwise,
there will be no way to use these imaging signs;
in some cases, imaging signs may narrow the
scope of DD. Most diseases are usually coexist-
ing with varieties of imaging signs; a single sign
could not indicate some disease. The more image
signs appear, the more adequate and conducive to
establish the diagnosis.
Image diagnosis relies on the imaging signs
of the disease. Some diseases could be shown as
typical imaging signs, which makes it easier for
radiologists to make a confident diagnosis. On
the other side, imaging signs are the reflection of
the comprehensive image information at differ-
ent pathological stages of the disease, which may
be affected by internal or external conditions,
random factors, and other effects; thus, atypical
appearances may present [11]. In clinical prac-
tice, we should not only focus on imaging signs,
that is, its directed diseases and exclusive diag-
nosis, but also master the essentials of DD, rela-
tively similarly featured appearances of different
diseases.
1.5 The Decision-Making
of Imaging Signs
The radiologists play a key role in the diagnosis
and care of patients, and diagnostic errors may
occur in interpreting hundreds of examinations
daily. The radiologists rely on heuristic principles
to reduce complex tasks of assessing probabili-
ties and predicting values into simpler judgmen-
tal operations. Heuristics in interpreting imaging
studies are generally helpful but sometimes may
result in cognitive biases or even significant errors
[12]. Awareness of the cognitive process that the
radiologists proceed in interpreting images would
contribute to recognizing the inherent biases in
decision-making. These mental shortcuts allow
rapid problem-solving based on assumptions and
cause of morbidity and mortality in the medical
field and are substantial contributors to medi-
cal costs. Errors can be categorized as a “miss”
when a primary or critical finding is not observed
or as a “misinterpretation” when errors in inter-
pretation lead to an incorrect diagnosis [14]. An
understanding of the causes of cognitive biases
can lead to the development of educational con-
tent and systematic improvements that mitigate
errors and improve the quality of care provided
by the radiologists [12]. Recognition of imag-
ing sign is a good way to implement to minimize
cognitive errors in daily practice, in which sys-
tem-level processes that can be implemented can
also minimize cognitive errors.
In the daily reading practice, image analysis
usually includes two basic steps: visualization
and interpretation. Generally, we need to follow
four steps: (1) perception – observing meaning-
ful imaging signs; (2) recognition – deciding the
pathological sign; (3) discrimination – character-
izing the specific lesion type; and (4) determina-
tion  – making the final diagnosis. Perception is
the basis of the diagnostic process. In the process
of making the final diagnosis, typical manifesta-
tions of common diseases should be considered
first, atypical manifestations of common diseases
second, then typical manifestations of rare dis-
eases, and lastly atypical manifestations of rare
diseases, which are the basic thinking principles
of imaging diagnosis. If only emphasize direct
image sign, typical image sign, primary image
sign, while ignoring indirect, atypical, second-
ary, rare, and possible image signs, which would
fall into the situation of “put the cart before the
horse.” If a radiologist misses an abnormality, it
1 Introduction
will lead to misdiagnosis and cause harm to the
patient. In many cases, one or several signs cannot
fulfill to make a diagnosis. Many common ethi-
cal dilemmas in radiology practices exist without
an appropriate, objective, and unified approach
to effectively guide the radiologist’s actions [15].
Medical ethics training should be highlighted
during residency and more uniform recommen-
dations to assist radiologists in addressing ethical
issues in an appropriate manner [16]. A com-
prehensive analysis of clinical laboratory tests
and therapeutic information would contribute to
reach the final diagnosis.
The Gestalt theory of modern psychology is
grounded in the ideas that holistic rather than
atomistic approaches are necessary to under-
stand the mind and that the mental whole is
greater than the sum of its component parts [17].
Although the Gestalt school fell out of favor due
to its descriptive rather than explanatory nature,
it permanently changed our understanding of
perception. For the radiologist, such fundamental
Gestalt concepts as figure-ground relationships
and a variety of “grouping principles” (the laws
of closure, proximity, similarity, common region,
continuity, and symmetry) are ubiquitous in daily
work, not to mention in art and personal life [17].
By considering the applications of these princi-
ples and the stereotypical ways in which humans
perceive visual stimuli, a radiology learner may
incur fewer errors of diagnosis.
As used by radiologists, an Aunt Minnie or
Aunt Minnie approach is a constellation of obser-
vations that the experienced reader finds virtually
pathognomonic of an entity, usually an unusual
or unexpected disease [18]. As a diagnosis based
on having seen similar images many times, it is
usually difficult to be explained systematically
to a less experienced and sometimes incredulous
colleague. This subliminal or subconscious pat-
tern recognition resembles a person being able to
recognize his or her Aunt Minnie among a large
group of similar women, although it is difficult to
analyze rationally or to explain verbally just how
this process was accomplished. An Aunt Minnie
is a diagnosis or recognition largely by Gestalt.
With the increase of publications and the popu-
5
larity of the Aunt Minnie, the original meaning of
the term has been expanded and been applied to
any classical constellation of findings.
It may take a long time to validate and famil-
iarize an imaging sign. Grasping the character-
istics of an imaging sign is the key to find the
question, and practice is the key of testing it.
Accurate diagnosis depends on correct thinking
and accurate understanding of the essence of the
signs. The cognition of signs must be accurate;
one-sided understanding of a certain sign will
unfortunately lead to the deviation from right
direction. Most studies on biases and heuristics
in medical decision-making are based on hypo-
thetical vignettes, raising concerns of applying
the scientific findings to actual decision-making
[19]. Radiologists motivate visual detection,
pattern recognition, memory, and cognitive rea-
soning to develop the final diagnosis of radio-
logical studies. This process is undergone in an
unfavorable situation in which there are unpre-
dictable distractors, increasing workloads and
consequent fatigue. Given the ultimate human
task of perception, some degree of error is likely
inevitable. An understanding of the causes of
interpretive errors can contribute to mitigating
errors and improve quality of radiological inter-
pretation [20].
In modern times, the fragmented information
from the Internet can’t replace systematic knowl-
edge learning and the organic combination of
which is conductive to enhance verification and to
deepen comprehension. Most importantly, build-
ing rigorous workstyle and scientific thinking
habits is the unique road to improve our academic
ability and diagnostic accuracy. Smartphones and
tablets can be used by diagnostic imaging profes-
sionals, radiographers, and residents and to intro-
duce relevant applications that are available for
their field [21]. There is a long list of common
radiology signs involving various body systems
from head to toe. Identifying the signs and recall-
ing their clinical relevance are crucial to not only
radiologists but also general practitioners with
access to clinical images. The apps can provide
a ready-to-use and convenient reference list for
radiologists via mobile phones [22].
6 B. Gao et al.
1.6 Radiomics and AI
Medical data is more and more likely to lead to
major changes in modern imaging. In contrast to
the traditional practice of treating medical images
as pictures intended solely for visual interpreta-
tion, the advances of modern medical imaging have
facilitated the development of high-­ throughput
extraction of quantitative features in converting
images into mineable data for subsequent analysis
in decision-making, which is coined “radiomics”
[3]. The models developed from combining imag-
ing features, patient data, and bioinformatics may
potentially improve diagnostic, prognostic, and
predictive accuracy. Radiomics are intended to
be conducted with standard data of images; the
conversion of digital images into mineable data
is conceivable to become practice. Radiomics
exploits sophisticated image analysis and image-
based signatures for precision diagnosis and
treatment. The standardized evaluation of the
numerous publications of radiomics is still lack-
ing currently [23]. Rigorous evaluation criteria
and reporting g­ uidelines of imaging signs need
to be established for investigations to meet urgent
requirement in the field of radiomics.
Imaging assessment of disease most com-
monly relies upon visual observations; advanced
computational analyses may extend the scopes of
interpretations [1]. Artificial intelligence (AI) has
the potential to make great strides in the qualita-
tive imaging interpretation by expert clinicians.
AI may automatically process image interpreta-
tion and shift the clinical workflow of imaging
detection, decision-making in intervention man-
aging, or subsequent outcome observation [24].
The algorithms of AI for workflow improvement
and outcome analyses are advancing. Using high-­
quality and high-quantity imaging data, AI can
provide assistance to radiologists in imaging
diagnosis and patient management [25]. AI may
reduce cost and improve value at the stages of
image acquisition, interpretation, and decision-­
making, but AI cannot yet be relied on or be
responsible for physicians’ decisions-making
that may affect survival. It is urgent for radiolo-
gists to receive the training and education of AI in
daily clinical practice [26].
References
1. O’Connor JP. Rethinking the role of clinical imaging.
elife. 2017;6:e30563.
2. Baker SR, Partyka L.  Relative importance of meta-
phor in radiology versus other medical specialties.
Radiographics. 2012;32(1):235–40.
3. Gillies RJ, Kinahan PE, Hricak H. Radiomics: images
are more than pictures, they are data. Radiology.
2016;278(2):563–77.
4. Baker SR, Noorelahi YM, Ghosh S, Yang LC, Kasper
DJ.  History of metaphoric signs in radiology. Eur J
Radiol. 2013;82(9):1584–7.
5. Gocmen R, Guler E, Kose IC, Oguz KK.  Power
of the metaphor: forty signs on brain imaging. J
Neuroimaging. 2015;25(1):14–30.
6. Dyer RB, Chen MY, Zagoria RJ. Classic signs in uro-
radiology. Radiographics. 2004;24(Suppl 1):S247–80.
7. Navarro-Sanchis EL, Sendra-Portero F.  Informatics
in radiology (infoRAD): album of radiologic signs:
a useful tool for training in radiologic semiology.
Radiographics. 2005;25(1):257–62.
8. Lewicki AM.  The Rigler sign and Leo G.  Rigler.
Radiology. 2004;233(1):7–12.
9. Mulroy E, Balint B, Adams ME, Campion T, Merello
M, Bhatia KP. Animals in the brain. Mov Disord Clin
Pract. 2019;6(3):189–98.
10. Koontz NA, Seltman TA, Kralik SF, Mosier KM,
Harnsberger HR.  Classic signs in head and neck
imaging. Clin Radiol. 2016;71(12):1211–22.
11. Raju S, Ghosh S, Mehta AC.  Chest CT signs in
pulmonary disease: a pictorial review. Chest.
2017;151(6):1356–74.
12. Itri JN, Patel SH.  Heuristics and cognitive error
in medical imaging. AJR Am J Roentgenol.
2018;210(5):1097–105.
13. Waite S, Grigorian A, Alexander RG, Macknik SL,
Carrasco M, Heeger DJ, Martinez-Conde S. Analysis
of perceptual expertise in radiology-current knowl-
edge and a new perspective. Front Hum Neurosci.
2019;13:213.
14. Busby LP, Courtier JL, Glastonbury CM. Bias in radi-
ology: the how and why of misses and misinterpreta-
tions. Radiographics. 2018;38(1):236–47.
15. Camargo A, Yousem K, Westling T, Carone M,
Yousem DM. Ethical dilemmas in radiology: survey
of opinions and experiences. AJR Am J Roentgenol.
2019;213(6):1274–83.
16. Camargo A, Liu L, Yousem DM. Radiology and ethics
education. AJR Am J Roentgenol. 2017;209(3):640–2.
17.
Koontz NA, Gunderman RB.  Gestalt theory:
implications for radiology education [published
correction appears in AJR Am J Roentgenol.
2008 Jun;190(6):1430]. AJR Am J Roentgenol.
2008;190(5):1156–60.
18. Hall FM, Griscom NT.  Gestalt: radiology’s aunt
Minnie. AJR Am J Roentgenol. 2008;191(4):1272.
19. Blumenthal-Barby JS, Krieger H.  Cognitive biases
and heuristics in medical decision making: a critical
1 Introduction
review using a systematic search strategy. Med Decis
Mak. 2015;35(4):539–57.
20. Waite S, Scott J, Gale B, Fuchs T, Kolla S, Reede
D.  Interpretive error in radiology. AJR Am J
Roentgenol. 2017;208(4):739–49.
21. Székely A, Talanow R, Bágyi P. Smartphones, tablets
and mobile applications for radiology. Eur J Radiol.
2013;82(5):829–36.
22. Yeung AW. Review of radiology signs app for android.
J Digit Imaging. 2016;29(5):523–5.
23. Lambin P, Leijenaar RTH, Deist TM, et  al.
Radiomics: the bridge between medical imaging
7
and personalized medicine. Nat Rev Clin Oncol.
2017;14(12):749–62.
24. Bi WL, Hosny A, Schabath MB, et al. Artificial intel-
ligence in cancer imaging: clinical challenges and
applications. CA Cancer J Clin. 2019;69(2):127–57.
25. Dey D, Slomka PJ, Leeson P, et al. Artificial intelli-
gence in cardiovascular imaging: JACC state-of-the-­
art review. J Am Coll Cardiol. 2019;73(11):1317–35.
26. Mendelson EB. Artificial intelligence in breast imag-
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2019;212(2):293–9.
 Brain
2
Alexander M. McKinney, Yang Wang,
and Ze Zhang

Contents
2.1 White Matter Buckling Sign  10
2.2 CSF Cleft Sign  12
2.3 Interhemispheric Fissure Sign  13
2.4 Gyral Gathering Sign  14
2.5 Lateral Ventricular Depressing Sign  16
2.6 Little Ventricle  17
2.7 The Swirl Sign  18
2.8 Spot Sign  19
2.9 Gray-White Matter Interface Displacement  20
2.10 The Dense or Hyperdense Artery Sign  21
2.11 The Middle Cerebral Artery Dot Sign  23
2.12 Middle Cerebral Artery Susceptibility Sign  24
2.13 The Cord Sign  27
2.14 The Insular Ribbon Sign  29
2.15 The Disappearing Basal Ganglia Sign  30
2.16 The Obscured Lentiform Nucleus Sign  32
2.17 Fogging Effect  33
2.18 Coarse Flecks of Calcification  35

A. M. McKinney (*)
Miller School of Medicine, University of Miami,
Miami, FL, USA
e-mail: mckinrad@umn.edu
Y. Wang · Z. Zhang
Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China

© Springer Nature Switzerland AG 2021 9

B. Gao, A. M. McKinney (eds.), Classic Imaging Signs,
https://doi.org/10.1007/978-3-030-56348-6_2
10 A. M. McKinney et al.

2.19 The Tram-Track Sign  37

2.20 The Tuft Sign  38
2.21 The Infundibulum Sign  39
2.22 Target Sign  41
2.23 Black Target Sign and White Target Sign  42
2.24 Multilocular Ringlike Enhancement  43
2.25 Hoop Sign and Popcorn Sign  45
2.26 Ivy Sign  47
2.27 Butterfly-Like Lesions  47
2.28 The Mount Fuji Sign  50
2.29 The Eye of the Tiger Sign  51
2.30 Aura Sign  52
2.31 Basilar Artery Encasement Sign  53
2.32 The Tau Sign  55
2.33 The Reversal Sign  55
2.34 The False Falx Sign  57
2.35 The Interpeduncular Fossa Sign  59
2.36 The Empty Delta Sign  60
2.37 The Parasagittal Sinus Sign  61
2.38 The Pulvinar or Hockey Stick Sign  62
2.39 The Radial Bands Sign  64
2.40 The Triangular Pattern  65
2.41 The Dural Tail Sign  67
2.42 The Acute Angle Sign  68
2.43 The Ependymal Dot-Dash Sign  69
2.44 The Hummingbird Sign and the Swallowtail Sign  71
2.45 The Hot Cross Bun Sign  72
2.46 The Molar Tooth Sign  74
2.47 The Caput Medusa Sign  75
References  77

2.1 White Matter Buckling Sign
Feature
The white matter collapse sign refers to the extra-
cranial occupying of growth under the inner plate
of the skull that has embedded in the gray mat-
ter. It causes the white matter to become flat after
compression subjacent to the gray matter. At the
same time, the distance increases between the
compressed white matter and the inner plate of
the skull.
Explanation
It is a reliable sign of extracerebral space-­
occupying lesions, especially meningiomas, that
grow under the inner plate of the skull and embed
2 Brain 11

a b

Fig. 2.1  A mass with low T1WI, slightly high T2WI sig- It buckles (displaces) the gray matter-white matter inter-
nal in the left frontal region on axial T1WI (a) and coronal face inwards
T2WI (b), and the basal region is flat to the dural surface.

in the gray matter of the brain to flatten the white CT and MRI signs of intracranial extra-cerebral
matter under the gray matter which protrudes into occupying effects can be observed [2]: (1) white
the brain like a finger and at the same time widens matter collapse sign and (2) displacement and
the distance between the compressed white matter compression of adjacent gyri. These refer to the
and the inner plate of the skull [1] (Fig. 2.1). gyral arcuate shift and compression change in
contact with the extra-cerebral occupying lesions;
Discussion this change forms a rim of increased attenuation
The white matter collapse sign is a reliable fea- around the tumor on CT. The shape of the tumor
ture of intracranial and extra-cerebral, extra-axial usually shows regular round or ovoid appear-
space-occupying lesion (particularly in menin- ance, while peripheral edema is usually mild. This
gioma). Gliomas, metastatic, and other intra-­ sign generally occurs in larger tumors and occurs
cerebral tumors mostly have infiltrative growth, in meningioma where the brain appears convex
where tumoral tissue is mixed with normal brain and adjacent to cerebral falx. Notably, this sign
tissue; hence, with intra-axial lesions such as glio- is related to not only the tumor size, growth pat-
mas, there is often no clear boundary, so we can’t tern, and speed but also its location. (3) Wide-base
see this sign in intra-axial tumors. Meningioma is sign occurs when the wide base of the tumor is
a common intracranial and extra-cerebral tumor closely connected with the skull and dura mater.
that arises from the arachnoid cell and arach- The junction between the tumor and dura mater
noid cap cell. The incidence of meningioma is an obtuse angle, so the typical contour of the
(97.5/100,000 persons) is greater than glioma tumor is hemispherical, but it can be presented
(4.7/100,000 persons). Meningiomas are typi- as round in some sections. (4) Pseudo-capsule
cally relatively well-circumscribed extra-cerebral sign: the pseudo-capsule is a thin layer structure
tumors with a hard texture and clear edge, being between the meningioma and adjacent brain tis-
slightly lobulated with a rich blood supply. sue on imaging. The pathological and anatomical
Meningiomas occur outside the cerebrum, basis of pseudo-capsule is the CSF-perivascular
and when the tumor grows into the brain, several space. In an extra-cerebral tumor, the incidence of
12
the capsule is approximately 50%. The existence
of a pseudo-capsule is a reliable sign for diagnos-
ing an extra-cerebral tumor. (5) Skull changes in
the attachment site: this is the site where the skull
undergoes thinning after compression, hyperos-
teogeny, and sclerosis; bone destruction can be
seen in some cases, or even extension through
the skull, forming a soft tissue mass outside of
the cranium in the deep scalp. Occasionally, the
bony skull tissue can be mixed with hyperplasia
and bone destruction. (6) Changes in the adjacent
basal cistern and cerebral sulci: basal cistern and
sulcal effacement in the tumor site and adjacent
basal cistern and sulcal expansion. The origin
of this sign is due to chronic and slow-growing
meningioma that compresses adjacent brain tissue.
In addition, meningioma can also exhibit a dural
tail sign, which is the adjacent meningeal thicken-
ing and enhancement after contrast enhancement;
however, the dural tail sign is not always charac-
teristic of meningiomas, as acoustic neuromas,
metastases. and chordomas also can appear as a
dural tail. Even though the majority of meningio-
mas can be diagnosed easily with MRI, the diag-
nosis can be challenging when meningiomas show
atypical imaging findings [1]. Diffusion-weighted
imaging/diffusion tensor imaging (DWI/DTI),
perfusion imaging, and magnetic resonance spec-
troscopy (MRS) can add value to help refine the
diagnostic considerations of a dural-based mass
and can also help further characterize the different
subtypes of meningiomas [3].
2.2 CSF Cleft Sign
Feature
On T2WI, the CSF cleft sign appears as a crescent
of bright fluid (CSF) surrounding and separating
the tumor margin from the cerebral or cerebellar
cortex.
Explanation
The CSF cleft sign can be used to distinguish
extra-axial lesion from intra-axial and is typi-
cally used in the description of meningioma.
The cleft is regarded as representing a thin rim
of CSF between tumor and brain parenchyma
(Fig. 2.2).
A. M. McKinney et al.
Fig. 2.2  A 33-year-old woman with a right occipital
space diagnosis of meningioma; a crescent of bright fluid
(CSF) surrounds the tumor margin (white arrow) on T2WI
Discussion
It is the most important factor for establishing
an appropriate differential diagnosis by deter-
mining whether an intracranial mass is intra-
axial or extra-axial. A majority of features
differentiate extra-axial tumors from intra-axial
tumors, such as the CSF cleft sign, interven-
ing cortex between the white matter buckling
sign and tumor, hyperostosis, and the dural tail
sign. Especially, the CSF cleft sign is a common
finding for meningiomas which makes it easier
to distinguish meningiomas from intra-axial
tumors. This sign is in conjunction with the
aforementioned “white matter buckling sign.”
On T2WI, where the CSF is depicted as bright,
benign extra-axial/extra-cerebral lesions (most
commonly meningiomas) may trap a crescent
of bright CSF, confirming its extra-axial nature.
The cleft can be confirmed as CSF by suppres-
sion (darkening) of the CSF signal on corre-
sponding routine FLAIR images. However, in
very large meningiomas causing severe amounts
of mass effect or herniation, this sign is occa-
sionally not present. The rim pattern of menin-
gioma on nonenhanced 3D-FLAIR can predict
surgical resectability and histological tumor
grading [4].
2 Brain
a b
Fig. 2.3 (a, b) Axial FLAIR shows DCC, longitudinal Probst-Bündel (white arrow) and typical typical lateral ventricu-
lar straightening and culpcephaly (stars)
2.3 Interhemispheric
Fissure Sign
Feature
On axial CT, interhemispheric fissure and ven-
tral/anterior portion of the third ventricle are
abnormally close at the continuous level, which
is called “interhemispheric fissure sign” of cal-
losal dysgenesis.
Explanation
The interhemispheric fissure sign is a character-
istic feature of dysgenesis of corpus callosum
(DCC) on CT. During the embryonic period, the
pseudocele between the bilateral lateral ventricle
is pouch shaped and connected with the inter-
hemispheric fissure. Later, it will be closed by the
mouth of the developed corpus callosum. If the
mouth of the corpus callosum is not developed,
the interhemispheric fissure will connect with the
pseudocele, direct or obviously close to the ante-
rior part of the third ventricle (Fig. 2.3).
Discussion
DCC is a form of dysplasia of posterior mid-
line structure in an embryonic period; it is one
of the most common congenital malformations
of the central nervous system, including hypo-
13
plasia or partial hypoplasia of the corpus callo-
sum, which may exist alone or be accompanied
by other craniocerebral deformities [5]. About
50% of the cases with DCC have been reported
to be accompanied by other types of malforma-
tion, such as holoprosencephaly, hypoplasia
of the septum, absence of the falx, gray matter
heterotopia, schizencephaly, interhemispheric
lipoma, interhemispheric arachnoid cyst, macro-
gyria, polymicrogyria, encephalomeningocele,
microcephaly, Dandy-Walker syndrome, Chiari
malformation, aqueduct stenosis, and other
anomalies.
CT features of DCC have been described: (1)
Interhemispheric fissure widens and is situated
abnormally close to the anterior part of the third
ventricle; hence, “the interhemispheric fissure
sign” is positive. Normally, the rostrum of the
corpus callosum, septum pellucidum, fornix, and
the anterior commissure separate the interhemi-
spheric fissure from the third ventricle. When the
corpus callosum and adjacent midline structures
develop abnormally, the interhemispheric fis-
sure and pericallosal artery will lie abnormally
close to the anterior part of the third ventricle,
and the hypoplasia of the adjacent white matter
results in the expansion of the interhemispheric
fissure. Because the rostrum of the corpus callo-
14
sum develops later, whether the corpus callosum
is dysplastic or partially hypoplastic, it is usu-
ally involved even in the mildest cases of callosal
dysplasia. (2) There is lateral ventricle dilation,
with bilateral lateral ventricular “inverted eight”
or “crescent” shape. The anterior horn of the lat-
eral ventricle is separated from the body, being
straightened. In severe cases, the trigone and
posterior horn of the lateral ventricle are irregu-
lar and asymmetrically enlarged, and the tempo-
ral horn can also be enlarged [6]. DCC is often
accompanied with deep white matter dysplasia,
so the lateral ventricle could also be enlarged. If
the splenium of the corpus callosum is absent,
the posterior horn will move up and enter dys-
plastic white matter, and occipital horn and tri-
gone of lateral ventricular are asymmetrically
enlarged, which is termed colpocephaly, i.e.,
lateral ventricular occipital horn enlargement.
The parahippocampal gyrus and medial hip-
pocampal formations are also often dysplastic,
causing the temporal horn to expand. (3) There
is enlargement and extension of the interven-
tricular foramen. (4) The third ventricle can be
enlarged, appearing raised, protruded, and to
varying degrees protrude laterally, even forming
interhemispheric fissure cysts.
The diagnosis of DCC does not generally
require advanced MRI or CT imaging, although
noninvasive angiographic imaging can be help-
ful to observe occasional associated anomalies of
the cerebral vessels. Severe DCC on CT is easy
to diagnose, but mild callosal dysgenesis may be
missed. Interestingly, in 39 cases of DCC reported
by Sarwar, the positive predictive value of the
interhemispheric fissure sign is 100%, and the
other signs were relatively low [7]. It is suggested
that some other signs may not be obvious in some
cases due to the CT technique, while the inter-
hemispheric fissure sign is a relatively reliable
sign and can be important in diagnosing DCC.
2.4 Gyral Gathering Sign
Feature
The sulci along the cerebral convexity narrow
or disappear, and the distance between the gyri
became smaller and close to each other.
A. M. McKinney et al.
Explanation
A chronic subdural hematoma along the convex
surface of the brain compresses the adjacent
gyri, narrows, and obscures the subarachnoid
space between the gyri, and the gyri become
closer to each other. The gyral gathering sign is
one of the important indirect signs of a chronic
subdural hematoma on the convex surface of the
brain (Fig. 2.4).
Discussion
The various components in chronic subdural
hematoma can affect CT density, especially
hemoglobin concentration. The speed of hema-
toma liquefaction is faster. After liquefaction,
the CT image shows low density, and the lesion
is clearly demarcated from brain parenchyma,
which is compressed and moved inward. When
there is fresh/hyperacute hemorrhage, particu-
larly if actively bleeding, the hematoma can
be iso-dense on CT due to the increase of pro-
tein content after hemolysis. The demarcation
between lesion and brain parenchyma is not clear
on CT, and the hematoma is not easy to identify.
However, it can show indirect signs such as the
convergence of cerebral gyri, displacement of
gray-white matter interfaces, lateral ventricu-
lar deformation, and medial displacement of
midline structures toward the opposite side [8].
Bilateral iso-dense chronic subdural hemato-
mas (CSDH) may cause considerable difficulty
in diagnosis on CT.  MRI can help in diagnos-
ing such lesions. MRI is more sensitive than
CT in determining the size and internal com-
position of CSDHs. Fresh bleeding, hemolysis,
and hemoglobin changes can also be observed
by MRI. Diffusion-tensor imaging (DTI) can
examine anisotropic changes of the pyramidal
tracts displaced by CSDH.  These anisotropic
changes are caused by a reversible distortion of
neuron and vasogenic edema by the hematoma.
These changes in the affected pyramidal tract
may correspond with motor weakness in CSDHs
[9]. CSDHs are hyperintense on both T1- and
T2-weighted images, in general. Notably, while
there are some pitfalls (particularly in pediatric
patients with abusive head trauma), in general,
the age of subdural hematomas can be estimated
using a combination of T1-, T2-, diffusion-­
2 Brain 15

a b

Fig. 2.4  A 75-year-old male presented with recurrent (2.4b), are shown in the right frontal lobe and left fronto-
headaches, accompanied by left eyelid droop. On MRI, parietal-occipital lobe. The brain parenchyma is shifted
arcuate areas of both hypo-intensity and iso-intensity, pri- inwards, and the cerebral gyri converge
marily with short T1 on T1WI (2.4a) and long T2 on T2WI

Table 2.1  The various phases of subdural and parenchymal hematomas can generally be classified based type of
blood/hemoglobin and characterized by age on MRI, based on the sequences above
Hemorrhage evolution on Tl, T2, DWI, SWI
Type of blood Age T1 T2 DWI SWI
Oxyhemoglobin (diamagnetic) Hyperacute Isointense Bright Bright Bright-ISO
Deoxyhemoglobin (paramagnetic) Acute Isointense Dark Dark Dark
Intracellular MetHgb (paramagnetic) Early subacute Bright Dark Dark Dark
Extracellular MetHgb (paramagnetic) Late subacute Bright Bright Bright Dark
Hemosiderin (paramagnetic) Chronic Dark Dark Dark Dark
Courtesy of Alexander M. McKinney, MD, University of Miami-Miller School of Medicine, Miami, FL

weighted imaging (DWI) and susceptibility-­
weighted imaging (SWI), as depicted in
Table 2.1. A symptomatic CSDH tends to have a
black band on the inner membrane of the CSDH
on T2*WI or SWI.  The subdural “hyperintense
bands” on DWI are intracellular and/or extra-
cellular methemoglobin (i.e., subacute stages),
based on T1- and T2-weighted imaging and
based on intraoperative surgical findings. The
subdural hyperintense band is an important find-
ing indicating relatively fresh bleeding from the
outer membrane [10]. Meanwhile, acute subdu-
ral hematomas are typically isointense on T1
and dark on T2, while hyperacute SDH may be
isointense on T1WI and slightly bright on T2WI;
however, note that hyperacute subdural hemato-
mas are not dark on SWI. Hence, utilizing DWI
and SWI may further help estimate the age of
subdural hematomas. As the soft tissue resolu-
tion of MRI is high, the signal of chronic sub-
dural hematoma is contrasted with that of brain
parenchyma, and MRI also has advantages over
CT in showing the convergence sign of cerebral
gyri. Hence, MRI has more utility in the diagno-
sis of chronic subdural hematomas. Hemorrhage
evolution on MRI is shown in Table 2.1.
16
2.5 Lateral Ventricular
Depressing Sign
Feature
The outer sidewalls of the lateral ventricles on
both sides move toward the midline, and the left
and right widths of the bodies of the lateral ven-
tricles become smaller.
Explanation
Subdural hemorrhage on both sides of the convex
surface of the brain pushes parenchyma, indi-
rectly compressing the lateral ventricle, resulting
in a narrowing of the widths of the lateral ven-
tricle (Fig. 2.5).
Discussion
Head trauma often leads to a subdural hematoma,
which is caused by traumatic tearing across the
cerebral arteriolar veins of the dura mater. An
acute subdural hematoma is a serious condition
and can progress rapidly and cause a worsen-
ing mass effect. The clinical symptoms such as
increased intracranial pressure and neurologic
deficits may appear earlier, but often, there is a
lack of localizing signs. In patients with a trau-
matic acute subdural hematoma, there has been
shown to be a strong correlation between the
degree of midline shift and the thickness of sub-
dural hematoma. Chronic subdural hematomas
(CSDH) are more common in elderly patients,
likely due to there being a more “brittle” blood
vessel wall, where the dura mater is rich in blood
a b
Fig. 2.5 (a) Acute right convexity subdural hematoma; (b) subacute left convexity subdural hematoma; (c) chronic left
convexity subdural hematoma
A. M. McKinney et al.
supply, and the presence of slight trauma can
lead to bleeding. CSDH composition and anat-
omy can be assessed using a modified Nakaguchi
classification. Postoperative CSDH volume and
the Nakaguchi classification subtypes may be the
most powerful predictors of recurrence, cure, and
the time to recurrence and cure [11].
Acute subdural hematoma on non-contrast
CT appears as high attenuation with a typically
crescentic shape. Subacute subdural hematoma
density usually gradually decreases with time,
due to the dissolution and absorption of hemo-
globin. Hence, iso-attenuation hematoma may
only exhibit indirect signs such as shift of the
gray-­white matter interface, shallow sulcus, and
narrowing of lateral ventricle. Contrast-enhanced
CT demonstrate punctate or linear enhancement
at the edge of the hematoma along the surface
of the brain, making the edge of the hematoma
appear more evident. CSDH is a mixture of
hemoglobin breakdown products, CSF and fresh
bleeding, which can exhibit low attenuation, iso-­
attenuation, high attenuation, or mixed attenu-
ation. Regarding bilateral subdural hematomas,
the thickness of bilateral subdural hematomas is
usually the same, the degree of compression of
the brain parenchyma is similar, and the degree
of narrowing of the lateral ventricle is not much
different relative to the presence of unilateral sub-
dural hemorrhage. If the bleeding range is large,
the width of the lateral ventricle can be slightly
reduced. When the pressure is applied to both
sides, the midline structure may not be displaced
c
2 Brain
a b
Fig. 2.6  A 5 year old male who suffered anoxic injury
from forced submersion. On the initial non-contrast CT
(a), there are small lateral ventricles, with early blunting
of the gray-white matter differentiation. On brain MRI
or the displacement may not be obvious. If the
thickness of the subdural hematomas on both
sides is more overt, the degree of narrowing of
the lateral ventricles may differ, and the midline
structures may be slightly deviated toward the
smaller hematomas [12]. CSDH can be more
extensive along the length of the cerebral con-
vexities due to epidural hematoma, and the mass
effect can be significant. If this occurs in com-
bination with intracranial hemorrhage or diffuse
brain swelling, the degree of compression of the
lateral ventricle can be more obvious and can be
prone to symptoms of increased intracranial pres-
sure. Hence, bilateral subdural hematomas can
have rapid clinical progression and poor progno-
sis and thus may have different degrees of clinical
and radiologic sequelae after treatment. Urgent
surgery for decompression of hematoma pressure
may be recommended for bilateral CSDH [13].
2.6 Little Ventricle
Feature
Its features are diffuse swelling of brain tissue,
decreased density, disappearance of the cerebral
sulci, and smaller lateral ventricles.
17
with diffusion-weighted imaging the next day (b), there is
diffuse brain swelling with cytotoxic edema, consisted
with hypoxic-ischemic (anoxic) injury involving the cere-
bral parenhcyma and basal ganglia throughout
Explanation
If brain blood-CSF barrier is destroyed, the intra-
vascular liquid diffuses and infiltrates into the
extracellular space, the amount of water in the
cerebral interstitium is increased, the intracranial
pressure is increased, and the lateral ventricles
pressures decrease (Fig. 2.6).
Discussion
Brain damage after head injury can be classified
by its time course. Primary damage includes
acute subdural hematoma (SDH), acute epidural
hematoma (EDH), and such intra-axial lesions
that include contusions, diffuse axonal injury
(DAI), and intraparenchymal hemorrhage (IPH)
which occur at the moments of impact and may
be irreversible. Secondary damage includes her-
niations, diffuse cerebral swelling, and secondary
infarction and hemorrhage; these evolve hours
or days after injury as consequence of systemic
or intracranial complications. The duration and
severity of secondary damage can influence the
clinical outcome [14]. Brain edema following
traumatic brain injury (TBI) often increases the
intracranial pressure and limits oxygen deliv-
ery. In severe brain edema, the cisterns will be
compressed or absent; a decrease in density,
18
as measured by Hounsfield Units (HU) of the
brain, suggests edema. Diffuse cerebral swelling
has a relatively high mortality rate, particularly
if severe. In children with head injury, bilateral
diffuse cerebral swelling is common; cerebral
blood flow and CT density studies suggest that
this is due to cerebral hyperemia. In comparison
to adults, the clinical prognosis in these chil-
dren is better if there are no secondary lesions
on CT. Rotterdam score is an independent factor
for predicting outcomes among patients with TBI
and can predict outcomes [15].
The non-contrast CT findings in diffuse cere-
bral swelling include homogeneous decreased
density, non-visualization of cortical sulcal
spaces, loss of the gray-white matter interface,
relative hyper-density of the cerebellum (white
cerebellum sign), effacement of the basal cis-
terns, especially the peri-mesencephalic cisterns,
and bilateral compression of the lateral ventricles.
Cerebral swelling may sometimes be associated
with fatal outcomes due to acute cerebral edema
[16]. As traumatic brain injury patients typically
have difficulty with daily tasks, physical and
occupational therapy is highly recommended as
patients attempt to regain a normal lifestyle.
2.7 The Swirl Sign
Feature
The swirl sign is sometimes visible on nonen-
hanced brain CT.  It is recognized as an area of
low attenuation within a larger high-density fluid
collection in the cerebrum or cerebellum.
Interpretation
The swirl sign is an ominous sign of an actively
bleeding epidural hematoma (extradural hem-
orrhage) that has two components: an actively
bleeding/hyperacute component and an older
one. The active component is usually a smaller,
rounded lesion that is iso-dense to the brain paren-
chyma and likely represents actively extravasat-
ing (un-clotted) blood. The older (usually acute
or subacute age) component is a h­ yperattenuating
extra-axial collection, which usually measures
50–70 HU (Fig. 2.7).
A. M. McKinney et al.
Fig. 2.7  An internal focus of low attenuation within a
high-density fluid collection along the left cerebral con-
vexity on non-contrast CT, representing the swirl sign
(arrow)
Discussion
The “swirl sign” (SS) has been previously
described as a tiny or smaller focus of hypo- or
iso-density within a larger region of a hyper-­
density that has been shown to represent active
hemorrhage on surgical evacuation [17]. The
swirl sign can be a reproducible predictor of
1-month mortality and functional outcome,
where it is first described in traumatic extra-
axial hematomas; correspondingly, Greenberg
et  al. and Al-Nakshabandi documented that
following surgical exploration, the swirl sign
correlates with areas of active hemorrhage in
subdural hematomas [18–20]. An epidural hema-
toma usually appears as a lentiform or biconvex
hyperattenuating collection along the cerebral
or cerebellar convexity. Epidural hematomas
may also occasionally present between the dural
sinuses and the skull in the setting of skull frac-
tures that cross the dural sinuses, and thus may
simulate dural sinus venous thrombosis [20, 21].
An arterial epidural hematoma usually results
from injury to the middle meningeal artery or its
branches. An arterial epidural hematoma in the
middle cranial fossa may compress the tempo-
2 Brain 19

ral, frontal, or parietal lobes, depending on the

size of the collection and the vessel injured. A
venous epidural hematoma commonly occurs
at the site of major dural sinuses (e.g., superior
sagittal sinus, transverse sinus, or confluence
of sinuses) [20, 21]. The black hole sign (BHS)
also seems to be a good predictor for hematoma
growth. The presence of the swirl sign on admis-
sion non-­contrast CT does not independently pre-
dict hematoma growth in patients with ICH. The
black hole sign and the swirl sign are both imag-
ing markers that reflect hemorrhage density het-
erogeneity. Hematoma growth may occur in a
cascaded pattern, with initial bleeding causing
secondary peripheral vessel rupture for ongoing
bleeding. The CT attenuation of blood is depen-
dent on the time course of the bleeding, so the
heterogeneity of the hematoma represents blood Fig. 2.8  Original CTA of head showing spot sign within
of different ages. In addition, the hypoattenua- hematoma high-density shadow in the shape of strip or dot
(arrow)
tion area may indicate fresh liquid blood bleed-
ing. SS has a vague definition, and the evaluation A spot sign is actual spotlike change caused by
of SS is more subjective. In BHS, a clear border contrast agent extravasation after enhancement.
and a delta of ≥28 HU between the two density It is an independent enhancement focus and has
regions can improve the reliability. Therefore, the no corresponding connection with blood vessels
inter-­rater reliability is higher than with SS. The (Fig. 2.8).
rigorous definition of the BHS results in a high
specificity of BHS (95.3%) but a low sensitivity Interpretation
(33.8%) [20]. Hematoma evolution in IPH is a dynamic process
that begins as a primary hemorrhagic insult, from
various causes, most commonly from trauma
2.8 Spot Sign or infarct. Multiple studies have shown that a
significant proportion of patients (~25–38%)
Feature undergo hematoma expansion on repeat CT
The spot sign is sometimes visible on dynamic imaging. The currently recognized clinical prog-
contrast-enhanced CT of the brain in the setting nostic factors (including initial hematoma vol-
of intraparenchymal hemorrhage (IPH), typically ume, neurologic deficit at presentation, age, and
in acute infarcts or IPHs of other causes, such infratentorial location) do not directly reflect
as trauma. It is recognized as an area of higher the dynamic nature of hematoma evolution.
attenuation within a larger high-density hemor- Hematoma growth is thought to be due to active
rhage within the cerebrum or cerebellum. hemorrhage and rebleeding and has been shown
to be a determinant of mortality and morbidity
Explanation [22–25]. Early identification and limiting hema-
The contrast-enhanced focus on the original CTA toma expansion have become the primary treat-
image of the head, i.e., spot sign, is caused by the ment goals; thus, identification of early signs of
rupture of the arteriole in brain parenchyma. It is hematoma expansion can help determine patient
defined as a single or multiple spotlike or line-­ prognosis. As such, the “spot sign” on dynamic
like enhanced high-density lesion in the hem- contrast CT, such as CT angiography, has been
orrhage substance on the original CTA image. shown to predict early/hyperacute IPH expan-
20 A. M. McKinney et al.

sion with 89–91% sensitivity and specificity; the

rate of IPH growth has also been identified as a
significant predictor of the patient’s prognosis
[25]. However, some patients may not undergo
contrast-­enhanced CT, whether due to iodinated
contrast allergy, intravenous access, renal fail-
ure, or for other reasons, and thus, the swirl sign
on nonenhanced CT may be more universally
applicable and not require the use of contrast.
Hence, the usage of either the swirl sign and spot
sign can predict patient’s likelihood of suffering
hematoma expansion and can help determine
patients’ prognoses. The nomogram model may
accurately predict hematoma expansion of spon-
taneous intracerebral hemorrhage in the recent
study [26].

2.9  ray-White Matter Interface

G Fig. 2.9  A 68-year-old woman presented with a crescent-­
Displacement shaped high-density hemorrhage (subdural hematoma)
overlying the left frontal and parietal lobes, with slight
inward displacement of the brain parenchyma, and blunt-
Feature ing (or blurring) with straightening of the gray-white mat-
When a subdural hematoma occurs, the gray-­ ter interface
white matter interface between the cortex and
medulla of the hematoma side is displaced
inward, and the distance between the hema- compression of the ipsilateral ventricle, dilata-
toma side and the skull’s inner table increases, tion of the contralateral ventricle, and efface-
which is called gray-white matter interface ment of the cortical sulci. Normally, the gray
displacement. matter of both hemispheres is of equal thickness
and, therefore, the gray-white matter interface
Explanation (G-WMI) of each hemisphere is equidistant from
Normally, the density of the gray-white matter the inner skull table. A small SDH with an atten-
(or “junction”) is readily visible. When an iso-­ uation value resembling gray matter will cause
attenuating subdural hematoma of equal occurs, an apparent thickening of the gray matter. This
the gray-white matter interface displacement is caused mainly by mechanical displacement
often appears. The so-called gray-white matter of the G-WMI [27]. Extracerebral lesions, espe-
interface sign refers to the change of the ipsilat- cially those with intact capsules, exert pressure
eral gray-white matter interface when an extra- on the brain tissue without destroying it, causing
cerebral space-occupying lesion is present. In the interface between gray matter and white mat-
such a situation, the interface becomes nearly ter to move inward, which is called gray-white
a straight line and becomes blunted, which is a matter interface (G-WMI).
characteristic appearance caused by extracerebral This sign is better displayed by T1WI, proton-­
space-­occupying lesions (Fig. 2.9). weighted image (PDWI), and 3D T1WI used in
recent years, as well as reversal sequences (such
Discussion as inversion recovery), that reverse the gray
The secondary signs of subdural hematomas and white matter signals. Subdural hematoma,
(SDH) have previously been documented and epidural hematoma, and extracerebral tumors
include midline displacement, small ventricles, such as meningiomas can affect the interface. It
2 Brain
should be noted that this sign can be seen on
both sides at the same time, especially in the
setting of bilateral subdural hematomas or sub-
dural effusions. It is easy to misdiagnose such
bilateral extra-axial lesions when the degree of
displacement is light [28]. SDH is a dynamic
lesion, and its appearance on computed tomog-
raphy is usually dependent on its age, as well
as other underlying factors (including hemoglo-
bin and hematocrit levels). Soon after a hemor-
rhage occurs (in the acute phase), the hematoma
appears hyperdense when compared with the
normal brain, due to the presence of fresh blood.
During the next few weeks, (subacute phase) res-
olution occurs due to fibrinolysis, so the hema-
toma appears iso-dense. After approximately
4  weeks (chronic phase), it appears hypodense
due to the resorption of fluid. However, repeated
micro-hemorrhages into SDH can increase the
density, giving rise to a heterogeneous and par-
tially hyperdense picture [29]. Hence, a hyper-
dense hematoma can be readily recognized,
but an iso-dense hematoma may be difficult to
visualize on the computed tomogram. A spe-
cific finding is the displacement of the brain
parenchyma away from the skull, and the usual
convex border appears flattened or even con-
cave. Also, several other indirect features may
occur due to the displacement of the brain; for
example, effacement of the sulci, compression
of the ipsilateral ventricle leading to midline
shift, and deformity of the normal ventricular
anatomy could aid in the diagnosis of subdural
hematoma.
2.10 T
 he Dense or Hyperdense
Artery Sign
Feature
The dense artery sign is characterized by an
increase in the density of the first to second seg-
ments of the middle cerebral artery (MCA) or
an increase in the density of other arteries in the
brain compared to the contralateral side. This can
be applicable to other major intracranial arteries,
such as the anterior cerebral artery (ACA) or the
posterior cerebral artery (PCA).
21
Explanation
The dense (or hyperdense) artery sign is an indi-
rect sign of cerebral infarction caused by occlu-
sion of a major cerebral artery (the MCA being
most common). The high attenuation component
represents a blood clot, thrombus, or emboli
lodged in the cerebral artery’s lumen. The CT
value of normal flowing blood is approximately
40  HU, whereas the CT value of a thrombus is
approximately 80  HU, thus showing a higher
attenuation than normal, un-clotted blood
(Fig. 2.10).
Discussion
The dense arterial sign, or the hyperdense artery
sign, which is believed to be caused by throm-
bus, has a density/attenuation (77–89 HU) that
lies between normal arterial (35–60  HU) and
calcified plaque (114–321  HU); it is common
in cardiogenic cerebral infarction, for example.
The M1 segment of MCA is located in the lat-
eral cleft, and there are more chances of arterial
obstruction, so there is a greater possibility of
this sign being exhibited in the setting of acute
ischemic stroke. Therefore, in this setting, it is
also called the “hyperdense MCA sign (HMCA
sign),” while ACA or PCA can less commonly
have a similar appearance [30]. Non-­contrast
CT is usually the first method of examina-
tion for acute cerebral infarction; however, in
the first few hours after infarction, CT usually
appears normal. When the image changes of
early ischemic infarction occur, they are often
concealed at first in the hyperacute phase but
usually become obvious over time. Hence, rec-
ognizing certain signs of acute infarction can
help to identify infarcts and lead to prompt
therapy [31]. Thus, early signs of MCA occlu-
sion include the HMCA sign, lenticular nucleus
sign, insular ribbon sign, low-density focus,
occupying effect, and the cortical effacement
sign. These signs can become more appar-
ent at approximately 6  hours after infarction.
In theory, the HMCA sign can be seen on CT
images when blood vessels are occluded and
earlier than the other changes in acute stroke. In
addition, as the HMCA sign is transient, most
patients with acute cerebral infarction who have
22 A. M. McKinney et al.

a b

c d

Fig. 2.10 An 81-year-old male patient. (a–c) Non-­
contrast CT shows increased attenuation of the left middle
cerebral artery (i.e. a “hyperdense MCA sign”) and
slightly low attenuation and blurred boundary in left fron-
tal, temporal, and parietal lobes; A few days later, cranial
MRI follow-up, FLAIR (d) shows a large area of abnor-
mal intensity in the left frontal, temporal, and parietal
lobes, while DWI (e) shows obvious hyperintensity with
restricted diffusion, indicating an acute cerebral
infarction
2 Brain
e
Fig. 2.10 (continued)
the HMCA sign have that sign disappear within
a few days post-infarct, or after thrombolytic
therapy, which confirms the mobility of such
blood clots within the hyperattenuating vessels.
When HMCA sign is seen, it should be
noted that it does not always represent vascular
obstruction; for example, when the specific vol-
ume level of blood cells is high, the CT value of
blood or calcification of blood vessel wall (often
associated with diabetes and hypertension) will
appear falsely positive for a thrombosed ves-
sel, but will usually involve multiple vessels,
and often appear bilaterally dense as regards the
MCA [32]. Thus, the high density of a unilateral
MCA is more reliable than bilaterally hyper-
dense MCAs. In one study, it is found that the
sensitivity and specificity of the dense artery
sign for arterial obstruction is approximately
52% and 95%, respectively, and the dense artery
sign is more commonly identified in the larger
proximal arteries, relative to the smaller distal
arterial segments [33]. Although false positive,
the dense artery sign has a higher diagnostic
value in patients with cerebral infarction symp-
toms and is a relatively highly specific sign.
When there are other early signs of early cere-
bral infarction, the reliability of the dense artery
sign is even higher.
23
2.11 T
 he Middle Cerebral Artery
Dot Sign
Feature
On non-contrast head CT, compared with the
contralateral or even with other vessels on the
same side, the hyperattenuating vascular shadow
located in the Sylvian fissure is called middle
cerebral artery dot sign.
Explanation
In non-contrast CT, normal vascular usually
shows soft tissue attenuation; when thrombo-
embolism and obstruction occur, the attenuation
of blood vessels increased. The middle cerebral
artery dot sign indicates thromboembolism in
a branch of the middle cerebral artery (M2 or
M3 segment) in the Sylvian fissure. In the axial
plane, the M2 or M3 segments are perpendicular
to the scanning plane; thus, these appear as a dot
on non-contrast CT. MCA dot sign and the hyper-
dense MCA (HMCA) signs are CT findings of
MCA occlusion occurring at different axial CT
levels (Fig. 2.11).
Discussion
Non-contrast CT is utilized to exclude intracra-
nial hemorrhage in an emergency setting and is
an invaluable tool in the evaluation of suspected
acute stroke. Beyond the detection of hemor-
rhage, early non-contrast CT can also be used
to detect direct or indirect signs of acute isch-
emia or infarction itself. The MCA dot sign is
an important indirect sign, which indicates a
high attenuation thrombo-embolus or occlu-
sion with an internal vascular shadow (appear-
ing as a filling defect). It refers to the dot of
high attenuation in the M2 or M3 segments of
the MCA of the Sylvian fissure, especially in
the annular sulcus [34]. It is generally believed
that atherosclerosis mainly involves the internal
carotid artery, MCA trunk (M1 segment), and
basilar artery and less commonly involves the
M2 segment of the MCA and smaller-diameter
distant arteries. Therefore, the high attenuation
shadows of M2 segment and distal artery are
considered mainly thromboembolic rather than
calcified atherosclerotic plaques. Some studies
24
a b
Fig. 2.11  An 81-year-old female with atrial fibrillation
had a left-sided facial droop, with unclear speech and
weakness of the left lower limb. (a) Non-contrast CT
shows a focus of high attenuation in the right Sylvian fis-
have found that in patients with MCA infarction
in the region of blood supply, patients with the
HMCA sign were found to have longer hospi-
talization times and worse short-­term progno-
sis, which is significantly worse than in patients
with MCA dot sign alone or in those lacking the
HMCA sign [34]. Although there is a report that
the MCA dot sign can be falsely positive due
to increased hematocrit, many scholars believed
that the MCA dot sign was still a highly spe-
cific CT sign. According to Leary et  al. [35],
MCA dot sign has a high specificity (100%) and
a moderate sensitivity (38%) in the diagnosis
of ischemic stroke in the blood supply area of
MCA, with a positive predictive value of 100%,
a negative predictive value of 68%, and an accu-
racy of 73%. Thus, the use of solely the MCA
dot sign suggests M2 or M3 segment of the
MCA is occluded, where the size of the injured
brain tissue by the ischemic injury is small, and
hence, there is a good short-term and long-term
prognosis; in such patients, the effect of throm-
bolytic therapy is greater than that of the proxi-
mal MCA trunk (M1 segment) [35].
The use of the MCA dot sign can be very
helpful in the diagnosis, treatment, and progno-
sis of MCA branch infarctions, and it has a bet-
ter prognosis than the HMCA sign. Therefore,
A. M. McKinney et al.
sure, suggesting MCA dot sign. (b) Contrast-enhanced
CT with 3D reconstructions shows occlusion of MCA M1
segment, with high-attenuation shadow thrombus extend-
ing into M2 segment
recognition of the MCA dot sign is vital for the
identification and quantification of the extent of
those acute ischemic lesions that have a better
prognosis. Incorporating multiplanar reconstruc-
tion may lead to a higher sensitivity of the middle
cerebral artery “dot” sign [36].
2.12 M
 iddle Cerebral Artery
Susceptibility Sign
Feature
On susceptibility-based MR images such as
susceptibility-­weighted imaging (SWI), T2*-
weighted gradient echo (T2*WI), or MR perfu-
sion imaging, the diameter of the apparently
low-­ signal middle cerebral artery (MCA) or
internal carotid artery (ICA) exceeds the diam-
eter of the corresponding contralateral artery,
which is called “middle cerebral artery suscep-
tibility sign.”
Explanation
The middle cerebral artery susceptibility sign
indicates acute thromboembolism in MCA or
ICA. In acute thromboembolism, the concentra-
tion of deoxyhemoglobin is very high, the value
of T2 in thrombus is shortened, and thus, the vis-
2 Brain 25

ible signal is lost on the imaging sequence based in other major intracranial arteries such as the
on susceptibility, showing overtly low signal with anterior cerebral artery (ACA) or posterior cere-
a “blooming effect” of the dark signal beyond the bral artery (PCA) as well, albeit less common in
expected MCA luminal diameter. This can occur those vessels (Fig. 2.12).

a b

Fig. 2.12  A 49-year-old male presented with the left MRA (c) demonstrates distal occlusion (arrow) of M2
middle cerebral artery susceptibility sign on SWI (arrow, branch of the left middle cerebral artery (inferior
a) and developed associated infarcts on DWI (b). On head division)
26
Discussion
In 2000, Flacke et  al. first reported that in MR
perfusion imaging (PWI) of stroke patients with
MCA occlusion within 6  hours after onset of
symptoms, the signal of MCA in the occlusive
segment is significantly reduced, and the diam-
eter of MCA is larger than that of the correspond-
ing contralateral artery, which is termed “middle
cerebral artery susceptibility sign” [37]. This is
related to the susceptibility effects from the para-
magnetic effect of intraluminal thrombus, usually
either in the acute phase of thrombus (deoxyhe-
moglobin) or subacute phase of thrombus (met-
hemoglobin). The value of high attenuation sign
of the middle cerebral artery on CT in the diagno-
sis and pre-thrombolysis evaluation of acute cere-
bral infarction has been recognized. However, its
application is limited due to the application of a
radiation dose, factors related to the possibility of
there being a false positive (such as due to dehy-
drations or beam hardening artifacts), and diffi-
culty in identifying lesions related to hyperacute
cerebral infarction. Compared with the hyper-
dense middle cerebral artery sign, the middle
cerebral artery susceptibility sign has the advan-
tages of no radiation and strong repeatability/reli-
ability, and is considered as good as or even a
better predictor of vascular occlusion; Payabvash
et  al. [38] found that there is greater than 90%
specificity and positive predictive value on SWI
MRI when this sign is demonstrated, while GRE
T2*WI is less sensitive.
Studies [39] have shown that the components
of emboli include red blood cells, platelets, fibrin
and nucleated cells (neutrophils, monocytes),
etc., but the proportion of the manifold compo-
nents of different emboli varies. Kimura et  al.
[40] suggested that the middle cerebral artery
susceptibility sign indicates that an embolus con-
tains a higher concentration of red blood cells.
White thrombi are typically rich in platelets and
resist intravenous thrombolysis of recombinant
tissue plasminogen activator (rt-PA), while red
thrombi are rich in red blood cells and elicit a
faster response to thrombolytics; hence, the
nature of the embolus determines the therapeutic
effect of revascularization. Therefore, the middle
cerebral artery susceptibility sign may have the
A. M. McKinney et al.
value of predicting vascular recanalization and
clinical prognosis [41]. However, the middle
cerebral artery susceptibility sign also has some
false positives as well. Of note, SWI is an imag-
ing technique developed on the basis of gradient-­
recalled echo (GRE), which can obtain both the
amplitude and phase maps of patients’ MRI;
ergo, SWI is more sensitive to the susceptibil-
ity effect induced by a substance, particularly
metallic agents, gas/air, and other substances or
agents that cause profound dephasing. With the
aging of thrombus, the presence of susceptibil-
ity within the middle cerebral artery varies in
patients with ischemic stroke at different stages.
The order of degradation of oxyhemoglobin in
erythrocyte, in approximate chronologic order
(although the stages can overlap) is deoxyhe-
moglobin, methemoglobin, and finally hemo-
siderin formed by macrophage phagocytosis.
The unpaired electrons of deoxyhemoglobin and
hemosiderin have a significant paramagnetic
effect (regardless of their bright or dark signal
on T1WI and T2WI), resulting in inhomogeneous
magnetic field and rapid proton spin dephasing
near them, which cause significant signal loss on
the SWI sequence. This “susceptibility effect”
can appear even as a small “blooming” effect
of the dark signal around the affected vessel
and can create difficulty in accurately measur-
ing the size of the vascular abnormality (such as
with an aneurysm). Manipulation of the time to
echo (TE) and time of repetition (TR) can also
alter the degree of susceptibility effect on SWI
and other GRE sequences. Thus, false positives
can occur simulating intraluminal thrombus,
due to susceptibility effects from artifacts (such
as whether from the adjacent scalp to metals
or foreign bodies or from the scalp or mastoid
air cell gas, pulsation effects, or even motion),
implants (e.g., adjacent clips or some stents),
biologic deposits (e.g., calcium or iron), or even
certain contrast agents (e.g., iron-containing).
Therefore, it is necessary to accurately confirm
that a middle cerebral artery susceptibility sign
is a true positive by correlating both with other
MRI sequences such as fast spin-echo T2WI,
which is relatively insensitive to susceptibility
artifacts), or FLAIR (which often has mildly
2 Brain
hyperintense vascular signal in acute stroke,
due to loss of the normal dark signal in normal
moving arterial flow); alternatively, retrospec-
tively correlating with the non-contrast CT can
reveal a subtle hyperdense middle cerebral artery
for confirmation. Less common signs such as
the prominence of either cortical or medullary
veins demarcating the territory of infarct on SWI
(present in 10–20% of acute stroke patients, pre-
sumably due to venous stasis) and the presence
of SWI-DWI mismatch (associated with lower
infarct volumes and better outcomes) can help
confirm and can help estimate the overall size
of infarct, as such secondary signs have been
shown to correlate with the eventual infarct size
[42, 43].
At present, cases of the middle cerebral artery
susceptibility sign are best visualized around
6  hours of stroke symptoms or later, while the
signal evolution of thrombus on SWI in  vivo is
not completely known, particularly with smaller
thrombi approximately a millimeter in size or
less. Therefore, while there is a lack of under-
standing of middle cerebral artery magnetic sus-
ceptibility within the first 3 hours of acute stroke
symptoms, there is not enough data to deter-
mine the shortest time that MRI can depict acute
thrombus on SWI. Therefore, the middle cerebral
artery susceptibility sign cannot yet be reliably
applied to patients with acute stroke within the
first 3 hours of symptom onset.
2.13 The Cord Sign
Feature
The cord sign is a homogeneous, hyperattenuat-
ing, cord-like appearance on non-contrast axial
CT of the brain.
Explanation
The cord sign appears as the result of increased
attenuation within either the dural sinuses or a
vein filled with thrombus. Thrombosis in veins
can be visualized directly on unenhanced exami-
nations as foci of increased attenuation within
the distribution of the affected veins. For veins
perpendicular to the transverse plane (including
27
the cortical vein, the vein of Galen, and parts
of the superior sagittal sinus), a round focus of
increased attenuation may appear on the succes-
sive sections. In veins parallel to the scanning
plane (including internal cerebral veins, med-
ullary veins, and the straight sinus), the linear
nature of the high attenuation may represent a
thrombosed blood vessel or venous sinus. This
appearance is termed the “cord sign” (Fig. 2.13).
Discussion
Cerebral venous thrombosis (CVT) is a type of
stroke where the thrombosis occurs in the venous
side of the brain’s circulation, leading to occlu-
sion of one or more cerebral veins and potentially
a dural venous sinus. CVT is more frequent in
women. The age distribution of CVT is different
from that of ischemic stroke, CVT being more
frequent in children and young adults. CVT has
a variable clinical presentation ranging from mild
cases presenting only headache, headache plus
papilledema or other signs of intracranial hyperten-
sion, focal deficits such as aphasia or paresis often
combined with seizures, to severe cases present-
ing with encephalopathy, coma, or status epilepti-
cus. The confirmation of the diagnosis of CVT by
imaging requires the demonstration of thrombi in
a dural sinus or cerebral vein [44]. The cord sign
appears as the result of increased attenuation in
either the dural sinuses or a vein filled with throm-
bus. Thrombosis in veins can be visualized directly
on unenhanced examinations as foci of increased
attenuation in the distribution of the affected veins.
For veins perpendicular to the transverse plane
(including the cortical vein, the vein of Galen, and
parts of the superior sagittal sinus), a rounded focus
of increased attenuation may appear on the succes-
sive sections. In veins parallel to the scanning plane
(including the internal cerebral veins, medullary
veins, and the straight sinus), the linear nature of
the high attenuation may represent a thrombosed
blood vessel or venous sinus [45].
On unenhanced CT, the most common cause
of a false-positive case is a high hematocrit
(e.g., in patients with polycythemia vera) caus-
ing a hyperdense sinus. However, the arteries of
such patients also frequently have a hyperdense
appearance, which is a clue to the correct diag-
28
a b
Fig. 2.13  In a 21-year-old male, axial unenhanced CT
image (a) showed the cord sign (arrow) in the straight
sinus. This was confirmed to be occlusive thrombus
nosis. The conundrum of a hyperdense appear-
ance of normal dural sinuses is also frequently
encountered in infants and young children, in
whom the relative density of the dural sinus com-
pared with brain tissue is typically high for two
reasons: first, a usually higher hematocrit value
than in adults and, second, a typically lower brain
density than in adults [46, 47]. Thus, other con-
ditions causing a hyper-dense appearance of the
vascular, such as dehydration or polycythemia,
can simulate a hyperdense venous sinus. The
diagnosis of CVT is often made through analy-
sis of source venographic and 3D images. The
diagnosis is based on confirmation of thrombus
A. M. McKinney et al.
(arrows) on postcontrast MR venography (b). Sagittal
T1WI postcontrast (c) confirms the straight sinus throm-
bus as well (arrows)
within the venous sinuses and identification of
any secondary effects of thrombosis on brain
parenchyma or CSF pathways. Unenhanced CT
is typically the most common initial imaging
modality for many of these clinical diagnostic
considerations. Unfortunately, unenhanced CT
examinations may often show only subtle find-
ings or appear normal, which necessitates the use
of 3D venographic images, if thrombosis is sus-
pected. Before the advent of MRI, conventional
CT is the best noninvasive method of diagnos-
ing CVT.  The cord sign is originally found in
only a minority of images of patients with cere-
bral venous thrombosis, and there were doubts
2 Brain
approximately the sign’s value in routine diagno-
sis. With thinner CT sections, however, this sign
is now detected more frequently with a higher
sensitivity on non-contrast CT.  Since the cord
sign demonstrates a newly formed thrombus, it
will seldom be visualized in patients with sub-
acute or chronic disease because the thrombus
ages, usually becoming iso-attenuating and then
hypoattenuating after the first 7–14 days. In other
cases, the thrombosed veins are too small for
the thrombi to be visualized, or the thrombi are
obscured by artifacts from adjacent bone [45].
2.14 The Insular Ribbon Sign
Feature
One of the earliest non-contrast CT findings of
cerebral infarction is the insular ribbon sign,
which consists of the disappearance of the vis-
ible boundary between the gray matter (usu-
Fig. 2.14 On non-contrast CT (a) in a 38-year-old
female, via bilateral comparison of the insular ribbon,
there is a right insular ribbon sign on the right (arrow),
29
ally slightly denser) and white matter (normally
slightly less dense) at the outer edge of the insu-
lar lobe. Thus, in acute infarction, the insular
ribbon becomes a blurred confluence of the gray
matter-white matter junction in the middle cere-
bral artery distribution.
Explanation
The claustral artery or insular artery from the
branch of the middle cerebral artery M2 segment
perfuses the insular ribbon area; alternatively,
lateral lenticulostriate branches can uncom-
monly supply this region. When the M2 seg-
ment becomes occluded, this region is prone to
infarction due to its being the furthest collateral
circulation from the arteria cerebri posterior and
arteria cerebri anterior. Hence, in the setting of
an acute insular region infarction (supplied by a
subdivision of an M2 segment), the loss of the
insular ribbon is a reaction to acute edema caused
by cerebral infarction (Fig. 2.14).
and the left side is normal. DWI (b) confirms an infarct
subsequently occurred in the right MCA distribution in
that location
30
Discussion
In 1990, Truwit et al. reported an early CT mani-
festation of acute cerebral infarction caused by
the disappearance of the insular zone from a
middle cerebral artery (MCA) or internal carotid
artery (ICA) acute occlusion [48]. Acute ischemic
stroke due to arterial occlusion on non-­contrast
head CT typically features the loss of gray-white
matter differentiation, followed shortly thereafter
by a confluent area of hypodense brain paren-
chyma representing the vascular territory of a sub-
sidiary artery from the MCA. In the early phase
of an MCA distribution infarct, this can usually
be observed first at the level of the insula and is
called the loss of the insular ribbon sign [49].
When the loss of the insular ribbon sign appears
alone, it is caused by occlusion of the M2 seg-
ment (insular segment and/or claustral branches)
of the MCA, and cortical infarction occurs. The
claustrum, external capsule, and the extreme cap-
sule together may be affected in this scenario, as
they constitute the insular ribbon, for which the
perfusion in this area is rich. However, when the
distal M2 segment of the MCA is occluded, this
area is prone to hemorrhage due to it having rela-
tively distant collateral flow from the anterior and
posterior cerebral arteries.
As mentioned earlier in this section, the early
CT signs of cerebral infarction (including both
direct and indirect signs) include the following:
(1) Hyperdense MCA sign: the blood clot can
often be observed on non-contrast CT, while
for other cerebral arteries or smaller vessels, the
sign can be termed the dense artery sign [49]. (2)
Obscured lentiform nucleus sign: after vasogenic
edema occurs in acute cerebral infarction, the
water in the blood vessel “leaks” into the extra-
cellular space, the total water content in brain tis-
sue increases, and thus, its CT value decreases,
where obscuration sign of the lentiform nucleus
hence appears in the early stage. (3) Loss of the
insular ribbon sign: the gray matter-white matter
boundary of the insular cortex becomes unclear
in early infarction, showing a confluent area of
hypoattenuation. (4) The boundary between the
cortex and the medulla is blurred (“blurred cor-
tex sign”): the CT Hounsfield units of the cortex
are slightly reduced, and the boundary of white
A. M. McKinney et al.
matter under the cortex along with the cortex is
blurred, which can be visible within 2–3  hours
of infarct onset; if the infarct size is large (often
quoted as being >3 cm diameter), the prognosis
is poor. After the lenticular nucleus is blurred,
the gray matter-white matter junction of the
infarct area may be slightly hypodense on CT
and can be visible within 2–3  hours of onset.
(5) Disappearance of the sulcus overlying the
cortex of an infarct, occurring within 3 hours of
onset, and being associated with larger areas of
infarction; if appearing alone, this suggests that
the infarct is irreversible and that thrombolytic
therapy may not be efficacious. Therefore, insu-
lar involvement is a well-established early sign
of ischemic MCA distribution infarct, whether
detected by loss of gray-white matter differen-
tiation on unenhanced CT, or restricted diffusion
on DWI. Functional studies have also suggested
that the insular ribbon has higher ischemic vul-
nerability relative to other cortical and deep gray
matter brain structures [50].
2.15 T
 he Disappearing Basal
Ganglia Sign
Feature
On non-contrast CT of the brain, this sign showed
that the normal basal ganglia disappeared, and
the affected basal ganglia showed abnormal mor-
phological features.
Explanation
The normal lenticular and caudate nuclei are
slightly higher in attenuation than the surround-
ing white matter, and they exhibit lower attenu-
ation on CT when ischemia occurs. The volume
of a normal cell requires a normal electrolyte
concentration and gradient inside and outside
of the cell, and cell damage occurs when blood
flow is interrupted. Such interruption causes
damage to the internal environment, causing an
influx of sodium ions, chloride ions, and calcium
ions, and thereafter, moisture enters the cells to
form metabolic acidosis. This net fluid flow into
the cells causes cytotoxic edema and the focal
edema noted on CT as hypoattenuation with loss
2 Brain
Fig. 2.15  A 70-year-old male lacking clear speech for
3 hours. The normal left basal ganglia contour has disap-
peared on CT, indicating acute infarction
of the distinction of the basal ganglia, which
normally are slightly more hyperdense on CT
relative to the anterior and posterior limbs of the
internal capsules (as the internal capsules nor-
mally have a higher concentration of myelin due
to their white matter tracts); this cytotoxic edema
usually later leads to cell lysis. On non-contrast
CT, the low attenuation zone of the basal ganglia
at this point is a sign of severe focal ischemia
and subsequent infarction (irreversible insult)
(Fig. 2.15).
Discussion
Non-contrast CT remains the primary initial
imaging modality for acute stroke presentations
because of its fast acquisition and widespread
availability, as well as the need to immediately
exclude intracranial hemorrhage. CT can quickly
differentiate between ischemic and hemorrhagic
stroke and can also be used to quantify the extent
of early ischemic changes (EICs); DWI can later
confirm the acute or early subacute infarct by hav-
ing a bright appearance on DWI that is accom-
panied by a corresponding dark signal in that
region on ADC maps. Non-contrast CT can be
31
reliably used for rapid clinical decision-­making
as well as prognostication given a standardized
image quality, in order to detect EIC. The disap-
pearing basal ganglia sign is a relatively common
manifestation of acute cerebral infarction. This
sign is often caused by incomplete or complete
occlusion of the middle cerebral artery from vas-
cular thromboembolic disease. Other differential
diagnoses leading to such focal basal ganglial
cytotoxic edema (also causing reduced diffusion
on DWI) include vascular occlusion from arte-
rial dissection, trauma, or rarely vasculitis, while
uncommon nonvascular congenital or metabolic
disorders can lead to basal ganglial cytotoxic
edema, such as mitochondrial disease, encepha-
litis, or rarely hemolytic uremic syndrome [51].
It is important to detect early ischemic stroke
on CT since the lack of early parenchymal hem-
orrhage or a larger (>3 cm size or 70 cc volume)
hypodense region of infarct suggests that the
patient may be amenable to thrombolytic ther-
apy, where thrombolytic therapy can improve
the patient’s prognosis [52]. Most ischemic cere-
brovascular accidents occur in the area of blood
supplied by the middle cerebral artery (MCA).
The most common cause of cerebral infarction
in industrialized countries is thromboembolism.
The basal ganglia (of which the lentiform nuclei
are part of) are very sensitive to ischemic injury
as their blood supply is typically derived directly
from small arteries, including the lenticulostriate
arteries. The basal ganglia are the deep gray mat-
ter structure of the cerebral hemispheres and over-
all include the corpus striatum (itself composed
of the nucleus accumbens of the basal forebrain
plus the caudate plus the lentiform nuclei), along
with the subthalamic nuclei and the substantia
nigra of the midbrain. The lenticular nucleus
(lentiform nuclei) includes the globus pallidus
and the putamen. Additionally, part of the ante-
rior limb of the internal capsule and the head of
caudate are together supplied by the medial len-
ticulostriate artery, which originates from the A1
segment of the anterior cerebral artery.
Notably, the recurrent artery of Huebner is
the main branch of the medial lenticulostri-
ate artery, which can be derived from the A1 or
A2 segments of the anterior cerebral artery, but
32
most often originates from the A2 segment in
proximity to the anterior communicating artery.
Meanwhile, the lateral lenticulostriate artery
supplies the lenticular nucleus, part of the cau-
date nucleus, and the posterior limb of the inter-
nal capsule. The area supplied by these arteries
varies in size and number, as there can be from
6–20 lenticulostriate arteries which may over-
lap in supply; these arteries are located along
the upper contour of the M1 segment of the
middle cerebral artery. Therefore, the early CT
signs of the infarction of the territory supplied
by the MCA include the high attenuation of the
middle cerebral artery (hyperdense MCA sign),
the disappearance of the lenticular nucleus’ bor-
der with the insula and Sylvian fissure (insular
ribbon sign), a focal unclear margin of cortical
gray matter at its junction with subjacent white
matter (blurred cortex sign), and the complete
disappearance of the outline of the basal ganglia
or basal nuclei by the internal capsules (disap-
pearing basal ganglia sign), as well as a lesser
degree and more focal loss of the outline of the
lentiform nuclei (obscured lentiform nucleus
sign, described next).
Fig. 2.16  On non-contrast CT 2 hours after the appear-
ance of the clinical stroke symptoms, there is initially a
normal appearance of the right basal ganglia (a: left
image), which appeared resembling the normal left basal
A. M. McKinney et al.
2.16 T
 he Obscured Lentiform
Nucleus Sign
Feature
Obscuration of the lentiform nucleus is a non-­
contrast CT finding of acute cerebral infarc-
tion. The attenuation of gray and white matter is
decreased due to focal cytotoxic edema within
the middle cerebral artery (MCA) distribution.
The capsula interna and its inner and outer bor-
ders are vague. The most obvious finding is vague
edges of the globus pallidus and putamen (which
together comprise the lentiform nuclei) due to the
decreased attenuation from acute ischemic infarct.
Explanation
When acute cerebral infarction leads to cytotoxic
edema, intravascular water enters into the extracel-
lular space, the total water content of the brain tis-
sue is increased, and the density/attenuation (HU)
is decreased on CT. At the same time, the obscured
lentiform nucleus sign is seen due to the vessels
supplying the lentiform nuclei being small termi-
nal arteries, where the process of infarction accel-
erates quickly when ischemia occurs (Fig. 2.16).
ganglia. One day later (b: right image), the contour of the
right lentiform nucleus disappeared. Note that this appears
more focal than the disappearing basal ganglia sign, as
the overlying right insular ribbon is intact
2 Brain
Discussion
Obscured lentiform nucleus sign can be one of
the earliest findings in patients with acute isch-
emic stroke within the MCA distribution. It occa-
sionally occurs in some patients within the first
hour of symptom onset, but mostly (73–92% of
MCA distribution infarct patients), it is visible
a bit later within the first 6 hours of onset [53].
This sign can be described as decreased attenu-
ation involving the lentiform nucleus (comprises
the globus pallidus and putamen) on CT, induc-
ing loss of the precise delineation of this area.
The lentiform nucleus is fed by the lenticulostri-
ate arteries from M1 segment of MCA; thus, this
sign is seen in patients with M1 segment or distal
ICA distribution infarctions. Whether in hyper-
acute, acute, or subacute cerebral infarction, low
attenuation of the affected cerebral parenchyma
is one of the most important early changes of
infarction. Within 6  hours of onset, the inci-
dence of the obscured lentiform nucleus sign in
MCA stroke patients is 92%. Besides this sign,
other early non-contrast CT findings of cerebral
infarction can be present, which include the fol-
lowing: (1) Hyperdense artery sign: an imaging
sign suggesting occlusion of a major cerebral
artery, usually the MCA, where the high-density
components represent arterial blood clot, throm-
bus, and embolism. (2) Loss of the insular rib-
bon sign: the insular ribbon is perfused by the
claustral/insular artery which separates the M2
segment of the MCA, and disappearance in gray-
white matter boundary may occur early in acute
MCA distribution infarction. Notably, the insular
ribbon sign and the obscured lentiform nucleus
sign have been reported to be relatively common.
Both signs are produced by infarction in a spe-
cific vascular distribution, which is the middle
cerebral artery and its subsidiary branches; thus,
evaluating for the presence of either of these
early signs can be helpful for the early diagnosis
of this disease.
Acute ischemic cerebral infarction has usu-
ally been defined as occurring within 72  hours
of symptom onset. It is generally believed that
cerebral infarctions that occur within hours are
considered hyperacute cerebral infarctions. There
is the need for early diagnosis and determination
33
of ischemic penumbra in the pathophysiologic
stage of acute cerebral infarction, as throm-
bolytic therapy for individuals in the effective
reperfusion time window can rescue some of
the impaired neurologic function from the isch-
emic penumbra. Non-contrast CT is still consid-
ered the preferred first-line imaging examination
in stroke, as its purpose is to eliminate cerebral
hemorrhage as well as to identify other CT signs
of impending cerebral infarction that would pre-
clude thrombolytic therapy [54]. Additionally,
CT angiography (CTA) and CT perfusion (CTP)
may play an important role in the early individual-
ized assessment of the clinical outcome and can
help to guide treatment decisions, via identifying
the degree of occluded vasculature or even col-
lateral circulation. Regarding CTP, various tissue
perfusion parameters can be used to differentiate
reversible from irreversible ischemic brain tissue
and to assess tissue at risk. It was reported the
measurement of maximum cerebral blood flow
of collateral vessels within the Sylvian fissure is
a feasible quantitative collateral assessment at
perfusion CT.  Maximum cerebral blood flow of
­collateral vessels was associated with clinical out-
comes in patients with acute ischemic stroke [55].
2.17 Fogging Effect
Feature
This sign can be seen on non-contrast CT and
MRI but initially is described on CT.  Patients
with cerebral infarction initially can have low
attenuation on CT or long T1 and T2 signal on
MRI; however, in the second and third weeks
after infarction, the infarct can become iso-dense
on CT or isointense on MRI (usually T1WI and
T2WI) to other more normal cortical regions.
Explanation
Fogging effect is typically noted in the subacute
phase of cerebral infarction. In the acute phase,
cerebral infarction-related cytotoxic and angio-
genic edema can lead to low attenuation on CT
or high signal on T2WI.  However, at the begin-
ning of the subacute phase of reabsorption and
repair, the edema of the infarcted area decreases,
34
the necrotic tissue is being cleared and replaced
by macrophages, and astrocytes and endothe-
lial cells proliferate to form new capillaries.
Therefore, the water content and cell composi-
tion in the area of subacute cerebral infarction
return to near-normal levels, so the subacute
infarct can appear isodense on CT or isointense
on MRI (usually T1WI and T2WI) to other corti-
cal regions, thereby obscuring the region of the
infarct. This can cause confusion as to the size of
the infarct if the patient is not imaged earlier in
the acute phase, particularly on MRI, since DWI
can appear “pseudo-normal” at 7–10 days post-­
infarct onset (Fig. 2.17).
a b
d e
Fig. 2.17 (a, b) A 64-year-old female is admitted to the
hospital because of “sudden left limb weakness for over
1  day,” where a non-contrast CT demonstrated low-­
density infarction in the right temporal lobe, insula, and
basal ganglia; (b) a non-contrast CT 11 days later in the
same patient showed that the area of infarction became
less clearly delineated. (c, d) In a 66-year-old female,
A. M. McKinney et al.
Discussion
Cerebral infarction is a common clinical cere-
brovascular disease. According to the onset time
of cerebral infarction, it can be divided into the
hyperacute stage (less than 6 hours), acute stage
(2–7  days), subacute stage (1–4  weeks), and
chronic stage (after 1  month). On non-contrast
CT, images obtained at more than 24 hours post-­
onset depict a significant decrease in density of
the region of cerebral infarction. Over time, the
density will continue to decrease, and the fogging
effect occurs at approximately 2–3  weeks. On
MRI, low signal on T1WI, high signal on T2WI,
c
f
admitted to hospital because of “hypertension over
2 months, but increased dizziness for the past 3 days,” an
MRI showed long T1 (hypo-intense) patches in the left
cingulate and occipital lobes, with long T2 (hyper-intense)
signal; (e, f) 10  days later, the infarct is not as clearly
visible
2 Brain
and fogging effect at 2–3 weeks were observed in
acute cerebral infarction.
Becker et al. [56] first described the increase
of relative density on CT in the second and third
weeks after cerebral infarction in 1979, which
has been termed the fogging effect. This fea-
ture can be seen in the whole infarct distribution
or part of the area; at the same time, it can be
accompanied by the disappearance of the space-­
occupying effect. If CT is performed during this
period, the diagnosis of cerebral infarction may
be missed. At this time, if contrast-enhanced
CT is performed, cerebral infarction with fog-
ging effect often shows homogeneous and overt
enhancement. Although the contrast resolution
of MRI is higher than that of CT, this phenom-
enon can also be seen in conventional T1WI and
T2WI. On MRI, the fogging effect is first reported
in 1990 [57]. At present, it is believed that there
are two reasons for the fogging effect of MRI:
(1) after cerebral infarction, small vascular endo-
thelial cells leak into the necrotic region fol-
lowing the onset of ischemia and hypoxia, and
hemoglobin is oxidized to deoxyhemoglobin and
methemoglobin; the latter two are paramagnetic
substances, which can reduce the signal intensity
of T2. (2) At 2–3 weeks after cerebral infarction
(subacute phase), the water absorption of necrotic
tissue decreases as large number of gitter cells
enter the necrotic area, which can also reduce the
signal of T2. Similarly, contrast-enhanced MRI
in the subacute phase can prevent missed detec-
tion by exhibiting avid cortical or parenchymal
enhancement. Recent studies have shown that
after cerebral infarction, with the passage of time,
through the space-specific regulation of neuro-
vascular function by the body itself, the patient’s
condition often shows some improvement, with
some having even complete recovery, depend-
ing on the size and location of the infarct [58].
Therefore, the prompt and accurate diagnosis and
treatment of subacute cerebral infarction patients
are particularly important. Hence, identifying
the fogging effect on CT and MRI, to exclude
that a patient’s imaging exam is “normal” on CT
and MRI in patients clinically having a cerebral
infarction at 2 or 3 weeks. Also, identifying the
fogging effect can prevent the underestimation
35
of the size of the infarct. Hence, in such cases,
attention should be paid to reexamination and the
potential of a follow-up contrast-enhancement
examination.
2.18 Coarse Flecks of Calcification
Feature
In the CT image, a curved strip of hyperdense
calcification is noted within the tumor.
Explanation
Calcification begins with smaller blood vessels
within the tumor, which create deposits along the
tumoral vascular bundle and surrounding tumor
tissue, forming a curved banded structure, which
is a characteristic CT feature of oligodendrogli-
oma (Fig. 2.18).
Discussion
Oligodendrogliomas are glial tumors, predomi-
nantly occurring in adults. Tumor growth is slow,
and the tumor calcification rate is approximately
70–90%, being one of the most prone to calcifi-
cation in the brain [59]. Notably, any glioma that
grows slowly can calcify, where OGs are just one
type that may exhibit slower growth; hence, it is
understandable that calcification is quite common
in these tumors. The calcification of tumors starts
from small blood vessels, and the calcification of
a certain number of tumor vascular bundles and
surrounding tissues leads to the coarse flecks of
calcification of the lesions on CT. On CT, many
studies report coarse flecks of calcification within
the lesion, and as such, coarse flecks of calcifica-
tion can be a characteristic feature of oligoden-
droglioma. However, the calcified regions may
not be clearly shown within smaller oligodendro-
gliomas on CT.  On MRI, the calcification may
be less prominent or not at all visible and may
have variable signal intensity adding to the het-
erogeneous appearance of the tumor. Also, it has
been suggested that c­ alcification is less common
in mixed oligoastrocytoma than in pure oligoden-
droglioma [59].
Their hallmark molecular feature is codele-
tion of the 1p/19q chromosome arms, which is
36 A. M. McKinney et al.

a b

Fig. 2.18 (a–c) Demonstrates a large area of low density, blurred edges, and uneven density in the right frontal lobe,
with multiple curved strips of higher density

not only of diagnostic but also of prognostic and
predictive relevance. Tumors with the 1p/19q
codeletion more commonly show heterogeneous
signal intensity, particularly on T2WI, calcifica-
tions, an indistinct margin, and mildly increased
perfusion and metabolism than 1p/19q intact
tumors [60]. Although multimodal MRI of oli-
godendroglial tumors has a lower contribution
to 1p/19q genotyping compared with cMRI
alone, it greatly improves the accuracy of grad-
ing of these neoplasms. Use of multimodal MRI
could thus provide valuable information in pre-
operative management and treatment decision-
making [61].
2 Brain
2.19 The Tram-Track Sign
Feature
The tram-track sign is seen on skull radiographs
as gyrus-like, curvilinear, and parallel calcifica-
tions. A similar appearance can be seen at CT.
Explanation
The tram-track sign is produced by cortical calci-
fications that result from vascular malformations
of the leptomeninges, as found in patients with
Sturge-Weber syndrome (SWS). The malforma-
tions consist of simple vasculature located in the
interspace between the pia mater and the arach-
noid. A simpler theory suggests that the primary
defect in Sturge-Weber syndrome occurs at the
early stage of formation of the venous vascula-
ture, when there should normally be a persistent
connection between the developing cortical veins
(cerebral circulation) and the superior sagittal
sinus (dura and calvarial circulation). If this con-
nection does not exist during the differentiation
and separation in these two areas of circulation,
the venous outflow from the cerebral cortex will
be impaired. Finally, the cerebral circulation in
the affected areas will be deficient in metabolism,
the cortex underlying the areas of leptomeningeal
malformation usually becomes dysfunctional,
Fig. 2.19  In a 44-year-old female with Sturge-Weber
syndrome (SWS), non-contrast CT (a) shows the typical
tram-track calcifications throughout the leptomeninges.
On MRI, non-contrast FLAIR (b) shows only focal right
37
and thus, the affected parenchyma progressively
atrophies and calcifies (Fig. 2.19).
Discussion
Sturge-Weber syndrome is a rare neurocutaneous
syndrome (a phakomatosis) that includes a facial
port-wine stain and associated leptomeningeal
angiomatosis. Weber demonstrated the char-
acteristic pyriform intracranial calcifications,
indicative of the pial venous malformation, lead-
ing to the tram-track sign [62]. The diagnosis of
Sturge-­Weber syndrome is based on typical clin-
ical symptoms, facial appearance, and character-
istic brain MRI findings. Gyriform calcifications
can be seen on the skull radiographs and clas-
sically described as the “tram-track sign.” CT
is the best modality to detect calcifications and
show the other changes such as cortical atrophy
and leptomeningeal enhancement on the post-
contrast studies. However, CT uses ionizing radi-
ation, and the routine use of CT in children is not
recommended. Therefore, MRI of the brain with
contrast is the recommended imaging modal-
ity of choice. The most common locations are
occipital and posterior parietal/temporal lobes.
The MRI findings depend on the stage of the dis-
ease and perhaps the patient’s age as well. In the
early phase, there is transient hyper-perfusion
frontal-parietal atrophy, but post-contrast FLAIR (c) illus-
trates that the leptomeningeal and dural enhancement
nearly follows the calcifications noted on CT
38
with accelerated myelin maturation, leptomenin-
geal enhancement (seen as serpiginous enhance-
ment along the sulci), and restricted diffusion
(the latter finding if there is associated acute
ischemic event). In the late phase, the increased
T2 signal is visible in the region of gliosis with
decreased pial enhancement and cortical atro-
phy. There is a lack of superficial cortical veins
with prominent deep medullary/subependymal
veins and at times an enlarged choroid plexus.
Gyriform calcifications (having the “tram track”
appearance) are best visualized on T2* or SWI,
appearing as areas of signal loss along the gyri in
a serpentine pattern. FDG-PET may be another
useful modality to study the cerebral metabo-
lism in patients with Sturge-Weber syndrome.
The affected area is usually hypermetabolic in
the early stages, with hypometabolism in the late
stage. PET may be useful in the surgical plan-
ning when cortical resection is required for the
treatment of intractable seizures. Given the high
incidence of epilepsy in patients with SWS, pre-
symptomatic prophylactic treatment has been
proposed. A prospective study has shown pos-
sible improvement in the cognitive impairment
in a group provided with prophylactic treatment,
so the use of anti-­seizure drug therapy prior to
seizure onset can modify the course of severe
epilepsy in SWS patients [63].
Fig. 2.20  Displacement or compression of the pituitary
capillary bed to the left on dynamic post-contrast MRI in
what is termed the “tuft sign.” After 30  seconds of
gadolinium-­based contrast administration, dynamic coro-
A. M. McKinney et al.
2.20 The Tuft Sign
Feature
Pituitary dynamic post-contrast coronal CT can
show a circular, punctate, or ribbon of intense/
hyperdense shadow in the center of the pituitary
gland approximately 10  s after contrast agent
reaching the supra-clinoid of carotid artery.
When it is replaced or oppressed (the tuft sign), it
can diagnose the tiny lesions within the pituitary.
This can also be noted on MRI.
Explanation
Dynamic CT can demonstrate the pressure shift
of the pituitary capillary bed (also called the sec-
ondary capillary bed), which is also called “the
tuft sign,” is an important sign of the diagnosis of
microadenoma. Histologically, vascular plexus is
vascular sinus formed by many small branches
of the hypophyseal-portal vascular system along
the stalk at the distal side of the pituitary gland
(Fig. 2.20).
Discussion
The two sides of the long and short portal veins
of the pituitary gland are capillary networks. One
side is called the primary capillary network, and
the other side is called the secondary capillary
network. The replacement and compression of
nal T1WI demonstrates the tuft of incomplete enhance-
ment of the pituitary on the right side of the gland (arrow,
a), which is confirmed on several minutes delayed post-­
contrast T1WI (arrow, b)
2 Brain
the capillary bed by a tumor on dynamic CT is
known as the tuft sign. This sign is an important
feature in diagnosing pituitary microadenoma
[64]. The superior hypophyseal arteries, of which
the trabecular arteries are among the most impor-
tant branches, arise from the supra-clinoid inter-
nal carotid and posterior cerebral arteries, while
the inferior hypophyseal artery arises from the
cavernous internal carotid artery and anastomo-
ses with its counterpart on the opposite side to
form a ring around the infundibular process of
the neurohypophysis. Components of the inferior
and superior hypophyseal arterial systems anas-
tomose freely. While the epithelial tissue of the
pars distalis receives no direct arterial blood, the
superior hypophyseal arteries supply the median
eminence and the infundibulum. The capillary bed
extending through these two structures is drained
by portal vessels of various lengths which open
into vascular sinusoids lying within the anterior
lobe of the pituitary gland. These sinusoids con-
stitute the secondary plexus of the pituitary portal
system. The portal system is of great functional
importance, since it carries hormone-­ releasing
factors that control the secretory cycles of the
adenohypophysis. Displacement or compression
of the pituitary capillary bed on dynamic CT or
MRI is what we term the “tuft sign,” being an
important feature in the diagnosis of pituitary
microadenomas [65].
The secondary hypophyseal capillary bed
becomes visible on dynamic CT and can begin
to appear approximately 10 seconds after optimal
opacification of the supra-clinoid carotid arteries,
appearing as a rounded vascular tuft in the mid-
line (just anterior to the pituitary stalk) and gen-
erally 3–4 mm in diameter, although occasionally
smaller in caliber. Rarely, the capillary bed
is spread along the upper surface of the gland,
where it appears as a horizontal, band-like den-
sity/intensity. The density-intensity of this vascu-
lar structure is greatest approximately 20 seconds
after optimal opacification of the carotid arteries
or 40  seconds following the beginning of the
contrast administration. Thereafter, the density-­
intensity of the vascular tuft progressively
diminishes, while the pituitary gland enhances
in a centrifugal fashion. Approximately 80  sec-
39
onds after the beginning of the administration,
pituitary enhancement is homogeneous, and the
hypophyseal capillary bed is no longer visible
[65]. Notably, the cavernous sinus enhancement
on coronal MRI or CT occurs very soon (usually
several seconds) of the cavernous internal carotid
artery enhancement. MRI is the first choice
for sellar and parasellar pathologies due to its
­superior soft tissue contrast, multiplanar capa-
bility, and lack of ionizing radiation. MRI also
provides useful information approximately the
relationship of the gland with adjacent anatomi-
cal structures and helps to plan medical or sur-
gical strategy. Dynamic contrast MRI has been
proven to be the best imaging tool in evaluating
pituitary adenomas [66].
2.21 The Infundibulum Sign
Feature
On thin-section non-contrast or contrast-­
enhanced CT or MRI of the sella, the pituitary
stalk is situated within the enlarged sella, being
the infundibulum sign.
Explanation
The infundibulum sign is the manifestation of an
empty sella, partially empty sella on coronal CT
or MRI, where the sellar fossa is filled with CSF
that has water-like attenuation on CT and CSF
signal on MRI, while the pituitary stalk with soft
tissue density/intensity can be displayed within
the enlarged bony sellar fossa. Because of the
enhancement of pituitary stalk after intravenous
administration of contrast, the contrast between
the pituitary stalk and surrounding CSF increases
and becomes clearly displayed (Fig. 2.21).
Discussion
The term empty sella refers to the sella being
occupied by the subarachnoid space. The pitu-
itary tissue either atrophies or is displaced or
compressed and flattened to the posterior and
inferior part of the sellar base. This entity is pres-
ent in about 5–10% of the population, may be
associated with clinical symptoms in the minor-
ity (approximately 20–40%), and is thought to
40
a b
c d
Fig. 2.21  In a patient with an empty sella, the pituitary
stalk in an enlarged sella can be seen on coronal enhanced
CT (a), suggesting that the infundibulum sign is positive.
On 3.0  T MRI in another patient who is a 28-year-old
have a higher incidence in obese patients, hyper-
tensives, and in women, particularly those with
multiple pregnancies [67]. An empty sella can be
classified as primary and secondary according
to the cause of disease. The former has no obvi-
ous etiology, which may be related to congeni-
tal sellar diaphragm development variation, CSF
circulation disorder, and other factors. The latter
is secondary to intrasellar or parasellar surgery,
radiotherapy in sellar region, pituitary apoplexy,
and intrasellar tumors [68]. Thus, an empty sella
may or may not be symptomatic, which depends
on the degree of sellar enlargement, pituitary
displacement, and size of the pituitary gland.
As such, the milder form, aka partially empty
sella, is usually not symptomatic. In addition to
empty sella, there can be solid or cystic masses
that involve the sella, such as arachnoid cyst, cra-
A. M. McKinney et al.
female (b–d), similar findings are noted on pre-contrast
sagittal T1WI (b), T2WI (c), and FLAIR (d), where the
signal surrounding the infundibulum follows CSF bright
signal on T2WI and suppresses on FLAIR
niopharyngioma, Rathke cyst, pituitary adenoma,
and third ventricular diverticulum in sella; the
most common to be confused with the empty sella
is the arachnoid cyst, since both have CSF signal.
In addition to the diagnosis of a symptomatic
empty sella, imaging of an empty sella is often
more important to exclude occupying lesions in
the sella, because the latter can cover the pituitary
stalk, resulting in the infundibulum sign being
negative [69]. Haughton et  al. have opined that
if the infundibulum sign is positive, it strongly
suggests an empty sella. At the same time, the
negative infundibulum sign does not rule out the
diagnosis of an empty sella or partially empty
sella. As such, there are many possible reasons
for a negative infundibulum sign occurring,
including a slim pituitary stalk or pituitary hypo-
plasia, weak enhancement of the pituitary stalk,
2 Brain
motion artifact, poor tissue contrast and spatial
resolution, and too thick of a slice acquisition, or
even the plane of imaging. In addition, the dis-
placement of the pituitary stalk can also lead to
a negative infundibulum sign [70]. MRI has the
advantages of high resolution of soft tissue, no
skeletal artifacts, and multidirectional, multipa-
rameter imaging. It also has high accuracy in the
diagnosis of an empty sella, particularly if utiliz-
ing isotropic imaging with 3D reconstructions.
Generally, non-contrast MRI can make a definite
diagnosis, and it has advantages in differentiating
empty sella from space-­occupying lesions of the
sella. If CT demonstrates an enlarged sella and a
negative infundibulum sign, further examination
by MRI should be performed.
2.22 Target Sign
Feature
On cerebral contrast-enhanced CT, there are
central, punctate, calcified, or spotted intracere-
bral ring-enhancing lesions, being called “target
signs.”
Explanation
Target sign is the feature of a mature tuberculoma
on post-contrast brain CT, characteristically with
focal punctate lesions in the center. Histologically,
the circular zone of enhancement corresponds to
the fibrous capsule containing inflammatory cells.
The non-enhanced zone corresponds to caseous
necrosis, where the mechanism of central spot
enhancement is unclear (Fig. 2.22).
Discussion
Intracranial tuberculosis is caused by the spread
of tuberculosis from other parts of the body via
the blood. The primary TB lesions are more com-
mon in the lungs and may also be extrapulmo-
nary tuberculosis such as lymph nodes, digestive
tract, bones, and kidneys. The disease can also
be secondary to remote primary infections that
have not been noticed, as they occurred many
years prior. The primary lesion in the lung may
be small, the conventional X-ray finding may not
be easy to show, and X-ray positive rate is only
41
Fig. 2.22  A 16-year-old female presented with a target
sign in the right cerebellar hemisphere, later proven to be
a tuberculoma
30%. It has been reported that approximately
10% of tuberculosis patients can be combined
with central nervous system tuberculosis, and its
incidence is directly proportional to the infection
rate of tuberculosis. With the increase in human
immunodeficiency virus (HIV) infection in recent
years, central nervous system tuberculosis has
gradually increased in prevalence in developed
countries, and the central nervous system of HIV-
infected people is more susceptible to infection
by Mycobacterium tuberculosis. Brain tubercu-
losis is a rare form of intracranial tuberculosis. It
refers to a tuberculous granulomatous lesion that
induces mass effect within the brain parenchyma.
Typically, M. tuberculosis spreads via the blood to
the brain parenchyma or, alternatively, via the CSF
along cortical veins and small penetrating arteries
that penetrate the brain parenchyma. The diameter
can be a few millimeters to 8 cm, round or ovoid, or
lobulated, via the fusion of multiple smaller nod-
ules. Cerebral tuberculosis can occur at all ages in
developing countries, more commonly in children
and younger people, while in developed countries,
it occurs mainly in adults. Cerebral tuberculosis
can have multiple or single/solitary lesions, with
differing reports regarding the incidence of the
multiplicity of lesions within the literature.
42
The CT features of brain tuberculosis are
varied, and non-contrast examinations can have
iso-­density (to cerebral parenchyma), high atten-
uation, or low-mixed attenuation; can be single
or multiple, round, or lobulated; can have mass
effect; and are often with moderate to severe
edema surrounding the lesion. On postcontrast-­
enhanced examinations, the lesions usually
show ring enhancement, homogenous or inho-
mogenous nodular enhancement, and a minority
of lesions do not enhance. The ring-enhancing
lesions are mostly continuous, thick, and thin
and have smooth or irregular edges. The tis-
sues in the ring are close to the attenuation or
low attenuation of brain tissue, and few of them
are calcified. Among them, the small circular
enhancement with the central point-like translu-
cent area is called the micro-ring sign. In 1979,
Welchman [71] first reported an enhancing CT
examination of four cases of cerebral tubercu-
losis, including three cases of central point cal-
cification with ring enhancement, and one case
of central point enhancement with ring enhance-
ment; thus, the target sign is considered char-
acteristic of cerebral tuberculosis. The results
of van Dyk’s [72] study supports this conclu-
sion, where lesions having target signs occurred
mainly in children, were less associated with
tuberculous meningitis, and were more sensitive
to drug treatment. On follow-­up CT, the lesions
could disappear completely or significantly,
and the mortality is low, with a good prognosis.
The tuberculosis necrotic material in the tuber-
culoma center may appear calcified, forming a
“target sign,” but the sign is not characteristic,
as the same feature can also be seen in other
granulomatous infectious diseases, such as cere-
bral cysticercosis and toxoplasmosis. Different
degrees of vasogenic edema can also occur in
tuberculomas, being caused by allergic reactions
caused by tuberculosis, where the degree also
reflects the activity of the lesion. The diagnosis
and treatment of brain tuberculoma remain a big
challenge even today. With the development of
imaging technology, CT perfusion and MRS
technology could be more helpful for the early
diagnosis of intracranial tuberculomas [73].
A. M. McKinney et al.
2.23 B
 lack Target Sign and White
Target Sign
Feature
MRI findings of neurocysticercosis (NCC) often
show small round cystic lesions, having a size of
4–6 mm, with T1-dark signal that has a spotlike
appearance of bright/enhancing T1-bright signal,
which is the black target sign; on T2WI, the white
target sign is the focally central T2-dark signal
within the larger area of bright/white high signal
on T2WI.
Explanation
The scolex of cysticercus cellulosae manifests
punctate high signal on T1WI and lower signal
than CSF on T2WI in the early vesicular stage
and colloidal-vesicular stage (Fig. 2.23).
Discussion
Neurocysticercosis (NCC), the central nervous
system form of cysticercosis, is caused by larvae
of the tapeworm Taenia solium and is commonly
associated with seizures, headache, and focal
neurologic deficits. The MR imaging evolution
of parenchymal NCC lesions recognizes four
stages: vesicular, colloidal vesicular, granular
nodular, and nodular calcified [74]. The imaging
findings in neurocysticercosis vary with the stage
of cyst development. The early vesicular stage is
typified by a smooth thin-walled cyst that is CSF-
like on MR image. Edema and contrast enhance-
ment are rare. A mural nodule is often present
that represents the viable larval scolex, the “cyst
with a dot” appearance. When cyst degeneration
begins (colloidal-vesicular stage) and the host
inflammatory response ensues, pericystic edema
and cyst wall enhancement are present. Cyst fluid
appears hyperintense to CSF on MR images dur-
ing this stage. In the healing, or granular nodular,
stage, nonenhanced CT show an iso-attenuated
cyst with a hyper-attenuated and calcified scolex.
Surrounding edema is still present, and enhance-
ment following contrast administration persists.
The residual cyst is isointense to the brain on
T1-weighted images and it is iso- to hypo-intense
on T2-weighted images. A nodular or micro ring
2 Brain
a b
Fig. 2.23  In this patient, there is high signal centrally
within black/lower signal intensity on T1WI (a), which is
the “black target sign”; the “white target sign” is shown as
of enhancement is common at this stage, suggest-
ing granuloma. In the quiescent or residual stage,
small calcified nodules without mass effect and
usually without enhancement are seen. Notably,
multifocal lesions and lesions in different stages
of development are common [75]. The diagno-
sis of NCC is complicated, and neuroimaging
is frequently required for a definitive diagnosis.
Currently, there are no standard treatment guide-
lines for NCC, and treatment is tailored to indi-
vidual cases, depending on factors such as the
location and viability of the cysts. Therapeutic
approaches might include symptomatic therapy,
anthelmintic treatment, or surgery, and often
more than one of these options is needed [76].
2.24 Multilocular Ringlike
Enhancement
Feature
On post-contrast CT or MRI, the wall of a multi-
locular brain abscess is well circumscribed, with
multiple circular or oval rings connected of mul-
43
the T2-darker focus within the larger area of bright/white
hyperintense signal on T2WI (b)
tiple lobulations/loculations; the rings can differ
in size, while the angle of adjacent rings is sharp.
Other names are large ring–small ring sign and
multilocular sign.
Explanation
Granulation tissue is formed around the lesion
during the capsule stage of a brain abscess. If
the wall/border is not complete, there will be a
smaller subordinate lesion (sub-lesion) around
the lesion, where a new abscess is eventually
formed by the sub-lesion. In CT or MRI post-
contrast examinations, the wall of the abscess
significantly enhances, forming numbers of inter-
connected rings of the same size or different sizes
(Fig. 2.24).
Discussion
The multilocular ringlike enhancement is seen
during the formation of the brain abscess and is
a specific sign of a brain abscess. The pathologi-
cal basis is the collapse of the weaker area of the
abscess wall, with the spread and limitation of
inflammation leading to the formation of walls
44 A. M. McKinney et al.

a b

c d

e f

Fig. 2.24 (a, b) Post-contrast CT shows the lesion the left cerebellar hemisphere, and the size of the rings
located in the left frontal lobe. Multiple elliptical rings varies, and they are interconnected. (e, f) Post-contrast
were found to be connected to each other. (c, d) Post-­ T1WI shows multiple interconnected high signal rings of
contrast T1WI shows multiple ring-enhancing lesions in the left frontal lobe, where the size of the rings varies
2 Brain
of sub-abscesses. According to the pathophysiol-
ogy of the disease, the pathological changes can
be divided into two periods: encephalitic period
and capsular period. Acute encephalitis consists
of inflammatory cell infiltration, with brain tis-
sue softening, liquefaction, and necrosis that
ultimately forms the abscess cavity. The develop-
ment of the abscess typically occurs over 2 weeks
to a few months. The surrounding abscess wall is
a membrane formed by the proliferation of gran-
ulation tissue. It is sometimes accompanied by a
wide surrounding rim of edema, causing signifi-
cant mass effect [77].
The lesion is typically located at the deep-
est portions of gray-white matter junction. The
brain abscess subring occurs mostly within the
white matter side of the lesion, with the theoreti-
cal reason being that the blood flow on the white
matter side is less than the cortical side, with
the white matter’s granulation tissue being less,
so the ring’s wall is relatively weak and thus is
easier to break. Post-contrast in a multilocular
abscess usually demonstrates a rim-enhancing
collection connected with one or several small
rings or several rings of similar sizes. The ring
is usually round or oval in shape, and the angle
with the adjacent ring is sharp, which is a distin-
guishing feature of multilocular brain abscesses.
Ring enhancement of the wall of brain abscess
represents granulation tissue; the formation of
granulation tissue is related to the number of
new blood vessels. The blood flow of cerebral
cortex is three to four times more than white
matter subjacent to the cortex, the terminal gran-
ulation tissue is thicker, and the deep portion is
relatively thin, so the spread of inflammation is
located in the deeper portion of an abscess and
the formation of sub-lesion is also often located
at that site. Thus, an abscess can extend deep
into the brain and form a pocket-like structure.
In the encapsulation period of a brain abscess,
granulation tissue forms the wall. If the encap-
sulation is incomplete, the abscess may break
through the defect area and form a sub-abscess
beside it. In post-­contrast CT or MRI, the weak
area of the abscess wall forms a localized defect,
and the adjacent lesions communicate with each
other via a gap, forming a sinus sign. When the
45
abscess wall between the two connected rings is
locally absorbed and the ring wall is incomplete,
a deep ring wall incisural appearance is formed.
The imaging features of brain abscesses are typi-
cal, but they still need to be differentiated from
metastatic tumors or gliomas, which are also in
the differential for rim-enhancing lesions of the
brain [77]. Patterned-approach in the form of
flowcharts for the purpose of quick reference is
intended as a guide to radiologists for quickly
narrowing the list of differentials when faced
with a clinical challenge [78].
2.25 Hoop Sign and Popcorn Sign
Feature
On T2WI or SWI sequences, the low signal ring
around the lesion in the brain parenchyma is
termed a hoop sign, where the blooming effect
of the hypo-intense ring widens gradually with
the increase of time. The popcorn sign is similar,
where the dark periphery is related to susceptibil-
ity/blooming effect on T2WI (sometimes T1WI)
with a slightly brighter center of the lesion.
Explanation
The hoop sign is the MRI finding of a cavernous
hemangioma in the brain parenchyma, where the
low signal ring surrounding the lesion is caused
by the accumulation of hemosiderin around the
lesion, as a result of repeated, small amounts of
chronic bleeding. The hemosiderin ring causes
blooming effects from susceptibility, which are
most prominent at the periphery of the caver-
noma (Fig. 2.25).
Discussion
“Hoop sign” and “popcorn sign” are MRI mani-
festations of cavernous hemangiomas within the
brain parenchyma, characterized by a low signal
ring around the lesion, which gradually widens
over time and can be seen in all sequences, but
it is most apparent on T2WI, GRE T2*WI, and
SWI.  The low signal ring around the lesion is
caused by the accumulation of hemosiderin
around the lesion, as a result of repeated and small
amounts of chronic bleeding. The low signal may
46
Fig. 2.25 (a–c) In a 43-year-old male, axial T2WI (a)
showed a centrally hyperintense lesion in the right cere-
bellum with a hypo-intense, lower signal ring surrounding
the lesion, measuring 10  mm transverse diameter (i.e.,
representing a “hoop sign” or “popcorn sign”). On MRI
with coronal GRE T2*WI (b), the lesion has a greater
degree of blooming (arrow), and measured 13 mm trans-
magnify, extend into the adjacent brain paren-
chyma when imaged with GRE and SWI due to
the “blooming effect” of hemosiderin, effectively
increasing the apparent size of the lesion [79],
and make the signs more obvious. The presence
of this susceptibility effect may make the lesion
appear larger on T2WI, GRE T2*WI, and SWI,
respectively (i.e., SWI may slightly overestimate
the size of the lesion if there is a large amount of
hemosiderin deposited).
A cavernous angioma (aka cavernoma or cav-
ernous hemangioma) is not a true tumor. It is one
of the low-flow congenital vascular malforma-
tions and accounts for 5–13% of intracranial cere-
brovascular malformations [80]. It can occur in
any part of the brain, where a single focus is obvi-
ously more common than multiple. The imaging
manifestations of cavernous angiomas are closely
related to its pathological structure and evolution
process. The main imaging basis of a cavernous
angioma is caused by slow blood flow, deposition
of hemorrhagic components in different stages
following repeated hemorrhages, and secondary
pathological changes such as thrombosis, calcifi-
cation, and gliosis. The characteristics of the MRI
A. M. McKinney et al.
verse diameter; on SWI (c) the lesion measures 16  mm
transverse diameter, demonstrating how susceptibility
effects can change the apparent size of the lesion. Also,
the presence of a large amount of susceptibility effect on
B and C obscures the centrally hyperintense region, so the
hoop and popcorn signs are not as evident
signal primarily depend on the timeline of intra-
tumoral hemorrhage. Repeated small amounts of
hemorrhage are the main factor for the forma-
tion of MRI features such as the “hoop sign” or
the “popcorn sign.” When macrophages are dis-
solved and hemosiderin is deposited around the
lesion, a ring-shaped low signal around the lesion
can occur, which is an identifying characteristic.
The typical MRI images of typical cavernous
angioma are as follows: (1) lesions show different
degrees of mixed-signal clusters; (2) hoop sign
is a rounded low-signal ring in the outer circum-
ference of the tumor, which is black in all imag-
ing sequences, being most evident on T2WI and
SWI; (3) reactive gliosis has long T1 and long T2
signal (i.e., dark on T1WI and bright on T2WI);
(4) there is no brain tissue edema and no obvi-
ous space-­ occupying effect around the tumor;
(5) the lesion enhances with intravenous contrast
to varying degrees. MRI is the preferred method
of examination for cavernomas, especially with
GRE T2*WI and SWI sequences, where the SWI
sequence is optimal, as it can detect likely dou-
ble to triple the number of cavernomas, if mul-
tiple [80]. The use of high field MRI can further
2 Brain
improve the detection of cavernomas by SWI. In
addition, SWI is superior to GRE in the screening
of multifocal familial cavernomatous malforma-
tions. Compared with GRE, SWI can also better
delineate the lesion edge and improve the sensi-
tivity in the setting of familial cavernous angio-
mas. SWI is especially useful in screening for
suspected cavernous angiomas to help solidify
the clinical diagnosis.
2.26 Ivy Sign
Feature
On T1WI post-contrast images and FLAIR
images, the signs appear as linear high-signal
shadows that are continuous or discontinuous
along the sulci and subarachnoid space.
Explanation
The ivy sign is seen in Moya-moya disease, from
diffusely prominent leptomeninges akin to ivy
crawling along stones. This characteristic appear-
ance of enhancement arises from the filling of the
leptomeningeal reticular formation following
chronic internal carotid artery (ICA) and/or ante-
rior cerebral artery (ACA) and middle cerebral
artery (MCA) occlusions; i.e., chronic anterior
circulation occlusion near the ICA terminus. The
reason for the high signal of the soft meninges
on the FLAIR image is more complicated. It is
probably due to the slow blood flow of the lep-
tomeninges attempting collateral flow, and the
hyperemia of the leptomeninges is also one of
the reasons for the high signal on FLAIR images
(Fig. 2.26).
Discussion
The “ivy sign” described in MDD is a finding
on postcontrast MRI images. This finding is
described in both post-contrast T1WI and FLAIR
images. On post-contrast T1WI images, the ivy
sign is prominently found along the cortical sur-
faces and potentially partially within the sulci,
due to the development of leptomeningeal collat-
erals, via an increased number of leptomeningeal
vascular network formations. The signal increase
within or along the sulci may also be evident to
47
a lesser degree on non-contrast FLAIR, which
originates from the slow arterial flow of the lep-
tomeningeal collateral vascular structures. This
leptomeningeal formation is prominent along
the cortical surface and resembles ivy growing
on a rock and, thus, this appearance is termed
the “ivy sign.” Moya-moya disease (MDD) is an
idiopathic disease characterized by progressive
stenosis and collateral development of the distal
internal carotid arteries. It is observed as being
1.8–2.2 times more common in women than in
men. Bimodal age in MDD has been reported to
show high peaks at ages over 5 years’ and lower
peaks at the age of 40  years. MDD shows dif-
ferent clinical features in children and adults.
While it typically presents with subarachnoid
and intraparenchymal bleeding in adults, in chil-
dren, it presents with transient ischemic attacks
with infarcts developing predominantly in the
frontal lobe. The typical symptoms in children
include monoparesis, hemiparesis, aphasia, and
dysarthria.
Studies evaluating the ivy sign on FLAIR MRI
in pediatric patients with MMD showed a strong
positive correlation between the hemispheric
TIS and the severity of the clinical hemispheric
symptoms. Also, a change in postoperative ivy
sign appearance can be an indicator of effec-
tive cerebral reperfusion in MMD [81]. Hence,
the prominence of leptomeningeal enhancement
overall appears to relate to the degree of collateral
perfusion, which is a current focus of research
involving dynamic CT and MR perfusion and
CT and MR angiography. The implementation of
arterial spin labeling (ASL) in a clinical setting
and the development of ASL can be considered to
have become mature and ready for clinical prime
time. Quantification of ASL as well as on new
technological developments of ASL for perfusion
imaging and flow territory mapping is the current
focus [82].
2.27 Butterfly-Like Lesions
Feature
The white matter around the trigone of the lat-
eral ventricle is symmetrical with a large area of
48
a b
Fig. 2.26 (a) Enhancement in an ivy-like fashion
(arrows) along the leptomeninges of the frontal sulci on
post-contrast T1WI, (b) FLAIR post-contrast images dem-
onstrating a similar appearance as in a. (c) CTA of the
head showed occlusion of the right internal carotid artery
reduced attenuation on CT. It has long T1 (dark)
and T2 (bright) signal on MRI; the lesions on
both sides are connected by the compression
of the corpus callosum, with a “butterfly-like”
distribution.
Explanation
Butterfly-like lesions are typical signs of CT/
MRI in children type with adrenoleukodystrophy
(Fig. 2.27).
A. M. McKinney et al.
and stenosis and occlusion of the lumen of bilateral ante-
rior cerebral artery, proximal middle cerebral artery, and
proximal posterior cerebral artery. Multiple hyperplastic
vascular network formation can be seen around, typical of
Moya-moya disease
Discussion
Adrenoleukodystrophy (ALD) is an X-linked
recessive hereditary disease that mainly affects
the white matter and adrenal glands and is the
most common form of leukodystrophy. The
disease is mainly seen in children, albeit occa-
sionally in adults, where affected patients are
almost all male and females are typically carriers
(heterozygous). They may exhibit symptoms of
neurologic deficits, mainly manifested by spinal
2 Brain 49

system tissues [85]. Most patients with cerebral

adrenoleukodystrophy die within a decade after
they receive the diagnosis if they are not treated
with hematopoietic stem-cell transplantation.
The children with ALD have characteris-
tic MRI features, where MRI depicts lesions
better than CT.  The lesions have low signal on
T1WI and high signal on T2WI. The high signal
pathologically represents the areas of myelin
loss (demyelination) and vasogenic edema. The
post-­contrast enhancing regions on MRI or CT
correspond to the areas of active demyelination
(so-called leading edge) and are characterized
by peripheral enhancement. The “butterfly”
lesions on MRI show a clearer distribution, best
depicted on FLAIR or T2WI. The lesions are dis-
tributed along the nerve conduction bundle, and
the lesions on both sides are connected by the
corpus callosum; typically, involvement begins
Fig. 2.27  A 8-year-old boy with bilateral temporal-pari- in the splenium of the corpus callosum. In the
etal-occipital lobe adrenoleukodystrophy on FLAIR MRI majority of patients, as the disease progresses,
has a symmetrical distribution of T2-hyperintensity poste-
riorly in the cerebrum, resembling a “butterfly” shape
the demyelinating lesions spread from posterior
to anterior, and the white matter region of the
parietal lobes gradually migrates to the temporal
cord involvement or mild pyramidal signs and lobes, basal nuclei, and frontal lobes and diffuses
urinary disorders. ALD is usually divided into downward to affect the brain stem. The afore-
four types: children, youth, adults, and adreno-­ mentioned appearance of posterior-predominant
myeloneuropathy. Allogeneic transplantation is involvement is present in the majority (80–90%),
the only effective therapy for cerebral adreno- whereas the minority (15–20%) have anterior
leukodystrophy that has been identified to date, predominance affect the genu of the corpus cal-
and it is more likely to be effective if it is per- losum and periventricular white matter and spar-
formed at an early stage of neurodegeneration. ing structures posteriorly in the early stages. In
Gene therapy with autologous hematopoietic the advanced stage, the lesions have much lower
stem cells has been investigated as an alternative T1WI signal and brighter T2WI signal, and at the
to allogeneic hematopoietic stem-cell transplan- late stage do not enhance on postcontrast T1WI,
tation [83]. Early results of this study suggest with resultant brain atrophy. Small calcifications
that Lenti-D gene therapy may be a safe and may occur, which are not easy to visualize on
effective alternative to allogeneic stem-cell trans- MRI.  Of note, recent research using advanced
plantation in boys with early-stage cerebral adre- MR imaging, including MR perfusion, and dif-
noleukodystrophy [84]. Adrenoleukodystrophy fusion tensor imaging (DTI) have shown that
is an X-linked genetic disease that is caused by the pretreatment (i.e., preceding transplantation)
a defect in the gene ABCD1, which encodes the Loes score measured on FLAIR/T2WI, the MRP
peroxisomal ABC half-transporter ALD protein. scores of the splenium, and certain DTI measures
Mutations in ABCD1 result in abnormal break- may predict the eventual patient outcomes [86,
down of very-long-chain fatty acids, a process 87]. In addition to adrenal leukodystrophy, but-
that predominantly affects adrenal and nervous-­ terfly lesions can also occur when central nervous
50
system lymphoma involving the corpus callo-
sum and spreading to the bilateral hemispheres.
Butterfly lesions can also occur when gliomas
originating in the corpus callosum invade the
cerebral hemispheres on both sides or when one
side of the cerebral hemisphere glioma invades
the contralateral cerebral hemisphere through
the corpus. However, in the setting of such “but-
terfly” lesions of high-grade gliomas, or alter-
natively tumefactive demyelinating lesions (i.e.
multiple sclerosis), the edema and accompanying
enhancement is usually overt and pronounced,
whereas edema and enhancement may be lack-
ing in ALD, and the cerebrum may actually be
significantly atrophied in cerebral ALD.
2.28 The Mount Fuji Sign
Feature
The mount Fuji sign is seen on CT scan as bilat-
eral subdural low density cause compression
and separation of the frontal lobes, the gaseous
tension on both sides make the frontal lobes
move back and the frontal lobes collapse and the
­interhemispheric space between frontal parietal
lobe expand,which looks like the Fujiyama (in
Japan).
Explanation
The low-density shadow is caused by the entry
of air into the skull, the condition caused by the
iatrogenic or non-iatrogenic disruption which
makes the skull base or calvaria rupture. The ten-
sion pneumocephalus leads to increased air pres-
sure within the subdural space. The increase of
air pressure is resembling the principle of ball
valve, air enters the subdural space through the
skull base or cranial fissure, and the way out is
blocked. Increased pressure leads to occupying
effect and compression of the frontal lobes. The
presence of air between the frontal-parietal lobe
suggests that the pressure of the air is at least
greater than that of the surface tension of cerebro-
spinal fluid between the frontal lobes (Fig. 2.28).
Discussion
The Mount Fuji sign on CT of the brain is use-
ful indiscriminating tension pneumocephalus
A. M. McKinney et al.
Fig. 2.28  A 71-year-old-woman. Axial CT scan demon-
strating a massive accumulation of air compressing the
frontal lobes
from non-tension pneumocephalus. Tension
­pneumocephalus can be a neurosurgical emer-
gency, unlike non-tension pneumocephalus.
Tension pneumocephalus occurs most com-
monly after the neurosurgical evacuation of a
subdural hematoma. The prevalence of tension
pneumocephalus following the evacuation of
chronic subdural hematomas has been reported
from 2.5% to 16%. Tension pneumocephalus
can also occur as a result of skull base surgery,
paranasal sinus surgery, posterior fossa surgery
in the sitting position, or head trauma. To diag-
nose tension pneumocephalus, the CT findings
should correlate with clinical signs of deteriora-
tion [88]. Pneumocephalus is most easily diag-
nosed on CT, which can detect quantities of air
as low as 0.5  ml. Air appears dark black (that
is, darker than CSF) with attenuation values of
−1000 Hounsfield units and will have a differ-
ent distribution pattern depending on the local-
ization. Depending on the underlying cause, the
intracranial air can be distributed in the epidural
space, subdural space or subarachnoid space,
intraventricular or intracerebral, or a combina-
tion of these [89]. Tension pneumocephalus
treatment includes a complex of manipulations
directed to removing of intracranial air mass
effect, adequate skull base defects closure, and
2 Brain 51

secondary posttraumatic meningitis prophy- Explanation

laxis. Initial treatment is usually conservative,
including bed rest in an upright position, high
concentration oxygen, avoidance of maneuvers
that might increase intra-sinus pressure (such
as nose-blowing or valsalva maneuver), and
antibiotics if there is evidence of meningism.
Surgical treatment is indicated when there is
recurrent pneumocephalus or signs of increas-
ing ICP suggesting the development of tension
pneumocephalus. Surgical options include direct
insertion of a subdural drain connected to under-
water seal or, indirectly, with the use of a saline-
primed Camino bolt [90].
2.29 The Eye of the Tiger Sign
Feature
When the eye of the tiger sign is found on T2WI
MRI, it shows significant hypo-intensity in the
globus pallidus bilaterally. In the center of the
hypo-intensity area, a hyperintensity area is vis-
ible on the anterio-medial side of the globus pal-
lidus, which is a tiger-eye appearance.
The eye of the tiger sign is most common in pan-
tothenate kinase-associated neurodegeneration,
or PKAN (formerly called Hallervorden-Spatz
syndrome). The significant ring-shaped hypo-­
intensity on T2WI in the globus pallidus is due to
excessive iron deposition (Fig. 2.29).
Discussion
PKAN involves extrapyramidal dysfunction
and a pathological triad (i.e., iron deposition,
axonal globules, and gliosis of the globus pal-
lidus). PKAN is a familial (autosomal reces-
sive) neurodegenerative disorder in children
that is characterized by stiffness, dystonia,
disruption of standard reflexes, and progres-
sive dementia. Mutations in the pantothenate
kinase gene (PANK2) have been reported to
be the cause of the neurodegeneration, at the
chromosomal locus 20p12.3-p13 [91]. The pan-
tothenate kinase is quite metabolically active
in the mitochondria, and this enzyme is also
vital in producing the molecule coenzyme A. In
patients with PKAN, the iron deposits increase
pathologically and rapidly disproportionate to

Fig. 2.29  Axial T2WI (a) of a 49-year-old female with giving an eye-of-the-tiger sign (arrows). On SWI (b),
worsening tremors showed bilateral symmetrical hypo-­ there is quite prominent iron deposition in that location
intensity in the globi pallidi with central hyperintensity,
52 A. M. McKinney et al.

the patient’s age, while iron levels in the blood adolescents, or young adults, such as with PKAN
and CSF remain normal. Superparamagnetic or INAD, this distinction in the degree of iron
iron materials (such as ferritin) have unpaired deposition for age should not be difficult, par-
electrons, which can lead to increased mag- ticularly on SWI.
netic sensitivity and hypo-intensity on T2WI.
Thus, the central hyperintensity in the globus
pallidus is caused by gliosis, increased water 2.30 Aura Sign
content, and disintegration of neurons and for-
mation of neurofibrous reticulum vacuoles, and Feature
central T2-hyperintensity of gliosis/edema is The aura sign can be seen on T1WI or post-­
surrounded by the T2-dark signal of the acceler- contrast T1WI, showing a bright ringlike high
ated iron deposition in the globi pallidi. The eye signal around the head of the patient.
of the tiger sign is the most common manifesta-
tion of PKAN, but it can also be seen in other Explanation
extrapyramidal Parkinson’s diseases and other When using clay or black beeswax to design
disorders of neurodegeneration from brain iron curly hair or long hair strands, the iron oxide
accumulation (NBIA’s), including cortico-basal content in clay or black beeswax can cause para-
ganglion degeneration, early-onset levodopa-­ magnetic effect. In MRI, T1WI or post-contrast
susceptible Parkinson’s syndrome, Steele-­ T1WI shows a bright ring high signal. Therefore,
Richardson Olszewski syndrome (progressive the aura sign is a kind of hair artifact in fact.
supranuclear paralysis), multisystem atro-
phy, neuroferritinopathy, aceruloplasminemia, Discussion
Kufor-­Rakeb syndrome, infantile neuroaxonal Duncan [94] first reported the aura sign of MRI
dystrophy (INAD), and Woodhouse-Sakati syn- in 2001. He believed that this kind of hair arti-
drome, to name a few. fact was related to national culture. It was mainly
Before the appearance of MRI, the diagnosis seen in women of southern African tribes, espe-
could only be suspected by clinical data, and the cially female healers, who often wove their hair
final diagnosis is dependent on autopsy. CT can with a local brown-red fabric made of clay,
only show nonspecific changes such as striatal because the ochre clay contained a large amount
atrophy and globus pallidus mineralization [92]. of iron oxide. The obvious paramagnetic effect
However, MRI with gradient-echo T2*WI or even was formed around the skull, which made the
better, SWI, can demonstrate the findings well; T1-weighted image of the patient show a bright
the eye of the tiger sign on MRI can solidify the ring around the skull. McKinstry et al. [95] had
diagnosis of PKAN or other NBIAs. As a certain also seen similar artifacts of MRI caused by
degree of normal iron deposition occurs with hair. Curly or long-haired hairstyles are popu-
increasing patient age, one way to discriminate lar among black American groups. Hairstylists
PKAN and other NBIAs from normal elderly use colorless beeswax or black beeswax colored
patients is the degree and location: the globus with iron oxide, which can cause paramagnetic
pallidus in adults and elderly should have more effects due to the iron oxide contained in black
than the surrounding portions of the lentiform beeswax. Therefore, the curled hair of these
nuclei and the caudate nucleus; if the caudate patients showed annular high signal artifacts
nucleus and lateral lentiform nucleus (the puta- on MRI images. Most radiologists know that
men) are darker than the globus pallidus, then iron-­containing pigments used in eye makeup
NBIA is a consideration [93]. Note: the putamen can cause MRI artifacts, but they do not know
and dentate nuclei can appear nearly as dark as much about the aura sign, because they have
the globi pallidi in the elderly at 70-plus years’ certain characteristics of ethnic and geographi-
age, so clinical correlation may be necessary, to cal distribution, so radiologists should also know
evaluate other structures. However, in children, something about it [96]. While the ferromag-
2 Brain
netic properties of metallic objects, implantable
medical devices, and cosmetics are well known,
sand is not generally considered a consequen-
tial substance. Beaches in specific geographic
regions have a propensity for ferromagnetic sand
because of their geologic history. MRI facili-
ties in areas where ferromagnetic sand is found
consider educating technologists and screening
patients for recent black sand exposure prior to
scanning [97].
2.31 Basilar Artery
Encasement Sign
Feature
Brain stem tumors can protrude forward into the
prepontine region and encase basilar artery. When
this occurs, it may have the shape of a circular or
linear with low density or low signal shadow on
transverse or sagittal sections of CT or MRI.
Explanation
Larger brain stem tumors or tumors originating
from the anterior part of the brain stem protrude
forward into the prepontine cistern, situated
just dorsal to the clivus. The cistern becomes
narrowed or occluded, and the basilar artery is
pushed forward and enclosed, forming a basilar
artery encasement sign (Fig. 2.30).
Discussion
Tumors originating in the pons, midbrain, and
medulla oblongata are collectively referred to
as brain stem tumors. The most common brain
stem tumor is astrocytoma, which is more com-
mon in children. Brain stem gliomas account for
10–25% of intracranial neoplasms in childhood
[98]. The growth patterns of brain stem tumors
are different, and Epstein et  al. have classi-
fied them into exogenous, disseminated, and
endogenous types. Exogenous tumors mostly
protrude from the brain stem. Disseminated
tumors spread along the longitudinal axis of
the brain stem, reaching up to the dorsal thala-
mus, the cerebellum, or the posterior part of the
third ventricle, and can travel even down to the
upper thoracic segment of the spinal cord. The
53
endogenous type is more common, in which
the tumor causes localized expansion of brain
stem or diffuses infiltrative growth. According
to the scope of its invasion, it can be divided
into the: limited type, diffuse type, or extended
neck type [99].
MRI has a unique value in the evaluation and
diagnosis of brain stem glioma. Its advantages
over other imaging modalities mainly include
the following: (1) Demonstration of the degree
of brain stem enlargement and swelling, which
can be expressed as a symmetry increase in size
with a round or fusiform configuration, which
can also increase the degree of asymmetry, and
the mass protrudes in all directions. (2) Signal
changes usually occur relative to the rest of the
brain stem, where gliomas on T1WI have slightly
lower signal or isointense signal relative to the
remainder of the brain stem, or occasionally
have mixed signals, being a mixture of hyper-
and hypo-intense signal on T2WI.  For children
with diffuse intrinsic pontine glioma, T2WI
demonstrates the greatest signal intensity vari-
ance suggesting tumor heterogeneity, and within
this heterogeneity, T2WI hypo-intensity is cor-
related with increased cellularity [100]. There
may be mild-moderate vasogenic edema around
the tumor, having T2- or FLAIR hyperintensity,
where the T2-bright tumor signal may not be
easy to distinguish from the vasogenic edema.
Cystic regions are also sometimes present,
which have lower T1WI signal and higher T2WI
signal. (3) On post-contrast, the larger tumors
are usually rounded with mass effect on adja-
cent structures if large enough, potentially with
peripheral/annular enhancement that is caused
by tumor liquefaction and necrosis (present in a
minority, and usually in larger tumors). On post-
contrast T1WI, if there is hypo-­intensity that is
non-enhancing surrounding the annular areas of
enhancement, this represents peritumoral edema.
(4) Regarding peritumoral edema, larger tumors
may induce disappearance of the posterior bor-
der of the pons, with deformation and displace-
ment of the fourth ventricle, and effacement of
the adjacent basal cisterns and quadrigeminal
plate cistern. (5) Regarding basilar artery encase-
ment sign, when the brain stem tumor advances
54
a b
Fig. 2.30  A 5-year-old boy with brain stem glioma with
obstructive hydrocephalus. The pons is significantly
enlarged and deformed, showing a nearly circular shape
with uneven signal shadows of T1-dark signal on axial
T1WI (a), and T2-bright signal on axial T2WI (b). The
anteriorly, the sign may occur (approximately
40–45%); some scholars believe that this sign
is one of the characteristic manifestations of a
larger brain stem tumor (such as those >2 cm in
size). Therefore, increased signal on T2WI and
marked enlargement of the pons with engulf-
ment of the basilar artery are typical imaging
findings of larger brain stem tumors. The pres-
A. M. McKinney et al.
fourth ventricle is compressed from mass effect, and the
cerebral aqueduct and the surrounding cisterns were nar-
rowed due to the compression, also depicted on sagittal
T2WI (c)
ence of enhancement on post-contrast MRI is
variable but, when present, is more concerning
for a higher grade or infiltrative tumor, poten-
tially with malignant degeneration, especially
if there is peripheral enhancement with necro-
sis and/or reduced diffusion on DWI.  Tumor
pseudo-­progression has been reported in brain
stem gliomas, which is characterized by an
2 Brain
increase in mass effect post-therapy, which usu-
ally occurs from 1.5  months to 2.5  years after
radiation therapy (mean 6  months); notably,
pseudo-­progression is sometimes associated
with new or worsening symptoms, being depen-
dent on the location of their tumor [101].
2.32 The Tau Sign
Feature
The tau sign is noted on coronal or sagittal MRI
images of the brain. The shape of the intracranial
artery near the sella and sphenoid’s clinoid pro-
cesses is similar to the Greek letter tau.
Explanation
In patients with persistent trigeminal arteries,
a sagittal MRI can reveal abnormal flow voids
that represent an abnormal carotid-basilar anas-
tomosis of blood vessels between the cavernous
segment of the internal carotid artery and the
basilar artery. The tau sign refers to a rare phe-
nomenon of a flow void formed by the saddle
anterior internal carotid artery and persistent
trigeminal artery on either paramedian sagit-
tal MRI or on maximum intensity projections
(MIP) reconstructions from MR angiography
(MRA) (Fig. 2.31).
Discussion
Persistent trigeminal artery (PTA), also known
as the persistent primitive trigeminal artery, is
a relatively uncommon anomalous variant con-
sisting of an anastomosis between the internal
carotid artery (ICA) and basilar artery. PTA is
the most common of the four primitive anasto-
moses that may exist between the carotid and
vertebrobasilar system that can persist in adults,
with an estimated angiographic incidence of
0.1–1.0%, and represent over 90% of persistent
carotid-­
vertebrobasilar anastomoses. The other
such anastomoses are the persistent otic, hypo-
glossal, and proatlantal intersegmental arter-
ies [102–104]. PTA often begins in the anterior
portion of the cavernous ICA, where the anas-
tomotic vessel (the PTA) often joins the basilar
at a point located between the superior cerebel-
55
lar artery and the origin of the anterior inferior
cerebellar artery. According to the characteristics
of angiography, Saltzman classified PTA into
three types. Type I: PTA supplies the entire dis-
tal vertebral-basilar system, where the proximal
basilar is often dysplastic with a lack of a pos-
terior communicating artery. Type II: PTA sup-
plies the circulation of both sides of the superior
cerebellar arteries, and the ipsilateral side of the
posterior cerebral artery is supplied by the devel-
oped posterior ­communicating artery. Type III:
PTA does not combine with the basilar artery,
but rather merges with the persistent longitudinal
neural arteries to supply the cerebellar artery on
the same side [103].
The clinical significance of PTA remains con-
troversial. Most cases have been found inciden-
tally on MRI, angiography, or autopsy. But there
are also reports that persistent trigeminal artery
can occasionally cause trigeminal neuralgia and
oculomotor paresis, even without a concomitant
aneurysm being present. Thus, it is important to
identify the presence of a PTA in the events that a
neurovascular intervention is necessary. Of note,
the persistent primitive trigeminal artery can also
become the collateral circulation pathway for
vascular obstructive disease.
2.33 The Reversal Sign
Feature
The CT sign of hypoxic-ischemic cerebral injury
in children manifests the attenuation of cerebral
cortex diffusely decreased and relatively high
attenuation of the basal nucleus, dorsal thalamus,
brain stem, and cerebellum.
Explanation
The reversal sign is a CT-based manifestation of
hypoxic-ischemic injury (HII) to the cerebrum
injury in children. There is a decrease in the atten-
uation of the cerebral cortex, caused by nerve cell
degeneration, necrosis, and axonal degeneration
following hypoxic-ischemic injury. There may
be resultant hyper-attenuation of the basal nuclei,
dorsal thalami, and the brain stem caused by a
combination of many factors, perhaps related
56
Fig. 2.31 (a, b) Coronal T2WI and MRA reformat (PA
view) demonstrate an artery connecting basilar artery
trunk below superior cerebellar artery origin, with hypo-
plasia of the vertebral-basilar junction below the site of
to the contrast of these structures with the mild
edema in the affected cortical regions, bleed-
ing at sites of vascular stasis, selective necrosis
of certain neural structures, or the existence of
calcium-containing neurons (Fig. 2.32).
Discussion
Han et al. first defined “reversal sign” as diffuse
loss of gray-white matter attenuation in chil-
dren with an unclear or disappearing boundary
between gray and white matter and a reversal of
the attenuation in gray and white matter, with
relative increasing attenuation of the dorsal
thalami, brain stem, and cerebellum [105]. The
reversal sign indicates diffuse cerebral injury
in patients who have suffered an ischemic/
anoxic insult and can be seen on CT of patients
with conditions such as birth asphyxia, head
trauma, status epilepticus, drowning, strangu-
lation, carbon monoxide poisoning, infection/
A. M. McKinney et al.
anastomosis in a patient with a left-sided persistent tri-
geminal artery. Hence, both the superior cerebellar arter-
ies and posterior cerebral arteries originate from the distal
basilar artery
inflammation of the brain and its meninges,
hypothermia, and other causes of global cere-
bral ischemia [106, 107]. The presence of a
reversal sign indicates irreversible damaged
neural tissue and is associated with poor prog-
nosis. Children displaying reversal signs on CT
have a high mortality rate (35%) [106], and
there is an increased incidence of profound
neurologic deficits with developmental delay
in those who survive. The III and IV layers of
nerve cells of the cerebral cortex are the most
vulnerable following hypoxic-ischemic injury.
Eosinophilic denaturation and coagulation
necrosis occur in cerebral cortical nerve cells
after more than 12 hours after ischemia, where
axonal cells begin to undergo denaturation at
2–3 days, glioblasts, fat granules, and neovas-
cularization occur at approximately 7 days, and
the formation of cavities and softening occur at
2–4 weeks. Regarding the attenuation increase
2 Brain 57

caused by the damage of basal nuclei and dorsal
thalami, the hyper-attenuation is associated with
the increased neovascularization that occurs
1–2  weeks after severe ischemia or relates to
the congestion of deep medullary veins in the
white matter of the brain, or the attenuation
is not actually increased, rather representing
normal brain tissue attenuation. Nonetheless,
regardless of etiology and pathophysiology, the
“reversal sign” is usually associated with poor
prognosis and irreversible brain injury.
According to the onset time of the reversal
sign, it is divided into two phases: acute and
chronic. The acute phase refers to the rever-
sal sign that occurs at the time of CT, while the
chronic phase demonstrates diffuse brain atro-
phy or encephalomalacia, which represents the
sequela of the reversal sign. Hence, the reversal
sign is an important CT sign of severe hypoxic-­
ischemic cerebral injury in children or in adults,
but it is not specific to an etiology. The cause can
be determined by means of the clinical history,
laboratory examination, and CT characteristics;
especially, it is important to note the chronic
imaging findings and sequelae of the reversal sign
as complications of hypoxic-ischemic encepha-
lopathy. The chronic reversal sign is character-
ized on NCCT by diffuse low attenuation of the
hemispheres, where the attenuation of central
regions such as basal ganglia and dorsal thalami
are markedly increased. Of note, common com-
plications of hypoxic ischemic ­encephalopathy
are diffuse brain atrophy and occasionally
hydrocephalus.
2.34 The False Falx Sign
Feature
Linear attenuation with an increased shadow-
ing in the interhemispheric fissure with a clear
boundary. The CT attenuation in this scenario of
“pseudo-hemorrhage” is lower than that of actual
hemorrhage.

a b

Fig. 2.32  The reversal sign represents severe anoxic-­ on non-contrast CT (a) and relative preservation of nor-
ischemic brain injury and can include diffuse, symmetric mal to high attenuation of central structures, such as bilat-
bilateral reversal of gray-white matter density relationship eral thalami (b)
58 A. M. McKinney et al.

Explanation images (the slope of the falx being best visualized

In patients with cerebral edema, there may be on coronal images) makes the falx cerebri and the
hyperemia of falx cerebri and/or venous sinuses, straight sinus appear to form a Y-shaped struc-
which may appear as linear high-attenuation in ture; the upper slice sections include the entire
interhemispheric fissure, which is false falx sign. falx cerebri. The appearance and visualization of
It should not be mistaken for subarachnoid hem- the falx cerebri on CT depend on its attenuation
orrhage (SAH) (Fig. 2.33). difference from neighboring structures as well
as its orientation to the section plane. Hence, if
Discussion there are low attenuation tissue and fluid around
“The false falx sign” manifests as linear high it, the un-enhancing falx cerebri can be identi-
attenuation shadow in the interhemispheric fis- fied and may even appear slightly hyperdense.
sure cistern, which can be seen in patient with Notably, more than 50% of children aged 4 years
anoxic brain injury and many other causes of dif- or younger have a complete or partial falx cere-
fuse cerebral edema [108]. In anoxic (hypoxic-­ bri that is visible on NCCT examinations. NCCT
ischemic) brain injury, the high attenuation with is widely accepted as the imaging standard for
adjacent shadowing appearance results from a the diagnosis of acute SAH, as it has a sensitivity
combination of a loss of cerebral gray-white and specificity that are reported to be as high as
differentiation, with narrowing and effacement 100% in the first 6 hours after a severe headache
of the subarachnoid spaces, and correspond- of acute onset [110]. Hyperemia of the falx cere-
ing engorgement of the superficial pial veins. It bri and venous sinus, especially in patients with
should not be mistaken for subarachnoid hemor- cerebral edema, may show the linear high attenu-
rhage. The CT attenuation values in pseudo-SAH ation shadow in the interhemispheric fissure,
are generally 30–45  HU but are 60–70  in true representing the false falx sign, which should not
SAH [109]. be mistaken for SAH. The differential diagnosis
Non-contrast CT (NCCT) at the level of the top or possible causes of this finding on NCCT are
of the tentorium cerebelli usually shows the pos- (1) a relative high attenuation boundary from the
terior falx cerebri, where the sloping falx on axial hyperemia in falx cerebri and venous sinuses, (2)

a b

Fig. 2.33  In the patient with ischemia and hypoxia, the cerebral hemispheric fissure (arrows), representing the
brain tissue is obviously swollen on axial non-contrast CT false falx sign, and should not be mistaken as subarach-
(a, b), and the linear high-attenuation shadow appears in noid hemorrhage
2 Brain 59

the CT attenuation values are also lower than that
in other intracranial hemorrhage sites of SAH,
(3) the hyperemia in a venous sinus can form a
solid triangular sign, where the high-attenuation
hemorrhage shadows on both sides of the tri-
angle (the base of the hyper-­attenuation being
the skull’s inner table) and presents as an empty
(black) triangle sign. Additional differentiating
features are a diffuse loss of gray-white differ-
entiation and effaced basal cisterns, indicating
diffuse cerebral edema [109]. MRI is a valuable
tool in the diagnosis of SAH, and SWI or FLAIR
sequence has higher sensitivity than CT in detect-
ing SAH [110], especially in the subacute phase
of SAH.
2.35 The Interpeduncular
Fossa Sign
Feature
On non-contrast CT (NCCT) examination, there
is a high attenuation shadow in interpeduncu-
lar fossa/cistern (IPF) in the form of an inverted
triangle, which is called interpeduncular fossa
sign.
the most fatal form of acute stroke, thus account-
ing for 5% of the total number of strokes. Many
survivors often later develop severe cognitive
impairment; thus, it can difficult to determine
the clinical prognosis immediately following
acute SAH, but it is critical to immediately iden-
tify signs of SAH on neuroimaging. Clinically,
the disease is generally divided into two types,
spontaneous and traumatic. Spontaneous can
be further divided into primary and second-
ary. When bleeding from vessels within the pia
along the surface of the brain enters directly into
the subarachnoid space, it is primary, whereas
intraventricular hemorrhage, considered to be
the hemorrhage from the brain tissue into the
ventricular system (also part of the subarach-
noid space), is considered secondary. The main
causes of SAH include ruptured intracranial
aneurysms, cerebrovascular malformations, fol-
lowed by hypertension, atherosclerosis, Moya-
moya disease, hematological diseases, and brain
tumors. As mentioned above, aneurysmal SAH
is the most devastating form of stroke. There
are many pathological changes after aneurysm

Explanation
The interpeduncular fossa sign suggests the pres-
ence of subarachnoid hemorrhage (SAH). The
interpeduncular fossa is situated between the left
and right cerebral peduncles, and the IPF appears
as an inverted triangle; at the anterior edge of the
IPF is the suprasellar cistern. The density of the
CSF in the interpeduncular fossa under normal
conditions is akin to that of water (−5 to 10 HU);
in the setting of subarachnoid hemorrhage, with
the NCCT obtained in the supine position, the
hemorrhage tends to accumulate dependently in
the IPF, resulting in interpeduncular fossa sign
(Fig. 2.34).

Discussion
SAH is a clinical syndrome caused by the rup-
ture of blood vessels in the brain or superficial
parts of the brain, leading to direct hemorrhage Fig. 2.34  A 38-year-old man involved in motor vehicle
into the subarachnoid space. It is an acute dis- trauma. Cranial NCCT reveals midline hemorrhage in the
ease, with high morbidity and mortality, being interpeduncular cistern
60
rupture, including hydrocephalus, endothelial
cell and neuronal apoptosis, cerebral edema, and
blood-brain barrier integrity loss with potential
microthrombus formation, neuronal depolariza-
tion, and vasospasm (usually the latter in the late
acute or early subacute phase) [111].
In SAH patients, the most common accumu-
lation sites of hemorrhage on imaging are usu-
ally within lateral/Sylvian fissures, cortical sulci,
and basal cisterns (including suprasellar cistern,
ambient cistern, and quadrigeminal plate cisterns,
to name a few); actually, the site of hemorrhage
most likely depends on the site of vascular rup-
ture (in the setting of aneurysmal-related SAH),
trauma (in the setting of contusional injury or
axonal injury) or the site of hemorrhagic stroke
(in the setting of parenchymal hemorrhage from
ischemic or non-thromboembolic hemorrhagic
stroke). In many cases, a small amount of blood
accumulation in interpeduncular fossa is the
main or only evidence of SAH; notably, IPF is
easily identified anatomically with either basi-
lar artery or anterior ponto-mesencephalic vein
(APMV) within interpeduncular fossa [112–
115]. Of note, a couple of scenarios can simu-
late SAH within IPF: first, as the basilar artery is
rounded and surrounded by CSF, it can be sepa-
rated from the wall of the interpeduncular fossa,
but due to slice thickness or slice orientation, it
can simulate SAH within the IPF, which can be
resolved by multiplanar reformats or noninva-
sive contrast-enhanced CT or angiographic CT
or MRI.  Regarding the normal variant APMV,
it is a normal, vertically oriented venous struc-
ture presenting in about 5% of the population,
which can simulate SAH on NCCT, particularly
if there are thicker slices of CT acquisition or
the venous structures are hyperdense (such as
from dehydration or polycythemia); this can be
discerned from true SAH using post-contrast CT
such as CT angiography or via MR angiography
[114, 115]. After injecting intravenously contrast
medium (whether via CT or MRI), the diagnos-
tic criteria for SAH in other parts become unreli-
able due to the degree of vascular enhancement
(often with normal contrast-enhancing veins
adjacent to arterial structures in some regions);
however, focal high density of the IPF with its
characteristic inverted triangular shape can be a
A. M. McKinney et al.
reliable sign, being easily identified relative to
surrounding enhancing vessels, even on post-
contrast CT or MRI. It should be noted that when
the cerebral herniation occurs, the IPF may be
displaced, be distorted, be deformed, or even
disappear in the most severe cases. Under such
circumstances, the interpeduncular fossa sign
becomes unreliable, but there are usually other
overt signs of SAH or other severe intracranial
injuries [113–115]. At the same time, due to the
angle of the NCCT acquisition (“slice selec-
tion”), the IPF can appear deeply situated in the
midbrain, for which multiplanar reformats can
help discern the IPF and confirm whether there
is actual hemorrhage.
2.36 The Empty Delta Sign
Features
On post-contrast CT or MRI T1WI, the empty
delta sign is manifested as when the superior
sagittal sinus has a triangular appearance of
enhancement or relatively low density/intensity
within the hyperdense region on multiple consec-
utive CT images (or on multiplanar post-contrast
T1WI).
Explanation
There is no universally accepted pathophysio-
logic explanation for the appearance of the empty
delta sign. However, potential hypotheses include
(a) intraluminal thrombus (static) with dynami-
cally flowing contrast surrounding a thrombus,
(b) recanalization of the thrombus within the
sinus, (c) organization of the clot/thrombus, (d)
blood-brain barrier breakdown with surrounding
enhancement, and (e) dilatation of collateral peri-
dural and dural venous channels around throm-
bosed dural sinus (Fig. 2.35).
Discussion
The so-called empty delta sign, which usu-
ally appears following contrast-enhanced CT
(CECT), is reliable in CT-based diagnosis of SSS
thrombosis, but it may not appear in all cases in
the hyperacute stage (<8  hours’ age). However,
the “empty delta sign” can also appear on non-­
contrast CT (NCCT) and disappear on postcon-
2 Brain
Fig. 2.35  Post-contrast CT indicates a triangle filling
defect in the superior sagittal sinus (white arrow)
trast CECT, representing the “pseudo-delta sign”
in the hyperacute stage of SSS thrombosis. On
the NCCT, blood surrounding the SSS can out-
line the thrombus; thus, when contrast is admin-
istered, the SSS becomes dense with enhancing
blood within the SSS in the venous phase of
enhancement [116]. However, up to 30% of initial
CT are normal. Unfortunately, the sign may be
absent when thrombosis does not affect the pos-
terior third of the sinus or when CT is performed
early (in the first 5 days after symptom onset) or
late (after 2 months) in the disease course. In the
acute stage, fresh clots exhibit increased attenu-
ation; in the chronic stage, the obstructed sinus
may show numerous channels of recanalization
within the thrombus. This may explain non-con-
trast why the sign is not apparent in the acute and
chronic stages [117].
The superior sagittal sinus thromboses are the
most frequently of all the cerebral veins, although
often, more than one vessel is involved. Cerebral
venous sinus thrombosis (CVST) is a challeng-
ing neurologic disorder because of the wide
variety of clinical manifestations. The annual
incidence is estimated at 2–7 cases per a popu-
lation of 1  million. There are numerous causes
and predisposing factors for CVST. The clinical
features are nonspecific, and brain CT is often
61
requested for the exclusion of CVST. Although
timely and correct anticoagulation or thrombo-
lytic therapy may improve clinical outcomes,
the diagnosis is often delayed. Non-contrast CT
is a cost-­effective and widely available imaging
technique in an emergency setting [118]. Various
imaging techniques are used to confirm the diag-
nosis with CT angiography and MRI/MRV being
most sensitive and specific. Nonspecific changes
such as focal edema, venous infarction, dilated
veins, small ventricles, and subtle diffuse edema
may be present. The “dense triangle sign” is a
hyperdense triangular or round shape in the
posterior superior sagittal sinus that has been
described in non-­contrast CT. The “empty delta
sign” seen with contrast-enhanced CT is a trian-
gular ring of enhancement with a central region
lacking contrast in the posterior superior sagit-
tal sinus. Emergency physicians who strongly
suspect CVST should obtain non-contrast CT,
followed by contrast-enhanced CT, and finally
MRI/MRV [119].
2.37 The Parasagittal Sinus Sign
Feature
The blood of subarachnoid hemorrhage accumu-
lates around the parasagittal sinus and the conflu-
ence of the sinuses (i.e., the torcular confluence)
as high density, and the flow of blood demon-
strates the relative low density in venous sinus,
hence the formation of a triangular shape.
Explanation
The parasagittal sinus sign is an important sign
of subarachnoid hemorrhage in neonates. The
blood accumulates around the parasagittal sinus
and the confluence of sinuses, which displays a
high-­density shadow on CT, forming relatively
low density called “the delta sign” around venous
sinus. If the blood is on one side, it is the “half
delta sign,” which is more significant (Fig. 2.36).
Discussion
Neonatal subarachnoid hemorrhage (SAH) is
a prominent cause of asphyxia and birth injury.
Beneath the arachnoid membrane is the sub-
arachnoid space, which contains vessels and
62
Fig. 2.36  The blood of subarachnoid hemorrhage accu-
mulates around the parasagittal sinus and the confluence
of sinuses in high density, and the flow of blood demon-
strates the low relative density in the venous sinus, which
is the parasagittal sinus sign (arrow)
cerebrospinal fluid. Hemorrhage into this space
is called SAH.  Overall, SAH results from the
shearing of bridging veins as they exit the brain,
cross the extra-axial spaces and membranes, and
continue to the venous sinuses. Blood accumu-
lates subjacent to the arachnoid membrane, in
the subarachnoid space, which normally con-
tains only cerebrospinal fluid; thus, SAH fills the
fissures and sulci in the region of hemorrhage.
SAH is best demonstrated in the acute or hyper-
acute phase with non-contrast CT (NCCT); the
use of MRI for detection of acute SAH remains
controversial, although the addition of special-
ized pulse sequences may increase the detection
rate, even relative to CT [120]. One direct sign
and four indirect signs are seen in subarachnoid
hemorrhage (SAH) of the newborn. The direct
sign is the high-density shadow caused by the
subarachnoid space of extra-axial SAH located at
the skull base or base of the cerebrum, including
the Sylvian cistern, the interhemispheric fissure,
and the cerebellar margin of the tentorium, along
the straight sinus; additionally, this direct sign
can be present along the superior sagittal sinus
(SSS) and along the surface of the brain. The four
indirect signs of newborn SAH are hydrocepha-
A. M. McKinney et al.
lus, other sites of intracranial local hemorrhage,
hypoxic-ischemic encephalopathy, and cerebral
infarction, which can be nonspecific as to their
etiology, albeit important to recognize each of
these signs.
In a study of the location and distribution of
subarachnoid hemorrhage, the authors found
three characteristic signs: the parasagittal sinus
sign (delta sign), the border sign (Y sign), and
the border blurring sign. After clinical follow-
up, they found that these three signs can have
great value in the identification of SAH. (1) In
the parasagittal sinus sign (delta sign), the blood
is concentrated around the sagittal sinus and the
confluence of sinuses in high density, and the
flow of blood in the sinus is relatively low, thus
forming the “delta sign.” If the blood is on the
one side, it is “half delta sign.” (2) The Y sign:
blood is concentrated along the upper and lower
edges of the cerebellar margin of the tentorium
to form a hyperdense shadow with the shape of a
“Y” or “V.” (3) The border blurring sign: blood is
concentrated within the interhemispheric fissure,
which can penetrate deep into the cerebral sulci
between the cerebral hemispheres.
CT angiography is recommended as the first
choice of imaging examination following the
detection of SAH, because of its fast speed and
convenience; however, it is associated with further
exposure to ionizing radiation and possible neph-
rotoxicity risks. MR angiography is free of these
problems and is therefore a promising alternative
[121]. Due to the advancement of multi-slice CT,
the sensitivity in detecting SAH on NCCT has
increased substantially. As such, recent literature
suggests that within 6  hours of symptom onset,
the sensitivity of NCCT approaches 100%.
2.38 T
 he Pulvinar or Hockey Stick
Sign
Feature
The dorsal thalamus (particularly the pulvinar
nucleus) may have symmetrical hyperintensity
on FLAIR MRI, or in some cases reduced dif-
fusion on diffusion-weighted imaging (DWI),
in the earlier phases of acute/subacute onset of
2 Brain 63

Creutzfeld-Jakob disease. The pulvinar sign is an

MRI finding of variant Creutzfeldt-Jakob disease
(vCJD), one type of prion-related disorder.

Explanation
The typical MRI feature of the variant is relative
symmetric density enhancement of the occipital
nucleus of the thalamus on T2WI, which is called
the “pulvinar sign” or “hockey stick sign. The
pulvinar sign can provide a reliable and accu-
rate diagnosis in clinically suspected vCJD.  By
detecting the pulvinar sign, the sensitivity of
FLAIR sequence is higher than T2WI or PDWI
(Fig. 2.37).

Discussion
In the appropriate clinical context, the presence of
the pulvinar sign on MRI is a highly accurate diag-
nostic sign for vCJD [123]. CJD is a rare progres-
sive fatal neurodegenerative disease. It is mainly
due to the accumulation of abnormal annexin and
prion virus proteins in neurons. There are four
clinical types: sporadic, iatrogenic, familial, and
variant types. The vCJD was described first in the
United Kingdom in 1996 [124]. It is also called
bovine spongiform encephalopathy (BSE) and
is a zoonotic form of human prion disease. The
MRI findings of sporadic CJD usually appear
first in the cerebral cortex, which is characterized
by strip-like high signal along the cortex, pre-
senting “streamer sign” or “lace sign.” The com-
mon sites include frontal (84%), parietal (72%),
and temporal (65%). Most of these studies did
not detect the vCJD agent outside of the nervous
system (central, peripheral, and autonomic) or
lymphoid tissues [125]. vCJD is mainly noted in
younger patients (usually <50 years of age, with
a median onset of 27 years of age), and there is
no definite difference in the incidence of vCJD
between gender. There is no clinical diagnostic
standard of vCJD, and the definitive diagnosis of
vCJD requires brain biopsy or autopsy for his-
topathological examination. Early MRI studies
showed diffuse cortical atrophy in the late stage
of CJD, followed by a reported T2 hyperinten-
sity in the basal nuclei, the dorsal thalami, and
the cortices. The sensitivity of hyperintensity in
basal ganglia T2WI and PDWI has been reported
Fig. 2.37  The pulvinar sign in vCJD on FLAIR in a
child, relatively mild hyperintensity in the caudate and
putaminal nuclei, but much greater hyper-intensity in the
posterior and medial thalamic regions (pulvinar sign)
to be about 75–80%. FLAIR and DWI sequences
reviewed together can increase the reported
sensitivity, especially when evaluating cortical
involvement. FLAIR sequence is more sensitive
than other sequences. Positive MR images may
obviate more invasive diagnostic tests in most
cases [126]. The WHO has thus used the pulvinar
sign on brain MRI as one of the most accurate
noninvasive methods for the diagnosis of vCJD.
Of note, this sign is based on the comparison
of the intensity of the dorsal thalami with other
cortical and deep cortical structures. For young
patients, the intensity of the normal basal gan-
glia region is relatively higher than the elderly on
T2WI.  Hence, in order to improve the accuracy
of MRI in diagnosing this disorder, it is neces-
sary to review the clinical history to determine if
the findings are consistent with vCJD, and axial
FLAIR and DWI sequences should be included
to help confirm the diagnosis of clinically sus-
pected vCJD. The differential diagnosis includes
bilateral dorsal thalamus infarction, perinatal
64 A. M. McKinney et al.

ischemic injury, iron or copper deposition, and
neoplastic infiltration (especially lymphoma and
glioma). Studies have also reported that the pul-
vinar sign is a highly specific sign of Fabry dis-
ease, found in male patients with cardiac signs
and severe kidney involvement [127].
2.39 The Radial Bands Sign
Feature
On MRI (usually FLAIR or T2WI), this sign
manifests as a linear or curvilinear abnormal sig-
nal radiating from the lateral ventricle to the sub-
cortical region of the cerebral hemispheres.
Explanation
Some authors believe that the “radial bands” in
patients with tuberous sclerosis represent abnor-
mal migration pathways of dysplastic neural cells
guided along the radial-glial unit (i.e., migrating
perpendicular to and centrifugal to the lateral
ventricles). These are also known as cortical
migrational anomalies or malformations of cor-
tical development, as the neurons were intended
to move from the ventricular/proliferative zone
(where they originated) out to the cortex; how-
ever, their migration is interrupted, and the cells
are dysplastic (hence, the general term “cortical
dysplasia”). The resultant abnormal, linear sig-
nals traversing the radial white matter represent
a variety of abnormal nerve differentiation and
astrocyte differentiation anomalies, and are not
classified simply by the presence of clusters of
giant cells (present in the multiple Type II cor-
tical dysplasia in tuberous sclerosis) or by the
presence of balloon cells (present in Type IIB
cortical dysplasia); notably, the same giant cells
can also be classified by different histological
techniques. This suggests that tuberous sclero-
sis may be due to developmental disorder and is
considered a form of multiple/multifocal cortical
dysplasia occurring at an early stage of develop-
ment (Fig. 2.38).
Discussion
The “radial bands” sign is a sign that sometimes
seen on brain MRI images of patients with sus-
pected tuberous sclerosis (from presumed cortical
dysplasia) or in patients with a history of seizures

a b

Fig. 2.38  In a young adult female with tuberous sclerosis, FLAIR MRI axial images (a, b) demonstrate linear high
signal from the lateral ventricular margins radiating out towards the cerebral hemispheres’ subcortical/cortical regions
2 Brain
[128]. The MRI finding is that of linear or cur-
vilinear areas of abnormal signal extending in a
radial fashion from the periventricular to subcor-
tical regions of the cerebral hemispheres, which,
in patients with tuberous sclerosis, are thought
to represent abnormal migration of dysplastic
stem cells along the radial-glial scaffolding used
to guide neuronal migration; these abnormali-
ties are also known as migration anomalies or
generally as “focal cortical dysplasia.” At pres-
ent, tuberous sclerosis is considered the second
most common neurocutaneous syndrome (after
neurofibromatosis type I) and is characterized by
organ dysplasia and potential tumors from three
embryonic layers. In the past, the diagnosis was
often based primarily on the presence of charac-
teristic skin manifestations and the typical clini-
cal triad (epilepsy, mental retardation, and facial
angiofibroma).
The four main intracranial manifestations
of tuberous sclerosis on neuroimaging are
subependymal nodules, subependymal giant
cell astrocytoma (usually called as such if
they are enhancing, enlarging, and potentially
causing hydrocephalus), cortical dysplasia,
and associated white matter abnormalities
[129]. Calcification of the subependymal nod-
ules can be seen in a few cases on CT.  Most
white matter abnormalities can be evident on
CT or MRI; these include cerebral focal areas
of edema (perhaps from cortical dysplasia or
hamartomas which usually do not enhance),
wedge-shaped or linear/curvilinear (resembling
bands) lesions, and multiple linear-­like lesions
adjacent to the fourth ventricle aggregating
near the cerebellar hemispheres. These migra-
tion bundle anomalies almost always show
hypo- or isointense signal on T1WI in adults,
being hyperintense on T2WI. Before the infant’s
myelin formation, white matter is a high sig-
nal on T1WI, and equal or low signal on T2WI
and FLAIR.  Occasionally, these enhance after
postcontrast administration, but the cause is
unknown, and is not considered a sign of malig-
nant degeneration, as that does not typically
occur from these “forme fruste” cortical dys-
plasia. The visualization of radial bands, which
65
is specific of tuberous sclerosis, may be helpful
in distinguishing this disease from other demy-
elinating or demyelinating diseases, infections,
tumors, or post-ischemic disorders. This is
especially important when the subependymal
nodules and subcortical nodules are not obvi-
ous. Abnormalities of the white matter may not
be evident on CT, but they are generally more
numerous and conspicuous on MRI.
Magnetization transfer and FLAIR images
are particularly sensitive to the detection of
these abnormalities. In recent years, MRI has
proved to have further utility in evaluating
patients with tuberous sclerosis, by evaluating
brain development via measuring cerebellar vol-
ume in tuberous sclerosis patients to help pre-
dict their prognosis [129]. Also, 7.0T MRI has
been used in the study of patients with tuber-
ous sclerosis, with improved spatial resolution
and better contrast as compared to 3.0T, as 7.0T
MRI can identify a greater number of smaller
lesions, and better delineation of cortical abnor-
malities [130].
2.40 The Triangular Pattern
Feature
This triangular pattern relates to the appear-
ance of supratentorial lesions arising from the
cerebral cortex or subcortical white matter,
with the surface of the brain as the base of the
triangle, and the tip of the triangle pointing
inward toward the deep regions of the brain.
The lesions are often well-circumscribed, with-
out peritumoral edema and without or with
mass effect.
Explanation
The triangular pattern and septations are rela-
tively characteristic manifestations of a dys-
embryoplastic neuroepithelial tumor (DNET).
The triangular sign may be related to the radial
distribution of glial fibrillary pathways, and the
septations may be related to branched capillaries
perpendicular to the surface of the cerebral cortex
(Fig. 2.39).
66
Fig. 2.39  MRI shows an unenhancing, multicystic lesion
located mainly in the left parahippocampal gyrus on axial
T1WI (a, derived from an inverted T2WI), and on axial
T2WI (b). There is very little mass effect, where there is
Discussion
First described by Daumas-Duport et  al. [131],
the dysembryoplastic neuroepithelial tumor
(DNET) is considered by some as a malforma-
tive, hamartomatous lesion and, given its pro-
liferative features, is considered by others as a
benign and extremely low-grade mixed glio-
neuronal neoplasm. It is included in the current
World Health Organization (WHO) classification
as a grade I glioneuronal tumor. They typically
occur in children and young adults, where three
histological forms of DNET have been described,
including simple, complex, and nonspecific.
Although DNET has been classically described
as a benign entity, there is increasing evidence
to suggest malignant transformation is possible,
albeit quite rare [132].
A cortical-based location and the lack of mass
effect and perilesional edema are common char-
acteristics of neuroimaging. In a large series of
DNET, a cystic appearance (23.9%), faint focal
enhancement (19.5%), and calcification (15.2%)
are common radiologic features. On non-contrast
CT, the tumors are typically quite hypodense,
appear nearly cystic in half of the cases, and
can at times have a focal calcific hyper-density
or exhibit slight focal contrast enhancement
A. M. McKinney et al.
slight posterior displacement of the hippocampal head and
anterior part of the temporal horn, as well as no significant
surrounding edema on T2WI
(the latter characteristic causing consternation
and potentially overlapping in appearance with
other low-grade tumors). MRI demonstrates a
well-­delineated tumor with a pseudo-cystic or
multicystic appearance, typically having very
low signal intensity on T1WI and quite high sig-
nal intensity on T2WI.  Focal ring enhancement
can rarely be noted on post-contrast T1WI [133].
MRI features in histologic variants of DNETs
were classified into three types [133]: type 1
(cystic/polycystic-like, well-delineated, strongly
hypo-intense on T1), type 2 (nodular-like, het-
erogeneous signal), or type 3 (dysplastic-like,
iso-/hypo-signal T1, poor delineation, gray-white
matter blurring). Simple or complex DNETs are
always seen as type 1 on MRI, whereas non-­
specific DNETs are seen either as type 2 or type
3 on MRI.  Epileptogenic zones are found to be
significantly different among MRI subtypes. The
epileptogenic zone co-localizes to the tumor in
type 1 and involves the peritumoral cortex in
type 2 MRI, while there are more extensive areas
involved in type 3. When a child, adolescent, or
young adult presents with a cortical epilepto-
genic lesion, including the triangular pattern of
distribution and the presence of septations, it may
aid in the diagnosis of DNET [134].
2 Brain
2.41 The Dural Tail Sign
Feature
The dural tail sign is visible on contrast-enhanced
MR images as postcontrast linear thickening
of the meninges that resembles a tail extending
from the larger mass; the visible range is typi-
cally from 0.5 to 3.0 cm in length.
Explanation
The dural tail sign is a common manifestation
of meningioma on post-contrast MRI. It was ini-
tially proposed that dural tails resulted from direct
tumor invasion, but investigators have not been
able to clearly demonstrate direct tumor involve-
ment. It is proposed that a dural tail represents
reactive changes to the dura mater. Currently, both
the mechanisms of tumor invasion and hyper-vas-
cular reaction may be responsible for the dural tail
sign or a combination of the two (Fig. 2.40).
Discussion
The dural tail sign was first described by Wilms
in 1989 [135]. The dural tail sign (DTS) repre-
sents thickening of the dura adjacent to an intra-
cranial pathology on contrast-enhanced T1WI
MRI, which was initially thought to be pathog-
nomonic of meningioma; however, many sub-
a b
Fig. 2.40  On a paramedian sagittal image (a) and on an
axial section (b), post-contrast T1WI in a 78-year-old
female demonstrates a left frontal cerebral meningioma
along the falx cerebri and on top of the planum sphenoi-
67
sequent studies demonstrated that this sign can
be present adjacent to various intra- and extra-­
cranial pathologies, as well as in spinal lesions,
including neuromas, chloromas, metastases,
lymphoma, glioma, pituitary diseases, and gran-
ulomatous disorders affecting the CNS [136].
Histologically, the exact nature of the dural tail is
still not clearly established. It has been ascribed to
the tumoral extension within or at the surface of
the dura. Conversely, it has also been attributed to
the presence of fibrous tissue with the prolifera-
tion of loose connective tissue, hypervascularity,
and vascular dilatation or to increased vascularity
within the tail [137]. Based on the histopatho-
logic and imaging findings, it has been concluded
that the greater degree of contrast enhancement
of the dural tail with respect to the larger body
of the tumor suggests that the dura (i.e., portion
involved by the tail) is histologically different
from the tumor. Indeed, a recent report aimed to
verify the histological appearance of the dural
tail accompanying meningioma on MRI, which
suggested that initially, the tumor cells invade
vessels and pack them together at the point of
tumor attachment; thereafter, vessel ­congestion
is induced in the adjacent dura mater, as a result
of which it enhances markedly, giving rise to the
dural tail sign [136].
dale. Post-contrast MRI showed a linear area of the
enhancement of the adjacent meninges posterior to the
tumor, which represents a dural tail (arrows)
68 A. M. McKinney et al.

In 1990, the triple criteria for DTS were estab-
lished by Goldsher et  al. as follows [137]: (1)
the presence of at least two consecutive sections
through the tumor at the same site in more than
one imaging plane, (2) the greatest thickness of
the tail being immediately adjacent to the tumor
and tapering away from it, and (3) enhancement
on postcontrast imaging is more intense than that
of the tumor itself. Nowadays, as imaging slices
tend to be less than 5  mm, there should always
be at least three sections showing the dural tail,
depending on the slice thickness. It remains con-
troversial as to whether the dura mater demon-
strating the tail sign should be resected to prevent
tumor recurrence. However, further studies are
needed to confirm this [138]. The DTS is not
always seen in a meningioma, as it is seen in
only 60–72%, and it is not entirely specific [139].
Despite this, it remains a useful sign in assess-
ing the morphology, as well as the enhancement
pattern of a lesion, and in helping confirm a sus-
pected meningioma.
2.42 The Acute Angle Sign
Feature
In axial post-contrast CT or MRI, the position
is located in the triangular area of the cerebello-
pontine angle (CPA), where the extra-axial tumor
grows around the internal auditory canal (IAC)
and forms an acute angle with the petrous bone,
being called the acute angle sign.
Explanation
The acute angle sign is the relative characteris-
tic of acoustic neuroma/vestibular schwannoma
(AN) on CT and MRI.  The tumor originates
from the Schwann cells of the vestibular nerve
in the IAC.  It begins to be confined within the
IAC and then grows along the nerve slowly out
of the IAC and into the CPA. Mostly, the center
of these lesions is located in the IAC, and the nar-
row base is attached to the petrous bone, so the
angle between tumor and petrous bone is an acute
angle (Fig. 2.41).

a b

Fig. 2.41 (a) A mixed low/low signal mass in the right cerebellopontine angle on T1WI. The angle between the right
cerebellopontine angle and the petrous bone is an acute angle. (b) The solid part of the mass enhances uniformly
2 Brain
Discussion
Acoustic neuromas are closely related to petrous
bone, and the site of contact between the lesion and
the very dense petrous bone is rather small, forming
an acute angle sign [140]. Acoustic neuroma is the
most common tumor in the CPA area, accounting
for 70–80% of the tumors in this region. Acoustic
neurinomas (AN, aka vestibular schwannomas) are
primary intracranial tumors of the Schwann cell
sheath surrounding the vestibulocochlear nerve
(eighth cranial nerve); these much less frequently
involve or arise from the seventh cranial nerve.
The CT findings of an acoustic neuroma can be
diverse. The tumor often grows into the CPA and
is centered on the IAC, where very few are not cen-
tered on the IAC; as such, approximately 80% of
patients have an enlarged IAC, with a difference
of >2.5 mm in width and diameter of the IAC as
compared to the contralateral side. Sometimes,
the IAC appears widened and shortened (“funnel-
shaped”), where the bone destruction may be seen
occasionally. Bilateral IAC enlargement is usually
caused by bilateral acoustic neuromas or chronic
intracranial hypertension, although normal variant
“bulbous IACs” on NCCT can simulate bilateral
schwannomas (and thus simulate neurofibromato-
sis type II), which may require MRI to confirm the
lack of tumors [141].
On MRI, as mentioned above, the main body
of the tumor typically grows into the CPA, cen-
tering on the IAC, and the IAC/porus acusticus is
enlarged, while the eighth nerve appears thick-
ened. The tumor’s morphology usually appears
round or oval, with a smooth edge, related to the
tumor envelope, where the envelope is low signal
on T1WI and T2WI. Acoustic neuroma is gener-
ally divided into three types: solid, cystic-solid,
and cystic. The tumors can have homogeneous
or inhomogeneous enhancement on post-contrast
T1WI and can also be irregular in shape. When a
vestibular schwannoma is large, adjacent struc-
tures can be compressed, such as the brain stem
and cerebellum and middle cerebellar peduncle,
and may cause deformation of the fourth ven-
tricle. Focal hyperintensity (FHI) in the dorsal
brain stem on T2WI of patients with CPA tumor
was thought to indicate degeneration of the ves-
69
tibular nucleus and is not a specific indicator of
­vestibular schwannoma and is related to not only
vestibular function but also other factors [142].
IAC does not necessarily have to be the center of
growth center; when a schwannoma is centered
primarily within the CPA and not the IAC, it may
be accompanied by hyperplasia of the adjacent
skull, such as of the adjacent petrous apex [143].
2.43 The Ependymal
Dot-Dash Sign
Feature
On sagittal thin-section FLAIR sequences, points
of irregular hyperintensity (the “dots”) can be
visible along the inner/lower surface of the cor-
pus callosum, and the middle is connected by a
linear hypo-intensity (the “dash”).
Explanation
The ependymal dot-dash sign is an MRI find-
ing of early-stage multiple sclerosis (MS); at
least two points are connected by lines to form
this sign. The point/dot is the irregular hyperin-
tensity on the subependymal surface, where its
size exceeds the thickness of the connecting line/
dash. The line/dash is a residual normal ependy-
mal streak (Fig. 2.42).
Discussion
MS is a common disease that affects brain func-
tion and can be progressively debilitating. The
presence of characteristic white matter lesions
on MRI, along with specific clinical manifesta-
tions, can be highly suggestive of the presence of
MS. The corpus callosum and pericallosal white
matter (WM) are the most frequently involved
regions in early MS. Early lesions can affect the
subependymal veins adjacent to the surface lining
of ventricles, and the corpus callosum is involved
in 55–93% of MS patients [144]. The histopatho-
logical basis of the ependymal dot-­dash sign is
that the early MS lesion begins in the subependy-
mal venous wall. Compared with other imaging
findings, this sign only involves the ependyma.
According to the Poser criteria, the incidence of
70
Fig. 2.42  In two
patients with multiple a
sclerosis (a, b), sagittal
FLAIR MRI
demonstrates a
“dot-dash sign”
subjacent to the corpus
callosum; the arrow
shows the “dot sign” and
the “line” is the “dash,”
a hypo-intense area
between the two points
the ependymal dot-dash sign is high in MS, and
the sensitivity is 91.4% in MS patients; however,
in the control group, the incidence of the epen-
dymal dot-dash sign is 34.4%. The ependymal
dot-dash sign is not the same as hyperintensities
that may be perpendicularly oriented to the epen-
dyma. These differences can be distinguished
from other signs of MS, such as striations, cin-
gulate stripes, or oval/fingerlike lesions. The sen-
sitivity and specificity of the ependymal dot-dash
sign in younger patients were reported as 95.7%
and 71.9%, respectively.
Despite the high correlation between the
ependymal dot-dash sign and the clinical mani-
festations of MS, as compared with other signs,
it still has a higher false-positive rate due to the
mediocre specificity; for example, 50% of the
false-­positive patients had a history of migraine
or chronic white matter changes in the elderly.
Typical manifestations of chronic white matter
A. M. McKinney et al.
lesions in the elderly are parallel to the ependy-
mal surface of the lateral ventricles; up to one
lesion per 10 years has been considered normal
for patients of advanced age. Thus, the pres-
ence of lesions perpendicular to the ependymal
is also a diagnostic criterion of MRI in MS and
being necessary in differentiating between these
two diseases. For migraine patients, the ependy-
mal dot-dash sign has more important diagnos-
tic significance. Without the occurrence of the
ependymal dot-dash sign, especially in patients
younger than 50  years old, the possibility of
MS can almost be completely ruled out, with a
sensitivity of about 95% [145]. Another poten-
tial sign of MS lesions is the presence of “sub-
callosal striations” on thinner section (≤2  mm
thickness) FLAIR images oriented perpendicular
to the ependyma of the lateral ventricles; these
are thought to represent the earlier sign of the
lesions that later become ovoid or “fingerlike,”
2 Brain
and the presence of these striations along with
another parenchymal WM lesion is highly sensi-
tive for representing MS [146]. Another potential
defect of the ependymal dot-dash sign is in the
differential diagnosis between MS and acute dis-
seminated encephalomyelitis (ADEM). Because
according to Poser criteria, the identified MS can
be repeated in time and location, while ADEM is
single-phase. Some patients in the control group
with the ependymal dot-dash sign are actual
ADEM, because the ADEM and MS are very
similar in the course of diseases. The ependy-
mal dot-dash sign in ADEM is actual immune-­
mediated demyelination, not the MS.  However,
the 2010 McDonald criteria for the diagnosis of
MS are widely used in research and clinical prac-
tice, and the criteria has been updated recently
[147]. The ependymal dot-dash sign is a charac-
teristic MRI finding of early MS.  An irregular
ependymal dot-dash sign in the sagittal thin-layer
FLAIR can improve the sensitivity of the diag-
nostic MS.
2.44 T
 he Hummingbird Sign and
the Swallowtail Sign
Feature
The hummingbird sign is seen in the median
sagittal position of MRI of the patients with
progressive supranuclear palsy (PSP). PSP is
characterized by atrophy of the tegmentum of
the mesencephalon. The atrophic superior edge
of the midbrain on MRI resembles a humming-
bird’s mouth, so it is termed the hummingbird
sign, where the superior edge of the midbrain
on sagittal images becomes flattened, rather
than the normal curved appearance. Meanwhile,
the swallowtail sign represents the normal
appearance of nigrosome-1 within the substan-
tia nigra on axial (or oblique axial) susceptibil-
ityweighted image MRI; thus, the lack of the
normal “swallowtail” sign (i.e. the presence
of confluent dark signal replacing the normal
wedge of isointense signal) within the substan-
tia nigra on SWI MRI is thought to represent a
sign of Parkinson’s disease.
71
Explanation
The hummingbird is a bird with a body length
of approximately 10  cm, mainly living in the
Americas, with a tall and thin and sharp mouth.
PSP patients can show the hummingbird sign in
the sagittal plane of MRI, where there is flatten-
ing of the superior midbrain’s profile (Fig. 2.43a).
The swallowtail is the normal appearance on axial
imaging of the sustantia nigra, with a normal
iso-intense/bright notch on SWI situated within
the larger, more confluent region of dark signal
within the cerebral peduncle and substantia nigra
on SWI MRI; the lack of the normal swallowtail
appearance on SWI on one or both sides is sug-
gestive of Parkinson’s disease.
Discussion
The hummingbird sign (or loss of the superior
midbrain profile) is a characteristic manifesta-
tion of midline sagittal MRI in PSP patients,
which is of great value in the diagnosis and
differential diagnosis of PSP from other neu-
rodegenerative disorders [148]. PSP is a rare
neurodegenerative disorder with pseudobulbar
palsy, vertical supranuclear ophthalmoplegia,
extrapyramidal muscle stiffness, gait ataxia, and
mild dementia as the main clinical features. The
main lesions are produced in the inner segment
of the globus pallidus, the subthalamic nucleus,
the red nucleus, the substantia nigra, the locus
caeruleus, the epithalamus, the cuneiform
nucleus, and the gray matter adjacent to the third
ventricle, as well as the pontine tegmentum, the
inferior olivary nucleus, and the dentate nucleus
of the cerebellum, etc. The pathological basis of
the hummingbird configuration is mainly due to
the increase in the width of the interpeduncular
fossa caused by the atrophy of the tegmentum
of the midbrain, including the tectum, with nar-
rowing of the front and back of the tegmentum.
Therefore, the appearance of the hummingbird
sign likely primarily reflects the atrophy of the
midbrain tegmentum, which strongly suggests
that the PSP patient is involved. This combi-
nation of findings appears as a “flattened” or
indented superior margin of the midbrain’s supe-
rior margin on sagittal MRI [149].
72
a b
Fig. 2.43 (a) A 65-year-old man with PSP. Note the flat
or concave appearance of the T2 sagittal midbrain contour
in a patient with PSP, indicating the hummingbird sign.
(b) A 61-year-­old man with Parkinson’s syndrome, and
the lack of the normal swallowtail appearance. On 3.0T
SWI MRI, on the left side, there is loss of the normal
PSP often needs to be differentiated from
other diseases, such as more typical Parkinson’s
disease (PD), Alzheimer’s disease, cortical
basilar degeneration, and multisystem atrophy
(MSA), each of which can variably cause eye
movement disorders, movement disorders, and
dementia. The hummingbird sign and the morn-
ing glory flower sign, reflecting midbrain pathol-
ogy on MRI, have previously been shown to
separate patients with PSP from those disorders.
Meanwhile, the swallowtail sign has recently
been suggested as being relatively accurate in
detecting typical Parkinson’s disease, and more
recently in detecting dementia with Lewy bodies;
this is presumably due to the result of abnormal
iron metabolism, where the increased iron depo-
sition at the site of nigrosome-1 within the sub-
stantia nigra ultimately leads to the disapperance
of the normal linear/wedge shape of intermedi-
ate-high signal on SWI [150]. This appearance
is often described as the “lack of, or loss of” the
normal swallowtail appearance on MRI interpre-
tations. The hummingbird sign rating scale is a
simple and measurable visual assessment tool to
identify the hummingbird sign, with adjustable
A. M. McKinney et al.
swallowtail due to prominent iron deposition in the sub-
stantia nigra (arrow), indicating Parkinson’s disease. Note
the normal right swallowtail (dotted line outlines the nor-
mal notch of the swallowtail and the arrow points at the
normal notch of the swallowtail)
diagnostic validity for PSP. It has been reported
that an MRI Parkinson’s index may be a good
tool for differentiating PSP from typical parkin-
sonism and vascular parkinsonism [151]. The
atrophy of the mesencephalic tegmentum often
occurs later than the widening of the third ventri-
cle and the lateral fissure and later than the fron-
tal lobe atrophy. Therefore, the change of subtle
midbrain atrophy should not be overemphasized
in the early phase, so as not to cause misdiag-
nosis; however, the indentation of the superior
midbrain causing the hummingbird appearance
does not happen until there is moderate-­severe
midbrain atrophy, and thus, an overdiagnosis
(i.e., a false positive) is unlikely in the presence
of the hummingbird sign [152].
2.45 The Hot Cross Bun Sign
Feature
The hot cross bun sign is noted on axial T2WI
or FLAIR, showing abnormal high signal that is
cross-shaped hyperintensity within the pons. Its
other name is the cross sign.
2 Brain 73

Explanation cerebellar peduncle causes increased water con-

The hot cross bun sign is commonly seen in
patients of multiple system atrophy (MSA). The
mechanism of this phenomenon is that the pontine
nucleus and its fibers (transverse pontine fibers)
which reach the cerebellum through the middle
cerebellar peduncle degenerate, while the fibers
and pyramidal bundles which constitute the upper
cerebellar peduncle from the dentate nucleus are
not damaged. The degeneration of pontine trans-
verse fibers and glial hyperplasia in the middle
tent that forms a cross-shaped T2WI or FLAIR
high signal on axial images of the pons (Fig. 2.44).
Discussion
The cross sign (or the “hot cross buns” sign)
refers to the cruciform-shaped hyperintensity
on axial T2WI MRI in MSA due to the selec-
tive loss of myelinated transverse pontocerebel-
lar fibers and neurons in the pontine raphe and
sparing of the pontine tegmentum and cortico-

a b

c d

Fig. 2.44  In a 67-year-old male clinically having multi- there is a quite dark signal of the entire lentiform nucleus,
ple system atrophy (MSA), on MRI, T2WI (a) and FLAIR and on sagittal T1WI (d), there is moderate-severe pontine
(b) both demonstrate hyperintense pontine signal (arrows) atrophy (arrow), both being secondary signs of MSA
that is cross-like (i.e., hot cross buns sign). On SWI (c),
74
spinal tracts [153]. MSA is a neurodegenerative
disorder that is classified as a type of parkin-
sonism plus syndrome with variable involve-
ment of the basal ganglia, the pontocerebellar
region, and the autonomic system. Striatonigral
degeneration, olivopontocerebellar atrophy,
and Shy-Drager syndrome are now considered
as subtypes of MSA.  The cross sign was first
reported by Savoiardo et al. in 1990. They found
the cross-­shaped high signal shadow of the pons
on the T2WI in patients with sporadic olivopon-
tocerebellar atrophy, but no similar changes were
found in other cerebellar degenerative diseases.
Therefore, they believed that the “cross sign”
was a characteristic change of sporadic olivo-
pontocerebellar atrophy. Later, it was reported
not only in OPCA but also in other subtypes of
MSA. Lee et al. [154] reported that a few patients
with spinocerebellar ataxia also showed such
cross signs. Recently, it was reported that there
are also cross signs in patients with encephalitis
[155]. Despite the appearance of the cross sign in
other disorders, it is still considered a character-
istic sign of MSA. Thus, in the clinical diagnosis
of MSA, the sensitivity of cross sign is not high,
but it has a high degree of specificity [156]. Once
the cross sign is positive, it is highly suggestive
of the diagnosis of MSA.  Additionally, through
dynamic observation, Horimoto et al. divided the
evolution process of the cross sign into six stages;
ultimately, in the later stages, the volumes of the
pons and midbrain are reduced [157].
Based on clinical features, MSA is classi-
fied into MSA-P with predominant parkinson-
ism symptoms and MSA-C with predominant
cerebellar and autonomic symptoms. MSA and
especially MSA-P must be differentiated from
Parkinson’s disease (PD). Atrophy of the puta-
men and brain stem and abnormal signal in the
middle cerebral peduncle are found in a signifi-
cant number of patients with MSA, while they
are almost never found in PD patients. The cross
sign is a feature of pontine atrophy in MSA and
is more commonly found in MSA-C. Hence, the
differential diagnosis of the cross sign includes
MSA, spinocerebellar ataxia type 2 and type 3,
and parkinsonism due to underlying vasculopa-
thy (when there is a significant load of subcortical
A. M. McKinney et al.
white matter lesions). In conclusion, subtentorial
atrophy with the presence of a cross sign can help
solidify the diagnosis of MSA when clinically
suspected, but only through histopathological
examination can the diagnosis be certain [158].
2.46 The Molar Tooth Sign
Feature
The molar tooth sign is visible on transverse CT
and MR images. The superior cerebellar pedun-
cle is lengthened at the level of the isthmus region
(i.e., the midbrain-hindbrain junction).
Explanation
The molar tooth sign (MTS) is a relatively charac-
teristic manifestation of Joubert syndrome, seen
in up to 85% of Joubert syndrome patients. The
sign is caused by a lack of the normal decussation
of the superior cerebellar peduncle (SCP) fiber
tracts, which is located deep to the interpeduncu-
lar fossa; thus, widening of the IPF often occurs in
Joubert syndrome. A lack of this decussation leads
to enlargement of the cerebral peduncles, which
follow a more horizontal course as they extend
perpendicularly to the brain stem. The absence
of crossing fibers is responsible for decreased
anteroposterior diameter and the depth of the
interpeduncular fossa. Combined with typically
hypoplastic or absent cerebellar vermis, the molar
tooth sign is formed on axial images (Fig. 2.45).
Discussion
JS is a rare autosomal recessive disorder with char-
acteristic clinical and neuroradiological findings
of midline structures of the brain stem. Extensive
brain stem malformation on non-­contrast exami-
nations can be present, with the patients having
clinical signs of oculomotor apraxia and hyper-
pnea; anomalies of the gracile nuclei and solitary
tract that are also present are thought to contrib-
ute to the abnormal respiratory pattern in these
patients. The breathing pattern in Joubert syn-
drome typically consists of effortless hyperven-
tilation (up to 200 breaths/min), which is more
conspicuous in the awake state, and intensifies
when the patient is stimulated, being interspersed
2 Brain
Fig. 2.45  A 7-year-old male who has mental retardation
since childhood. MRI shows prolongation of the superior
cerebellar peduncle (the MTS) and a deepened interpe-
duncular fossa, with an absent cerebellar vermis at the
midline
with central apnea [159]. Maria et  al. reported
the MTS as the characteristic neuroimaging find-
ing of “pure” JS. However, the MTS can also be
noted uncommonly in other syndromes. The term
“JSRD” (Joubert syndrome-­ related disorders)
has been coined to group all conditions sharing
the MTS [160], which include syndromes such
as the COACH, Varadi-Papp, Dekaban-Arima,
Senior-Loken, Joubert with polymicrogyria, and
Malta syndromes, where MTS and other features
of JS may be variably seen [159].
Though the diagnosis of JS is generally based
on the presence of typical clinical features and
the presence of the “molar tooth sign” (MTS), as
seen on an MRI, the definitive diagnostic crite-
ria for JS are yet to be established. However, the
clinical features frequently considered as essen-
tial for the diagnosis of classic JS comprise the
following: (1) hypotonia in infancy, (2) delayed
developmental milestones with mental retarda-
tion, and (3) one or both of the following: (a)
an irregular breathing pattern in infancy and (b)
abnormal eye movements [161]. After the diag-
nosis of Joubert syndrome is made, therapy is
75
usually started immediately, after a neuropedi-
atric evaluation to quantify the degree of motor
and speech deficits. Typically, only symptomatic
therapy is available for patients with pure JS.
2.47 The Caput Medusa Sign
Feature
On noninvasive post-contrast CT or MRI, several
enhancing umbrella-shaped or radial small blood
vessels in the brain parenchyma converge into a
larger blood vessel (an anomalous draining vein),
called the “caput medusa sign” (this can also
resemble a jellyfish).
Explanation
The caput medusa sign is the characteristic
manifestation of cerebral developmental venous
anomalies (DVA, also termed a “venous angi-
oma”) on post-contrast CT or MRI and can be
noted on post-contrast CT or MR angiography,
as well as on catheter angiography in the venous
phase. Umbrella-shaped or radial convergence
of small vessels represents the dilated medul-
lary vein, with the convergence of the larger ves-
sels into the anomalous draining vein. Recently,
non-­contrast susceptibility-weighted imaging
(SWI) has been shown to demonstrate this sign
adequately as well (Fig. 2.46).
Discussion
The term cerebral “developmental venous anom-
aly” (DVA), coined by Lasjaunias et al. [162], is
now widely used as a synonym for venous angi-
oma, cerebral venous malformation, or cerebral
venous medullary malformation. DVAs are clas-
sified as a subtype of cerebral vascular malforma-
tions, along with brain capillary telangiectasias
(BCTs), cavernous malformations (CMs), and
arteriovenous malformations (AVMs). Cerebral
DVAs are the most frequently encountered cere-
bral vascular malformation and, as such, are fre-
quently reported as incidental findings on CT
and MRI studies. DVAs are generally considered
extreme anatomical variations of the cerebral
vasculature and follow a benign clinical course in
the vast majority of cases [164].
76 A. M. McKinney et al.

a b

c d

Fig. 2.46 A 5-year-old girl presented with a DVA demonstrated its enhancement as a vascular lesion with a
(arrows) of the right cerebellum, suspected initially on prominent draining vein, with multiple branches of
an MRI with axial T2WI (a) and SWI (b). (c, d) blood vessels at the edge of the lesion that converge cen-
Postcontrast T1WIs in axial (c) and sagittal (d) planes trally into that vein

On MRI, DVAs typically have a central flow
void, particularly on T1WI, T2WI, and SWI. Non-­
contrast MRI images may demonstrate flow
voids and phase-shift artifacts produced by the
central draining/collecting vein of a DVA. T1WI
may yield normal results in the presence of
small DVAs, where the central collecting vein is
detected as a linear or small, round, signal-void
structure on all sequences and is demonstrated
best on postcontrast T1WI or on SWI. Resembling
CMs, low flow and low resistance almost always
typify DVA hemodynamics. After the adminis-
tration of gadolinium, significant enhancement
of the medullary veins and venous collector is
2 Brain
observed on postcontrast T1WI because of the
slow flow. On contrast-enhanced T1WI, the clus-
ter of veins in DVAs has a spoke-wheel appear-
ance; the veins are small at the periphery and
gradually enlarge as they approach and converge
on the central draining vein. This appearance has
been referred to as caput medusae (or the head of
the mythical Gorgon Medusa) [163]. The charac-
teristic caput medusae appearance of a DVA can
also be visible on noninvasive post-contrast CT
or MR angiography or on catheter angiography.
DVAs consist of thin-walled, dilated medullary
veins draining into a large, central trunk lack-
ing a smooth muscle or elastic layer and without
direct arterial supply. The collecting vein can be
identified by contrast-enhanced CT (CECT), but
it is best visualized using gadolinium-enhanced
MRI and more recently has been shown to be
well demonstrated on SWI.  MRI with SWI (or
alternatively gradient-echo T2*WI) is particularly
useful for identifying associated malformations,
such as cavernous malformations (aka cavernous
hemangioma), typically appearing in proxim-
ity to the DVA. As such, cavernomas have been
found in 20–60% of patients with DVAs (the
large range likely being due to the variability
of the technique used to evaluate for caverno-
mas), whereas the incidence of DVAs is 8–33%
in patients with cavernomas [165]. Diagnostic
cerebral angiography is typically not applied for
further characterization of lesions identified on
CT or MRI, especially since the associated cav-
ernoma is angiographically occult, unless a very
large DVA (aka “hemispheric DVA”) is present,
or if the lesion (usually a large DVA) was initially
suspected to be an arteriovenous malformation
based on noninvasive CT or MRI [166]. SWI uses
paramagnetic deoxyhemoglobin in the cerebral
vein as intrinsic contrast, which is useful for the
demonstration of the cerebral venous anatomy.
Thus, on SWI, a DVA is demonstrated as a sig-
nal void lesion akin to the normal cerebral veins.
Some authors have proposed that elevated venous
pressures may exist within the territory of a DVA,
suggesting that this may be a key factor in the sub-
sequent development of a cavernoma-like lesion.
The authors observed that these cavernoma-­like
lesions appear to arise at the distal contributing
77
veins of such venous malformations. In fact, the
close association of the cavernous malformation
and DVAs is explicitly described in one report, in
which surgery demonstrated a dark reddish mass
embedded in xanthochromic subcortical white
matter, where the lesion was partially adherent to
a dilated vein [166].
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 Head and Neck
3
Zhongxiang Ding, Guoyu Chen,
and Alexander M. McKinney

Contents
3.1 Progressive Enhancement Sign  85
3.2 Tendon Sign  86
3.3 V-Shape Sign  88
3.4 Teardrop Sign  90
3.5 Tram-Track Sign  91
3.6 Double-Ring Sign  92
3.7 Salt-and-Pepper Sign  93
3.8 Steeple Sign  95
3.9 Bitten Cookie Sign  97
3.10 Prominent Ear Sign  98
3.11 Gas Bubble Sign  98
References  100

3.1 Progressive
Enhancement Sign

Feature
Z. Ding (*) On dynamic contrast-enhanced CT or MRI,
Department of Radiology, Affiliated Hangzhou First orbital cavernous hemangioma exhibits nodular
People’s Hospital, Zhejiang University School of and small, focal patchy enhancement, where the
Medicine, Hangzhou, China range of enhancement gradually spreads to the
G. Chen center of the tumor and then eventually expands
Department of Radiology, Affiliated Hospital of to the entire tumor over time.
Guizhou Medical University, Guiyang, China
A. M. McKinney Explanation
Miller School of Medicine, University of Miami,
Miami, FL, USA The “progressive enhancement sign” is a specific
e-mail: mckinrad@umn.edu CT or MRI sign in the diagnosis of cavernous

© Springer Nature Switzerland AG 2021 85

B. Gao, A. M. McKinney (eds.), Classic Imaging Signs,
https://doi.org/10.1007/978-3-030-56348-6_3
86
hemangioma on postcontrast imaging. Cavernous
hemangiomas are composed of vascular cavities
and stroma of differing sizes, where fibrous tis-
sue separation exists between the cavities. The
contrast medium enters the tumor via the junc-
tion between blood vessels and the tumor and
then gradually fills each vascular cavity through
the fibrous tissue separation (Fig. 3.1).
Discussion
Cavernous hemangioma is the most common pri-
mary orbital tumor in adults. These tumors
develop slowly and are more common in women
than in men, with the highest incidence in the
fourth and fifth decades of life. They may enlarge
during pregnancy [1]. The main clinical manifes-
tations are progressive, painless unilateral exoph-
thalmos leading to different degrees of hyperopia,
transient amaurosis, and other ocular symptoms.
The involvement of orbital apex could cause
compressive optic nerve neuropathy, albeit rare,
occasionally resulting in monocular vision loss.
Other less common symptoms include pain,
swelling, diplopia, or a palpable lump [2].
Cavernous hemangiomas are usually solitary;
rarely, they may be multiple. Pathologically, cav-
ernous hemangiomas have a clear boundary with
the fibrous capsule and do not invade the extra-
ocular muscles.
On non-contrast CT, most of these tumors
appear round or elliptical. Also, some are lobu-
lated with clear boundaries, having equal attenu-
ation with the extraocular muscles; occasionally,
these tumors have uneven attenuation and calcifi-
cation. After contrast administration, the progres-
sive enhancement sign can be seen within the
lesion. On non-contrast MRI, the lesion is isoin-
tense or slightly hypointense on T1WI and
­hyperintense as compared with the extraocular
muscles on T2WI; the lesion is also notably isoin-
tense to the vitreous body. This is mainly due to
the slow blood flow and greater concentration of
liquid materials in the interstitium. Progressive
enhancement sign is specific for the diagnosis of
a cavernous hemangioma. In the early phase of
postcontrast dynamic MRI, the contrast enhance-
ment is most likely to start from multiple points
in patchy or geographical regions, with a wide-
Z. Ding et al.
spread pattern. In comparison, the starting points
of enhancement on CT are likely to be one or
more focal points situated along the periphery of
the lesion [3]. The enhancement pattern help dif-
ferentiate cavernous hemangiomas from other
tumors that may occur in the orbit, such as
schwannomas and meningiomas. Schwannomas
typically occur in the extraconal space, while
cavernous hemangiomas usually occur in the
intraconal space; meningiomas are usually intra-
conal as well but typically abut or surround the
optic nerve due to the typical origin from the
optic nerve sheath. After contrast enhancement,
schwannomas show obvious inhomogeneous
enhancement with nonenhanced necrosis and
cystic areas, while meningiomas vary in their
degree of enhancement, as well as the degree of
calcification.
3.2 Tendon Sign
Feature
The typical CT findings of orbital myositis are
thickening of the extraocular muscles, which
extends forward to the attachment of the tendon
to the globe. The attachment may be irregular or
have nodular thickening, called the “tendon sign”
or “muscle tendon sign.”
Explanation
Orbital myositis is a nonspecific orbital inflam-
mation that causes irregular thickening of the
extraocular muscles and the attachment of the
tendon to the globe. Both non-contrast and post-­
contrast CT reveal irregular thickening of the
extraocular muscles and the attachment of the
tendon to the globe, which is called the tendon
sign, because intra-orbital myositis involves the
tendinous membrane of the tendon that attaches
to the globe. The appearance of this sign can be
considered as a specific diagnostic clue for orbital
myositis (Fig. 3.2).
Discussion
The “tendon sign” is characterized by thickening
of the extraocular muscles and at the site of
attachment of the tendon to the globe on pre- or
3  Head and Neck 87

a b

c d

e f

Fig. 3.1 (a, b) Axial and coronal T2WI demonstrates an early punctate enhancement within the mass. (e, f) The
oval, lobulated, and homogeneously hyperintense mass entire lesion showed more homogeneously at a point
within the cone of left orbit’s extraocular musculature 10 minutes after intravenous injection of contrast medium
superomedially. (c, d) Post-contrast T1WI demonstrates
88
Fig. 3.2  In a patient with orbital myositis, non-contrast
CT reveals the enlargement of the bilateral medial rectus
and lateral rectus, like tubular configuration, with the
thickened muscles at the site of attachment to the globes
(arrows)
post-contrast CT. The attachment site of the ten-
don to the globe may be irregular or have nodular
thickening, indicating the diagnosis of orbital
myositis. Orbital myositis is a nonspecific orbital
inflammatory disease that mainly affects the
extraocular muscles. The pathological manifesta-
tion is the thickening of one or more extraocular
muscles. The site of attachment of the tendon to
the globe that may appear irregular or have nodu-
lar usually has extensive inflammatory cell infil-
tration (mainly lymphocytes) on histopathology.
The typical clinical symptoms of orbital myositis
are acute periorbital pain, diplopia, ocular protru-
sion, swelling of the orbits, conjunctival hyper-
emia, and conjunctival edema adjacent to the
affected extraocular muscle.
On both pre- and post-contrast CT, orbital
myositis usually involves a unilateral extraocular
muscle but sometimes with bilateral involvement
with the spread of the lesion along the tendon.
The hyperdense appearance can appear much
more pronounced after intravenous contrast
administration, which can even involve more of
the extraocular muscles (sometimes all of them)
than noted on non-contrast CT; such diffuse
enhancement may be related to the vascular accu-
mulation and inflammation throughout the
affected musculature. However, MRI is the pre-
ferred method for the diagnosis of orbital myosi-
Z. Ding et al.
tis. Post-contrast T1WI combined with fat
suppression can clearly depict the inflammation
of the muscles, tendons, and orbital fat [4], which
contributes to the diagnosis of the disease. The
differential diagnosis of extraocular muscle
thickening mainly includes thyroid dysfunction,
internal carotid cavernous fistula, cavernous
sinus dural arteriovenous malformation, and neo-
plasms [5]. Thyroid dysfunction myopathy is
manifested as bilateral muscle involvement and
typically as thickening of the extraocular muscles
into a spindle shape, with tapering at the attach-
ment site of the tendon to the globe [5], while
orbital myositis manifests as the tendon sign.
Irregular or nodular thickening of the extraocular
muscles and localized enhancement contribute to
the differentiation of intraocular myositis from
thyroid dysfunction. Internal carotid cavernous
fistula and cavernous sinus dural arteriovenous
malformation are usually manifested as diffuse
thickening of the unilateral orbital musculature.
High-resolution CT shows that if the findings of
superior orbital venous dilatation are combined
with the expansion of the ipsilateral cavernous
sinus, then the findings are highly suggestive of
internal carotid cavernous fistula or cavernous
sinus dural arteriovenous malformation. Finally,
neoplastic lesions can directly invade or metasta-
size to the orbit, resulting in extraocular muscle
thickening; the thickened muscles are usually a
result of direct tumoral invasion.
3.3 V-Shape Sign
Feature
The typical retinal detachment shows a “V” shape
with its tip on the optic disk and the end point
toward the ciliary body. A subretinal effusion typ-
ically has high attenuation on CT, while on MRI,
T1WI and T2WI show hyperintensity, without
overt enhancement after injecting contrast agents.
Explanation
Retinal detachment refers to the separation of the
retinal neuroepithelial layer from the pigment
epithelial layer. The liquid leaks into the potential
gap between the two layers, forming subretinal
effusion (Fig. 3.3).
3  Head and Neck
a b
c d
Fig. 3.3 (a, b) On MRI, a rounded lesion of abnormal sig-
nal intensity is noted of the right globe on T1WI (a) and on
T2WI (b), where the vitreous body around the lesion was
isointense-hypointense on both sequences, and the signal
intensity internally within the lesion was a bit inhomoge-
neous on T2WI. (c, d) Following contrast administration,
Discussion
Retinal detachment is a common manifestation
of subretinal effusion or other disorders (such as
inflammation, trauma, and vascular disease). It
can be divided into two major categories based
on its causes: primary retinal detachment and
secondary retinal detachment. The former refers
to the absence of other diseases in the eye and is
solely due to the formation of holes in the retina.
The latter is caused by other diseases of the eye,
such as retinal exudative inflammation, trauma,
tumor, and proliferative lesions; also, any choroi-
dal lesion can lead to retinal detachment [6].
Because a subretinal effusion contains pro-
teins, CT shows a crescent-shaped or curved, uni-
form, high-attenuation shadow in the globe
(compared with the vitreous matter’s attenua-
tion). Regarding MRI, the concentration of pro-
tein affects T1 and T2 values. Hence, MRI
intensity of the subretinal effusion is varied and
mostly exhibits hyperintensity on T1WI/
T2WI. The typical retinal detachment sign shows
a “V” shape on CT or MRI with its tip at the optic
disc and the end pointing toward the ciliary body.
The detached retina is very thin and cannot be
89
on axial (c) and sagittal (d) postcontrast fat-suppressed
T1WI, there was slightly inhomogeneous enhancement
within the lesion, and the “V-shaped” hypo-­intensity was
visible (arrows). The tip of the arrow points to the optic
disc, while the opposite end points toward the ciliary body;
the “V” sign was more clearly seen in the sagittal plane
completely displayed on CT or MRI, but the con-
tour of the retina can be depicted between the
subretinal fluid and the liquid in the vitreous cav-
ity. Retinal detachment is thus manifested on CT
or MRI as an increase in density or signal inten-
sity, respectively, of the entire vitreous cavity. A
small number of retinal detachments can be
expressed as spheres, termed “spherical” retinal
detachment. Following contrast administration, a
subretinal effusion does not enhance. Secondary
retinal detachment appears not only with the
imaging findings described above of retinal
detachment but also often with visible primary
lesions on CT or MRI [7]. Hence, MRI showing
a subretinal effusion can demonstrate the primary
lesion of secondary retinal detachment. However,
the primary lesion may not be well-visualized on
CT, although the diagnosis of certain entities
causing the retinal detachment and subretinal
effusion, such as choroidal osteoma, can be
apparent. Of note, a detached retina is not directly
visible on CT/MRI images, but ultrasound can
depict a detached retina. Ultrasonographic
assessment of the vitreous body, retina, and sub-
retinal space adds a significant dimension to the
90
diagnosis of retinal detachment and the manage-
ment of patients with vitreoretinal abnormalities
[8]. The main differential diagnosis for retinal
detachment includes choroidal detachment and
choroidal tumors. Regarding choroidal detach-
ment, due to the limitation of the short posterior
ciliary short artery and vortex vein, a posterior
choroidal detachment appears as one or several
hemispheres, and the detachment cannot reach
the optic disc area; hence, the vicinity of the optic
disc is not affected. Regarding a choroidal tumor,
it can be distinguished from subretinal effusion
by the intensity of the tumor and the subretinal
fluid on MRI, as well as the degree of contrast
enhancement on post-contrast images.
3.4 Teardrop Sign
Feature
When the inferior wall of the eyelid is fractured,
the contents of the eyelid penetrate the maxillary
sinus through the fracture, shaped like tears.
Therefore, it is called a “teardrop sign,” which is
a specific indirect sign for the diagnosis of infe-
rior wall fracture.
Explanation
The wound is around the eyelids, causing the
pressure of the eyelids to rise. This indirectly
leads to a fracture of the inferior orbital wall, or
alternatively, there is injury to the infraorbital
margin directly, thus causing the inferior wall
fracture. The soft tissue in the orbit is embedded
in the fracture and falls into the sinus, forming a
teardrop sign (Fig. 3.4).
Fig. 3.4  A 37-year-old female with a fracture of the left inferior orbital wall. The left orbital content herniated inferi-
orly through the fracture site (arrow) into the left maxillary sinus, resembling teardrops (the “teardrop sign”)
Z. Ding et al.
Discussion
Multi-slice CT (MSCT) is the most effective
method of initial examination for ocular trauma.
The horizontal axis image shows not only the
location and displacement of the fracture but
also changes in the optic nerve, eye muscles, and
intra-orbital fat. Multiplanar reformat (MPR)
image is an important supplement. Volume
reconstruction images can also be utilized to
visualize the periorbital fractures. It is an impor-
tant reference value for clinically determining
whether to develop and operate a reasonable sur-
gical plan. When the globe and the surrounding
soft tissues are subjected to a blunt trauma such
as a direct blow, the pressure acting on it is con-
verted into hydraulic pressure. This pressure
may cause an increase in the internal pressure
within the bony orbital socket, resulting in the
breakage of the platelike bone wall of the middle
one-third, especially the weaker inner and lower
sidewalls, which are the walls most prone to
fracture. Typical clinical manifestations and
signs of orbital burst fractures are enophthalmos,
diplopia, vision decrease and loss, infraorbital
nerve sensory loss, supracondylar syndrome,
and globe shift.
The CT signs of orbital burst fractures include
direct and indirect signs. Direct signs include the
following: the continuity of the inferior orbital
bone is interrupted and comminuted, with no
fracture in the lower margin of orbit. The fracture
ends are angled or curved into the maxillary
sinus, typically resulting in a sinus effusion.
Indirect signs include thickening, displacement,
and incarceration of the extraocular muscles
adjacent to the fracture. In such instances, the
3  Head and Neck
orbital contents may prolapse through the frac-
ture into the maxillary sinus, forming a teardrop
sign, which is a specific, indirect sign for the
diagnosis of inferior orbital wall fracture. The
main purpose of orbital repair is to reconstruct
the orbits, restore them to the pre-traumatic state,
and repair the invaginated globes, particularly so
vision with its required extraocular muscle
motion is not impeded. CT scan demonstrates not
only the extent of the fracture but also the extent
of fracture displacement; it also shows the
embedded soft tissue. These factors provide the
basis for conservative clinical treatment or surgi-
cal treatment, as well as the choice of the surgical
plan and implant size. If the burst fracture causes
an increase in the volume of the orbit of
>2.25  cm3, it can be assumed that the globe
invagination is >2 mm after the orbital swelling
subsides. Therefore, an increase in the orbital
volume of >2.25 cm is a new standard for the sur-
gical treatment of orbital fractures [9]. Another
study aimed to find an accurate and reliable CT
measurement that could be used to identify
patients with orbital inferior wall fractures requir-
ing surgery to prevent subsequent diplopia and/or
globe retraction. The results showed that a
cranial-­caudal dimension greater than 0.8  cm
could predict the development of diplopia and/or
enophthalmos; such patients then require surgical
correction [10].
Fig. 3.5  A 58-year-old man with a progressive decline in
vision. MRI shows optic nerve of the right eye appearing
as low signal in relation to the surrounding, circumferen-
tial enhancement (arrows) of the optic nerve sheath on
91
3.5 Tram-Track Sign
Feature
The “tram-track sign” is most pronounced on
post-contrast CT or fat-suppressed T1WI of the
orbit. The optic nerve appears as low density or
low signal, in relation to the surrounding, parallel-­
appearing enhancing tumor of the optic nerve
sheath.
Explanation
The “tram-track sign” is most commonly used
to describe optic nerve sheath meningiomas.
Meningiomas tend to cause segmental or diffuse
circumferential thickening of the optic nerve
sheath. Once intravenous contrast material is
administered, the optic nerve can be seen on CT
or MRI as an unenhanced central linear struc-
ture (negative defect) surrounded by enhancing
meningioma. Transverse or sagittal images
demonstrate that this defect produces a “tram-
track sign” consisting of two parallel enhanced
regions of the tumor separated from each other
by the negative contrast defect of the optic
nerve. The corresponding finding on coronal
images is a doughnut configuration. Though less
common, when linear calcification occurs
within the optic nerve sheath meningioma, the
tram-track sign may be apparent on non-con-
trast CT (Fig. 3.5).
axial (left) and coronal (middle) fat-suppressed post-­
contrast T1WI.  This represents the “tram-track” sign of
optic meningioma. On non-contrast FLAIR with fat sup-
pression (right), a corresponding appearance is noted
92 Z. Ding et al.

Discussion kemia/lymphoma, and Erdheim-Chester disease

The tram-track sign is described as a feature to (a form of non-Langerhans cell histiocytosis).
help distinguish between optic glioma and optic
nerve sheath meningioma. In optic nerve sheath
meningiomas, the tumor sheath demonstrates 3.6 Double-Ring Sign
increased attenuation compared with the optic
nerve on post-contrast CT, and may not be read- Feature
ily visible on non-contrast CT.  Notably, optic Cochlear otosclerosis (also called oto-­spongiosis)
gliomas are derived from glial cells within the appears as an inhomogeneous hypodense ring
optic nerve and closely related to the optic nerve, surrounding the bony labyrinth of the basal turn
regardless of the pattern of growth. Hence, no of the cochlea on high-resolution CT (HRCT),
clear separation is present between the tumor and representing peri-cochlear erosions. Thus, the
the nerve on non-contrast CT images [11]. Optic appearance of a typical double-ring shape of
nerve sheath meningiomas (ONSMs) arise from lucency on HRCT at the bottom of the cochlea is
meningothelial cells of the arachnoid mater, called the “double-ring sign.”
being situated along the optic nerve sheath.
Histologically, the cell of meningioma is usually Explanation
of the meningotheliomatous type, but it may The trabecular meshwork in the region of peri-­
occasionally be of the transitional type. The early cochlear lucency on HRCT is, on histopathology,
subdural growth causes the tumor to surround the sparse and irregular, with large numbers of blood
nerve. Since the nerve is only surrounded, and vessels, osteoblasts, and osteoclasts, which is the
not completely covered or invaded by the tumor, basis of the double-ring sign (Fig. 3.6).
the optic nerve can usually be identified as a
“negative defect” within the tumor [11]. Discussion
Post-contrast CT also reveals the changes of Otosclerosis/oto-spongiosis is a chronic, progres-
optic canal area, such as bone destruction and sive hearing loss originating from the unknown,
bone hyperplasia in the case of expanding optic originally reported by Valsalva in 1735.
meningioma. Johns et al. described three distinct Otosclerosis is an osteodystrophic disorder of the
density changes in ONSMs on post-contrast CT otic capsule that results in abnormal resorption of
[12]: (1) the low-density optic nerve (the “nega- the endochondral bone, with deposition of abnor-
tive contrast” defect described above); (2) the
denser meningiomatous tumor mass; and (3) the
denser, parallel linear enhancing areas adjacent
to the optic nerve. This linear enhancement is
believed to be related to the linear spread of the
tumor along the subarachnoid space. Other retro-
bulbar masses usually do not exhibit perineural
dissemination along the dura and arachnoid in
such a focal fashion. On non-contrast MRI, an
ONSM is usually isointense or slightly hypoin-
tense on T1WI and isointense or slightly hyperin-
tense on T2WI, relative to the optic nerve itself.
On gadolinium-based postcontrast imaging, the
contrast enhancement is obvious, especially on
fat suppression sequences [13]. Other conditions
that can theoretically exhibit a tram-track sign
Fig. 3.6  Cochlear otosclerosis presents as a rounded peri-
include sarcoidosis, optic neuritis, orbital pseu- cochlear lucency that parallels the basal turn of the cochlea
dotumor, perioptic hemorrhage, metastases, leu- on HRCT, forming the double-ring sign (Black arrow)
3  Head and Neck
mal vascular bone. Otosclerosis usually appears
in the third to fifth decades of life, being more
common in women. On HRCT of the temporal
bone, otosclerosis/oto-spongiosis is typically
considered of two types based on their anatomic/
topographic location and imaging appearance:
fenestral (involving the fissula ante fenestram
just anterior to the oval window, ultimately result-
ing in stapes fixation) and retrofenestral
(hypodense bone within the otic capsule sur-
rounding the cochlea); of note, the fenestral vari-
ant is often limited to the region anterior to the
oval window. Typically, fenestral (i.e., stapedial)
otosclerosis presents with conductive hearing
loss (CHL), although it can also present as mixed
or sensorineural hearing loss (SNHL) in the
absence of CHL. It is often called “cochlear oto-
sclerosis”; fenestral otosclerosis/oto-spongiosis
is notably the more common type, representing
about 75–80% of oto-spongiosis cases, and is not
always detectable on imaging [14]. The fenestral
lesion is located along the lateral wall of the otic
capsule focally at the fissula ante fenestram (just
anterior to the oval window) and the tympanic
segment of the fallopian canal. The retrofenestral
type is more diffuse, affecting the labyrinthine
capsule and peri-cochlear regions, and is
described in more detail in the following para-
graph [15].
As described above, the retrofenestral type is
less common (about 20–25% of otosclerosis) and
more commonly presents as sensorineural hear-
ing loss (although also can present as a mixed
hearing loss). It nearly always involves fenestral
otosclerosis as well and can be much more exten-
sive and overt on HRCT. This subtype can poten-
tially involve the semicircular canals, internal
meatus, vestibule, and cochlear and vestibular
aqueducts in more severe cases; in such severe
cases, these can clinically present rarely as a
“third window” phenomenon causing hearing
loss or vestibular symptoms. HRCT abnormali-
ties are usually evident, which are visualized as a
disease within the peri-labyrinthine bone and
particularly along the cochlea in the retrofenes-
tral subgroup. HRCT highlights differences in
the density of the capsule outline, called the
double-­ring sign, which is a low-density, demin-
93
eralized endochondral defect outlining the
cochlea. Thus, this appearance on HRCT can be
considered a “gold standard” in the diagnosis of
otosclerosis, where active oto-spongiosis, as
described above, is visualized on HRCT as
reduced bone density/radiolucency throughout
the otic capsule; this appearance is also known as
the fourth ring of Valvassori). HRCT can also be
used to distinguish between otosclerosis and
other pathological conditions such as tympano-
sclerosis, cholesteatoma, ossicular fixation, and
congenital malformations [15]. As above, tempo-
ral bone HRCT using 1  mm (or less) thickness
sections is the modality of choice for assessing
the labyrinthine and peri-cochlear regions. MRI
is useful for assessing the cochlear lumen prior to
cochlear implantation in patients with profound
hearing loss, via assessing their patency on heavy
T2WI, preferably using 3D isotropic reconstruc-
tions of the labyrinthine structures [16].
3.7 Salt-and-Pepper Sign
Feature
The salt-and-pepper sign is a typical MRI sign of
paraganglioma (“glomus tumor”). On non-­
contrast T2WI, there is high-signal tumor tissue
and low-signal vascular flow void intertwined,
showing a characteristic “salt-and-pepper sign.”
This appearance may variably be present on
T1WI and post-contrast imaging as well.
Explanation
The typical appearance of a salt-and-pepper sign
is best shown on T2WI and also can be demon-
strated on T1WI and even on post-contrast
T1WI.  The “pepper” predominately represents
the intratumoral vascular flow voids, and the
“salt” is the hyperintensity of the lesion caused
by slow-flowing blood vessels or intratumoral
hemorrhage on T2WI, enhancing tumoral stroma
on post-contrast T1WI (Fig. 3.7).
Discussion
The salt-and-pepper sign was first described by
Olsen et  al. in 1987 [17]. On T2WI, the tumor
exhibits high signal, with multiple spotted intra-
94
a b
e f
Fig. 3.7  Paragangliomas in two different patients. (a–d)
A 43-year-old male with a right skull base mass, showing
dynamic enhancement on CE MRA (top left, a), a “salt-­
and-­pepper sign” on coronal postcontrast T1WI (top mid-
dle, b), and intermediate reduced diffusion on axial ADC
(top right- top image, c) and DWI (top right-bottom
image, d), consistent with a paraganglioma (glomus jugu-
lare). (e–g) In a 46-year-old male with bilateral paragan-
tumoral vascular flow voids, which is manifested
as the salt-and-pepper sign. The sign is consid-
ered a characteristic feature of paraganglioma.
Those authors believed that the incidence of this
sign was related to the size of the tumor; with a
tumor diameter of >2  cm size, the overall inci-
dence of this sign was reported to be 80%. Of
note, this sign can also be visualized on non-­
contrast T1WI and contrast-enhanced T1WI
scans. On histopathology, a paraganglioma is
composed of type I chief cells and type II sup-
Z. Ding et al.
c
g
gliomas (arrows in each image) splaying the carotid
bifurcations (“carotid body tumors”), there is characteris-
tic avid enhancement with a slight “salt-and-pepper sign”
on axial postcontrast CT (bottom left, e), having avid
metabolic uptake on 18F-FDG PET (bottom middle, f);
several months after right paraganglioma resection, there
was a “salt-and-pepper sign” of the residual left glomus
tumor on axial non-contrast T2WI (bottom right, g)
porting cells. The chief cell cluster is separated
by a fibrous matrix rich in large numbers of vas-
cular lumens; these blood vessels form many
extremely small capillary-level arteriovenous fis-
tulas. These histopathological features likely
form the basis for the MRI signal changes with
the salt-and-pepper signs in this type of tumor,
which again is found in paragangliomas with a
diameter of >2 cm. Similar appearances are also
found in other blood-rich vascular tumoral
lesions such as metastatic adrenal adenoma and
3  Head and Neck
metastatic thyroid carcinoma. Additionally, cer-
tain malignant tumors of the temporal bone, such
as adenoid cystic carcinoma of the e­ ndolymphatic
sac, may also have this sign. Also notable is that
glomus tumors may be bilateral in 5–10% of
patients, particularly in the region of the carotid
bodies.
Diffusion-weighted imaging (DWI), contrast-­
enhanced MR angiography (CE-MRA), and
dynamic contrast-enhanced (DCE) MRI have
shown great potential in oncologic applications
for head-and-neck tumors and can at times be
used to help distinguish paragangliomas from
other tumors. For paraganglioma, a higher signal
is often visible on DWI, with corresponding
mildly lower values on the ADC maps as related
to that expected for other benign tumors [18].
The mildly lower ADC values are not related to
cellularity or malignant potential as might be
inferred; rather, the bright DWI/low ADC signal
has been attributed to the inner texture of the
lesion, where benign solid tumors lacking necro-
sis can sometimes have higher DWI signal and
lower ADC values [19]. Regarding CE-MRA, it
has been utilized to distinguish paragangliomas
from other benign head/neck tumors such as
meningioma and schwannoma, with a sensitivity
and specificity of 100% and 90–95%, respec-
tively [20]. On CE-MRA, in over 90% of para-
gangliomas, there are both earlier dynamic
enhancement and much more prominent intratu-
moral flow voids as compared to meningiomas
and schwannomas [20]. Regarding DCE-MRI, it
has been used for the detection and evaluation of
paragangliomas, where malignant tumors tend to
exhibit a strong initial signal increase followed
by a washout effect, whereas benign lesions
(such as paragangliomas) mostly demonstrate a
slower initial signal increase combined with a
continuous signal increase [18]. Also, at present,
morphological and functional imaging has
become an important step in the diagnosis and
staging of paraganglioma in multidisciplinary
applications. Somatostatin receptor imaging and
positron emission tomography are the most reli-
able examinations currently approved for this
disease, while 18F-FDG PET usually demon-
strates elevated uptake in the large majority [21,
22]. These functional imaging methods use
95
highly specific tracers (specificity close to 100%).
The major advantage of metabolic imaging is that
it allows whole-body examination, which is very
useful for detecting multifocal forms of paragan-
glioma, which happen in a minority [21].
3.8 Steeple Sign
Feature
X-ray plain films of the posterior and anterior
soft tissues of the neck show that the normal con-
vexity on both sides of the trachea in the subglot-
tic region disappears, and the narrow subglottic
cavity leads to an inverted V-shape appearance of
this region. The apex of the inverted V-shape is
located at the level of the lower edge of the true
vocal cords. The narrow subglottic cavity changes
the shape of the tracheal air column, which
resembles a steep inclined roof or church spire,
hence being called the “steeple sign” (Fig. 3.8).
Explanation
Regarding the steeple sign, the adjacent area
affected by airway stenosis is 1 cm proximal to
the trachea, between the elastic cone and the true
vocal cord. At this level, the mucosal junction is
loose. The steeple sign is caused by tracheal
edema, which can elevate the tracheal mucosa,
leading to the disappearance of the shoulder of
the air column.
Discussion
Viral howling (also known as acute laryngotra-
cheobronchitis) is often caused by parainfluenza
or respiratory syncytial viruses. It is the most
common cause of upper-respiratory distress in
infants and young children, with a peak incidence
at 6 months to 3 years. Typical clinical manifesta-
tions are inspiratory wheezing and barking
cough. The diagnosis of the viral roar is usually
made clinically rather than radiologically. The
purpose of the radiological examination is to
exclude other diseases causing wheezing, such as
foreign body inhalation, esophageal foreign
body, congenital subglottic stenosis, diphtheria,
glottitis, or subglottic hemorrhage, which have
clinical symptoms resembling those of viral
wheezing. The viral roar can be manifested as a
96
a b
d e
Fig. 3.8  A 70-year-old male; there was a question of sub-
glottic stenosis in two locations (upper stenosis = arrows,
lower stenosis  =  dotted arrows), resembling a “steeple”
sign on chest X-ray (left, b), CT scan coronal reformat
(left middle, c), virtual airway 3D reconstruction AP plane
steeple sign, which can also be seen in some
other lesions. Differential diagnosis includes
glottitis, scald, neurovascular edema, and bacte-
rial tracheitis. In viral roar, the glottis is normal
on the lateral X-ray of the upper respiratory tract
and has a 1–1.5  cm long subglottic stenosis.
Z. Ding et al.
c
(middle, d), and descending “fly-through” images (right,
e–f). Note the normal true vocal cords in each image (*)
and that the more inferior subglottic stenosis is more
severe (dotted arrows) relative to the more proximal ste-
nosis (arrows)
Whether lateral X-rays of the soft neck tissue
should be included in evaluating viral roar is still
controversial. If glottitis cannot be ruled out clin-
ically, the absence of illumination to the lateral
film may result in misdiagnosis. Therefore, if
viral roar is suspected in a clinic, anterior and
3  Head and Neck 97

lateral radiographs of the trachea and chest radio- Explanation

graphs should be performed at the same time. On a plain CT image, the normal thyroid gland is
Usually, viral howling is a self-limiting disease replaced by a low-density tumor and form a
with a good prognosis [23]. To improve the gas “bite-like shape” defect (Fig. 3.9). Axial or mul-
exchange function, nonsurgical treatment, such tiplanar reconstructions show the largest tumor
as aerosol inhalation of racemic adrenaline and diameter at the edge of the thyroid gland.
corticosteroids, is usually used.
Further imaging can be necessary in some Discussion
cases, preferably utilizing low-dose, non-contrast Bitten cookie sign can be used as a useful indica-
CT. In questionable cases or in adults with more tor for the diagnosis of PTC.  PTC is the most
complex anatomy and post-surgery, non-contrast common subtype of thyroid carcinoma with low
CT with thin-section (<1  mm) and “virtual air- malignancy [25]. The disease can occur at any
way” reconstructions with “fly-through” images age. The tumor grows slowly, and the main symp-
can be helpful to confirm a subglottic stenosis tom is a painless mass in the neck that moves up
(Fig.  3.8). Such 3D reconstructions (also called and down with swallowing. Complications are
“virtual laryngoscopy”) can be helpful to the sur- asphyxia, impaired laryngeal nerve, impaired
geon in visualizing the site and degree of steno- recurrent laryngeal nerve, low calcium level, and
sis, particularly if multiple [24]. hypothyroidism. Bitten cookie sign is an impor-
tant sign of CT diagnosis of papillary thyroid car-
cinoma, which is highly specific and sensitive. On
3.9 Bitten Cookie Sign a plain CT image, the normal thyroid gland is
replaced by a low-density tumor to form a “bite-­
Feature like shape” defect. Axial or multiplanar recon-
Bitten cookie sign means that the normal thyroid structions show the largest tumor diameter at the
high-density contour is locally replaced by a low-­ edge of the thyroid gland [26]. The development
density tumor on plain CT scan, forming a “bite-­ of a bitten cookie sign may be related to the tumor
like shape” defect, which can be used as an occurring at the edge of the thyroid gland and
indication for the diagnosis of papillary thyroid involving the capsule. If the capsule is not
carcinoma (PTC). involved but the thyroid tissue in the capsule is

a b

Fig. 3.9 (a) Low-density lesion of the right thyroid mar- tumor margin is more blurred than the plain scan, and the
gin, corresponding to the right thyroid margin interruption relatively low-density area of the tumor shrinks
and defect, in a 49-year-old female patient. (b) Enhanced
98
thin, it cannot be distinguished on CT. This needs
to be differentiated from nodular goiter, which
involves expansive growth, with peripheral thy-
roid tissue showing external pressure and most of
the thyroid margin intact. After enhancement,
some tumors show significant peripheral enhance-
ment, while the sign of thyroid edge interruption
disappears completely or partially, masking the
true contour of the tumor. Hence, a plain CT scan
is more objective to reflect the contour of the
tumor compared with contrast-­ enhanced scan.
Hence, it is valuable for the differential diagnosis
of benign and malignant tumors. Also, the irregu-
lar shape of the nodules and microcalcification are
also important CT signs of PTC. Han et al. showed
that each sign had high sensitivity in the diagno-
sis, but the specificity was low. The combination
of different CT signs would improve the specific-
ity of diagnosis of PTC and reduce the occurrence
of misdiagnosis.
3.10 Prominent Ear Sign
Feature
Relapsing polychondritis (RP) is an autoimmune
disease that involves recurrent inflammation of
the cartilage in multiple areas of the body (includ-
ing the auricles). Central nervous system lesions
are rare. RP with encephalitis can be diagnosed
by a distinctive appearance of the auricle of
hyperintensity on DWI, which has been termed
the “prominent ear sign.”
Explanation
In patients with RP also having encephalitis,
DWI depicts hyperintensity in the temporal lobe
and adjacent auricles. Histopathology shows
inflammatory cell infiltration, predominately
lymphocytes, consistent with RP. Therefore, the
brain inflammation is also attributed to RP.  On
MRI, the sign related to the auricular inflamma-
tion is called the prominent ear sign.
Discussion
In RP with encephalitis, Kuwabara et  al. have
reported that it can be diagnosed based on the
prominent ear sign of the auricle on DWI [27].
Z. Ding et al.
Regarding RP, it is a rare disease with unknown
etiology, usually characterized by recurrent
inflammation of the cartilage in multiple body
parts, such as the auricle, nose, trachea, and joints
[28]. The lesion can occur at any age, but the
peak of incidence occurs in the fourth and fifth
decades of life, with nearly equal gender distribu-
tion. On biopsy of the auricle, histopathology
shows inflammatory cell infiltration, mainly lym-
phocytes, consistent with RP.  Therefore, the
encephalitis in this entity is attributed to
RP. Immunofluorescence studies have confirmed
the involvement of autoantibodies in specific col-
lagen types limited to cartilage.
CT and MRI reveal the affected preauricular
soft tissue swelling and thickening, where the
T2WI signal hyperintensity of the auricular carti-
lage manifests as edema and inflammation. In RP
patients with encephalitis, CT shows low-density
areas in the temporal lobe, which has a high sig-
nal on T2WI and abnormal enhancement on
contrast-­enhanced T1WI, suggesting encephali-
tis. DWI shows hyperintense in the enhanced
region and the adjacent auricle. The differential
diagnosis should include necrotizing external oti-
tis, which may be due to the presence of bony
erosions on imaging, a complication in elderly
patients with diabetes. On the contrary, the signal
abnormality of the prominent ear sign is limited
to the auricle without bone erosion.
3.11 Gas Bubble Sign
Feature
In the case of hangings and other cases of direct
blunt injury to the larynx, when a fracture occurs,
gas bubbles are observed in the tissue near the
laryngeal structures, called the “gas bubble sign,”
as a diagnostic indicator of neck trauma.
Explanation
The gas bubble sign can be used as a diagnostic
indicator of neck trauma, which strongly sup-
ports the assessment of injury to the larynx. This
finding not only helps those who survive an
attack to the neck but also contributes to postmor-
tem (Fig. 3.10).
3  Head and Neck
a b
Fig. 3.10  A 36-year-old female with (a) an axial slice at
the level of the thyroid cartilage. In (b), there is a coronal
reconstruction demonstrating the thyroid cartilage. Gas
Discussion
The appearance of vacuum phenomena (also
known as minute gas) is well known on radiogra-
phy [29]. It is most common in degenerative joint
disease and is also found in osteomyelitis,
abscesses, joint effusion, multiple myeloma, iat-
rogenic causes, bone fractures, and other causes
of trauma, such as ligament tears. The enclosed
tissue space can expand as a rebound phenome-
non after external impact, in which the volume
increases, the pressure decreases, and thus the
solubility decreases, causing the gas to leave the
solution [30, 31]; this then appears as a vacuum
phenomenon, which can be identified near trau-
matic lesions. The gas bubble sign is a distinctive
indicator of diagnosing traumatic neck injury,
usually to the laryngeal structures.
Non-contrast CT is sufficient to diagnose this
type of injury and is usually adequate in the
assessment of acute neck trauma, although post-­
contrast CT may be necessary for dedicated cer-
99
bubbles (arrows) at the site of the thyroid cartilage and
surrounding soft tissues are demonstrated
vical vascular evaluation. The assessment of the
larynx includes the location of the fracture (hyoid
with the small and large cornua, upper and lower
horns, thyroid cartilage, etc.). A “gas bubble
sign” can be visualized in the tissue adjacent to or
within the cartilage/bone itself potentially with
malformation and/or dislocation of the thyroid
membrane, the thyroid cartilage, and/or the hyoid
bone. The diagnosis of gas in a laryngeal struc-
ture not only helps evaluate and delineate the site
of injury in those who survive an attack to the
neck but also contributes to the assessment of
postmortem cases of trauma (for example, it may
help determine the etiology or mechanism of
injury). As such, the gas bubble sign can be used
as a diagnostic indicator for detecting laryngeal
trauma. In the case of variants of the larynx bone,
especially the thyroid cartilage, the difference
between cartilaginous or fatty osseous changes
versus gas in the thyroid must be accurately
noted.
100 Z. Ding et al.

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3  Head and Neck 101

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Stack BC Jr, Tolley NS, Bartel TB, et  al. AHNS series:
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Szymańska A, Szymański M, Gołąbek W, Drelich-Zbroja
Pan C, Yarbrough WG, Issaeva N. Advances in biomarkers
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neck cancer. Onco Targets Ther. 2018;5(5–6):140–1.
Widmann G, Henninger B, Kremser C, Jaschke
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the art. MRI-Sequenzen in der Kopf-Hals-Radiologie-­
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Payabvash S.  Quantitative diffusion magnetic resonance
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 Chest
4
Tao Jiang, Yanling Zhang, Shanshan Wu,
and Jujiang Mao

Contents
4.1 Multinodule Accumulation Sign  105
4.2 Lobulation Sign  106
4.3 Spinous Protuberant Sign  107
4.4 Vacuole Sign  108
4.5 Coarse Spicules Sign  109
4.6 Pleural Indentation Sign  110
4.7 Beaded Septum Sign  112
4.8 Honeycomb Sign  113
4.9 Withered Tree Sign  114
4.10 CT Angiogram Sign  114
4.11 Air Bronchiologram Sign  115
4.12 Air Bronchogram  116
4.13 Positive Bronchus Sign  117
4.14 Mucous Bronchogram  118
4.15 Gloved Finger Sign  119
4.16 Feeding Vessel Sign  120
4.17 Vascular Convergence Sign  121
4.18 Silhouette Sign  122
4.19 Luftsichel Sign  123

T. Jiang
Department of Radiology, Changhai Hospital,
Shanghai, China
Y. Zhang · S. Wu · J. Mao (*)
Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China

© Springer Nature Switzerland AG 2021 103

B. Gao, A. M. McKinney (eds.), Classic Imaging Signs,
https://doi.org/10.1007/978-3-030-56348-6_4
104 T. Jiang et al.

4.20 Golden S Sign  124

4.21 Hampton’s Hump Sign  125
4.22 Square Sign  126
4.23 Peach-Tip Sign  128
4.24 Comet Tail Sign  129
4.25 Reversed Halo Sign  130
4.26 Halo Sign  131
4.27 Air Crescent Sign  132
4.28 Water-Lily Sign  133
4.29 Mosaic Pattern  135
4.30 Ground-Glass Opacity  136
4.31 Tree-in-Bud Sign  138
4.32 Double-Wall Sign  139
4.33 Crazy Paving Appearance  140
4.34 Black Pleural Line Sign  141
4.35 Sarcoid Galaxy Sign  142
4.36 Diaphragm Sign; the Interface Sign; the Bare Area Sign; the Displaced
Crus Sign  144
4.37 Split Pleura Sign  147
4.38 Subpleural Line; Subpleural Curvilinear Shadow  148
4.39 Signet Ring Sign  149
4.40 Fallen Lung Sign  150
4.41 Ring Around the Artery Sign  151
4.42 Deep Sulcus Sign  152
4.43 Scimitar Sign  154
4.44 Bulging Fissure Sign  155
4.45 Air–Fluid Level Sign  156
4.46 Incomplete Border Sign  157
4.47 Grey Snow Sign  158
4.48 Ace-of-Spade Sign  160
4.49 SAM Sign  161
4.50 Linguine Sign  163
4.51 Peripheral Washout Sign  164
4.52 Spicular Sign  166
4.53 Tiny Calcium Sign  167
4.54 Tattoo Sign  169
References  170
4 Chest
4.1 Multinodule
Accumulation Sign
Feature
On high-resolution computed tomography
(HRCT), three forms of the multinodule accumula-
tion sign are seen. (1) Petal shape: lesion less than
or equal to 2 cm. In the mediastinal window can be
seen 3 to 5 small nodules of about 1–5  mm size
nodule aggregation, which can show a petal shape.
There is a narrow, clear, low-attenuation septum
between each small nodule. (2) Mulberry-­ like
structure: lesion usually more than 2  cm in size,
composed of several or perhaps 10 small nodules in
aggregation. (3) Gourd-like structure: the lesion
shows multiple nodules arranged in an oval. The
largest nodules are near the pleura, of which the
diameter can reach 3–5 cm, and the smallest nod-
ules are near the hilum, with diameter to 3–5 cm. In
the shape like a pagoda, the tip points to the hilum.
Explanation
Petal-shape accumulation may be a specific sign
of a relatively early peripheral pulmonary carci-
noma. With growth, the tumor gradually shows
the other two characteristic appearances. The for-
mer is the early manifestation of the latter two
structures. It is helpful to strengthen the under-
standing of the multinodule accumulation sign
and can improve the early diagnosis of peripheral
pulmonary carcinoma (Fig. 4.1).
Discussion
The formation of the mulberry-like multinodule
accumulation sign may be attributed to interlobu-
lar septum fibrosis. (1) The lung cancer originates
from the bronchioles and invades one or more
adjacent lobules, stimulating the alveolar septum
and causing interlobular septum hyperplasia. The
tumors can be temporarily obstructed at the
thickened interlobular septum and develop in the
direction of no or less resistance. (2) The growth
rates of the parts of a lung cancer are not uniform.
Each part of a lung cancer may have different his-
tological types, but some share the same kinds of
tissue (common type). However, the tumors usu-
ally have multiple nuclei at onset and the degree
of differentiation is different, so the growth rates
105
Fig. 4.1  On computed tomography (CT) mediastinal
window, an irregular nodular mass is shown in the upper
lobe of the right lung; multiple round nodules are aggre-
gated and the nodules are smaller
of tumors are inconsistent. (3) Tumors meet
resistance in growth: during the growth process,
the tumor encounters the obstruction of adjacent
blood vessels and scar tissue, so the obstructed
part becomes concave, and the cancer tissue pro-
trudes on both sides [1].
The pathological basis of pagoda-like multi-
nodule accumulation sign is the spread of the
tumor to the surrounding tissues in a continuous
infiltrating way. With the growth of the tumor, the
tumor cells from the primary tumor invade and
destroy the surrounding normal tissues and con-
tinue growth through the interstitial space, lymph
vessels, blood vessels, and further. Formation of
a gourd-like or pagoda-like structure leads to the
normal structure of the lymph nodes becoming
partly or completely involved. The pagoda-like
multinodule accumulation sign is commonly
seen in poorly differentiated tumors; when the
tumor growth appears in tracking (the tumor cells
fill the alveolar cavities in clusters and grow
along with the alveolar pore) or the tumor growth
occurs along the alveolar wall (cancer cells cover
the alveolar wall and continue to grow along
alveolar walls), this sign can be formed. The mul-
tinodule accumulation sign has important clinical
value in the diagnosis and differential diagnosis
of benign and malignant lung diseases. The pres-
ence of the multinodule accumulation sign sug-
gests malignant tumor of the lung.
106
4.2 Lobulation Sign
Feature
The lobulation sign, which is present when the
edge of the nodule shows an uneven lobulated
contour, is a nonspecific CT sign of peripheral
lung cancer. It can be divided into shallow lobes,
middle lobes, and deep lobes. Measured by the
ratio of arc–chord distance to chord length, lob-
ules with the ratio of 4:10 or more are defined as
deep lobules, those of 2:10 or less are defined as
shallow lobes, and those equal to 3:10 are defined
as middle lobes. The deep lobule is more com-
mon in malignant tumors.
Explanation
The formation of lobulation is the result of dif-
ferent degrees of differentiation of tumor cells;
some cancer tissues grow faster outward, thus
protrude more clearly and form lobulation. In
addition, the resistance of the tumor is different
when it expands outward. In the soft lung group,
the resistance is smaller. When it encounters the
pulmonary artery, bronchus, and fibrous scar tis-
sue, the resistance is greater, and growth is tem-
porarily limited; thus, the lobulation sign will be
formed. Fibrous hyperplasia of interlobular
septa, which has a limited effect on tumor
growth, can be seen on pathological sections of
lung cancer. The arc protrusion of the interlobu-
lar septum reflects the size and depth of the
tumor lobulation. If the tumor breaks through the
interlobular septum and expands outward, merg-
ing multiple interlobular septa form larger lob-
ules, which also is a factor in the formation of
lobulation (Fig. 4.2).
Discussion
The lobulation sign is an appearance of multiple
pronounced uneven arcs in the edge of tumors
caused by the different degrees of differentia-
tion of tumor cells [2]. Lobulation in a nodule is
attributed to different or uneven growth rates, a
finding that is highly associated with malig-
nancy. In part-solid nodules, a lobulated border
suggests invasiveness. The finding is not uncom-
mon in carcinoids. Benign lobulation is the
result of hyperplasia of adjacent connective tis-
T. Jiang et al.
Fig. 4.2  Man aged 74 years presented with chest pain for
1 week. On chest CT, a lesion in the lower lobe of the right
lung was shown having a lobulated border with moderate
enhancement on post-contrast CT
sue and cicatricial contraction. The margin
should be carefully evaluated on thin-slice CT
to differentiate it from satellite micronodules. In
benign nodules, lobulation is often seen in ham-
artomas. A special form of lobulation is the
“notch sign.” A notch is defined as an abrupt
bulging of the lesion contour. This finding is
relatively frequent in malignant nodules but can
also be seen in benign conditions such as
granulomatous.
Assessing the likelihood of malignancy in pul-
monary nodules remains a challenging task.
Morphological assessment is only one part of the
diagnostic puzzle, but its role should not be
underestimated. A smooth border, triangular or
polygonal shape with peri-fissural location, fat,
and popcorn calcifications indicate a benign
nature. Features that suggest a malignant nature
include a persistent subsolid morphology, spicu-
lation, lobulation, and pleural retraction. More
complex findings such as bronchial abnormali-
ties, bubble-like lucency, an associated cystic air-
space, and vascular convergence sign are also
indicative of a high likelihood of malignancy. In
subsolid nodules spiculation, lobulation, and
pleural retraction indicate an invasive adenocar-
cinoma rather than a preinvasive lesion.
Lobulation is associated with the size of tumors.
Round or round-like appearance of lobulation
could be observed in small tumors, and lobula-
4 Chest
tion genesis might be induced by a 1–1.5  cm
tumor. In response to the increase in tumor size,
lobulation might become continuously obvious
and deepened [3].
4.3 Spinous Protuberant Sign
Feature
On CT scans, the edge of a solitary pulmonary
nodule has one or more pointed spinous protu-
berances, called spicule sign, which make the
edge of the lesion irregular. If the spinous protu-
berances are arranged densely, forming serrated
teeth, it is called serrated sign. If the spinous pro-
tuberance is longer, and its thickness and length
are different, it resembles crab feet.
Explanation
Malignant tumor cells produce tumor angiogen-
esis factor and induce neovascularization.
Usually, malignant tumors with active growth are
rich in blood vessels and are tortuous and thick. It
is generally believed that the lobular spinous pro-
tuberance of the tumor is caused by its uneven
growth rate, which results from differential resis-
tance and blood supply in different parts of the
tumor at different locations during its growth and
development (Fig. 4.3).
a b
Fig. 4.3 (a) Peripheral lung cancer in the right upper lobe. (b) Peripheral lung cancer in the left upper lobe. Spicule
sign is seen at point of arrow
107
Discussion
A spicule is a kind of thick and blunt structure
between lobulation or spiculation, sometimes
called special lobulation. The target scan can
show the edge and spinous protuberance of the
mass well, and the three-dimensional (3D) scan
can also show better this “mallet” structure, a
proximally wide, distally narrow, triangular soft-­
tissue protrusion. The spicule sign is an impor-
tant sign of lung cancer: central lung cancer and
peripheral lung cancer can be seen, with the high-
est incidence of peripheral lung cancer, followed
by benign nodules, such as tuberculosis, inflam-
matory pseudotumor, and other organic inflam-
mation [4]. The main pathological basis is the
infiltrative growth of malignant tumor cells. The
blood supply of lung cancer mainly comes from
the bronchial artery, with some from the pulmo-
nary artery and other collateral vessels. The blood
vessels around the tumor are abundant, dense,
and numerous, and the proliferation of cancer
cells is active. Therefore, the lobular spinous pro-
cess around the tumor is the anterior aspect of
tumor growth. Because the blood supply of
­different parts of the tumor is different, some tis-
sues grow rapidly. Tumor cells infiltrate or spread
along lymphatic vessels in connective tissues
adjacent to bronchi and pulmonary arteries, caus-
ing tumor nests or tumor infiltration in adjacent
108
lung tissues, resulting in edema, fibrosis, thicken-
ing of connective tissues, and the formation of
spinous protuberances. Second, in the process of
tumor growth, the sign is caused by the resistance
of various spaces, such as the interlobular septum
and other connective tissue barrier factors. In
benign lesions, spinous protuberance may also
occur. The pathological basis is that caseous and
inflammatory secretions invade the interlobular
septum, resulting in acute or subacute inflamma-
tion of local bronchi and blood vessels.
The CT features of peripheral small lung can-
cer and inflammatory nodules are solitary nod-
ules. The occurrence and development of lung
cancer is a gradual process. The growth pattern of
lung cancer mainly includes solid growth and
wall-accumbent growth. Wall-accumbent growth
is regarded as the early pathological change of
lung cancer, which gradually forms a solid mass
with the continuous progress of the tumor.
However, lobulation and small spinous protuber-
ances may form when the growth rate around the
tumor is different or obstructed by adjacent lung
stents. There was a significant correlation
between the appearance of spicule sign on CT
and peripheral lung cancer that was associated
with interstitial lung disease and chronic obstruc-
tive pulmonary disease [5]. Inflammatory nod-
ules are usually caused by inappropriate treatment
of acute inflammation or chronic formation at the
beginning. Consolidation, granuloma formation
with slight exudation, and fibrosis are pathologi-
cal manifestations of inflammatory nodules. With
the gradual development of fibrosis in the lesion,
a b
Fig. 4.4 (a) A nodular increased attenuation shadow can be seen in the left lower lobe. (b) Vacuole sign is seen in the
lesion and shallow lobulation and burr growth at the edge of the lesion
T. Jiang et al.
it may eventually lead to contraction of the lesion,
further lobulation, and spinous protuberances.
4.4 Vacuole Sign
Feature
The vacuole sign refers to a small round, oval, or
strip-shaped reduced attenuation zone in the
dense mass or nodule. Its diameter, less than
5  mm, can be distinguished from a pulmonary
carcinoma cavity (>5 mm is called a cavity), and
vacuole sign can be single or multiple.
Explanation
The pathological basis of vacuolar sign includes
(1) gas-filled lung tissue that was not occupied
by tumor tissue; (2) unclosed or dilated bronchi-
oles; (3) gas-filled cavity between papillary car-
cinoma structures; (4) cancer tissue growing
along the alveolar wall that does not close, dis-
solve, destroy, or enlarge the alveolar space; or
(5) formation after small focal necrosis dis-
charge in the tumor. This sign is more common
in bronchioloalveolar carcinoma and adenocar-
cinoma, but is also seen in squamous cell carci-
noma. In some cases, the presence of mucus
causes exfoliated tumor cells in the vacuoles.
The CT value can be increased and be similar to
the attenuation of water. On the CT lung win-
dow, it appears as a small bubble-like fuzzy
low-attenuation shadow, or a small bubble-like
radiolucent shadow on the mediastinum window
(Fig. 4.4).
4 Chest
Discussion
According to the foregoing definition, it is neces-
sary to pay attention to the air bronchogram. The
air bronchogram can show a thin strip of air
attenuation shadow and can also be a small-­
diameter, 1-mm bubble air attenuation shadow. It
can be seen on several consecutive levels, so the
two signs should not be confused. In the process
of image analysis, if the low-attenuation shadows
in the nodules are localized, located within the
nodules, and do not reach the edge of the nod-
ules, it should be considered as a vacuole sign.
The vacuole sign is most common in bronchio-
loalveolar carcinoma, adenocarcinoma, and
occasionally in other lung benign nodules such as
tuberculosis and bronchiolar cysts [6]. There are
differences in the location of vacuolar signs
between pulmonary carcinoma and benign nod-
ules. The vacuole sign of pulmonary carcinoma is
mostly located in the middle two thirds and outer
part of the nodule, and the vacuole sign of benign
nodules is mostly located in the middle two thirds
and inside part of the nodule. The vacuole sign is
an important imaging sign in the differentiation
of pulmonary carcinoma and other benign nod-
ules and quite importantly in the differential
diagnosis of early lung cancer. When seen in sub-
solid nodules, particularly part-solid nodules, it is
likely to suggest to a malignancy [7, 8].
4.5 Coarse Spicules Sign
Feature
The coarse spicules sign is a thin, short line of
radial unbranched shadow that extends from the
edge of the tumor to the surrounding lung paren-
chyma and is not connected to the pleura.
Explanation
The coarse spicules sign is more common in
peripheral pulmonary carcinoma. The pathologi-
cal basis is the infiltration of tumor cells into an
adjacent bronchial sheath or local lymphatic ves-
sels or fibrous band of the tumor that promotes
connective tissue formation. Benign nodules,
such as inflammatory pseudotumor and tubercu-
losis, can also be seen on the edges of coarse
109
spicules, but longer and softer, often formed by
hyperplastic fibrous connective tissue (Fig. 4.5).
Discussion
The coarse spicules sign has high clinical value
in the diagnosis and differential diagnosis of
peripheral pulmonary carcinoma, especially for
isolated lung nodules [9]. The pathological basis
is (1) invasive growth of cancer tissue, peripheral
exudation, fibrosis, and interstitial reaction; or
(2) obstructive pneumonia or pulmonary infarc-
tion caused by cancer cells infiltrating small
bronchi and small blood vessels. When analyzing
the coarse spicules sign, it should be noted that
(1) it is not connected with the pleura (otherwise
it is defined as pleural indentation: pleural line
shadow, rabbit ear sign); (2) it shows radial but
no branch, thus can be distinguished from vascu-
lar shadow; and (3) the sharp, triangular, or ser-
rated shadows at the edge of the lesion are called
the spinous process sign. For the convenience of
description, the coarse spicules with length less
than 5 mm are called short coarse spicules, and
coarse spicules with length more than 5 mm are
called long coarse spicules.
The coarse spicules sign can be displayed on
both plain radiography and CT, but CT has a
greater advantage in displaying fine coarse spic-
ules. When there is a coarse spicule sign in the
isolated nodules in the lung, the possibility of
pulmonary carcinoma should be considered.
Short coarse spicules are more useful, but the
absence of coarse spicules cannot rule out the
possibility of pulmonary carcinoma [10].
Numerous reports in the literature have shown
the coarse spicules sign is not a specific sign of
malignant lesions. Benign nodules can also have
coarse spicules, but the benign nodules have
fewer coarse spicules, and this sign is more com-
monly seen in malignant nodules. Moreover, the
coarse spicules sign is more likely to appear in
peripheral pulmonary carcinoma associated with
interstitial pneumonia and chronic obstructive
pulmonary disease. For some cases that are diffi-
cult to identify and show little change in
­short-­term follow-up observation, biopsy should
be suggested to avoid the delay in optimal time of
treatment.
110
a b
Fig. 4.5 (a) A 66-year-old woman: chest CT shows a
nodular increased attenuation in the right upper lobe; mul-
tiple long and thin coarse spicules can be seen. (b) A
4.6 Pleural Indentation Sign
Feature
On CT, the pleural indentation sign shows more
than one or two linear shadows on the edge of
the pulmonary lesion, terminating in the pleura
with small triangular or trumpet-shaped
shadows.
Explanation
The main pathological basis of pleural depres-
sion is fibrous tissue hyperplasia, scar formation,
and connective tissue septum thickening in
lesions, without local pleural thickening or adhe-
sion. Inflammatory lesions and tumors with such
pathological basis may show the pleural indenta-
tion sign (Fig. 4.6).
T. Jiang et al.
78-year-old woman: chest plain CT shows a nodular
increased attenuation in the left upper lobe and multiple
short coarse spicules
Discussion
Pleural indentation (PI) is an imaging sign sec-
ondary to peripheral lung lesions. In the past this
image was called the rabbit ear sign, or pleural
tail sign, which some scholars described as char-
acteristically V-shaped, X-shaped, or star-shaped.
Currently, the appearance of adjacent pleural
changes in these peripheral lung lesions is col-
lectively referred to as the pleural indentation
sign. The PI is an important imaging manifesta-
tion in the diagnosis and differential diagnosis
of solitary pulmonary nodules. Although PI and
intrapulmonary nodules occur simultaneously
as a malignant phenomenon, PI is not unique to
lung cancer. It is very easy to misdiagnose if the
diagnosis and differential diagnosis are based on
PI alone. Because inflammatory lesions and lung
4 Chest
a b
c d
Fig. 4.6 (a, b) Pleural indentation sign: lesion in left
lower lobe terminates in pleura with a linear shadow and a
trumpet shape. (c, d) Pleural indentation sign: right lower
cancer are very similar, it is difficult to distin-
guish them. For example, the linear shadow can
be seen in tuberculoma, mycotic globules, silico-
sis fusion, and metastasis, so PI is limited in the
diagnosis of lung cancer [11]. PI was previously
used as one of the principal signs of malignant
tumor diagnosis. Recently, the benign and malig-
nant nodules of the lungs are said to cause PI,
but the pathological basis is not completely the
same, so the morphological manifestations on the
multi-slice CT (MSCT) images are also different.
The pathological basis of benign pulmonary nod-
ules is the inflammatory cells in various inflam-
matory lesions, which are directly infiltrated
into the pleural side along the interstitial space
of the pulmonary lobule or the subpleural lym-
phatic vessels, involving the visceral pleura and
even the parietal pleura to make the pleural reac-
111
lobe lesions terminate in pleura with multiple linear shad-
ows that appear as a small triangle
tion. Sexual thickening, followed by cellulose
exudation, and adhesion, cause lung tissue con-
traction, and finally lead to pleural thickening,
traction, and adjacent subsegmental atelectasis.
Concurrent pleural attachment and indentation
are risk factors for visceral pleural invasion, and
the odds increase with a larger solid portion in the
subsolid nodules. Early surgical resection could
be encouraged for these patients to decrease the
risk of recurrence [12].
On MSCT are seen thickening and twisting
pull lines near the pleura, thick basal thickening
adjacent to the pleura, pleural fat depression, and
pleural effusion. The pathological basis of PI in
malignant pulmonary nodules may be the con-
tractile force of some component of fibrous scar
tissue in the mass. It is transmitted to the free
visceral pleura through the elastic fibrous reticu-
112
lar structure of the alveolar stent, which causes
the visceral pleura to collapse without thicken-
ing and adhesion along the traction direction. On
MSCT, one or more thin and rigid stretch lines
were seen at the edge of the lesion and termi-
nated in visceral pleura with a triangle-like or
trumpet-­like shadow. A linear pleural tag with
soft-tissue component at the pleural end on CT
can increase the accuracy of early diagnosis of
visceral pleural invasion by non-small cell lung
cancer (NSCLC) that does not abut the pleura
[13]. Pleural depression is considered as a non-
specific sign of malignant solitary pulmonary
nodules on HRCT. Pleural thickening and adhe-
sion in pleural depression are common in inflam-
matory lesions, resulting in uneven linear
thickness, which is the key to differentiating PI
from lung cancer. Comprehensive consideration
of these factors of pleural indentation, sex, tumor
density, and distance between the lesion and
pleura might improve the diagnosis of pleural
invasion [14].
4.7 Beaded Septum Sign
Feature
On high-resolution computed tomography
(HRCT), irregular and nodular thickening of
interlobular septum is called beaded septum sign,
mainly occurring in the periphery or in one third
of the outer part of lung.
Explanation
Beaded septum sign is a feature of pulmonary
metastases on HRCT. An irregular, nodular thick-
ened interlobular septum represents the irregular
expansion of tumor cells in capillaries and lym-
phatic vessels, as well as secondary perivascular
and interstitial edema and fibrosis [15] (Fig. 4.7).
Discussion
The interlobular septa of peripheral pulmonary
interstitial tissue are composed of pulmonary
veins, lymphoid tissue, and interstitial tissue. The
smallest anatomical unit displayed on HRCT is
the secondary lobule. Metastatic tumor cells or
tumor thrombi stay in the capillary and lymphatic
vessels around the lung through hematogenous
T. Jiang et al.
Fig. 4.7  A 63-year-old woman presented with multiple
metastatic tumors in both lungs. The beaded septum sign
was seen in the left lung
dissemination, lymphatic dissemination, or retro-
grade lymphatic metastasis. There may be two
major factors in the formation of this sign. (1)
Metastatic foci should be located at the edge of
the lung; if a metastatic focus is located in the
middle of the lung, this focus is prone to subseg-
ment or segmental lymph nodes to form a mass,
and it cannot form the beaded septum sign. (2)
Tumors with a high degree of malignancy, and
rapid growth, present easy to early metastasis
along the lymphatic system, so that lung metasta-
ses and lung and hilar lymph nodes can form
nodules or masses at the same time [16]. The
pathological mechanism is tumor cells spread
along the lymphatic vessels of the lungs and dif-
fusely in the lymphatic vessels. The lymphatic
vessels are highly dilated, and the tumors are
silted into a single embolus or cluster of tumor
emboli with variable degrees of edema, fibrosis,
and inflammation. The cells infiltrate, causing the
bronchial vascular bundle to be irregularly nodu-
larly thickened and showing beaded changes.
The appearance of beaded septum is highly
suggestive of pulmonary metastases and is con-
sidered as the most specific CT feature for this
diagnosis. However, the beaded septum sign is
occasionally seen in pulmonary sarcoidosis and
should be differentiated from this [17]. The typi-
cal early stage of sarcoidosis is bilateral hilar
lymphadenopathy, mostly accompanied by ade-
nopathy in the right superior mediastinum; and
metastatic tumors often have unilateral hilar and
multiple lymph nodes involved in the mediasti-
num. In sarcoidosis, eggshell-like and spotted
4 Chest
calcification are seen in lymph nodes, whereas
metastatic lymph nodes are enlarged and fused
into a mass, with necrosis and nonhomogeneous
enhancement. The nodule boundary of sarcoid-
osis is unclear, and the lesion can occur in either
lobe, although the upper lobe is more common.
The lesions are distributed along the bronchial
vascular bundle, which is characterized by thick-
ening of this bundle, which is bead like with
pleural thickening and a small amount of pleural
effusion; the metastatic tumor has bead-like
changes caused by irregular thickening of inter-
lobular septa.
4.8 Honeycomb Sign
Feature
The CT appearance of bronchioloalveolar car-
cinoma (BAC) is mainly characterized by light
consolidation. On the mediastinum window or
intermediate window, multiple vesicles are
integrated into the honeycomb shadows or
shown as grid patterns, which is called “ honey-
comb sign.”
Explanation
The pathological basis is tumor cells taking the
alveolar wall as the stromal scaffold and diffus-
ing along the local peripheral air cavity; that is,
incumbent growth. The pulmonary structure is
not destroyed and the alveolar cavity still exists,
because the bronchioles are infiltrated by the
tumor to form valvular stenosis, which results in
varying degrees of dilatation, and the remaining
gas or mucus can be seen in the dilated alveolar
cavity or bronchioles (Fig. 4.8).
Discussion
Honeycomb sign is usually seen in pulmonary
adenocarcinoma with inflammatory consolida-
tion. It is manifested as a bubble-like airy
shadow in consolidation involving one or more
lobes or segments of the lung. Many pathogen-
esis mechanisms result in the honeycomb sign.
The mechanism of a check valve after airway
stenosis is accepted by most scholars; that is,
cancer cells grow along the alveolar wall or sep-
tum and spread to bronchioles, or cancer cells
113
Fig. 4.8  In an 83-year-old man, HRCT showed honey-
comb shadows in upper lobe of the right lung
directly destroy the walls of bronchioles, thus
forming a single bronchiole. Because of the
valve, the pressure in the alveoli increases as the
gas forms in the alveoli, which then break down
and fuse into larger cavities. The remaining
alveolar wall or septum forms the septum of the
honeycomb. The findings suggest a common
underlying mechanism that drives thin-wall cav-
ity formation in p­ rimary lung cancer, particu-
larly in adenocarcinoma containing mixed
BAC.  Thin-wall cavitation is most common in
adenocarcinoma containing mixed BAC.  The
high incidence of cavity formation in this histo-
logical subtype further supports the notion that
thin-wall cavity formation is directly related to
the infiltration of tumor cells into a bronchiole,
resulting in the establishment of a unidirectional
check valve [18].
The ground-glass component of a tumor usu-
ally corresponds to a partially aerated lung that
bears cells of BAC, whereas the solid component
may correspond to other adenocarcinomas. The
frequency of the nodule type may depend on the
frequency of the histopathological subtype of
carcinoma. The relatively lower frequency of
ground-glass nodules may reflect the lower fre-
quency of BAC [19]. Likely the most significant
change is the discontinuation of the term “BAC”
in the 2004 WHO Classification, which was pre-
viously used for at least five different entities
with disparate clinical and molecular properties,
leading to great confusion in routine clinical care
and research [20].
114
4.9 Withered Tree Sign
Feature
There are inflatable bronchial images in the
shadow of large patches; the larger bronchus can
be seen and the smaller bronchi cannot. The bron-
chial wall is irregular, uneven, generally narrow,
rigid, twisted, and takes the shape of withered
arborization. Other name: withered tree sign.
Explanation
An air bronchogram as commonly seen in diffuse
bronchiolar carcinoma differs from general
inflammation. This sign is characterized by irreg-
ular thickening and rigidity of the bronchial wall.
Other air bronchial signs are manifested as inflat-
able bronchial development in large consolida-
tion shadows, and the wall of the bronchi is not
rigid (Fig. 4.9).
Discussion
An air bronchogram is an important radiologic
sign of air–space consolidation, in which the nor-
mally invisible bronchial air column becomes
visible because of the contrast with surrounding
tissues. Two situations may exist for an air bron-
chogram to be identified: the bronchus must con-
tain air (it cannot be occluded completely at its
origin) and the surrounding lung parenchyma
must have reduced air content or be airless.
Although most commonly seen in the presence of
air–space consolidation, a severe degree of inter-
Fig. 4.9  A 55-year-old woman with no obvious discom-
fort. Chest CT shows patchy density enhancement shadow
in the right lung, with “air bronchogram sign”
T. Jiang et al.
stitial lung disease can also present as an air
bronchogram. Lung cancer of the bronchioloal-
veolar cell type may produce air bronchograms
on radiographs or CT. It was suggested that the
presence of pseudo-cavitation in small peripheral
bronchioloalveolar cell carcinoma may represent
air bronchograms in cross section. However, air
bronchograms have been considered uncommon
in other types of lung cancer [21].
Bronchioloalveolar carcinoma (BAC) is one
of the few lung tumors known to demonstrate the
air bronchogram sign. Production of this valu-
able radiologic sign by this tumor has been
ascribed to an “alveolar” filling process in which
the tumor grows along alveolar walls with pres-
ervation of the architecture and secretes copious
amounts of mucus. Thus, aerated bronchi are
surrounded by alveoli that are filled with mucus
and tumor [22]. BAC accounts for about 4% of
all primary lung malignancies; it is more com-
mon in females and never-smokers. The radio-
logic presentations of BAC are diverse and vary
from solitary or multiple pulmonary nodules to
cystic disease, cavitation, and consolidation.
Most consolidations in BAC are peripheral
in location, and can persist for a long duration,
making it difficult to differentiate from consoli-
dation of an infective origin [23].
4.10 CT Angiogram Sign
Feature
Enhanced CT shows hyperattenuation dendritic
pulmonary vasculature in the area of uniform and
consistent pulmonary consolidation, with the
shape of branching or punctiform shadows.
Explanation
CT angiogram sign is mainly seen in bronchoal-
veolar carcinoma (BAC), followed by lung con-
solidation caused by diseases such as primary
pulmonary lymphoma, obstructive pneumonitis,
and infectious pneumonitis. The homogeneous
and consistent consolidation lung tissue is the sac
cavity filled with mucus, and the high-density
dendritic angiography is the shadow of undam-
aged pulmonary vessels, which is the result of the
difference between the two tissues (Fig. 4.10).
4 Chest
Fig. 4.10  Enhanced chest CT shows pulmonary vascular
shadows in uniform hypoattenuation area of lung paren-
chyma with the shape of branching or punctiform shadows
Discussion
The CT angiogram sign was first proposed by Im
et al. in 1990 and is considered as a characteristic
manifestation of BAC [24]. According to the study
of Im et al., “CT angiogram sign” is described as
the enhancement of normal vascular trees in the
uniformly low-density atelectasis (or consolida-
tion) of the lung, during peripheral intravenous
contrast agent and chest dynamic CT scans. The
CT angiogram sign must meet three conditions: (1)
uniform consolidation or atelectasis of the unit lung
(segment, lobe, and whole lung); (2) normal vascu-
lar network in the lesion area; and (3) appropriate
injection of contrast agent and CT scanning proto-
cols. The CT angiogram sign consists of enhancing
pulmonary vessels in a homogeneous low-attenuat-
ing consolidation of lung parenchyma relative to
the chest wall musculature at the mediastinal win-
dow. This sign has been described in the lobar form
of bronchoalveolar cell carcinoma. Pneumonia is
another important cause of CT angiogram sign.
The low-attenuating area has been considered as
the result of mucus production by tumor cells. CT
angiogram sign has also been reported in pulmo-
nary edema, obstructive pneumonitis caused by
central lung tumors, lymphoma, and metastasis
from gastrointestinal carcinomas [25].
BAC represents a subgroup of adenocarcinoma
and accounts for 5% of all bronchogenic carcino-
mas in most series. BAC can be separated into two
basic morphological types: mucinous and Clara
115
cell, and two spread pattern types: tumors with
aerogenous spread and those without aerogenous
spread. The mucinous tumors account for 20% to
30% of BAC and are characterized by tall, mucus-
filled columnar cells. The mucinous tumors tend to
spread aerogenously, infiltrating along the preex-
isting normal framework of the lung (i.e., lepidic
growth). Four clinical manifestations are reported:
(a) single nodule, (b) multiple nodules, (c) single
consolidation, and (d) multiple lobar consolida-
tions. Single and multiple lobar consolidations are
more common in the mucinous tumors. BAC in a
patient with alveolar consolidation remains diffi-
cult to diagnose clinically and radiologically. In
cases of obstructive pneumonitis and primary pul-
monary lymphoma, investigators have suggested
that it is the relative difference between the attenu-
ation of the pulmonary vessels and that of the con-
solidated lung parenchyma rather than an absolute
low attenuation value of the consolidated lung that
is responsible for the CT angiogram sign. Although
CT angiogram sign is not specific for BAC, it still
may be considered a useful sign in imaging. The
sign is seen with a limited number of entities, all of
which involve the enhancement of unaffected pul-
monary vessels coursing through low-attenuating
consolidated lung parenchyma. Correlation of the
imaging findings with the clinical findings may
help to further narrow the differential diagnosis to
a specific entity [26].
4.11 Air Bronchiologram Sign
Feature
Air bronchiologram sign refers to the air density
shadow (the inflatable bronchus , which is paral-
lel to the CT scan plane of a small tubular or
small strip (diameter < l mm) in lesions (nodules
or lumps), which is most commonly seen in bron-
chioloalveolar carcinoma (BAC).
Explanation
BAC originates from epithelial cells of bronchi-
oles and alveoli, often for wall-type growth; the
bronchioles can be preserved because of the struc-
ture of the lung, which does not show damage by
the tumor, so there is no segmental atelectasis. At
the same time, the tumor and the surrounding lung
116
fiber tissue proliferate (BAC has connective tissue
formation), causing intact air-filled cavities near
fibrous cords to dilate, leading to localized
emphysema or bronchioliectasis (Fig. 4.11).
Discussion
BAC has varied growth patterns, mixed histologi-
cal features, and confusing clinical symptoms
and evolution. Generally, it is classified as a sub-
type of adenocarcinoma and is characterized by
its tendency to spread locally. The pathological
and epidemiological features of BAC include
peripheral location, desmoplastic reaction, mucin
production, high occurrence in non-smokers, and
tendency to appear in multiple foci [27]. The
spectrum of radiologic findings is divided into
three patterns: (1) solitary nodule or mass; (2)
localized consolidation; and (3) multicentric or
diffuse disease. CT patterns suggestive of BAC
include cystic air spaces; star pattern and pleural
tag, reflecting the tendency for the tumor to
retract; angiogram sign; and bulging of fissures.
An air bronchogram is an important radiologic
sign that shows high suspicion of malignancy in a
small peripheral lung nodule: an air bronchogram
or bronchiologram was seen in 78% of patients
with adenocarcinomas. Air bronchiologram with
disruption and/or irregular dilatation was signifi-
cantly more prominent in invasive adenocarci-
noma than adenocarcinoma in situ (AIS).
Conversely, characteristics of the air broncho-
gram in AIS may be without any disruptions and
Fig. 4.11  A 70-year-old woman with BAC.  CT shows
consolidation shadow of the lower lobe of right lung, in
which the air bronchiologram sign can be seen
T. Jiang et al.
irregular dilatations. Bubble-like areas of hypoat-
tenuation caused by small air-­containing bronchi
within the mass was reported to be sufficiently
characteristic to suggest the diagnosis of adeno-
carcinoma with lepidic growth. The evaluation of
an air bronchiologram in nodules might be useful
for predicting pathological invasion [28].
4.12 Air Bronchogram
Feature
On lung CT, the air bronchogram is shown as a
thin strip of air density shadow in a large area of
solid lesions, which also can be a small bubble-­
like air density shadow with a diameter of 1 mm.
Dilated bronchioles in lesions can appear on sev-
eral successive levels.
Explanation
When parenchymal lesions occur in the lungs, the
gas below the bronchioles is squeezed and emp-
tied by the lesions. The remaining gas-­bearing
bronchi are shown as a negative bronchial image
in a background of high-density images. This phe-
nomenon is absent in pulmonary interstitial
lesions and is common in pneumonia (Fig. 4.12).
Discussion
The main pathological changes of pneumonia are
exudation, infiltration, hyperplasia, and meta-
morphism of inflammatory cells. In pathological
gross specimens, nodular consolidation, irregular
consolidation, or consolidation of lung segments
Fig. 4.12  A 45-year-old woman presented with an “air
bronchogram” sign in the middle lobe of the right lung
4 Chest
and lung lobe are seen. CT can accurately reflect
the general shape and distribution of lung inflam-
mation. Clinically, the early clinical manifesta-
tions of pneumonia and consolidation
bronchioloalveolar carcinoma are nonspecific
and similar in imaging, so the identification of
the two is often difficult. Air bronchography is
now used to evaluate the prognosis of lung cancer
and is considered as a prognostic factor for lung
cancer. Because an air bronchogram reflects a
condition in which intratumoral bronchi remain
intact without destruction by tumor invasion or
expansion, the presence of an air bronchogram
would indicate a less aggressive tumor. Onoda
et al. assessed the relationships between CT fea-
tures and the histological components of tumors,
including their percentages, and found that air
bronchogram on CT was associated with adeno-
carcinoma components showing papillary and
lepidic growth patterns and adenocarcinoma-­
dominant tumors [29]. Dai et al. believe that air
bronchography is the main histological subtype
of squamous cells and is seen less commonly in
other patterns because the solid-density type
would obscure the bronchi [30]. A subsolid nod-
ule with air bronchogram is supposedly more fre-
quent with epidermal growth factor receptor
(EGFR) mutation. As a typical sign of pneumo-
nia, the air bronchography sign is important in
the definitive diagnosis [31].
a b
Fig. 4.13 (a) A nodular increased attenuation shadow
can be seen in the left lung; bronchial passage is visible in
the nodule. (b) A nodular increased attenuation shadow
117
4.13 Positive Bronchus Sign
Feature
On chest CT, a positive bronchus sign can directly
approach to the mass or as an air bronchogram
contained within the mass.
Explanation
This sign indicates that one or more bronchi lead
to or are contained within the mass and nodule.
The presence of this sign is valuable for the dif-
ferentiation of benign or malignant mass and
nodule in the lung (Fig. 4.13).
Discussion
Bronchogenic pulmonary carcinoma is the most
common malignant tumor, and its incidence has
been increasing in recent years. Judging the rela-
tionship between bronchogenic pulmonary carci-
noma and bronchus is important for bronchial
biopsy. Studies have shown there are five types of
relationship between solitary nodules or lumps
and bronchus in lung: (1) bronchus is cut off by
the tumor when it reaches the edge of the tumor;
(2) bronchus extends into the tumor and the
tumor infiltrates along the bronchial wall; (3)
bronchus is pushed by the tumor; (4) bronchial
wall thickening with lumen smoothly stenotic;
(5) bronchial wall thickening with lumen irregu-
larly stenotic. If CT findings fall in types 1 or 2,
can be seen in the left lung; a bronchial shadow is visible
near the edge of the nodule
118
they are classified as bronchus sign positive; if
CT findings fall in types 3, 4, or 5, they are clas-
sified as bronchus sign negative [32].
Benign and malignant lesions in lung can
lead to a positive bronchus sign. The pathologi-
cal basis of this is normal or slightly dilated tra-
chea or bronchioles. Positive bronchus sign is
more common in malignant nodules in lung, and
adenocarcinoma is more common. Pathological
findings reveal bronchial cartilage is destroyed
and tumor cells are infiltrated into the bronchus.
Benign lesions in lung are more common in
parenchyma and interstitially; they have less
effect on the bronchus, and the incidence of pos-
itive bronchus sign is lower. Incidence is
reported as about 27%, mainly in tuberculosis,
inflammatory pseudotumor, and infarction. The
presence of positive bronchus sign indicates a
larger bronchus is connected to the mass. In
tumors less than 3 cm in diameter, in 90% only
one bronchus is connected to the mass, whereas
in tumors of diameter greater than 3  cm, in
about 60% three or more bronchi are connected
to the mass. CT should be performed before
bronchoscopy to confirm whether there is bron-
chus sign, thus making the assessment of posi-
tive rate of bronchoscopy more objective. Once
this sign occurs, the positive rate of fiberoptic
bronchoscopy is higher; however, a negative
bronchus sign is not eligible for bronchoscopy
[33].
a b
Fig. 4.14 (a, b) A 58-year-old woman with repeated sputum
coughing for 7 years. Postcontrast CT showed patchy density
T. Jiang et al.
4.14 Mucous Bronchogram
Feature
Mucous secretions filling the bronchial tree may
be identified on contrast-enhanced CT as low-­
density, tree-like branching structures within a
hyperattenuated collapsed lung resembling air
bronchograms, called a mucous bronchogram.
Explanation
Mucous bronchial sign is the finding of atelecta-
sis with bronchial mucous embolism on CT. An
enhanced high-density shadow represents atelec-
tasis whereas an unenhanced low-density shadow
represents mucous emboli in the bronchus
(Fig. 4.14).
Discussion
The basic pathological change of mucous bron-
chial sign is bronchial mucous embolism in atelec-
tasis, which is caused by bronchial stenosis
obstruction, abnormal mucus secretion, or dys-
function of ciliary movement [34]. Mucoid impac-
tion of bronchi has been reported to occur from a
variety of causes of bronchial obstruction, most
notably bronchial atresia and obstructing tumor,
and from a variety of conditions without bronchial
obstruction. If the involved portion of lung is not
aerated by collateral ventilation, pulmonary atel-
ectasis ensues, obliterating the shadow of impacted
bronchi. Variable amounts of atelectasis may occur
enhancement in the left lower lobe of the lung with dilated
bronchus and filling of attenuated intraluminal density
4 Chest
distal to the obstruction of a segmental or lobar
bronchus. A combination of pathological features
in the lung (e.g., mucous plugging, intraalveolar
fluid, interstitial pneumonitis, interstitial fibrosis,
and infection) may account for the opacification
seen on plain chest radiographs. Mucus glands
continue to function after an obstruction of a bron-
chus unless destroyed by tumor or infection.
Mucus is p­ roduced until the bronchial pressure
exceeds the secretory pressure. Cilia transport the
mucus proximally to the site of obstruction, where
it overdistends the bronchi. Changes of bronchial
impaction may be less apparent with neoplasms
seen at an early stage or with only partial bronchial
obstruction. With segmental bronchial impaction,
one or more tubular structures with the long axis
pointing toward the pulmonary hilum are seen on
radiographs or CT [35].
Mucoid impaction is a relatively common
finding at chest radiography and CT. On the CT
scan plane of hilum and near hilum, the long axis
of the bronchus forms a banded or branched
image 0.2–0.6 cm wide, which is consistent with
the direction of the bronchus and extends from
the hilum to the periphery of the lung. In the apex
or bottom of the lung and its adjacent layers, CT
cross section of the bronchus shows oblong and
nodular images. CT is more useful than chest
radiography for differentiating between mucoid
impaction and other disease processes, such as
arteriovenous malformation, and for directing
further diagnostic evaluation [36]. The mucous
bronchial sign on postcontrast CT shows a low-­
density area without enhancement in atelectasis,
and atelectasis tissue is obviously enhanced.
Knowledge of the patient’s medical history, clin-
ical symptoms and signs, and predisposing fac-
tors is quite important to make the final
diagnosis.
4.15 Gloved Finger Sign
Feature
The gloved finger sign, which is visible on chest
radiograph and CT, is characterized by branching
tubular or finger-like opacities originating from
the hila and are directed peripherally. It is fan
shaped in the center of the hilum, with a V shape,
119
Y shape, or grape-like shape, looking like the fin-
ger of a glove, so it is called finger sign.
Explanation
The branching tubular or finger-like opacities
extending out from the hila represent dilated
bronchi filled with mucus (mucoid impaction).
Once bronchial obstruction has occurred, the
mucous glands continue to secrete until bronchial
pressure exceeds the secretory pressure. Mucous
secretions are transported by ciliary action up to
the site of obstruction. The secretions become
inspissated, and the mucus and inflammatory
debris accumulate distal to bronchial obstruction,
causing bronchial dilatation. If atelectasis occurs
in the surrounding lung tissue, there is no indica-
tion of the sign; if the distal lung tissue is venti-
lated through the alveolar foramen and Lambert
tube, the sign may appear (Fig. 4.15).
Discussion
Both congenital and acquired abnormalities may
cause mucoid impaction of the large airways,
which often manifests as tubular opacities known
as the finger-in-glove sign. The congenital condi-
tions in which this sign most often appears are
segmental bronchial atresia and cystic fibrosis.
The sign may also be observed in many acquired
conditions, such as inflammatory and infectious
diseases, broncholithiasis, and foreign-body
aspiration, benign neoplastic processes, and
malignancies.
Finger-in-glove sign is the chest radiographic
finding of tubular and branching tubular opaci-
Fig. 4.15  In a 50-year-old woman, chest CT showed
enlarged right lower lobe bronchus with finger-like changes
120
ties that appear to emanate from the hila, said to
resemble gloved fingers. The tubular opacities
represent dilated bronchi impacted with mucus.
CT is more useful than chest radiography for
differentiating between mucoid impaction and
other disease processes, such as arteriovenous
malformation, and for directing further diagnos-
tic evaluation. The CT finger-in-glove sign is
branching endobronchial opacities that course
alongside neighboring pulmonary arteries [37].
The finding is classically associated with aller-
gic bronchopulmonary aspergillosis (ABPA),
seen in persons with asthma and patients with
cystic fibrosis, but may also occur as an imaging
manifestation of endobronchial tumor, bron-
chial atresia, cystic fibrosis, and postinflamma-
tory bronchiectasis. Bronchoscopy may be
necessary to exclude endobronchial tumor as
the cause of the finger-in-glove sign. The tubu-
lar opacities that occur in ABPA result from
hyphal masses and mucoid impaction and typi-
cally affect the upper lobes. Pathologically,
ABPA is characterized by bronchocentric gran-
ulomas within both bronchi and bronchioles,
with associated mucoid impactions.
Bronchiectasis, mainly in the upper lobes, is a
hallmark of the disease.
a b
Fig. 4.16 (a–c) Man, 52 years old, with pulmonary aspergillosis. On chest CT plain scan, multiple nodular hyperat-
tenuation is seen in the left upper lobe, and feeding vessel sign was seen in one of the larger air-forming nodules
T. Jiang et al.
4.16 Feeding Vessel Sign
Feature
The feeding vessel sign is shown as multiple nod-
ules and vascular passages through the nodular
shadows on chest CT.  These vascular shadows
passing through the nodules do not really pass
through, but occur mostly around the nodules,
and the other vessels passing through the nodules
are mainly pulmonary veins.
Explanation
Feeding vessel sign indicates pulmonary hematog-
enous pyogenic infection. Multiple nodules in the
lung field represent septic embolus. Similar signs
are also seen in pulmonary metastasis (Fig. 4.16).
Discussion
Septic pulmonary embolus is most common in
infective endocarditis, central venous catheter-
ization infection, pacemaker-induced infection,
or suppurative periodontal disease [38]. CT find-
ings of the disease mainly include multiple pul-
monary nodules, subpleural gas or gasless
shadows, and blood feeding vessel sign. The
main finding of feeding vessel sign is a clear and
visible vascular shadow directly entering the
4 Chest
nodule. It has been reported the sign highly sug-
gests pulmonary septic embolus, with the occur-
rence rate 67% to 100%. Similar signs can also
be seen in metastatic nodules of the lung. A case-­
control study of metastatic nodules under a ste-
reomicroscope showed only 18% of the nodules
have definite pulmonary artery blood supply into
the nodules, whereas 58% of the nodules do not
show blood vessels entering the nodules under
stereomicroscope, but going along their margins,
which suggests the blood vessels are shifted by
nodules. Dodd et al. found in most lesions show-
ing feeding vessel sign that the blood supply ves-
sels are mostly veins [39]. The author believes
that the feeding vessel sign observed on axial CT
scan may be the blood vessels through two adja-
cent nodules at the early stage; as the nodule
grows, it gradually becomes the result of blood
vessels passing through the center of the nodule
[39]. The clinical presentations of septic pulmo-
nary embolus range from insidious illness with
mild respiratory symptoms to respiratory failure
and septic shock. Further study on the structure
of multiple pulmonary nodules and peripheral
blood vessels would contribute to improving the
understanding of specific manifestations of septic
emboli and metastatic nodules [40].
4.17 Vascular Convergence Sign
Feature
The vascular convergence sign refers to the phe-
nomenon that one or several blood vessels (arter-
ies or veins) around the lung nodules reach the
inside of the tumor, or are cut off at the edge of
the tumor, or pass through the tumor. On HRCT
it can be divided into three types: (1) one or sev-
eral intrapulmonary vessels reach the nodules or
pass through the nodules, (2) a number of blood
vessels around the lesion in the lung are pulled
into the lesion and are cut off at the edge of the
lesion, or (3) increased blood vessels and thick-
ening on the upper and lower levels of the lesion.
Explanation
Vascular convergence sign is mainly seen in lung
cancer, especially adenocarcinoma and alveolar
121
Fig. 4.17  In an 84-year-old man, a space-occupying
lesion in the upper lobe of left lung and a vascular conver-
gence sign (arrow) are seen
cell carcinoma. Pathologically, tumor tissue infil-
trates into the vascular bronchial sheath or inter-
lobular septa, with proliferation or scar formation
of fibrous tissue in the tumor, leading to concen-
tration of adjacent vessels toward the tumor
(Fig. 4.17).
Discussion
Small cell lung cancer (SCLC) is a neuroendo-
crine tumor of the lung, accounting for 10% to
15% of lung cancer. SCLC is prone to diffuse in
the lung lobe or submucosal area of the main
bronchus and to form giant hilar masses with
mediastinal lymph node metastasis [41]. The
vascular convergence sign is of great value in the
diagnosis of SCLC. The pathological basis and
imaging features of the vascular convergence
sign are (1) tumor angiogenesis factors produced
by malignant tumor cells induce neovasculariza-
tion of tumors, especially those with active
growth. The blood supply of malignant tumors is
especially abundant, resulting in compensatory
thickening of blood vessels supplied by tumors.
These vessels are often dilated or accompanied
by infiltration of bronchial artery sheath or tumor
thrombus. Therefore, thickening of peripheral
vessels is of great significance in differentiating
benign from malignant. (2) Closely related to
fibrotic foci (scar formation) in lung cancer, the
formation of fibrotic foci and the proliferation
and destruction of tumor nests in lung cancer
have an important role in the formation of pleu-
ral indentation and vascular convergence. (3)
The appearance of this sign is related to the size
122
of the tumor; it is rarely seen in lung cancer nod-
ules less than 1 cm [41]. (4) The vascular conver-
gence sign of adenocarcinoma is more obvious
than that of other types of lung cancer, because
of the greater blood supply of adenocarcinoma,
and the formation of fibrotic foci is more obvi-
ous in general. (5) One-vessel-oriented nodules
are not only seen in malignant nodules, but also
in more benign pulmonary nodules [42].
It should be regarded as a vascular connec-
tion only, not as a vascular convergence sign.
The incidence of multiple-vessel-oriented nod-
ules is higher in malignant nodules. Although
the incidence of vascular convergence sign in
lung cancer is high, it is not a unique sign.
Tuberculoma, spherical pneumonia, and inflam-
matory pseudotumor can also appear as vascular
convergence sign.
4.18 Silhouette Sign
Feature
Silhouette sign refers to the obscure contour of the
central shadow (heart, aorta or diaphragm) which
is obscured by the adjacent lung tissue (pathologi-
cal condition) with the same density. If the lesion
causes central shadow edge blurring, the silhou-
ette sign is positive. If the central shadow edge is
clear, the silhouette sign is negative.
Explanation
Most silhouette sign is positive when the lesion is
adjacent to the heart or aortic arch, and most sign
is negative if the lesion is far away from heart or
aortic arch (Fig. 4.18).
Discussion
The boundary of soft-tissue structures such as
mediastinum, hilum, and one side of the dia-
phragm can be clearly seen on chest X-ray
because of the adjacent pneumatic lung tissue.
When a consolidated lung (or soft-tissue mass) is
connected to one of these structures, its boundary
disappears or is not clearly visible, which is called
silhouette sign [43]. Silhouette signs are used to
diagnose the presence of pulmonary abnormali-
ties (such as consolidation, atelectasis, mass) and
to locate them in a specific lobe or region of the
T. Jiang et al.
Fig. 4.18  On X-ray chest films, the boundary of the right
cardiac margin is blurred, and silhouette sign (arrow)
appears because of lesions of middle lobe of right lung
lung. Silhouette sign has many names and is
widely used, but it is used to determine the lesions
in the right middle lobe and left lingual lobe. Here
are some specific features. (1) When inflamma-
tion or atelectasis occurs in the right middle lobe
and left lingual lobe, the adjacent cardiac margin
is blurred on the conventional posterior and ante-
rior views. If the cardiac margin is clear, the
lesion is located in the pulmonary tissue of the
posterior lower lobe of the heart. (2) If the lesion
is located in the anterior segment of the right
upper lobe, the ascending aorta and left hilum can
be blurred, but it is clear in the posterior segment.
(3) The middle and lower segment of ascending
aorta and the upper segment of right cardiac mar-
gin were not visualized, and the silhouette sign
indicated that the lesion was in the dorsal seg-
ment of the right lower lobe of the lung. (4) All
the right cardiac margins were not visualized, and
the silhouette sign suggested that the lesion was
located in the middle lobe of the right lung. (5)
The lower segment of aorta and pulmonary artery
were not visualized, and the contour sign sug-
gested the lesion of the anterior segment of the
left upper lobe. (6) The blurred edge of the aortic
node was caused by the lesion of the posterior
segment of the left upper apex or the change of
adjacent lymph nodes. (7) The upper half of the
4 Chest
left cardiac margin was not visualized, and the
contour sign suggested lesions in the upper part
of the left lobe of the lung and tongue. (8) The
middle and lower segments of the left cardiac
margin were not visualized, and the silhouette
sign suggested that the lesion was in the lower
segment of the left lung and lingual lobe. (9) The
margin of the descending aorta is unclear, sug-
gesting that the lesion is the posterior basal seg-
ment of the left lower lobe; the tumors in the
posterior mediastinum are far away from the
heart and ascending aorta, and the heart shadow
and ascending aorta margin are clear; if blurred,
the lesion is located in the anterior mediastinum
[44]. In a word, the significance of silhouette sign
is to indicate the existence of lesions.
Familiarization with this sign would help reduce
missing diagnosis of lesions. Most importantly, if
suspicion is found on X-ray chest film, CT would
be further suggested [45].
4.19 Luftsichel Sign
Feature
On the posteroanterior view of a chest radio-
graph, luftsichel sign manifests as a paraaortic
crescent of hyperlucency with sharp margins that
extend from the apex of the left hemithorax to the
a b
Fig. 4.19  A 63-year-old man with obsolete pulmonary
tuberculosis with collapse of the left upper lobe. (a)
Posteroanterior chest radiograph demonstrates a paraaor-
tic hyperlucency (arrows) representing a hyperinflated
superior segment of the left lower lobe positioned between
the mediastinum and the collapsed left upper lobe, the
123
left superior pulmonary vein and outline the
medial aspect and sometimes the upper aspect of
the opaque collapsed left upper lobe. CT scans of
left upper lobe collapse show a homogeneous
opacity that extends from the anterior chest wall
to the mediastinum. The hyperexpanded superior
segment of the left lower lobe is positioned
between the collapsed lobe and the aortic arch;
this is the luftsichel sign.
Explanation
Luftsichel sign is a well-documented radiographic
sign seen on the images obtained in patients with
collapse of the left upper lobe. The sign represents
the hyperexpanded superior segment of the left
lower lobe interposed between the atelectatic left
upper lobe and the aortic arch. As the left upper
lobe collapses, it moves anteriorly and superiorly
to lie against the anterior chest wall, with the
hyperexpanded left lower lobe located behind the
upper lobe. The superior segment of the left lower
lobe expands upward to the apex of the left hemi-
thorax and is positioned medially between the
mediastinum and the collapsed left upper lobe,
thus producing the luftsichel sign. The appearance
and extent of the luftsichel depend on the severity
of the collapse. The inferior and medial extents of
the luftsichel are delineated by the left superior
pulmonary vein (Fig. 4.19).
luftsichel sign. (b) CT scan helps to confirm medial inter-
position of the hyperexpanded superior segment of the left
lower lobe (black arrows) on the back side of the aortic
arch. White arrows outline the medial and posterior
aspects of the opaque collapsed left upper lobe
124
Discussion
Luftsichel is a German word that means air cres-
cent (luft means air, sichel means sickel).
Luftsichel sign may be seen on posteroanterior
chest radiographs obtained in patients with left
upper lobe collapse. This paraaortic area of
hyperlucency was once thought to represent a
herniated anterior part of the right lung that is
compensating for the loss of volume in the left
hemithorax. However, careful evaluation of the
radiographic anatomy and correlation with bron-
chographic and CT findings clearly demonstrate
that expansion of the superior segment of the left
lower lobe accounts for this finding [46]. There is
usually no minor fissure in the left lung. In left
upper lobe collapse, the major fissure is displaced
anteriorly and parallels the anterior chest wall on
the lateral radiograph. The left upper lobe col-
lapses against the mediastinum anteromedially
and can obliterate the left cardiac border on the
posteroanterior chest radiograph. The volume
loss in the left hemithorax results in posterior and
leftward rotation of the heart. On the posteroante-
rior radiograph, the collapsed lobe produces a
hazy opacification that is distributed about the
hilar area and that fades superiorly, laterally, and
inferiorly. Luftsichel sign/shovel sign can be seen
on the right or left side, typically on the left [46].
Collapse of lung may present in varied combina-
tions of direct and indirect signs. One such indi-
rect sign is the luftsichel sign. Along with this
sign, other direct and indirect signs of collapse
will be evident. The direct signs include displace-
ment of fissures, loss of aeration, and crowding
of vessels. Indirect signs such as shift of trachea,
mediastinal shift, rib crowding, compensatory
overinflation of the remaining lung, and hilar dis-
placement may also be visualized [47].
The differential diagnosis of luftsichel sign
includes herniation of the right lung and mediasti-
nal pneumothorax. Right lung herniation occurs in
left lung collapse. Left lung collapse causes medi-
astinal shift and shift of aorta to the left. Right lung
herniates behind the sternum to fill the space, and
it produces a parasternal hyperlucency. However,
in luftsichel sign there is paraaortic lucency.
Mediastinal pneumothorax can be differentiated
from luftsichel sign as there will be no other signs
of collapse, although there may be pneumothorax
T. Jiang et al.
or subcutaneous emphysema accompanying it.
Recognition of luftsichel sign as a finding of left
upper lobe collapse is important in the adult
patient, because the cause of the collapse may be
caused by phasm. Luftsichel sign is a helpful sign
of the diagnosis of left upper lobe collapse, but its
absence does not exclude this diagnosis [48].
4.20 Golden S Sign
Feature
On the posteroanterior chest radiograph, when
volume loss occurs in the right upper lobe, lobe
volume is reduced and shifted upward. Because of
the limitation of the minor fissure, the lower mar-
gin of the concave face connected with the lower
margin of the lower convex of the hilar mass.
Because this sign resembles a reverse S shape, it is
also referred to as the “reverse S sign of Golden.”
Explanation
Golden S sign is a finding that can be seen not
only on the posteroanterior views of chest radio-
graphs, but also on CT. The right upper lobe lies
anterior to the major fissure and is bordered infe-
riorly by the minor fissure and posteriorly by the
major fissure. The lobe is also bordered laterally
by the chest wall and medially by the mediasti-
num. When volume loss occurs in the right upper
lobe, the resultant anatomical changes include
fissure displacement, a shift of structures, and an
increased lung opacity, depending on the sever-
ity of the volume loss. During right upper lobe
collapse, the minor and major fissures move
superiorly and medially toward the mediasti-
num, and there is a compensatory hyperexpan-
sion of the right middle and lower lobes. The
result can be seen on chest radiograph as a down-
ward concavity of the minor fissure and a trian-
gular opacity that represents the collapsed lobe,
with the apex of the lobe located at the elevated
hilum and the broad base of the lobe located
against the chest wall. With severe right upper
lobe collapse, the minor fissure may either lie
parallel to the mediastinum to simulate a wid-
ened mediastinum or be compressed superiorly
to resemble an apical cap. Golden S sign can be
seen on posteroanterior chest radiographs of
4 Chest
Fig. 4.20  Central type carcinoma of right lung with right
upper lobe atelectasis. Posterior and anterior X-ray
showed “transverse S sign”
right upper lobe collapse when a large enough
central mass is present to produce a downward
convexity of the medial or proximal portion of
the minor fissure (Fig. 4.20).
Discussion
This sign was first described by Golden in 1925
to describe cases of lobar collapse caused by lung
carcinoma [49]. A reverse S-shaped curve of the
horizontal fissure is sometimes seen on the fron-
tal radiograph in cases of upper lobe collapse.
The superolateral concave segment of the S is
formed by the elevated horizontal fissure. The
inferomedial convex segment is formed by the
central tumor or lymph node enlargement.
Although not pathognomonic of bronchial carci-
noma, it is very suggestive of the diagnosis [50].
Although typically seen with right upper lobe
collapse, the S sign can also be seen with the col-
lapse of other lobes and has been demonstrated
on lateral chest radiograph [51]. The Golden S
sign is created by a central mass and should raise
suspicion of a central neoplasm, such as primary
bronchial carcinoma. Other central masses to be
considered include metastasis, primary mediasti-
nal tumor, or lymph nodes. Bronchial carcinoma
is one of the leading causes of cancer deaths
among men and women. Eighty percent of lung
cancers are non-small cell lung carcinomas,
which include adenocarcinoma, squamous cell
carcinoma, and large cell carcinoma. Small cell
lung carcinoma is the most aggressive and has the
125
worst prognosis. However, sometimes patterns of
upper lobe collapse can result in an apparent
Golden S sign in the absence of a mass [52].
4.21 Hampton’s Hump Sign
Feature
Hampton’s hump sign is a typical X-ray sign of
pulmonary infarction. It refers to the conical or
wedge-shaped shadow truncated by the apex of a
uniformly increased density in the infarct area
during pulmonary infarction. It is often located in
the periphery of the lung, in which the bottom is
often located in the pleura or costophrenic angle
side with a convex apex directed toward the
hilum, likely a hump.
Explanation
Hampton’s hump is seen on the chest radiograph
as a wedge-shaped opacity with a rounded con-
vex apex directed toward the hilum. The conical
or wedge-shaped shadow represents the focus of
pulmonary infarction. The Hampton’s hump
occurs within 2 days of a pulmonary infarction,
whereby subsequent alveolar necrosis and hem-
orrhage into an incomplete infarct accounts for
the opacity. After a few months, the pulmonary
infarct will resolve and a residual scar remains
(Fig. 4.21).
Discussion
Hampton’s hump represents pulmonary infarc-
tion secondary to pulmonary embolism (PE). PE
is caused by an embolic obstruction of the pul-
monary arteries, which can impair blood flow to
the lung, leading to a ventilation perfusion (V/Q)
mismatch. This obstruction can then result in a
spectrum of cardiorespiratory complications
from hypoxemia to cardiac arrest, depending on
the size and the chronicity of the emboli. Even
though Hampton’s hump has a high specificity of
82%, it has a low sensitivity of 22%, which limits
its usefulness in the diagnosis of PE.  The low
sensitivity of the sign can be explained by the
dual blood supply of the lungs, which is present
in most people. With collateral vascular supply
from both the pulmonary and bronchial arteries,
the bronchial arteries protect against a pulmonary
126
Fig. 4.21 (a) Chest radiograph shows uniform density of
the wedge in right lung field (red arrow), associated with
pulmonary infarction, known as “Hampton’s hump sign.”
(b) Computed tomography pulmonary angiogram (CTPA)
infarction in the event of a PE.  However, the
Hampton’s hump can sometimes be misdiag-
nosed as pneumonia with an alveolar consolida-
tion. Hence, importance should be placed on
accurate recognition of the sign on chest radio-
graphs [53]. Hampton’s hump is seen more com-
monly in patients with certain comorbidities
affecting the cardiopulmonary system such as
chronic obstructive pulmonary disease, left heart
failure, and venous pulmonary hypertension.
Common clinical presentations of acute PE
include chest pain, tachycardia, hypotension,
dyspnea, cough, and hemoptysis. About 90% of
the emboli originate from deep vein thrombosis
of the proximal lower limbs and pelvis. From
another perspective, about 50% of deep vein
thrombosis in the legs embolize to the lung [53].
PE is a condition that is treatable if suspected
and diagnosed early. The diagnosis of PE is typi-
cally shown on CTPA, other diagnostic modali-
ties such as ventilation-perfusion scan, D-dimer,
ultrasound of the lower extremities, echocardio-
gram, electrocardiogram, chest radiograph, and
clinical decision rules. The chest radiograph is
still the first investigation that is ordered in
patients presenting with cardiorespiratory symp-
toms or symptoms suggestive of PE [53]. The
various features of chest plain radiography in PE
include Hampton’s hump, Westermark sign (oli-
gemia), Palla’s sign, pleural effusion, and ele-
T. Jiang et al.
shows widening of right pulmonary artery descending
branch with filling defect, an occlusive thrombus (black
arrow), and a corresponding segmental wedge infarction
(red arrow) [54]
vated diaphragm. Palla’s sign was described and
represented with engorgement of right descend-
ing pulmonary artery. Combination of Hampton’s
hump and Palla’s sign is rare, but early interpreta-
tion can remind the emergency physician to raise
suspicions for PE [54]. CTPA is the current gold
standard in the diagnosis of acute PE with high
accuracy, wide availability, and rapid turnaround
time. V/Q scanning is indicated in patients who
are young, pregnant, or cannot use contrast
media. Magnetic resonance pulmonary angiogra-
phy (MRPA) can provide good accuracy in cen-
ters with adequate expertise. In pregnant patients,
lower-extremity ultrasound is recommended as
the initial imaging modality. Echocardiography
is useful in triaging high-risk PE patients.
Invasive pulmonary angiography is reserved for
those patients needing endovascular intervention.
In patients with Hampton’s hump, computed
tomographic angiography (CTA) will confirm the
diagnosis, showing a three-dimensional infarc-
tion distal to the embolus [55].
4.22 Square Sign
Feature
When the lesion is adjacent to the pleura, both
sides of the lesion are perpendicular to the pleura,
showing a knife cut-like edge, the lesion is
4 Chest
a b
Fig. 4.22 (a) A 38-year-old man with “square sign” in the posterior basal segment of the right lower lobe. (b) A
65-year-old man with “square sign” in the right lung
square, known as square sign. Other name: knife
cut sign.
Explanation
Square sign is the characteristic manifestation of
spherical pneumonia. The pathological basis of
its formation is still unclear. It is estimated that
obstruction of the pleura or interlobular septum
leads to limited diffusion of inflammatory exu-
dates, which is the main cause of the change
(Fig. 4.22).
Discussion
Square sign is a more specific CT feature of
spherical pneumonia. Spherical pneumonia is an
acute and chronic nonspecific inflammation of
the lungs caused by viruses or bacteria. Bacterial
infections (Pneumococcus or Staphylococcus)
are common. Its pathological basis is inflamma-
tory exudation, which can be completely
absorbed or basically absorbed after antiinfective
treatment. Alveolar wall and other lung structures
do not cause damage or necrosis, which is differ-
ent from organic pneumonia, inflammatory pseu-
dotumor, and spherical atelectasis formed after
pneumonia. The latter exists for a long time and
remains unchanged. Spherical pneumonia is
named for its shape, resembling a sphere. It may
be formed by pneumococcal exudate along the
alveolar pores up and down, left and right, and
before and after, forming an inflammatory lesion
with equal diameters [56].
127
On CT scans, it is more common in the pos-
terior and outer basal segments, dorsal seg-
ments, and pleural surfaces of the lower lobes of
both lungs. It is characterized by focal wedge-
shaped or quasi-circular lesions with rough long
burrs or blurred margins. Most of the lesions are
homogeneous in density. Blood vessels on the
side of the hilum, local congestion of the bron-
chus, and patchy inflammatory exudation on the
margin of the lesion are seen. Spherical pneu-
monia should be differentiated from the follow-
ing diseases [57]: focal organizing pneumonia,
pneumonia pseudotumor, tuberculosis, hamar-
toma, and peripheral lung cancer. Focal organiz-
ing pneumonia occurs in the outer zone of the
lung field and under the pleura. Its density is
mostly inhomogeneous, and the anti-halation
sign is visible. The edges are often irregular, and
the long burr sign, the spine-like sign, or the
bow-shaped sag sign can be seen. There is a
necrotic cavity in the enhanced lesion, and the
necrotic cavity seems to have a certain sense of
tension. The pulmonary vascular passage can be
seen in the lesion, and the lesion is mostly
delayed enhancement. Pneumonia pseudotumor
is a group of intratumoral tumor-like hyperpla-
sia: it is not a true tumor. Most patients have a
history of pulmonary infection. It is spherical or
clumpy, with slow growth, inhomogeneous den-
sity, and irregular shape. The edge is not smooth;
the typical patient shows the sharp angle sign or
the trimming sign, and the lesion is unevenly
128 T. Jiang et al.

enhanced after the scan. The tumor margin of Discussion

peripheral lung cancer is often not smooth, with Peach-tip sign was first proposed by a Chinese
small burrs and/or deep lobulation and/or pleu- radiologist in 1988. They believe that this is
ral indentation. The surrounding edge of the caused by the adhesion of the envelope of inflam-
clear ground-glass halo sign, vascular concen- matory pseudotumor of the lung, which is char-
tration sign, uneven tumor density, mediasti- acteristic of benign masses, especially
num, and hilum can be seen in enlarged lymph inflammatory pseudotumor of the lung. It should
nodes. Neither the accumulation of growth nor be noted that the peach-tip sign is distinguished
the lung tumors of the sulcus growth shows a from the lobulated sign. The difference between
knife-like edge (square sign) as formed by the peach-tip sign and the lobulated shape is that
spherical pneumonia. the tip of the former is an acute angle and the tip
of the latter is an obtuse angle. Inflammatory
pseudotumor of the lung is a benign lung lesion
4.23 Peach-Tip Sign that is rare in clinical practice. The clinical mani-
festations include cough and phlegm, and in
Feature severe cases, even blood in the sputum. It mainly
On CT images, a sharp horn-like change resem- occurs in the middle and lower lung lobe and the
bling a peach tip can be seen at the edge of the peripheral part of the lung. It is an intrapulmo-
mass. Other name: peach-cusp sign. nary mass caused by chronic inflammatory gran-
uloma, fibrous connective tissue hyperplasia, and
Explanation mechanical changes in the lungs [58].
Peach-tip sign is a specific sign of inflammatory Pathologically, according to its main cellular
pseudotumor of the lung (IPL). Because most of components, it is divided into five types: histio-
the pseudotumor is located in the superficial part cytosis type, sclerosing hemangioma type,
of the lung, there is often an inflammatory reac- plasma cell granuloma type, cell epithelial papil-
tion adjacent to the pleura, followed by localized lary hyperplasia type, and pseudolymphoma.
pleural thickening and adhesion. A sharp horn-­ Knife-cutting, peach-tip sign, and continuous
like appearance of a pleural-like adhesion can be enhancement of delayed period can be used as
seen at the edge of the mass. This sharp horn-like important imaging data for differential diagnosis
expression combines with the mass to resemble a of inflammatory pseudotumor of the lung [58].
peach tip (Fig. 4.23). Fibrotic traction at the edge of the lesion of the
inflammatory pseudotumor of the lung, or the
lesion along the edge of the lobe or the segment
of the lung, may cause a layer of lesion at one
side of the lesion with flat knife-shaped changes;
the “knife-shaped” sign has important clinical
value in the diagnosis of pulmonary inflamma-
tory pseudotumor. In addition, the adhesion and
traction of the capsule of the lesion of inflamma-
tory pseudotumor of the lung causes a sharp apex
on the edge of the mass, similar to “peach tip,” so
it can be used as an important imaging feature in
the diagnosis of inflammatory pseudotumor of
the lung. Inflammatory pseudotumor of the lung
Fig. 4.23  A 63-year-old man. In middle lobe of the right
is moderately enhanced, and the enhancement is
lung, peach tip sign at the edge suggests inflammatory homogeneous or inhomogeneous. Continuous
pseudotumor enhancement in the delayed phase is the
4 Chest
enhancement characteristic of inflammatory tis-
sue. Therefore, delayed continuous enhance-
ment can be used to differentiate pulmonary
inflammatory pseudotumor from lung cancer.
Inflammatory changes can occur around pneu-
monia pseudotumor or surrounding lung cancer,
but the distribution characteristics of the two are
very different. The inflammation of peripheral
type carcinoma of lung is distributed at the dis-
tal end of the mass. The distribution of inflam-
mation of inflammatory pseudotumor of the
lung is not characteristic [59].
4.24 Comet Tail Sign
Feature
Comet tail sign is a finding visible on chest CT
scans. It consists of a curvilinear opacity that
extends from a subpleural mass toward the ipsi-
lateral hilum.
Explanation
Comet tail sign is produced by the distortion of
vessels and bronchi that lead to an adjacent area
of round atelectasis, which is the mass. The bron-
chovascular bundles appear to be pulled into the
mass and resemble a comet tail (Fig. 4.24).
Discussion
Comet tail sign was originally described on chest
radiographs. It is formed by distorted blood
vessel(s) and a focal area of atelectatic lung adja-
Fig. 4.24  In a 23-year-old woman, chest CT shows con-
solidation in the lower lobe of right lung; the edge con-
nected with cord-like density increased shadow shows
comet tail sign
129
cent to pleural thickening. The vessel(s) is seen
as a curvilinear soft-tissue density or densities,
extending from the medial margin of the atelec-
tatic lung to the pulmonary hilum. When the ves-
sels are multiple, thus there are multiple tails; if
the vessels are more like a parachute, then name
parachute sign may be used [60]. CT can demon-
strate the comet tail sign. Crowded and converg-
ing bronchovascular bundles are seen entering
the mass from all sides, giving the appearance of
crow’s feet or a talon sign. Overlying pleural
thickening is invariably seen and is well demon-
strated on CT. Although homogeneous enhance-
ment occurs with the intravenous administration
of contrast material, it cannot be used as a dif-
ferentiating sign because it also occurs with some
carcinomas. The appearance of round atelectasis
at magnetic resonance imaging (MRI) is
described as a lesion with a signal intensity simi-
lar to that of the liver on T1WI, with bronchovas-
cular bundles curving into the mass [60].
The characteristic feature of round atelectasis
is the comet tail sign. Rounded atelectasis is a
pulmonary entity that is increasingly recognized
but underdiagnosed and sometimes misdiag-
nosed. Although the exact pathophysiology
remains debatable, characteristic imaging appear-
ances of round atelectasis have remained consis-
tent [61]. Round atelectasis is a form of chronic
collapse of the lung that usually follows an old
pleural injury in the form of effusion or pleuritis,
which results in entrapment of the subpleural
lung, thereby giving it a rounded appearance
radiologically. The disease is known by several
names such as “Blesovsky’s syndrome,” “folded
lung syndrome,” “atelectatic pseudotumor,” and
“shrinking pleuritis with atelectasis.” Round atel-
ectasis has most often been reported in cases with
a history of asbestos exposure. The patients are
usually not symptomatic, and the lesion is most
often detected incidentally on radiography.
However, this feature does not help to differenti-
ate it from malignancy. The lesion does not
require any treatment and usually remains stable;
hence, interval radiography may be suggested to
look for progression or regression of the lesion.
Characteristic CT signs help in the diagnosis of
the lesion; however, in equivocal cases fine-­
130
needle aspiration or biopsy may be done to rule
out malignancy [62].
4.25 Reversed Halo Sign
Feature
On HRCT, when the lung window appears as the
center of the lesion with a ground-glass-like
attenuation, surrounded by a crescent-shaped or
circular high-attenuation strip that is in contrast
to the slightly low attenuation ground-glass-like
shadow around the halo sign, it is called reversed
halo sign.
Explanation
The central ground-glass-like attenuation is
alveolar septal infiltration and cell debris on
histopathology. The surrounding crescent or
circular high-attenuation band is a dense air
cavity consolidation caused by alveolar orga-
nizing pneumonia or dense, uniform interalveo-
lar cell infiltration (no organizing pneumonia)
(Fig. 4.25).
Discussion
The “reversed halo sign” is a sign on chest CT
that is characterized by a central ­ground-glass-­like
attenuation surrounded by a crescent-shaped or
a b
Fig. 4.25  A 80-year-old man with pulmonary tuberculosis. Axial (a) and coronal (b) noncontrast CT images show a
reversed halo sign with nodular walls in the apicoposterior segment of the right upper lobe
T. Jiang et al.
circular high-attenuation band. The sign was ini-
tially discovered in patients with cryptogenic
organizing pneumonia. In the past the central
ground glass-like attenuation was considered
alveolar septal infiltration and cell debris in histo-
pathology, and the surrounding crescent or circu-
lar high-attenuation band was pulmonary alveolar
organizing pneumonia. Now it has been proved
that reversed halo sign can exist in a variety of
lung diseases, including tuberculosis, invasive
pulmonary aspergillosis, pulmonary infarction,
noninvasive fungal infections, and granulomato-
sis. Infections are more likely to cause reversed
halo sign than noninfectious pathology in immu-
nocompromised patients [63]. Histopathology
confirmed the central ground-glass-like attenua-
tion lesions contained alveolar septal inflamma-
tory infiltration, macrophages, lymphocytes,
plasma cells, and some giant cells, and the alveo-
lar cavity was relatively intact. The surrounding
high-attenuation band is a dense, uniform interal-
veolar cell infiltration with no evidence of orga-
nizing pneumonia. Therefore, the reversed halo
sign cannot be considered as a specific sign of
cryptogenic organizing pneumonia.
The reversed halo sign is widely present in
various diseases and is considered a nonspecific
sign, but it has certain morphological features
that can aid differential diagnosis. When the wall
4 Chest 131

or inside of the reversed halo sign has nodules,

and the tree bud sign is combined, it is highly
suggestive of the diagnosis of tuberculosis. If
there is a reticular shadow in the reversed halo
sign, and the thickness of the peripheral margin
of the lesion is greater than 1 cm, accompanied
by pleural effusion, it strongly suggests pulmo-
nary muctomycosis [64]. It has been found in
clinical practice that the attenuation of reversed
halo sign in organizing pneumonia is often lower
than that in mucoid fungal disease; the circumfer-
ence is small and the wall is thin [64]. The Fig. 4.26 A 54-year-old man in immunosuppression.
reversed halo sign was first reported in crypto- Chest CT shows scattered pulmonary nodules, surrounded
by ground-glass shadow, mainly diagnosed as
genic organizing pneumonia, but this sign can
aspergillosis
also occur in the pathology of nonmechanized
pneumonia, so it is not specific. Recently it was
more common, especially invasive pulmonary
also reported in patients infected with coronavi-
aspergillosis. Invasive aspergillosis occurs in
rus disease-19 (COVID-19) [65].
patients with suppressed immune function, such
as acute leukemia, chronic wasting disease,
malignant tumor, kidney transplant, or radiation
4.26 Halo Sign exposure, and its mortality rate is 30% to 90%.
The main pathological changes of this disease are
Feature allergic reactions, acute inflammation, suppura-
On CT, a halo-like ground-glass opacity may be tive lesions, and even the formation of chronic
seen around the nodules or masses in the lungs. granuloma. Hemorrhagic pulmonary embolism
Its density is lower than that of the central mass, occurs when pulmonary aspergillosis invades the
but higher than that of normal lung tissue, with pulmonary blood vessels and the necrotic nod-
shape like a halo. Other name: CT halo sign. ules in the center of the early lesion are sur-
rounded by the bleeding area. In pathological
Explanation examination, the nodule represents the center of
Halo sign is a CT sign in the early stages of inva- the infarct, and the ground-glass-like halo is the
sive pulmonary aspergillosis, with hyperattenua- result of intraalveolar hemorrhage. Late necrosis
tion of nodules and masses in the center. dissolves to form a gas-containing crescent-­
Pathologically, it is necrotic lung tissue. Ground-­ shaped cavity (air crescent).
glass halo refers to a hemorrhagic area around the On chest X-ray the density of the halo is
focus (Fig. 4.26). lighter because of the small difference in tissue,
and the halo around the small nodules is often not
Discussion displayed. The X-ray film has no diagnostic
CT halo sign consists of an area of ground-glass value. In the late stages of aspergillosis, the
opacity surrounding a pulmonary nodule or mass. appearance of the air crescent can be typical in
The halo sign was first described in 1985 by high-kV photography. Chest CT is the most
Kuhlman et al., who reviewed chest CT scans of important diagnostic tool for invasive aspergillo-
nine patients with acute leukemia who developed sis and is a means of detecting early changes. CT
invasive pulmonary aspergillosis [66]. Its patho- findings of early lesions (with clinical symptoms
physiology usually involves one of three mecha- and signs within 10 days) have higher sensitivity
nisms: hemorrhage, inflammation, or neoplastic and specificity. In recent years, with the popular-
growth. Many diseases can cause halo signs, ization of MSCT and the wide application of
among which pulmonary fungal infections are HRCT technology, it can display the halo change
132
at the edge of the nodule. It appears on the CT
transverse image as a shadow around the mass or
nodule between the mass and the surrounding
normal lung tissue and surrounding the mass. It is
placed under the background of a higher density
of the mass, its surrounding density is relatively
low, and the circular band shadow is like a halo.
The incidence of CT halos in the early stages of
invasive pulmonary aspergillosis is quite high; it
occurs less frequently over time. In the early
stages of invasive pulmonary aspergillosis, MRI
is not as characteristic as the solar halo sign of
CT. However, in the late stage of the lesion, the
edge of the lesion after MRI enhancement is sig-
nificantly enhanced on T1WI, and the antihalo
sign on T2WI is strong evidence for the diagnosis
of invasive pulmonary aspergillosis. Although
many scholars are studying the application of
MRI in this sign, MRI cannot be used as a means
of early diagnosis.
The halo sign can also occur in tumor or
inflammatory cells infiltrating the lung paren-
chyma [67]. Metastases, Wegener’s granulomato-
sis, pulmonary Kaposi’s sarcoma, eosinophilic
pneumonia, obliterative bronchiolitis and organic
pneumonia, tuberculosis and Mycobacterium
avium complex, Q-febrile rickettsia, cytomegalo-
virus, herpes simplex virus, myxovirus infection,
lung transplantation, intrathoracic lymphoprolif-
erative disease, and an occasional halo can also
occur. Wegener’s granulomatosis, a necrotizing
vasculitis involving the respiratory tract, can be
characterized by pulmonary hemorrhage fol-
lowed by a halo. It is reported that a thicker halo
a b
Fig. 4.27 (a, b) In a 45-year-old man with pulmonary aspergillus infection, chest CT images show cavity lesion with
an air crescent sign in the right lower lobe and an intracavitary fungus ball-like mass
T. Jiang et al.
is associated with infectious diseases and a thin
halo with tumor diseases [68]. In summary, the
ground-glass halo on CT is mainly pathologically
representative of intraalveolar hemorrhage, but
tumor or inflammatory cells infiltrating the lung
parenchyma can also appear in halo sign; thus,
this sign can appear in many diseases. However,
the CT halo sign is most common in pulmonary
fungal infections, especially in the early stage of
invasive pulmonary aspergillosis.
4.27 Air Crescent Sign
Feature
On chest X-ray or CT, the appearance of a mar-
ginal, crescent-shaped translucent area within the
mass or nodule is called the air crescent sign.
Explanation
Air crescent sign is common in invasive pulmo-
nary aspergillosis. The mycelium of the fungus
invades the pulmonary blood vessels, causing
pulmonary hemorrhage, arterial embolism, and
infarction. The center of the lesion forms a
necrotic nodule. After that, the central infarct
component shrinks and the surrounding necrotic
tissue is absorbed by the white blood cells to
form a thin-walled cavity. The aspergillus ball
formed by the mixture of aspergillus mycelium,
fiber, and mucus is parasitic in the cavity lesion.
When the gap between the aspergillus ball and
the thin-walled cavity is filled with air, the air
crescent sign is formed (Fig. 4.27).
4 Chest
Discussion
“Air crescent sign” is a sign on chest X-ray or
chest CT that is characterized by a marginal,
crescent-shaped translucent area within the mass
or nodule [69]. It is common in invasive pulmo-
nary aspergillosis, mostly in people with impaired
immune function, especially in patients with leu-
kemia, lymphoma, bone marrow transplantation,
or organ transplantation, as it is an opportunistic
infection. In the early stage of the disease, the
chest X-ray can be normal, and with the progress
of the infection, there are single or multiple
peripherally plaque-like shadows with unclear
borders. Finally, it can become large, sometimes
nodular, lumpy, or miliary. The air crescent sign
occurs about 2 weeks later, with an incidence of
about 50%. It usually appears 15  days after the
initial infiltration of the lung, which is a sign of
the late stage of the disease, and the representa-
tive to enter the recovery period.
CT is more sensitive and specific than chest
X-ray. CT halo sign can be found at an early
stage, with high specificity. The typical CT find-
ing in the late stage is the appearance of the air
crescent sign. The presence of the air crescent
sign in pulmonary aspergillus infection has cer-
tain characteristics. However, in reports in the
literature, air crescent sign can also occur in other
fungal infections, tuberculosis, actinomycosis,
lung abscess and a small number of lung cancers
[70]. Differential diagnosis should be based on
characteristic imaging findings such as cavity
thickness, enhanced performance, nodular mobil-
ity, and intracomponent attenuation [71]. The
aspergillus ball is a soft-tissue attenuation mass,
which is parasitic in the cavity of the lung and is
easily secondary to the tuberculous cavity.
Therefore, it is more common in the posterior
segment of the upper lung. Usually, the lesion in
the cavity is separated from the wall by air, result-
ing in the air crescent sign. Changing the patient’s
position (between supine position and prone
position), the lesion in the cavity is movable,
which is a good indicator of differential diagnosis
[71]. Clinicians should understand this feature
and propose a possible diagnosis of invasive pul-
monary aspergillosis based on its characteristic
133
air crescent sign and CT halo sign. In addition, a
detailed clinical history, including immunosup-
pression, past medical history, and the history of
the epidemic area, is also essential for the diag-
nosis of the disease. Accurate diagnosis is essen-
tial and may have a significant impact on disease
management and prognosis.
4.28 Water-Lily Sign
Feature
When the inner and outer cysts of the pulmonary
echinococcosis, partial liquid coughing out of the
cysts and gas entering the inner cysts, the inner
cysts wall collapse and float on the liquid level. It
is shown as a soft-tissue attenuation on the liquid
level that moves with the change of body posi-
tion, which is similar with the floating of a lotus
or lily on water.
Explanation
Water-lily sign is a typical X-ray or CT sign of
complete rupture of inner and outer cysts of pul-
monary echinococcosis; the liquid is the cystic
fluid of hydatid, the float lotus is the ruptured
inner cyst wall that floats above the liquid level
after collapse (Fig. 4.28).
Discussion
Pulmonary echinococcosisis also known as pul-
monary hydatid disease. It is a chronic parasitic
disease caused by human-infecting larvae of the
dog tapeworm. This disease is mainly prevalent
in the animal husbandry area, with the highest
incidence rate in Northwest China. About 75%
of the disease occurs in the liver; about 15%
occurs in the lung and forms pulmonary hydatid
cysts [72]. The hydatid cysts are mostly spheri-
cal or elliptical. The cyst wall is divided into
two layers: the inner layer is the germinal layer,
having reproductive ability and secreting toxic
protein solution; the outer layer is the cuticle,
which has a protective effect. When the cysts
increase, the cysts wall may rupture; if commu-
nicating with the bronchus, the contents of the
cysts can be coughed up and air enters the cysts.
134
a b
Fig. 4.28 (a) Chest CT shows left lung lesions of patients
with echinococcosis by “water-lily sign,” through the
mediastinal diaphragm window. Collapsed inner capsule
is floating above the gas–liquid level. (b) Chest CT scan of
The pulmonary hydatid cysts grow slowly, and
are generally asymptomatic when small. When
the cysts increase to a certain extent, they cause
compression symptoms to surrounding tissues
and organs. The symptoms that can appear are
cough, mild chest pain, hemoptysis, or short-
ness of breath [73]. The Casoni test and the
complement fixation test of the pulmonary
hydatid cysts are mostly positive and can appear
eosinophilic.
Pulmonary echinococcosis is more common
in the lower lobe. If the cysts are not ruptured,
X-ray and CT show a typical fluid cysts sign,
which are round or oval in homogeneous attenu-
ation and sharp edges. The shape and size can
change with respiratory movement. The lesion
can be single or multiple, but a single lesion is
more common. Calcification and daughter cyst
formation are rare in lung hydatids [74]. In addi-
tion to the water-lily sign, the following findings
can be seen after the pulmonary hydatid cysts
rupture [2]. (1) Crescent sign: If the outer cyst
rupture, air enters between the inner and outer
cyst through the bronchus that form a crescent
radiolucent shadow at the top of the cyst. (2)
Two-bow sign: If both the inner and outer cysts
are ruptured, part of the contents discharge in the
cysts and air enters the inner and outer cysts at
the same time. Next, a fluid level appears in the
cyst, and two arc-shaped radiolucent bands
appear above the cyst, the two-bow sign. (3)
T. Jiang et al.
the mediastinum window shows a mass of low-density
shadow in the left lower lobe of patients with echinococ-
cosis, with multiple “balloon” or “bubble” signs, accom-
panied by marked thickening of the lesion wall
Float-egg sign: When a large inner wall or an
incompletely broken asci fall off and float on the
liquid level, it has a smooth semicircular attenua-
tion shadow, like an egg floating on water, the
float-egg sign. Its diagnostic significance is the
same as the water-lily sign. (4) Annular eclipse
sign: If the inner and outer cysts rupture and com-
pletely discharge, air enters between the inner
cyst and the inner–outer cyst, and the inner cyst is
still in an expanded state. The air band between
the inner cyst and the inner–outer cyst form a
double-layer air band that resembles the annular
eclipse. (5) Intracavitary snake shadow sign: If
both the inner and outer cysts are ruptured, all the
fluid is discharged. The inner cyst wall shrinks
and attaches to the outer cyst wall, causing the
intracavitary snake shadow sign. (6) Air bubble
sign: When the smaller hydatid cyst ruptures into
the bronchus, all the fluid discharged. After the
air enters, it looks like an air bubble. If there is no
infection, it can heal spontaneously. (7) Pleural
effusion or empyema: rupture of the cyst into the
chest forms a pleural effusion. If it is accompa-
nied by a bronchial fistula, a secondary infection
may result in an empyema. The imaging findings
of pulmonary hydatid cysts after rupture are com-
plex and various. Only the water-lily sign has a
characteristic diagnostic significance. Therefore,
the diagnosis should be combined with the clini-
cal manifestations and analyzed in many aspects
to make a correct diagnosis.
4 Chest 135

4.29 Mosaic Pattern

Feature
On HRCT, because of small-airway disease, vas-
cular lung disease, and infiltrative disease, which
cause differences of adjacent lung area in blood
perfusion, uneven lung density appears; it is char-
acterized as between increased pulmonary den-
sity area and reduced area. When the pattern is
the irregular shape of a patch or map, the arrange-
ment of the adjacent parts of different density
resemble the mosaic building material. Other
name: Mosaic perfusion; mosaic oligemia.

Explanation
Decrease of persistent pulmonary capillaries or
reflex vasoconstriction, and low perfusion of
blood flow in the dyspnea area, manifest local
reduced density and internal blood vessels appear
thinner on HRCT.  To maintain cardiac output,
reduced blood flow is redistributed to unblocked
areas of adjacent blood flow, with increased
blood perfusion, increased lung density, and
thickened internal blood vessels (Fig. 4.29).
Discussion
A mosaic pattern of lung attenuation on chest CT
scan is defined by the Fleischner Society glossary
as a patchwork of regions of differing attenuation
seen on CT of the lungs. The density of normal
lung parenchyma reflects the comprehensive
image of gas volume, blood volume, extravascu-
lar fluid volume, and lung tissue biological den-
sity in the lung, of which about 80% is gas, 10%
is liquid, and 10% is tissue structure. Any factor
that causes an increase in the amount of gas in the
lungs, as well as a decrease in the amount of fluid
or tissue composition, can produce a low-density
shadow of the lungs. There are many reasons for
the formation of mosaic pattern, the main reasons
being of three types: small-airway disease,
vascular lung disease, and infiltrative disease.
­ seen in association with pulmonary hypertension,
Small-­airway disease can be a primary disorder,
such as respiratory bronchiolitis or constrictive
bronchiolitis, or be part of parenchymal lung dis-
ease, such as hypersensitivity pneumonitis, or
large-­airways disease, such as bronchiectasis and
asthma. Diseases of the pulmonary vasculature
Fig. 4.29  Chest CT shows uneven opacity of the right
lobes, in which the perfusion looks like a mosaic shape
contribute to the remaining cases. In patients
with small-airways disease, air cannot readily
escape in the regions where the small airways are
obstructed. Because of this, the attenuation of the
involved segments remains relatively unchanged
in comparison with that at inspiratory imaging.
With air being normally conducted through the
noninvolved areas, the difference in attenuation
between the normal and abnormal areas becomes
much more pronounced and air trapping can be
diagnosed [75].
Primary pulmonary vascular disease results in
mosaic attenuation from regional differences in
lung perfusion. Mosaic attenuation is commonly
which will lead to enlargement of the pulmonary
trunk and remodeling of the right heart, including
right ventricular enlargement and hypertrophy.
The mosaic pattern related to pulmonary hyper-
tension (PH) consists of relative hypoattenuation
and hyperattenuation from adjacent areas with
136
disparate perfusion. The chest CT findings in
patients with PH may also demonstrate enlarge-
ment of the main pulmonary artery (PA) with
peripheral tapering. As a mosaic pattern is
believed to represent disparate pulmonary blood
volume in adjacent lung segments, the areas with
relative oligemia are thought to have more severe
pulmonary vasculopathy. More recent attention
to ventriculoarterial coupling mechanisms with
methods to access pulmonary impedance and PA
distensibility may offer opportunities for future
research to understand the link between pulmo-
nary vasculopathy and the upstream impact on
the right ventricle and main PA [76]. Primary
parenchymal disease causes ground-glass appear-
ance; in these lung diseases, there is a patchy
infiltrative process within the interstitium of the
lung on partial filling of the air spaces by fluid,
cells, or fibrosis so that the CT attenuation of the
affected lung increases compared with that of
normal parenchyma. The caliber and number of
vessels are not appreciably different between the
normal and abnormal regions of the lung.
Diseases that can produce such a CT pattern of
mosaic lung attenuation include Pneumocystis
carinii pneumonia, chronic eosinophilic pneu-
monia, hypersensitivity pneumonia, bronchiolitis
obliterans organizing pneumonia, and pyogenic
pneumonia [77]. Mosaic pattern is a nonspecific
sign that can occur in small-airway disease, vas-
cular lung disease, and infiltrative disease.
Although differentiation can be difficult, the dif-
ferential diagnosis can be narrowed by recogniz-
ing various imaging manifestations, which can
help guide management [75].
4.30 Ground-Glass Opacity
Feature
Ground-glass opacity (GGO) is a high-resolution
CT (HRCT) sign of the lung, which shows slight
increase in lung attenuation, with visible bron-
chial and vascular contours. The morphology of
GGO includes (1) diffuse type, which is more
common in severe acute lung transplantation
rejection, early adult respiratory distress syn-
drome, cardiogenic and noncardiogenic pulmo-
T. Jiang et al.
nary edema, acute and subacute allergic
pneumonia, pulmonary hemorrhage, and infec-
tions of various causes; (2) patch type, which can
be seen in all kinds of pneumonia, pulmonary
alveolar proteinosis, adult respiratory distress
syndrome, lipoid pneumonia, and Cysticercus
cellulosae; (3) focal type, which overlaps with
diffuse and patchy etiology, may occur in focal
tumors, trauma, pulmonary infarction, or lobar
pneumonia; (4) halo type, most of which are
found in early invasive pulmonary aspergillosis
or after pulmonary nodule puncture; and (5)
bronchovascular type and centrilobular type.
Eosinophilic pneumonia and sarcoidosis were the
most common types of bronchovascular type,
whereas exogenous allergic pneumonia and
respiratory bronchiolitis were the most common
lobular centroid type.
Explanation
GGO is a nonspecific chest CT imaging feature.
Any factor that causes consolidation of the lung,
reduction of air content in the distal air chamber,
and no total alveolar occlusion can produce
GGO. Histologically, the alveolar wall is slightly
thickened or the alveolar cavity is partially filled
with fluid, macrophages, neutrophils, and amor-
phous substances (Fig. 4.30).
Discussion
GGO is a nonspecific finding that can be caused
by a variety of diseases, including inflammatory
diseases or fibrosis. However, GGO lesions are
also thought to be closely related to primary ade-
nocarcinoma (AIS) or minimally invasive adeno-
carcinoma (MIA) [78]. The clinical history helps
to differentiate the diagnosis of GGO.  For
patients with acute history such as inhalation of
organic dust, the presence of GGO combined
with corresponding symptoms may indicate the
diagnosis of exogenous allergic alveolitis.
Multiple systemic lesions or patients with a his-
tory of collagen vascular disease strongly suggest
the cause of GGO. For patients who smoke and
have clinical symptoms of interstitial lung dis-
ease, GGO may be the manifestation of bronchial
inflammation-related interstitial lung disease
(RB-ILD). Patients with a history of pulmonary–
4 Chest
a b
c d
Fig. 4.30 (a–d) Ground-glass opacity (GGO) in bilateral lungs (white arrow)
renal syndrome and CT showing multiple or dif-
fuse ground-glass shadows may be considered
pulmonary hemorrhage. In patients with sickle-­
shaped erythrocyte anemia, if there is acute onset
and fever and chest pain, chest CT showing a
glass-like shadow is most likely an acute chest
syndrome. In patients with leukemia, AIDS with
cystic pneumonia, acute lung rejection, and
immunosuppressive cytomegalovirus infection
after lung transplantation, diffuse grinding with
diffuse ground-glass shadows as the main mani-
festation of alveolar hemorrhage may be seen on
CT.  Localized GGO-enhanced density nodules
strongly suggest leukemia with invasive aspergil-
losis, nodules after biopsy in lung transplants,
and patients with low-immunity lymphocytosis.
The anatomical distribution of pulmonary lob-
ular in GGO contributes to its differential diagno-
sis. (1) When it is distributed in the center of the
lobules, it is indicated as early air cavity consoli-
dation, infection by bronchial distraction, allergic
pneumonia, or desquamation interstitial pneumo-
nia. (2) If the ground glass is distributed in the
whole leaflet, the edge of the lesion is clear. If
only part of the pulmonary lobule is involved, the
137
edge of the lesion is blurred; the ground glass of
the whole leaflet distribution can be seen in alve-
olar proteinosis and drug toxicity. Lung injury,
lipid-like pneumonia, sarcoidosis, cystic pneu-
monia, and hemorrhage occur in the absorption.
(3) Ground glass is a peripheral distribution of
the lobules in early idiopathic pulmonary fibro-
sis. The distribution of the gross anatomy of
GGO is helpful to narrow the scope of differen-
tial diagnosis. Peripulmonary GGO may indicate
pulmonary contusion if there is a history of blunt
chest wall injury. Without a recent history of
trauma, the diagnosis of peripheral GGO may be
eosinophilic pneumonia, obliterative bronchiol-
itis with organized pneumonia, sarcoidosis, or
drug toxicity. CT scans in patients with sarcoid-
osis show nodules along bronchovascular distri-
bution, with mediastinal and hilar
lymphadenopathy. The distribution of GGO in
bilateral basal and subpleural regions is charac-
teristic of common interstitial pneumonia, des-
quamated interstitial pneumonia, and other
interstitial pneumonia. If there is a corresponding
history of isolated GGO in the middle lobe of the
right lung, it can be explained by the residual
138 T. Jiang et al.

fluid after bronchoalveolar lavage. Single local- linear, branching opacities that have more than
ized GGO may indicate early bronchioloalveolar one contiguous branching site, resembling a tree
carcinoma, or patients with known lung cancer in bud.
complicated with bronchioloalveolar adenomas.
Combined with other CT manifestations of Explanation
GGO complications, it is helpful to narrow the Tree-in-bud sign represents bronchiolar luminal
diagnostic range. The reticular shadow overlap- impaction with mucus, pus, or fluid, which
ping with GGO, showing polygonal lines, or demarcates the normally invisible branching
crazy paving, suggests alveolar proteinosis. course of the peripheral airways. Dilated and
Pulmonary edema was suggested when vascular thickened walls of the peripheral airways and
shadow thickened, heart shadow increased, with peribronchiolar inflammation can contribute to
pleural effusion, thickened septum, and ground-­ the visibility of affected bronchioles (Fig. 4.31).
glass opacity gravity distribution. When GGO is
combined with traction bronchiectasis and hon- Discussion
eycomb lung, pulmonary fibrosis is suggested. The tree-in-bud sign was described by Im et al. in
The manifestations of pneumatic injury such as 1993 [81], indicating the endobronchial spread of
interstitial emphysema, pneumothorax, mediasti- Mycobacterium tuberculosis. The tree-in-bud-­
nal pneumatosis, or pulmonary balloon can be pattern of images on thin-section lung CT is
seen in adult respiratory distress syndrome defined by centrilobular branching structures that
(ARDS). GGO and consolidation can also occur resemble a budding tree. The tree portion corre-
in these patients at an early stage. Follow-up is of sponds to the intralobular inflammatory bronchi-
great significance for GGO patients. It has been ole, and the bud portion represents filling of
pointed out that the curative effect of GGO
patients after operation is good and the recur-
rence is less, suggesting that GGO patients do not
need to be resected immediately [79]. Surgical
resection of the lesion is usually recommended
after the growth of GGO has been found. Sawada
et al. reported that for patients with partial solid
GGO lesions, a 3-year follow-up should be suf-
ficient to judge the growth of the tumor [80]. For
simple GGO lesions, a long follow-up time may
be required. In a word, the etiology of GGO is
various, and a comprehensive and systematic
analysis of GGO lesions is very important to
determine the etiology. It is meaningful to follow
up patients with GGO until the cause of the dis-
ease is determined.

4.31 Tree-in-Bud Sign

Feature
Tree-in-bud sign is a finding seen on thin-section
CT images of the lung. Peripheral (within
3–5 mm from pleural surface), small (2–4 mm in
Fig. 4.31  CT scan in a 69-year-old man shows multiple
diameter), centrilobular, and well-defined nod- small centrilobular nodules of soft-tissue attenuation con-
ules of soft-tissue attenuation are connected to nected to linear branching opacities (arrow)
4 Chest
inflammatory substances within alveolar ducts,
which are larger than the corresponding bronchi-
oles. Inflammatory bronchiole per se represents
the “tree” and inflammatory alveolar ducts con-
stitute the “buds” or clubbing. The tree-in-bud
pattern or sign should be used in case of visible
“tree” and “bud” [82]. The appearance of the
tree-in-bud sign is closely linked to the anatomy
of the secondary pulmonary lobule. Each second-
ary lobule is supplied by a lobular bronchiole and
a lobular artery located in the center of the lobule.
Under normal circumstances, the intralobular
bronchiole is less than 1 mm in diameter and is
not normally visible on CT. Diseased bronchioles
with mucous plugging, wall thickening, or dilata-
tion can be visualized on thin-section CT, dis-
playing the tree-in-bud phenomenon [83]. This
pattern is analogous to the larger airway “finger-­
in-­glove” appearance of bronchial impaction but
on a much smaller scale [84]. The tree-in-bud
sign has primarily been used as a descriptive term
for abnormalities found on CT scans of the lung
in patients with endobronchial spread of
Mycobacterium tuberculosis [85]. In the past sev-
eral years, however, it has become clear that the
finding of a tree-in-bud sign on a CT scan is not
specific for a single pulmonary disease entity, but
it can be found with a large number of conditions,
primarily those of infectious origin, but also with
immunological disorders, congenital disorders,
neoplasms, aspiration of irritant substances, and
disease entities with idiopathic causes [83].
In contrast to endobronchial tuberculosis, in
acute bacterial or viral infection, the inflamma-
tory process in and around the bronchioles tends
to be more exudative, spread into the adjacent
alveolar space. This phenomenon explains why
the tree-in-bud pattern in acute infection is less
common and less conspicuous than in endobron-
chial tuberculosis. The relative frequency of tree-­
in-­bud opacities in the clinical setting has been
evaluated by some scholars. The most common
causes were respiratory infections (72%), includ-
ing mycobacterial (39%), bacterial (27%), viral
(3%), and multiple (4%) infections [82]. In
patients with ‘tree-in-bud’ sign, pulmonary infil-
trations of chronic lymphatic leukemia (CLL)
should also be considered. Bronchoalveolar
139
lavage can be used to exclude differential diagno-
ses, but the diagnosis of pulmonary infiltration of
CLL may be missed. Transbronchial biopsies can
lead to the diagnosis [85]. In summary, tree-in-­
bud sign is a characteristic and easily detectable
CT finding in patients with disease of the small
airways. It is a useful sign, which, in the appro-
priate context of clinical findings and laboratory
features, almost invariably points to inflamma-
tory disease of the small airways [83].
4.32 Double-Wall Sign
Feature
On CT lung window, the linear hyperdensity
shadow parallels the chest wall and the abnormal
bright area of the lung field. This sign is mani-
fested by an unusually bright outline of the air in
the lung field showing the sides of the bullae par-
allel to the chest wall.
Explanation
Double-wall sign is a sign of pneumothorax in
patients with giant bullous emphysema (GBE).
One side is the wall of the bulla and the other is
the wall pleura. This sign occurs when one sees
air outlining both sides of the bulla wall parallel
to the chest wall. The double-wall sign may not
be evident on all CT slices, particularly with
compression of adjacent bullae; careful observa-
tion of multiple images may reveal this sign when
a pneumothorax is present (Fig. 4.32).
Fig. 4.32  A 71-year-old man with right lung bullae and
right pneumothorax with double-wall sign (arrow)
140
Discussion
Giant bullous emphysema (GBE) (also called
“vanishing lung syndrome”) is a rare condition
that typically presents in young male smokers
with a history of cannabis use or α-1 antitrypsin
deficiency [86]. GBE is characterized by large
bullae that involve at least one third of one or
both hemithoraces. The bullae are mostly unilat-
eral or asymmetrical and limited to the upper
lobes. Clinical presentations of GBE usually
include dyspnea, hemoptysis, chest pain, or spon-
taneous pneumothorax [87]. Most GBE patients
are often diagnosed as giant (large) pulmonary
bullae when clinicians lack understanding of the
concept of GBE, but this disease differs from, or
belongs to, a special type of pulmonary bullae.
The diagnosis of GBE mainly depends on imag-
ing studies. The imaging features of GBE patients
[88] include (1) large vesicular translucent shad-
ows in the upper and middle lobes, thin wall,
single or multiple, unilateral, partial double side
incidence. (2) Lesions are large, occupying more
than one third of the entire thoracic cavity, severe
cases with varying degrees of mediastinum and
heart shadow to the contralateral displacement
and diaphragmatic reduction. (3) Lesions can be
seen in a variety of slender strips separating the
shadow. (4) Adjacent lung tissue is compressed
and the lung texture is relatively concentrated,
and the edge of the lesion shows a little collapsed
lung tissue. (5) The lung tissue surrounding most
lesions is accompanied by different degrees of
emphysema.
GBE is easy to be misdiagnosed as pneumo-
thorax on a chest X-ray film. The following signs
are used to diagnose pneumothorax in patients
with bullous emphysema: compression of lung
tissue, abnormal areas of light, and relief of pul-
monary distension immediately after placement
of drainage tubes. The separation in GBE vesi-
cles is often slim, and the distribution is random;
the relationship with pleura is not very close. In
addition, patients with pneumothorax have a
complete pleural line, parallel to the chest wall,
showing a “double line sign,” the compressed
lung tissue converged toward the hilum; whereas
GBE showed a circular or oval transparent
T. Jiang et al.
shadow with greater tension, and the surrounding
lung tissue was compressed and gathered, but no
obvious centripetal areas showing uneven com-
pression to the mediastinum or around it. In addi-
tion, pulmonary tissues around GBE lesions are
often accompanied by different degrees of
emphysema, which should be differentiated from
bullous emphysema. Another sign of differentia-
tion between pneumothorax and giant bullae is
the double-wall sign. The absence of this sign can
negate the diagnosis of pneumothorax and reduce
unnecessary placement of a chest tube. The
double-­wall sign may not be clearly shown on all
CT images, especially with compression of adja-
cent pulmonary bullae, but when pneumothorax
is present, careful examination of multiple slices
of the image will show this sign. The predomi-
nant findings on HRCT scans are extensive para-
septal emphysema coalescing into giant bullae.
HRCT is helpful in confirming the diagnosis of
vanishing lung syndrome, assessing the degree of
the disease, and providing information to guide
treatment [89]. Emphysema commonly accom-
panies various complications such as pneumonia.
These comorbidities sometimes look strange on
images because destroyed airspaces could change
the usual disease progression. Awareness of vari-
ous findings of emphysema with commonly
coexistent diseases may aid in the proper diagno-
sis and management of emphysema patients [90].
4.33 Crazy Paving Appearance
Feature
On the thin-layer CT or high-resolution CT
(HRCT) of the chest, it appears as a diffuse or
scattered ground-glass shadow, superimposed
with a smooth thin line shadow of the mesh,
resembling a crazy paving.
Explanation
In pulmonary alveolar proteinosis (PAP), which
is believed to be the result of thickening of the
interlobular septa, interstitial thickening of the
lobules is also involved in the formation of this
sign (Fig. 4.33).
4 Chest
a b
Fig. 4.33 (a, b) A 50-year-old woman with PAP. Chest CT shows diffuse ground-glass opacities and a crazy paving
appearance
Discussion
“Crazy paving appearance” is a sign on the chest
thin-layer CT or high-resolution CT (HRCT). It
was first discovered and reported by Murch et al.
in a case of PAP in 1989 [91]. The sign appears as
a diffuse or scattered ground-glass shadow,
superimposed with a smooth thin line shadow of
the mesh, resembling crazy paving. In PAP, the
corresponding pathological changes of crazy
paving appearance are caused by the filling of
phospholipid-like substances in the alveoli, alve-
olar septal lymphocytic infiltration, edema, fibro-
blast proliferation, and collagen deposition,
resulting in interlobular septal and lobular septal
thickening. Crazy paving appearance is common
in patients with PAP, characterized by ground
glass with a clearly defined map-like distribution,
in which the mesh shadows are uniform in size,
homogeneous in attenuation, and smooth on the
edges [92].
It was once considered to be a characteristic
chest CT manifestation of PAP, but it was later
found that many other diffuse diseases of the lung
also showed this imaging change. Histologically,
three changes lead to the crazy paving appear-
ance: alveolar consolidation, interstitial fibrosis,
and a combination of the two [93]. So long as the
disease conforms to the histological changes it
can cause a crazy paving appearance, such as
pneumocystis carinii pneumonia, bronchioloal-
veolar carcinoma, nonspecific interstitial pneu-
monia, organizing pneumonia, exogenous lipid
pneumonia, acute respiratory distress syndrome,
pulmonary hemorrhage, radiation pneumonitis,
and congestive heart failure [93]. In the identifi-
141
cation, PAP is mostly subacute, chronic onset,
patchy or diffuse, map-like changes; pulmonary
edema, pulmonary hemorrhage, and pneumocys-
tis pneumonia are acute onset; and bronchioloal-
veolar carcinoma consolidation nodules are
common. In addition, the range of radiation
pneumonitis is often consistent with the radiation
field; mechanized pneumonia lesions, which can
be nodules, are more common in the periphery of
the lungs. The crazy paving appearance is a non-
specific imaging manifestation that occurs in a
variety of diseases. However, it is often possible
to make an appropriate diagnosis by acknowledg-
ing the location, characteristics, and other imag-
ing findings of various diseases, combined with
the patient’s medical history and clinical
manifestations.
4.34 Black Pleural Line Sign
Feature
This sign refers to a thin strip of low-density
shadow between the lung parenchyma and the
ribs on chest X-ray films, which can be seen from
the apex of both lungs to the angle of the rib dia-
phragm, against the backdrop of small stones in
the chest wall and lung parenchyma.
Explanation
Black pleural line sign is an X-ray sign of pulmo-
nary alveolar microlithiasis (PAM). It is con-
firmed by HRCT that subpleural microcysts are
arranged along the pleural surface. HRCT has
confirmed that the black pleural line sign seen in
142
Fig. 4.34  In a 72-year-old man, bilateral lower lobes
show the black pleural line sign (arrow)
X-ray is a thin-walled cyst under the pleura. Its
diameter is about 5–10 mm, along the wall pleura
and mediastinal pleura, from the apex of the lung
to the bottom of the lung. The ribs and lung
parenchyma on both sides of the pleura make the
band of the subpleural cyst more clearly visible.
The black pleural line sign is more common in
cross-sectional imaging (Fig. 4.34).
Discussion
The black pleural line sign, first described by
Felson et al. [94] in 1967, is considered a charac-
teristic sign of pulmonary alveolar microlithiasis
(PAM). PAM is a rare disease characterized by
numerous diffused calcareous (calcium and
phosphorus) microlithiases in the alveoli. PAM is
considered a familial hereditary disease [95].
Post studies confirmed the disease is caused by
autosomal recessive inheritance of a mutation in
the gene that produces the protein that is the only
known sodium-dependent phosphate transporter
in the lungs. As a result of this mutation, the pro-
tein is unable to transport phosphorus ions from
the alveolar space into type II pneumocytes, and
this failure leads to the development of calco-
spherites in the alveolar space. PAM is character-
ized by diffuse small calcareous nodules
involving both lungs in the form of typical dust
storms. In the lower lobes of both lungs, the
increase of calcification density is more obvious,
which is attributed to the larger surface area of
the lower lobes and the thicker parenchyma of the
lungs. The course of the disease can be divided
T. Jiang et al.
into four stages: stage 1 (pre-calcification): atypi-
cal early imaging; stage 2: diffuse sandy granular
changes in both lungs, clear boundary between
heart shadow and diaphragm; stage 3: increased
number and volume of microlithiases, interstitial
thickening, subpleural high-density calcification
in the mediastinal window and patchy calcifica-
tion in the dorsal subpleural fusion, under sharp
edge of heart shadow and diaphragm in the lower
and middle lung fields; stage 4: most of the lung
fields are filled with microlithiasis, and “white
lung” manifestations have appeared. In this stage,
emphysema, bullae, and pneumothorax could be
combined.
Black pleural line sign often appears in the
early stage of PAM, which is characterized by
long and narrow transparent shadows between
the mediastinum, chest wall and lung margin.
The presence of various forms of lesions reflects
the pathological process of chronic progression
of PAM.  CT is superior to X-ray radiography,
which is helpful for early detection of small cal-
cifications, follow-up, qualitative diagnosis of
lesions, and the determination of small cysts.
HRCT is preferable because it can detect mini-
mal structural changes in the pulmonary paren-
chyma that cannot be assessed with radiograph or
other CT techniques. HRCT could clearly show
the subpleural transparent zone, that is, the cysts
arranged in series [96]. The radiologic manifesta-
tions of PAM have characteristic diagnostic sig-
nificance, but the final determination still needs
to be based on thoracotomy biopsy. Early diagno-
sis is mainly based on radiologic examination.
The appearance of black pleural line sign indi-
cates the formation of subpleural cyst, which is
the radiologic manifestation of the destruction of
lung parenchyma and the further development of
PAM lesions.
4.35 Sarcoid Galaxy Sign
Feature
The large nodules in the pulmonary parenchyma
of sarcoidosis (diameter >1 cm) are composed of
numerous nodules on CT images. There are small
satellites points around large nodules with rela-
4 Chest
tively clear boundary. The characteristic pattern
of large nodules in the pulmonary parenchyma
resembles a galaxy consisting of millions or even
billions of stars.
Explanation
The galaxy sign is the characteristic CT appear-
ance of large nodules in the pulmonary paren-
chyma of sarcoidosis, which is standard for
noncaseating granuloma lesions from the conflu-
ence of numerous nodules (Fig. 4.35).
Discussion
The galaxy sign, also called the sarcoid galaxy, is
used to describe pulmonary parenchymal nodules
seen in sarcoidosis that are composed of several
smaller interstitial nodules. The appearance of a
central dense mass with tiny peripheral satellite
nodules is akin to a galaxy cluster [97]. It is most
often between 1 and 2 cm in diameter but can be
larger. The galaxy sign represents interstitial
granulomas that have coalesced and become
a b
Fig. 4.35  CT plain scan shows small nodules around the large nodules, with typical sarcoid galaxy sign (a, b)
143
inseparable, simulating the appearance of a larger
nodule [98]. The galaxy sign was initially
described in sarcoidosis but is not specific for this
condition. The galaxy sign may also be present in
active tuberculosis (TB). Findings mimicking the
galaxy sign may be present in progressive mas-
sive fibrosis (PMF) and neoplasm. The location
and number of conglomerated nodules as well as
the overall pattern of parenchymal disease and
presence of associated findings such as lymph-
adenopathy must be taken into consideration
when formulating a differential diagnosis. The
presence or absence of lymphadenopathy can
also be very helpful. Bilateral hilar lymphade-
nopathy is a hallmark of sarcoidosis and occurs
either alone or with mediastinal lymphadenopa-
thy in 95% of patients with sarcoidosis.
Calcification within hilar and mediastinal lymph-
adenopathy is also helpful as it is common in sar-
coidosis but rare in untreated malignancy. Active
TB can also present with a conglomerate nodule
surrounded by smaller nodules. The location and
144
number of the nodules as well as associated find-
ings are useful in differentiation from sarcoid-
osis. The galaxy sign in active TB favors the
upper lobes and the superior segments of the
lower lobes, although it does not demonstrate a
specific lobar distribution in sarcoidosis.
Therefore, a single isolated focus of the galaxy
sign favors TB. Lymphadenopathy is more com-
mon in sarcoidosis whereas tree-in-bud opacities
are characteristic of TB. PMF in pneumoconiosis
can loosely mimic the appearance of a galaxy
sign, but distinguishing PMF from the galaxy
sign in sarcoidosis is usually not difficult.
PMF is characterized by extensive architec-
tural distortion, traction bronchiectasis, paracica-
tricial emphysema, and nodules mixed with
haphazardly arranged bands of fibrosis. In the
galaxy sign, fine nodules emanate from a larger
central nodule without these extensive fibrotic
changes. The satellite nodules must be distin-
guished from the spiculated lung nodules typical
of malignancy. Extensive mediastinal and bilat-
eral hilar lymphadenopathy is rarely seen in non-­
small cell lung cancer, especially in lesions less
than 3 cm [97]. Clinical history and demograph-
ics can be helpful in troublesome cases.
Sarcoidosis can affect patients at any age but is
commonly diagnosed before the age of 40 years,
with the peak incidence in the third decade of
life. Malignancy is more common in older
patients; tuberculosis risk factors or occupational
exposure can lead one to more strongly consider
active TB or PMF, respectively. The galaxy sign
favors a benign etiology and in the context of
appropriate demographics, history, and associ-
ated findings can be quite helpful in establishing
a specific diagnosis [98].
4.36 Diaphragm Sign;
the Interface Sign; the Bare
Area Sign; the Displaced
Crus Sign
Feature
In conventional upper abdominal CT scans, free
pleural effusion is sometimes difficult to distin-
guish from peritoneal effusion. Especially when
T. Jiang et al.
the volume of effusion is small, the following
four signs can be used to differentiate pleural and
peritoneal effusion [99]. (1) The diaphragm sign
means the pleural effusion and peritoneal effu-
sion are located in different positions of the dia-
phragm. Pleural effusion is located around the
diaphragm, whereas peritoneal effusion is located
in the center of the diaphragm, surrounded by the
diaphragm. (2) In the interface sign, the interface
between pleural effusion and adjacent liver or
spleen is blurred, and the interface between peri-
toneal effusion and adjacent liver or spleen is
clear. (3) The bare area sign refers to the area near
the posterior abdominal wall of the right lobe of
the liver, which lacks peritoneal tissue, and the
liver directly contacts the posterior abdominal
wall, so there is no peritoneal effusion on the pos-
terior edge. (4) The displaced crus sign refers to
the pleural effusion located between the dia-
phragm angle and the spine, pushing the dia-
phragm angle forward, causing diaphragm angle
displacement. This is not the case with peritoneal
effusion.
Explanation
In conventional upper abdominal CT scans, free
pleural effusion is sometimes difficult to distin-
guish from peritoneal effusion. Halvorsen et al.
have summarized four signs for the differential
diagnosis of pleural and peritoneal effusion. In
peritoneal effusion patients, any patients lack
adequate perihepatic fat to identify the dia-
phragm. Because the attenuation of ascites is
less than that of the diaphragm and the liver, the
diaphragm sign is visible in patients with perito-
neal effusion, and because of the small effect of
partial volume, the boundary between ascites
and surrounding organs is clear. Not only that,
peritoneal effusion is prevented from extending
behind the liver at the level of the bare area.
When pleural effusion occurs, the interface
between pleural effusion and adjacent liver or
spleen is blurred. This appearance is presumed
to be caused by the diaphragm separating pleural
effusion from the liver. Pleural effusion can
extend behind the liver at this level because the
posterior sulcus of the right pleural space extends
behind the liver. Therefore, fluid behind the liver
4 Chest 145

at the level of the bare area is in the pleural
space, not intraperitoneal. In practical work,
these four signs are inseparable. If only one of
them is used, it will lead to difficulties in identi-
fication or misjudgment. Taking the four signs
into consideration, the correct rate of diagnosis
can be significantly increased. Usually these
four signs are collectively referred to as pleural
and peritoneal effusion differential quadruple
sign (Fig. 4.36).

a b

c d

e f

Fig. 4.36  Diaphragm sign (a): the diaphragm is clearly
visible between the pulmonary and peritoneal effusions.
Interface sign (c, d): the interface between pleural effu-
sion and liver is blurred. (e, f) The interface between peri-
toneal effusion and liver is clear. Bare area sign (g):
peritoneal effusion diffuses to the front and side edges of
the liver but does not enter the bare area of the liver. (h, i)
Pleural effusion can be seen into the bare area. Displaced
crus sign (j): in the right pleural effusion, the diaphragm
angle is displaced to the outside
146
g h
i j
Fig. 4.36 (continued)
Discussion
CT diagnosis of pleural and peritoneal effusion is
generally clear, but sometimes it is difficult to
differentiate a small amount of pleural and peri-
toneal effusion. The CT value of peritoneal effu-
sion is lower than 0–15 HU, which often gathers
around the liver and spleen and pushes the latter
forward. However, when pleural effusion is in the
lateral posterior recess of the pleural cavity, it can
also be in the lateral posterior part of the liver and
spleen and push the liver and spleen forward.
Therefore, pleural effusion should be differenti-
ated from peritoneal effusion in CT scan of the
upper abdomen [100]. The location of the dia-
phragm is easy to observe when peritoneal effu-
sion occurs. However, in many patients with
pleural effusion, because the diaphragm is insep-
T. Jiang et al.
arable from the liver, it is difficult to see, so the
diaphragm sign is more useful for identifying
peritoneal effusion.
The boundary between the pleural effusion
and the liver or the spleen is blurred, possibly
because of the insertion of the diaphragm between
the effusion and the liver or the spleen. Because
the diaphragm is obliquely transected during
transverse scanning, a partial volume effect is
inevitable, leading to blurring of the interface
between the effusion and the liver or spleen
[101]. The peritoneal effusion is generally at a
low position, and there is no partial volume effect
from diaphragmatic insertion between the perito-
neal effusion and adjacent organs, so the inter-
face is clear and well defined. If the thickness of
the scanning layer is thinned, the interphase
4 Chest
between pleural effusion and liver or spleen can
be clearer, but it cannot achieve the interface clar-
ity of the peritoneal effusion. The posterior of the
liver is attached directly to the posterior abdomi-
nal wall. This part of the liver without peritoneal
coverage is called the bare area. The upper and
lower layers of the hepatic coronary ligament are
attached to the posterior part of the liver and the
lower part of the liver. They form the bare area of
the liver, occupying the lower and posterior of the
right lobe of the liver and to the last third of the
liver. Although the abdominal cavity is blocked
by the bare area, the peritoneal effusion cannot
reach the side of the spine. However, it is worth
noting that the blocking scope of the bare area of
the liver is limited, and it can flow freely above
and below the bare area.
4.37 Split Pleura Sign
Feature
The split pleura sign is seen on postcontrast chest
CT images with enhancement of the thickened
inner visceral and outer parietal pleura, separated
by a collection of pleural fluid.
Explanation
Thoracic empyema is defined as purulent content
in the pleural cavity. Empyema most commonly
occurs in the setting of bacterial pneumonia. It
typically develops from transformation of a parap-
neumonic effusion (not infected) into a compli-
cated effusion (features of infection but not
purulent) and then into empyema. In parapneu-
monic effusion, fluid moves in the interpleural
space by the increased capillary vascular permea-
bility. Proinflammatory cytokines facilitate the
fluid entry into the pleural cavity and cause hyper-
emia. With increasing fluid accumulation and bac-
terial invasion through the damaged endothelium,
transudative effusion progresses to empyema. As
empyema progresses, a fibrin peel coats the sur-
faces of the visceral and parietal pleural layers
with ingrowth of capillaries and fibroblasts and
subsequent thickening, forming the basis of the
split pleura sign: thickened visceral and parietal
pleural layers separated by empyema (Fig. 4.37).
147
Fig. 4.37 Postcontrast CT shows empyema between
thickened parietal and visceral pleural layers
Discussion
Normal visceral and parietal pleura are indistin-
guishable on CT images. In the presence of an
exudative pleural effusion with loculation,
inflammatory changes may thicken both the vis-
ceral and parietal pleura that surround the fluid
collection and may become evident as the split
pleura sign, suggesting the presence of empy-
ema. A loculated effusion may have an atypical
chest radiographic appearance when located
within a fissure. The split pleura sign may be seen
in combination with the air–fluid level sign when
a bronchopleural fistula occurs within empyema.
Empyema should be considered when a patient
presents with fever, cough, and chest pain and CT
shows split pleura sign [102]. The split pleura
sign is not specific for empyema but rather indi-
cates the presence of an exudative effusion. Other
important causes of this sign include parapneu-
monic and malignant effusions, hemothorax, and
sequelae of previous talc pleurodesis, lobectomy,
or pneumonectomy. Hemothorax usually has
associated heterogeneously high attenuation, and
talc pleurodesis has attenuation resembling that
of calcium and is often clumped [102]. About
half of empyema are caused by gram-positive
bacteria (Staphylococcus aureus, Streptococcus
pneumoniae); the remainder are gram-negative
organisms commonly growing together with
other gram-negative organisms or anaerobes. In
summary, the split pleura sign refers to thicken-
ing and increased contrast enhancement of the
148
visceral and the parietal pleura separated by
empyema or an exudative effusion [103].
Increased attenuation of extrapleural fat and
thickening of the fat layer of 3  mm or more is
seen in 60% of empyema. Pneumonia, lung
abscess, or obstructing malignancy are readily
evident on contrast-enhanced studies. In patients
with fibrinopurulent pleural infections, the under-
lying lung often shows multiple alternating out-
pouchings and indentations from fibrin strands
that produce intrapleural adhesions. Septations
within an infected effusion are less readily
imaged as compared with ultrasonography.
Pleural-based lung abscesses may be difficult to
distinguish from loculated empyema. On CT
scan, lung abscesses tend to be round rather than
lenticular in shape as are empyema, have thick,
irregular walls, and do not displace adjacent lung.
If ineffectively treated, empyema can progress to
a fibrothorax that appear as uniform smooth
thickenings of the pleurae with hypertrophy of
the extrapleural fat and reduced volume of the
affected empyema with narrowing of the inter-
costal spaces and shift of the mediastinum to the
affected side. Chest CT scan cannot predict the
likelihood that pleural thickening during the
fibrinopurulent phase of pleural infections will
progress to fibrothorax [104].
4.38 S
 ubpleural Line; Subpleural
Curvilinear Shadow
Feature
Subpleural line refers to the linear within 1  cm
below the pleura on chest CT, and parallels the
pleura with a length of 1–5 cm.
Explanation
Subpleural curvilinear shadow is one of the CT
findings of interstitial lung disease, which is a
manifestation of the flattening of alveoli and atel-
ectasis caused by peribronchiolar interstitial
hyperplasia and pulmonary fibrosis (Fig. 4.38).
Discussion
Subpleural curvilinear shadow (SCLS) is com-
monly seen in the posterior part of the lung on
T. Jiang et al.
Fig. 4.38  In a 76-year-old woman, chest plain CT shows
subpleural fibrous cords of inferior lobe of the right lung,
the subpleural curvilinear shadow (arrow)
HRCT, but the shadow is more than one lung seg-
ment in scope and located in the non-pendent part
of the lung. When the position changes, its shape
does not change and will not disappear. Most of
the SCLS have a smooth, continuous surface; a
few are irregular and discontinuous. SCLS has
originally been visible in the lower dorsal lung
field on chest CT scan in patients with pulmonary
fibrosis and asbestosis. Some scholars described
that SCLS in the lower dorsal lung field might be
chronic changes such as fibrosis, and it might
somewhat be attributed to the effect of gravity.
Arai et  al. [105] showed two cases of transient
SCLS caused by pulmonary congestion, and they
speculated that SCLS was not a specific finding
in pulmonary fibrosis and asbestosis. SCLS in a
patient was located lateral to anterior parts of
both upper lobe of the lungs. Therefore, it might
not be a gravity-related chronic parenchymal
abnormality. Histopathological findings of SCLS
in a patient were alveolar septal thickening and
marked infiltration of eosinophils. There was no
fibrosis or organizing change. In addition, the
shadow responded dramatically and disappeared
soon after corticosteroid therapy. This response
implied that the shadow might be a transient
change such as plate-like atelectasis or inade-
quate lymphatic flow from an exudative lesion
[106].
In the past, some scholars thought that the
subpleural curvilinear shadow was more com-
mon in asbestosis, or that this sign was the unique
4 Chest 149

manifestation of asbestosis patients, but research Discussion

now shows that the subpleural curvilinear shadow Signet ring sign is a finding seen on chest CT,
can be seen in a variety of pulmonary interstitial which is characterized by small circular soft-­
fibrosis diseases, such as chronic bronchitis with tissue attenuation shadow connected with a
pulmonary interstitial fibrosis, coal worker pneu- large soft-tissue attenuation ring with circular
moconiosis, idiopathic pulmonary interstitial hypoattenuation area and shaped like a signet
fibrosis, or collagen disease caused by interstitialring [107]. In histopathology, the soft-tissue
lung pulmonary changes from fibrosis and sar- attenuation ring represents the dilated bronchial
coidosis. In addition, the subpleural curvilinear wall, the low attenuation of which is the air
shadow is also seen in inflammation, pulmonary contained in the dilated bronchus, and the small
congestion, and inspiratory conditions. In the circular soft-­tissue attenuation shadow repre-
case of pulmonary interstitial fibrosis, the sub- sents the pulmonary artery associated with the
pleural curvilinear shadow represents an early dilated bronchus. Bronchiectasis refers to the
change in pulmonary interstitial fibrosis. The unrecoverable abnormal expansion of the local
length of the subpleural curvilinear shadow is bronchi caused by destruction of the elastic tis-
associated with the severity of pulmonary inter- sue and muscle tissue of the bronchial wall,
stitial fibrosis, and some are reversible. Current often accompanied by thickening of the bron-
research shows that the total percentage of all the chial wall. Bronchiectasis is often divided into
interstitial lung features was then determined by cystic, columnar, varicose, and mixed types.
combining the reticular, centrilobular nodule, lin- Columnar bronchiectasis is the lightest type,
ear scar, nodular, subpleural line, ground glass characterized by mild and consistent expan-
and honeycombing subtype volumes and divid- sion; variceal bronchiectasis refers to moderate,
ing by the total volume of all subtypes including irregular bead-like dilatation; cystic bronchiec-
normal, interstitial, and emphysematous. There tasis is most severe; and bronchus is saclike.
was no significant difference in the morphology The clinical manifestations of bronchiectasis
of subpleural curvilinear shadow in different dis- are nonspecific, manifested as chronic cough,
eases. However, the subpleural curvilinear massive purulent sputum, repeated lung infec-
shadow lacks the value of differential diagnosis tions, and hemoptysis.
for most diseases. Chest X-ray scan is the first step in the diagno-
sis of bronchiectasis. X-ray findings in 80% to
90% of patients with bronchiectasis can occur
4.39 Signet Ring Sign with lung texture aggregation, unclear edges, cir-
cular light transmission, and thickening of the
Feature bronchial wall to form two parallel linear shad-
Signet ring sign is formed by a small circular ows, also called the track sign. Although the chest
soft-tissue attenuation shadow and large soft-­ X-ray can detect lesions, suggesting the possibil-
tissue attenuation ring with circular low-­ ity of bronchiectasia, it cannot make the diagno-
attenuation area shaped like a signet ring on chest sis of bronchiectasis. The manifestations of
CT. bronchiectasis CT vary widely, depending on the
type of bronchiectasis and the relationship
Explanation between the direction of bronchial travel and the
The soft-tissue attenuation ring represents the scan plane. Normally, the diameter of the pulmo-
dilated bronchial wall, the low attenuation of nary artery is slightly larger than the bronchial
which is the air contained in the dilated bronchus, tube of the same level. When the ratio of the
and the small circular soft-tissue attenuation bronchial artery is increased, that is, when the
shadow represents the pulmonary artery associ- diameter of the bronchial tube is larger than that
ated with the dilated bronchus (Fig. 4.39). of the adjacent pulmonary artery, and the signet
150 T. Jiang et al.

a b

c d

Fig. 4.39 (a–d) A 72-year-old woman with bronchiectasis. Chest CT shows the bronchial wall of the left lower lung is
thickened, cystic dilated, with signet ring sign

ring sign appears. Then, bronchiectasis is consid-
ered [108]. The diameter of a cystic dilated bron-
chial tube is generally greater than 1  cm. The
relationship between the trachea and the scan-
ning plane is different, resulting in different CT
findings of bronchiectasis. Parallel to the direc-
tion of bronchial movement, it manifests as track
sign, and if perpendicular to the direction of
bronchial movement, it appears as the signet ring
sign. The CT findings of bronchiectasis include
the signet ring sign, track sign, clustered sac,
beaded shadow, and branching shadows from
mucous caulking. The first three diagnoses are
most useful.
4.40 Fallen Lung Sign
Feature
On sitting or standing chest films, lung tissue is
collapsed and droops in a mass in the cardio-
phrenic angles or retrocardiac region.
Explanation
X-ray findings of the fallen lung sign are specific
for bronchial rupture. With bronchial rupture,
lung displacement is posterior and lateral in a
supine position and inferior in a standing posi-
tion. Symptoms that progress within hours raise
the index of suspicion; a pneumothorax that per-
4 Chest
Fig. 4.40  A 24-year-old man had no improvement in
pneumothorax after chest tube. A large amount of gas was
seen in the right thoracic cavity; lung tissue was collapsed
and drooped in a mass in the cardiophrenic angles
sists or progresses despite a correctly placed
chest tube is a valuable sign in the diagnosis of
bronchial rupture (Fig. 4.40).
Discussion
The fallen lung sign was first described by Oh
et al. in 1969 [109], indicating complete rupture
or transection of the main bronchi. The term
“fallen lung” refers to the peripheral displace-
ment rather than the usual central displacement
of the collapsed lung, which is usually the result
of complete rupture of a bronchus. X-ray findings
of the fallen lung sign are specific for bronchial
rupture [110]. However, later it was reported that
incomplete rupture also may produce this sign on
CT and that the collapsed lung is displaced
toward the dependent portions, or posteriorly in a
supine patient. Although pneumothorax, pneu-
momediastinum, and soft-tissue emphysema may
indicate a bronchial rupture, these signs may not
be observed in early examination of most patients
presenting with pneumothorax and pneumomedi-
151
astinum following blunt trauma. Such ruptures
are difficult to diagnose in an emergency, and the
diagnosis is often delayed. Although fallen lung
sign is rarely seen, it is highly specific for bron-
chial rupture. The specific signs of tracheal injury
include deformity of the tracheal outline, an out-­
of-­place endotracheal tube, and an endotracheal
tube cuff protruding beyond the outline of the
trachea.
Fallen lung sign is considered pathognomic of
mainstem bronchial injury, in which the detached
lung tends to collapse laterally and posteriorly,
inferior to its attachment at the hilum, instead of
being collapsed inward as in other cases of pneu-
mothorax. Even partial injuries of the bronchus
can produce this sign, and the changing position
of the lung on patient repositioning can confirm
the detachment [111]. Bronchial wall irregularity
and surrounding air leakage may be seen in par-
tial ruptures. The diagnosis in the rarely seen tra-
cheobronchial rupture is generally established
with CT or bronchoscopy. However, when the
typical fallen lung sign is present, the diagnosis
of bronchial rupture may be established on radio-
graph [112].
4.41 Ring Around the Artery Sign
Feature
On the lateral chest X-ray film, a clear and trans-
parent image along or around the right pulmo-
nary artery is called the ring around the artery
sign.
Explanation
Pneumomediastinum refers to the accumulation
of abnormal gases in the mediastinum. A gas
shadow can delineate the boundary of the normal
structure. When the gas surrounds the mediasti-
num (outer pericardium) of the right pulmonary
artery, the lateral chest X-ray shows a clear
shadow around the right pulmonary artery, which
is called ring around the artery sign (Fig. 4.41).
Discussion
The ring around the artery sign was first reported
by Hammond et al. in 1984 [113]. This sign is the
152
Fig. 4.41  In a 20-year-old man with spontaneous pneu-
momediastinum, lateral chest X-ray shows a clear and
transparent area (arrow) along the right pulmonary artery,
called the ring around the artery sign
characteristic feature of pneumomediastinum in a
lateral chest X-ray film. Pneumomediastinum
refers to the accumulation of gas in the mediasti-
num, which can have various causes, the most
common of which is the Macklin effect. Alveolar
rupture is caused by the increase of intrapulmo-
nary pressure. Gas spills into the interstitium
around the alveolar through the rupture mouth.
Under the compression of respiratory movement,
gas can continue to move along the interstitium
to the hilum of the lung, and finally enters the
mediastinum to form a pneumomediastinum; this
is the Macklin effect. Gases in the mediastinum
can delineate different anatomical structures and
have different imaging features. In addition to the
circumferential sign around the mediastinum of
the right pulmonary artery, the gas can also sur-
round the thymus and elevate its position as sail
sign; it can surround the ascending aorta, aortic
arch, and the main branches of the aorta, as artery
cannula sign; it can surround the trachea and
proximal bronchus, as double bronchial wall
sign; it can also surround the diaphragm and the
T. Jiang et al.
cephalobrachial vein. The ring around the artery
sign is only used to describe patients with sec-
ondary asthma, trauma, subclavian artery intuba-
tion, and cocaine use or no definite inducement
[114]. This sign is usually accompanied by other
signs of pneumomediastinum. When pneumato-
sis occurs in the mediastinum, gas travels along
the fascial space and accumulates around the pul-
monary artery. Because only a small segment of
the right pulmonary artery is located in the peri-
cardium, the peripheral ring sign on lateral radio-
graph is only the extrapericardial segment of the
pulmonary artery.
In the differential diagnosis of pneumomedi-
astinum, traumatic pneumomediastinum should
be distinguished from spontaneous pneumomedi-
astinum [115]. The former has a clear history of
trauma, whereas the latter has no history of
trauma and often accompanies basic pulmonary
diseases. Second, traumatic pneumomediastinum
should be differentiated from traumatic rupture
of trachea and esophagus, because the former
usually needs no treatment, and the gas can be
absorbed by itself. Traumatic tracheal rupture
often occurs near the bronchial bulge, showing
continuous interruption of the tracheal wall.
Pneumatosis is mostly around the end of the rup-
ture without interstitial pneumatosis. When
esophageal rupture occurs, if esophagography
shows spillover of contrast medium, the diagno-
sis can be prompted. In a word, pneumomediasti-
num is caused by various reasons, and X-ray can
make a diagnosis. On the lateral radiograph, the
ring around the artery sign of pneumomediasti-
num can be displayed, and other signs of pneu-
momediastinum can also be observed.
4.42 Deep Sulcus Sign
Feature
A deep sulcus sign is seen on chest radiographs
obtained with the patient in the supine position. It
represents lucency of the lateral costophrenic
angle extending toward the hypochondrium. The
abnormally deepened lateral costophrenic angle
may have a sharp angular appearance.
4 Chest
Explanation
When the patient is in the supine position, air in
the pleural space (pneumothorax) collects anteri-
orly and basally within the nondependent portions
of the pleural space; when the patient is upright,
the air collects in the apicolateral location. If air
collects laterally rather than medially, it abnor-
mally deepens the lateral costophrenic angle and
produces the deep sulcus sign (Fig. 4.42).
Discussion
In a supine film, a deep sulcus sign may be the
only indication of a pneumothorax because air
collects anteriorly and basally within the nonde-
pendent portions of the pleural space, as opposed
to the apex when the patient is upright. Air enters
the pleural space by crossing any of its boundar-
ies, such as the chest wall, mediastinum, lung, or
diaphragm. Recognition of a pneumothorax
depends on the volume of air in the pleural space
and the position of the body. The visceral pleural
line, which is visible as a thin curvilinear opacity
along the lung and is separated from the chest
wall by air in the apical pleural space in the
upright patient, is commonly not identifiable on
radiographs of supine patients unless there is a
sizable pneumothorax. Approximately 30% of
Fig. 4.42  Chest X-ray image of a newborn in the supine
position: the indicated narrow, sharp, and black air-line
forward to the abdominal region at the left costophrenic
angle represents the deep sulcus sign in pneumothorax
153
pneumothoraces are undetected on supine radio-
graphs. The deep sulcus sign of pneumothorax
may be present following severe chest injury
[116]. However, false-positive deep sulcus signs
have been described in chest radiographs of
patients with chronic obstructive pulmonary dis-
ease and those receiving mechanical ventilation
with high tidal volumes [117]. In addition to the
deep sulcus sign, other clues may suggest the
presence of a pneumothorax on supine radio-
graphs: (a) relative lucency in the hypochondrial
region or the entire hemithorax; (b) depression of
an ipsilateral hemidiaphragm; (c) double-­
diaphragm appearance caused by air outlining of
the anterior costophrenic angle and aerated lung
outlining the diaphragmatic dome; (d) improved
sharpness of the cardiomediastinal border by
anteromedial collection of air, which may appear
as a lucency; (e) increased sharpness of the peri-
cardial fat pads; (f) visible inferior edge of a col-
lapsed lower lobe or of the undersurface of the
heart from air in the pleural space; (g) band of air
in the minor fissure bounded by two visceral
pleural lines; or (h) visible lateral edge of the
right middle lobe caused by medial retraction in
the presence of anterior pneumothorax [116].
The deep sulcus sign is a useful clue in the
diagnosis of pneumothorax in neonates or in criti-
cally ill patients such as those who have under-
gone major trauma or are in intensive care units.
This finding is also important in the intensive care
setting for procedures such as insertion of a sub-
clavian central venous catheter and for the use of
positive pressure ventilation [116]. Pneumothorax
is a common and important clinic condition in
polytraumatized or critically ill patients. It is
important that the lateral costophrenic angles are
included on the radiograph, as failure to diagnose
pneumothorax may be life threatening because of
the risk of tension. However, up to 76% of all
pneumothoraces may be occult when interpreted
by trauma teams at the time of admission. In a
retrospective review of 44 severely injured
patients identified with occult pneumothoraces,
the deep sulcus sign is the most commonly
‘missed’ radiologic sign [118]. Thoracic ultraso-
nography, as a part of extended focused assess-
ment with sonography for trauma, can be utilized
154 T. Jiang et al.

promptly at the bedside for early detection. The
CT scan is the gold standard for the diagnosis of
occult pneumothorax [118]. Nonetheless, identifi-
cation of the deep sulcus sign on chest X-ray
images obtained in the supine position can be use-
ful for early diagnosis of pneumothorax.
4.43 Scimitar Sign
Feature
Scimitar sign is seen on the posterior and anterior
chest X-ray film. It is a curved vascular shadow
on the right side of the heart, moving downward
toward the diaphragm.
Explanation
The curved knife sign is formed by an abnormal
pulmonary vein draining the right lung, which
resembles a short curved Turkish knife
(Fig. 4.43).
Discussion
Congenital pulmonary vein syndrome (CPVS)
includes a group of congenital abnormalities of
the chest that often occur simultaneously. CPVS

a b

c d

Fig. 4.43 (a) CT angiography shows right pulmonary and draining into the RA in (c) [119]. (d) Chest X-ray
vein (RPV, arrow) draining into right atrium (RA). pulmonary artery (PA) view shows scimitar sign in right
Angiography shows scimitar sign (arrows) of RPV in (b) lung field
4 Chest
consists of many different developmental abnor-
malities, each representing a different congenital
malformation of the chest. The main malforma-
tions of CPVS include pulmonary hypoplasia,
partial anomalous pulmonary venous reflux
(PAPVR), absence of pulmonary artery, pulmo-
nary sequestration, unsegregated pulmonary
artery blood supply, absence of inferior vena
cava, repetitive diaphragm (accessory dia-
phragm); the secondary malformations of CPVS
include tracheal triple, diaphragm bulge, partial
absence of diaphragm, diaphragmatic cyst, horse-
shoe lung, esophagogastric lung, abnormal supe-
rior vena cava, and absence of left pericardium.
Abnormalities associated with the heart and spi-
nal cord are more common. The deformities just
mentioned can occur alone or in combination.
However, the most common deformities of CPVS
are pulmonary hypoplasia and PAPVR.  When
pulmonary hypoplasia and PAPVR coexist, it is
called scimitar syndrome. Its characteristic mani-
festation is that a curved knife vein drains into the
inferior vena cava from the upper or lower right
diaphragm [120]. The scimitar syndrome is more
common in women (1.4:1.0). Most of the patients
were asymptomatic; in adulthood, this syndrome
is only found accidentally after taking posterior
and anterior chest X-rays. The symptoms of
childhood are recurrent chest infections or dys-
pnea. Symptomatic patients have obvious left-to-­
right shunts or severe congenital heart disease. In
most cases, this vein drains the whole right lung.
However, in some cases, this vein may drain only
the lower or middle lobes, and the upper lung
may drain normally into the left atrium. Almost
all blood from abnormal pulmonary venous
drainage flows back to the inferior vena cava
under the right diaphragm, and some to the por-
tal vein, hepatic vein, and even left atrium.
Because this abnormal pulmonary vein often
drains unquantified blood flow from the right
lung to the inferior vena cava, a left-to-right
shunt is formed. Usually, this shunt is asymp-
tomatic, unless the shunt reaches 2:1 or higher,
and the cardiac cavity is normal, but 25% of
patients have congenital heart disease, the most
common being atrial septal defect. Other com-
155
mon types are patent ductus arteriosus, aortic
stenosis, tetralogy of Fallot, and ventricular
septal defect [121].
The X-ray signs of the scimitar syndrome
have diagnostic significance. The scimitar sign is
common on posterior and anterior chest radio-
graphs, but this sign may sometimes be blurred
by overlapping with the heart, especially when
the right heart is visible. This vein can be bent
like a knife, straightened or thinned, and some-
times multiple veins are seen. Most of these are
accompanied by right lung dysplasia, and the
severity of this dysplasia determines the extent of
heart and mediastinal displacement. The right
lung is not only small, but also usually has tra-
chea, bronchus, lobe, and deformities of interlo-
bar fissure. Therefore, the upper or middle lobes
and transverse fissures may be absent, and the
right main bronchus may be elevated. These
abnormalities make the right lung similar to the
left lung [122]. Traditionally, angiography has
been the best choice for displaying vascular
anomalies when scimitar syndrome or pulmonary
sequestration is suspected. CT angiography
(CTA) as a noninvasive angiography is increas-
ingly used in CPVS.  The scimitar syndrome
rarely requires surgical treatment. Surgery is
mainly intended for patients with left-to-right
shunt, which can be treated by reorienting the
curved vein into the left atrium. Recurrent pul-
monary infections can be treated by lobectomy or
pneumonectomy.
4.44 Bulging Fissure Sign
Feature
Bulging fissure sign represents expansive lobar
consolidation causing fissural bulging or dis-
placement by copious amounts of inflammatory
exudate within the affected parenchyma.
Explanation
Classically associated with right upper lobe con-
solidation caused by Klebsiella pneumoniae, any
form of pneumonia can manifest the bulging fis-
sure sign (Fig. 4.44).
156
Fig. 4.44  Posteroanterior (left) and lateral (right) radio-
graphs show right upper lobe consolidation causing infe-
rior bulging of minor fissure (black arrows), posterior
Discussion
The sign is frequently seen in patients with pneu-
mococcal pneumonia [123]. The prevalence of
this sign is decreasing, likely because of prompt
administration of antibiotic therapy to patients
with suspected pneumonia [124]. The bulging
fissure sign is also less commonly detected in
patients with hospital-acquired Klebsiella pneu-
moniae than in those with community-acquired
Klebsiella infection [125]. Other diseases that
manifest a bulging fissure include any space-­
occupying process in the lung, such as pulmo-
nary hemorrhage, lung abscess, and tumor.
4.45 Air–Fluid Level Sign
Feature
In a patient with pneumonia, detection of an air–
fluid level on chest radiographs or CT images
suggests the presence of a lung abscess or empy-
ema with bronchopleural fistula. The former typi-
cally requires medical treatment with antibiotics
and the latter usually requires insertion of a chest
tube for drainage.
T. Jiang et al.
bulging of major fissure (white arrow), and inferomedial
displacement of bronchus intermedius (asterisk)
Explanation
Lung abscess is commonly associated with aspi-
ration pneumonia and septic pulmonary emboli.
Common causative organisms include anaerobes,
Staphylococcus aureus, and Klebsiella pneu-
moniae. Lung abscess is associated with increased
morbidity and mortality. Prompt detection at
imaging studies may improve patient care,
enabling clinicians to treat patients with an
appropriate course of antibiotic therapy
(Fig. 4.45).
Discussion
Detection of an air–fluid level at chest radiogra-
phy should prompt evaluation of its location as
being in the lung parenchyma or within the pleu-
ral space. A lung abscess with an air–fluid level
can be differentiated from empyema with bron-
chopleural fistula by measurement and compari-
son of the lengths of the visualized air–fluid level
on orthogonal chest radiographs [126]. Because
of the characteristic spherical shape of a lung
abscess, an associated air–fluid level typically
has equal lengths on posteroanterior and lateral
chest radiographs. By contrast, empyema typi-
4 Chest
a b
Fig. 4.45 (a) Posteroanterior (left) and lateral (right)
radiographs show right lower lobe cavity with air–fluid
level (arrows) of equal length on both orthogonal views.
Thick, irregular wall typical of lung abscess is evident. (b)
cally forms lenticular collections of pleural fluid,
and an associated air–fluid level (e.g., broncho-
pleural fistula) usually exhibits length disparity
when compared on posteroanterior and lateral
chest radiographs. In addition, both entities typi-
cally display a difference in the angle of their
interface with an adjacent pleural surface. A lung
abscess usually forms an acute angle when it
intersects with an adjacent pleural surface, and its
wall is often thick and irregular. By contrast,
empyema typically forms obtuse angles along its
interface with adjacent pleura and usually has
smooth, thin, enhancing walls [127]. Other dif-
ferential diagnostic considerations for an intra-
thoracic air–fluid level include hemorrhage into a
cavity, lung cancer, and metastatic disease.
4.46 Incomplete Border Sign
Feature
The incomplete border sign is a manifestation of
an abdominal X-ray film or chest X-ray positive
film, which means that the overall contour of a
soft-tissue mass is clear and sharp on one side
157
Axial CT image shows parenchymal location of right
lower lobe cavity with air–fluid level, irregular internal
contours, and associated bronchus (arrow) coursing to
lesion
and blurred on the other side, and the border is
submerged in the adjacent tissue shadow.
Explanation
The sign is an X-ray sign of extraabdominal mass
and extrapulmonary mass. The blurred, incom-
plete border of the mass is because the soft-tissue
mass fixed to the abdominal wall (or chest wall)
has little difference in attenuation from the adja-
cent abdominal wall (or chest wall). On the other
hand, the X-ray tangential line passes through the
other side of the soft-tissue mass (free from the
abdominal wall or protruding into the lung field),
which can form a clear, sharp border (Fig. 4.46).
Discussion
In 1964, Mendelson et  al. first studied the “the
incomplete border sign” and later it was dis-
cussed in some foreign textbooks [128]. It is a
manifestation of abdominal radiograph or chest
X-ray positive film, which means the overall con-
tour of a soft-tissue mass is clear and sharp on
one side and blurred on the other side, and the
border is submerged in the adjacent tissue shadow
[129].This sign may indicate that the mass origi-
158
a b
Fig. 4.46 (a) Chest film in the left-upper lung field (clav-
icle and first rib overlap) showed circular nodular shadow;
the inner and lower boundary of the lesion was clear, the
nates from an extraabdominal or extrapulmonary
site and is important for identifying the origin of
the mass.
On radiograph the border of the lesion is clear
and sharp, depending on (1) the difference in
attenuation between the lesion and the adjacent
structure; or (2) the edge tangent to the X-ray
beam [130]. Intraabdominal or intrapulmonary
lesions satisfy these two conditions, the tissue
attenuation is much larger than the surrounding
air, and the edge is tangent to the bundle in any
projection; while the extraabdominal and extra-
pulmonary lesions do not meet these criteria,
often causing partial border blurring, resulting in
the “incomplete border sign.” It is well known
that a mass originating from the abdominal wall
is easy to palpate. An incomplete border on the
supine abdomen radiograph on a plain radiograph
suggests that the mass is located outside the
abdominal cavity (including hernia and masses),
and this sign is more helpful in diagnosis when
there is no gas in the hernia. When the extrapul-
monary mass forms an incomplete border sign, it
usually appears as a partial border smoothing of
the lung field, and the border of the part con-
nected to the chest wall is unclear. The most com-
mon extrapulmonary lesions are localized pleural
effusion, rib lesions (fractures, primary or meta-
static tumors, plasmacytoma), interstitial tumors,
neurological tumors, hematoma, and intradermal
T. Jiang et al.
outer upper edge was blurred, and showed the “incom-
plete border sign”; (b) CT showed that the lesion was a
node protruding from the posterior chest wall [131]
lesions. Any extrapulmonary lesions can pro-
duce incomplete border signs, but the most com-
mon is rib metastases, and the mediastinal mass
can also have incomplete border sign. Pulmonary
nodules are sometimes confused with the nip-
ples. In addition to the position, the nipple
shadow usually showed a sharp outer border and
the inner border is unclear. The reason is that the
nipples protrude out due to the compression of
the film box, which is consistent with the forma-
tion mechanism of incomplete border sign. In
short, in actual work, lesion localization is the
first step in clinical practice and an indispensable
step. Incomplete border sign is an important fea-
ture of extraabdominal or extrapulmonary
masses. Understanding this sign can help radi-
ologists correctly locate lesions and guide subse-
quent diagnosis and treatment.
4.47 Grey Snow Sign
Feature
In a patient with COVID-19 (CoronaVirus
Disease 2019), an area of ground-glass opacity
(GGO) with interlobular septal thickening or
reticulation is detected on chest CT images. The
GGO was defined as a hazy increase in lung
attenuation with no obscuration of the underlying
vessels on chest CT images.
4 Chest
Explanation
The pathological basis of COVID-19 is exudative
inflammation. Histology shows bilateral diffuse
alveolar damage with cellular fibromyxoid exu-
dates. Interstitial mononuclear inflammatory
infiltrates are seen in both lungs dominated by
lymphocytes [132]. CT imaging shows pulmo-
nary parenchyma and interstitium changes simul-
taneously, which are consistent with pathological
changes. In the early stage, the distribution of
lesions is mostly located in the subpleural periph-
eral pulmonary cortex; then gradually develops
from the parenchyma of the lower peripheral to
the interstitial in the center, involving alveoli and
pulmonary lobules (Fig. 4.47).
Discussion
COVID-19 is a new type of pneumonia caused by
the SARS-CoV-2 (Severe Acute Respiratory
Syndrome Coronavirus 2) that broke out in
December 2019 in Wuhan City, Hubei Province,
China [133]. COVID-19 is highly contagious.
Currently, the main source of infection is patients
with COVID-19, and asymptomatic infected peo-
ple may also become the source of infection.
Respiratory droplets and contact transmission are
the main way of transmission, and the population
is generally susceptible. The 2019-nCoV infec-
a b
Fig. 4.47 (a, b) Grey snow sign. HRCT images of two
confirmed COVID-19 patients showed lesions distributed
in the subpleural peripheral pulmonary cortex, with single
159
tion was of clustering onset, is more likely to
affect older males with comorbidities, and can
result in severe and even fatal respiratory dis-
eases such as acute respiratory distress syndrome;
it is associated with intensive care unit (ICU)
admission and high mortality [134]. The
nasopharyngeal swab test for the COVID-19
­
nucleic acids had been positive. The diagnosis of
COVID-­19 should be based on comprehensive
analysis of epidemiological history, clinical
manifestations, laboratory tests, and imaging
characteristics. Radiologic examination and
diagnosis are an important part of the diagnosis
and treatment. The hallmarks of COVID-19
infection on imaging were bilateral and periph-
eral ground-­glass and consolidative pulmonary
opacities. There were more consolidated lung
lesions in patients 5 or more days from disease
onset to CT scan versus 4 or fewer days. Patients
more than 50  years old had more consolidated
lung lesions than those 50  years or younger.
Notably, 20/36 (56%) of early patients had a nor-
mal CT.  With a longer time after the onset of
symptoms, CT findings were more frequent,
including consolidation, bilateral and peripheral
disease, greater total lung involvement, linear
opacities, “crazy paving” pattern, and the
“reverse halo” sign [135].
(a, black arrow) or multiple (b, black arrow) GGO accom-
panied by interlobular septal thickening (b, white arrow)
and thickened bronchial vascular bundle (b, arrow)
160
Grey snow sign is often observed in the mild
cases on HRCT. It is observed in single or bilat-
eral GGOs with interlobular septal thickening or
reticulation and thickened bronchial vascular
bundle. The lesions are distributed in the sub-
pleural peripheral pulmonary cortex, looking
like a wedge or trapezium. Because the corona-
virus is inhaled through the respiratory tract,
most cases first reach the region of subpleural
lung periphery for gas exchange, which also
explains the characteristic distribution of
lesions. The presence of GGO on CT often indi-
cates inflammatory exudation and edema,
mainly in the lung interstitium. Meanwhile, the
parenchyma can also be involved, and the alveo-
lar cavity can contain half liquid and gas. In
severe cases, gas exchange is affected, and the
partial pressure of oxygen drops seriously. The
majority of patients with mild cases tend to be
stable and improve through isolation treatment,
showing that the range of lesions is narrowed,
the density is gradually reduced, the number of
lesions is reduced, and the GGO can be fully
absorbed. A small number of patients with basic
underlying diseases or elderly patients can be
more seriously affected. The COVID-19 still
needs to be differentiated from viral pneumonia
(influenza virus pneumonia, avian influenza
a b
Fig. 4.48  Two-chamber (a) and three-chamber (b) long-axis cine-MRI can demonstrate apical hypertrophy. The nar-
rowed portion of the ventricular cavity forms the cusp of the spade
T. Jiang et al.
pneumonia, SARS), mycoplasma pneumonia,
bacterial pneumonia, and other viruses [136].
4.48 Ace-of-Spade Sign
Feature
The “spade-like” configuration of the left ventri-
cle (LV) cavity at end-diastole on ventriculogram
or cardiac MRI (CMRI) is a typical finding of
apical hypertrophic cardiomyopathy (HCM)
without left ventricular outflow tract (LVOT)
obstruction.
Explanation
Differing from the hypertrophic obstructive
counterpart, apical HCM does not have LVOT
obstruction, and apical obliteration and prolifera-
tion are the characteristic pathological changes of
this kind of myocardiopathy (Fig. 4.48).
Discussion
Apical HCM is an uncommon variant of nonob-
structive HCM in which the hypertrophy is pre-
dominantly at the apex of the left ventricle.
Sakamoto et al. initially described the electrocar-
diographic (ECG) pattern and echocardiographic
characteristics in 1976 in Japan [137], but it was
4 Chest
Yamaguchi who described the syndrome subse-
quently and demonstrated the typical “spade-­
like” appearance on ventriculogram, so apical
HCM is also known as Yamaguchi syndrome
[138]. The prevalence of apical HCM has been
difficult to quantify, for the data vary with region
and ethnicity. Some studies have suggested that
apical HCM is particularly common in East Asian
populations (41% of Chinese with HCM and
15% Japanese with HCM) [139, 140]. Recently,
another study directly compared findings in
Japanese and European centers showing that pre-
dominantly distal and apical hypertrophy is seen
in almost similar percentages of Japanese (13%)
and European (11%) patients, suggesting there
may not be significant differences in prevalence
of apical HCM between Asians and other racial
groups [141]. Apical HCM is generally asymp-
tomatic because of the lack of LVOT obstruction
classically seen in HCM, although presentation
with angina, heart failure, myocardial infarction,
and atrial fibrillation has been reported [142].
Audible and palpable fourth heart sound can be
heard reflecting impaired LV relaxation. Deep
T-wave inversions are usually picked up on ECG,
typically in the left precordial leads. Some ST-T
abnormalities and atypical angina could be con-
fused with coronary ischemia. “Giant” negative
T-waves (defined as 10 mm deep) can be seen in
half the patients with T-wave inversions on ECG
[143].
Although echocardiography detects left ven-
tricular hypertrophy and obstructive HCM well,
it performs poorly in evaluating localized apical
hypertrophy, apical pouches, or aneurysms,
which are characteristics of apical HCM. Apex of
the heart is often not well visualized, and the
echo density of the hypertrophied apex may not
be significantly different from the near ventricu-
lar cavity. Contrast echocardiography could be
used to make the diagnosis but is not often per-
formed [144]. Without noninvasive imaging
modalities, apical HCM was once diagnosed
based on left ventriculographic appearance of a
“spade-like” ventricle, but it is no longer rou-
tinely performed in present clinical practice.
Multislice CT (MSCT) evaluates the coronary
161
artery when excluding coronary artery disease
(CAD) if patients have atypical chest pain, show-
ing the morphology of the LV wall and shape of
the LV cavity. However, radiation and contrast
exposure must be considered and the tissue fibro-
sis is not as well demonstrated as by CMRI. CMRI
is the accurate imaging modality of choice to
detect apical HCM. It provides good spatial reso-
lution and can show the tight spade shape charac-
teristic in cine-imaging. The quantitative
diagnosis can be made when apical thickness is
greater than 15 mm or a left ventricular apex to
base wall thickness ratio of 1.3 or more is deter-
mined by CMRI. Late gadolinium enhancement
(LGE) on CMRI confirms the existence of patchy
fibrosis in the hypertrophied segment. LGE is
associated with a higher risk of sudden cardiac
events caused by fibrotic tissue, which can affect
heart rhythm [145]. So, establishing the type of
HCM and ruling out CAD is very important to
the diagnosis and differential diagnosis, because
apical HCM is generally benign and frequently
asymptomatic [146]. The benign clinical course
and long-term prognosis require us to make accu-
rate diagnosis via the various imaging modalities
and genetic markers available to offer credible
guidance for follow-up management.
4.49 SAM Sign
Feature
Patients with hypertrophic cardiomyopathy
(HCM) frequently have systolic anterior motion
(SAM), which can be observed via transthoracic
echocardiography (TTE) or cardiac MRI (CMRI)
[147].
Explanation
“SAM” means the position of mitral valve moves
anteriorly into left ventricular outflow (LVOT) in
systole, recognized as the main cause of LVOT
obstruction. There is contact between the mitral
valve and the septum in patients with obstructive
HCM; the more prolonged the duration of mitral–
septal contact, the higher the LVOT obstruction
(Fig. 4.49).
162 T. Jiang et al.

(ECG), cardiac imaging modalities to identify

LV hypertrophy (LVH) should be performed in
all patients to acquire evidence supporting the
diagnosis. ECG should be checked in all patients
with susceptible HCM. Although 90% of patients
shows abnormalities such as prominent abnormal
Q waves in inferior (II, III, aVF) and lateral (I,
aVL, V4–V6) leads, the test is still specific
enough for further diagnostic evaluation [147].
Two-dimensional echocardiography can be
used to reliably diagnose patients with HCM. A
clinical diagnosis of HCM is confirmed when
unexplained increased LV wall thickness of
15  mm or more is imaged anywhere in the LV
Fig. 4.49 Apical three-chamber long-axis cine-MRI wall [149]. A wall thickness of more than 13 mm
shows minimal systolic anterior motion (SAM) of the may also be considered diagnostic of HCM, par-
mitral valve (black arrow) and LVOT obstruction
ticularly for patients with a family history. The
most common location for LVH is the basal ante-
Discussion rior septum in continuity with the anterior free
HCM is a genetic cardiomyopathy caused by wall, with the posterior septum the third most
mutations of the cardiac sarcomere, leading to common location. When detecting the presence
heterogeneous phenotypic expression with of LVH, among various of views, the parasternal
respect to the extent, location, and distribution of short-axis plane is primarily used in diastole at
left ventricle (LV) wall thickening. The clinical the level of the mitral valve and papillary muscle
course may include sudden death (often younger [148]. Other echocardiographic findings sugges-
than 30  years of age), heart failure (HF), or tive of HCM include increased LVOT gradient,
stroke. The prevalence of HCM in the general SAM of mitral valve, and increased LA size asso-
population is 1  in 500. Patients may remain ciated with atrial fibrillation (AF) [150]. For the
asymptomatic for a long time and then develop assessment of anatomic structures, CMRI may
one or more atypical symptoms such as HF with provide additional information that is not avail-
resultant dyspnea, fatigue, atypical chest pain, able from echocardiography [151, 152]. CMRI,
syncope, and palpitation [148]. Physical exami- emerging as a modality particularly well suited
nation in a patient with HCM may be normal or for characterizing the diverse subtype of HCM,
reveal nonspecific abnormalities such as a fourth has higher spatial resolution and tomographic
heart sound or systolic murmurs. Significantly, imaging capability without the burden of expo-
LVOT obstruction, often caused by a combina- sure to radiation and contrast [151]. Areas of seg-
tion of SAM of mitral valve and LV upper septal mental LVH that are not reliably visualized by
hypertrophy, results in a harsh systolic murmur echocardiography can be accurately identified
beginning slightly after S1. The murmur may via CMRI.  In the study performed by Hindieh
reflect both aortic outflow obstruction and mitral et al., 195 patients underwent both echocardiog-
regurgitation in patients with large ventricle-to-­ raphy and CMRI within a 6-month period, and in
aorta gradients. A variety of tests have been used half the patients, maximal LV thickness was sim-
in the evaluation of patients with possible ilar, whereas in the other 97 patients there was a
HCM. By performing these tests, we can estab- discrepancy greater than 10% discrepancy in
lish the diagnosis, identify the presence of sever- maximal LV thickness between the two imaging
ity of LVOT obstruction or mitral regurgitation, modalities, for the majority of echocardiography
and assess the overall LV function. Based on the overestimated the thickness. In instances where
physical examination and electrocardiogram the determination of massive LVH thickness
4 Chest
would impact the follow-up clinical management
decisions, CMRI should be performed more reli-
ably [153]. Structural abnormalities of the myo-
cardium, mitral valve (i.e., elongation leaflets),
and papillary muscles (i.e., accessory and api-
cally displaced or anomalous insertion into the
mitral valve leaflets) can be clearly demonstrated,
meanwhile precisely identifying the mechanisms
responsible for LVOT obstruction [151, 154–
156]. Because of the importance of mitral valve
and papillary muscle anatomy in patients with
LVOT obstruction who are being considered to
undergo invasive septal myectomy, CMRI should
be performed as a part of the evaluation [149].
Myocardial fibrosis can be shown with late gado-
linium enhancement (LGE). In a prospective
multicenter cohort of almost 1300 patients with
HCM who underwent contrast CMRI, extensive
LGE was an independent predictor of sudden
death [157]. Once the diagnosis of HCM is estab-
lished, based on clinical and echocardiographic
modes or CMRI, ambulatory ECG monitoring
should be performed for 24–48 h as a part of risk
assessment for arrhythmias and other cardiovas-
cular events [158]. Nowadays, the diagnosis of
HCM can generally be made via noninvasive
imaging modalities, and invasive diagnostic
assessments have been rarely necessary. Cardiac
catheterization is reservedly used for patients
with suspected HCM to exclude coronary artery
diseases and sometimes for the precardiac trans-
plantation assessment.
4.50 Linguine Sign
Feature
The linguine sign can be seen on T2WI. Breast
implants are characterized by multiple curvilin-
ear low signal lines in hyperintense silica gel.
Hypointense lines are often scattered, long-stripe
low-signal lines, which are tortuous between
each other looking like linguine.
Explanation
The linguine sign prompts the rupture of the
breast implant envelope. The coating and filling
of silica gel prosthesis consist of dimethyl sili-
163
cone with different degrees of polymerization.
The coating of a silica gel prosthesis adds some
chemical bonds between methyl and silicone to
form an elastic solid. The signal intensity of this
polymer is lower than that of silica gel on MRI,
with hypointensities on each sequence. On T2WI
the elastic silica capsule showed a low signal and
silica gel showed a high signal. Silica gel is
released after the rupture of the silica gel capsule,
forming a fibrous capsule (scar tissue) around the
breast implant. Layers of coiled wire represent
the elastic capsule floating in the silica gel
(Fig. 4.50).
Discussion
The linguine sign was first put forward by Safvi
in 2000 [159] and was named because it resem-
bles Italy’s linguine. More and more women now
have breast implants for cosmetic or reconstruc-
tive reasons, the most common of which is silica
gel. Complications associated with silicone
breast implants include cystic fibrosis or calcified
contracture, rupture and leakage, local pain,
deformation, and sensory abnormalities. Breast
implant rupture is common. The rupture of the
implant is mainly divided into two types: intra-
capsular and extracapsular. Intracapsular rupture
refers to the destruction of the implant envelope,
a small amount of silicone leakage but not beyond
the fibrous capsule; extracapsular rupture refers
to the implant envelope damage, amounts of sili-
cone leakage beyond the fibrous capsule.
On MRI, the surface of normal implants is
smooth and the boundary clear. Silica gel is
homogeneous in hypointensity on T1WI and
hyperintensity on T2WI. Because of the cross-­
linkage of methyl, the envelope is low signal in
all sequences. Radial folds are normal features of
the capsule, usually with one end connected to
the fibrous capsule. There are several types of
breast prostheses, the most common of which is a
single-lumen silicone implant wrapped in an
elastic silicone film, with a smooth or woven sur-
face. Silicone bleeding refers to a small leakage
of silica gel through the capsule, which is com-
mon after surgery. In intracapsular rupture,
fibrous capsules encapsulate silica gel, and in
extracapsular rupture, silica gel leaks from the
164 T. Jiang et al.

a b

c d

Fig. 4.50 (a–d) Line-like low-signal shadows can be seen on T2 (arrow)

ruptured fibrous capsule into breast tissue. The Explanation

linguine sign often indicates intracystic rupture. A malignant mass has a faster blood flow speed
This MRI sign is the most sensitive of all diag- in the periphery, larger capillary diameter, more
nostic modalities for fibrous capsule rupture, but capillaries, and higher capillary permeability,
sometimes needs to be differentiated from larger making the flow of contrast medium in the
folds [160]. Folds can be extended to the edge of periphery faster than in the center (Fig. 4.51).
the implant. Extracapsular rupture of the prosthe-
Discussion
sis is often a further development of intracapsular
rupture. All signs of intracapsular rupture can beThe sensitivity of the peripheral washout sign to
seen, and free silica gel signals can be seen out-diagnosis malignancy is quite low, but the speci-
side the fibrous capsule. ficity is very high. Factors that determine this
include capillary permeability, the number and
size of capillaries in tumors, and the speed of
4.51 Peripheral Washout Sign blood flow. Some of these factors are directly
related to tumor vascularity. Some studies have
Feature shown that tumor cells release vascular growth
The degree of enhancement around the lesion is factors, resulting in increased number and size of
reduced relative to the central lesion on delay-­ capillaries and increased capillary permeability.
phase dynamic contrast-enhanced MRI. Faster blood flow speed in the periphery, larger
4 Chest 165

a b

c d

Fig. 4.51  Woman, 47 years old, with right breast cancer. (a–d) In the early and delayed phase of dynamic enhance-
ment, a nodular abnormal enhancement was seen in the right breast. The edge is coarse and the shape is irregular [161]

capillary diameter, more capillaries, and higher
capillary permeability mean the contrast medium
of the periphery has a high turnover rate com-
pared with the center; it can be transported rap-
idly from the blood vessels to the tissues. There is
another mechanism for the flow of contrast
medium in the tumor. If the transport occurs
between parts of the tissue that have different
hydrostatic force, the contrast agent will flow
from the high-pressure area to the low-pressure
area. Some studies suggest that the center of the
malignant tumor is high pressure, and the periph-
eral area of the malignant tumor is low pressure.
Between these two different pressure zones, there
is a radial pressure gradient around the tumor.
This gradient causes the flow of interstitial fluid.
The flow of interstitial fluid pushes the contrast
medium from the peripheral zone to the outside
of the tumor, whereas the contrast medium in the
central of the tumor remains current from lack of
a pressure gradient.
On MRI most breast cancers have unclear
margins, irregular shapes, and edges that are nee-
dle like or radial. Tumors showed hypointensity
on T1WI, heterogeneous internal signal on T2WI,
and mixed with hypointensity and hyperintensity.
After contrast enhancement, the tumor shows
moderate enhancement, the internal signal is still
irregular, and there is no enhancement area. The
lesions often present hyperintensity on DWI
[162]. The structure of normal ductal tissue
around the tumor is obviously disordered. After
injecting the contrast medium, the peripheral and
central features of malignant breast lesions
showed different enhancement characteristics. In
some malignant tumors, the peripheral enhance-
166 T. Jiang et al.

ment was more obvious than the central enhance- on radiomics can improve the diagnosis of breast
ment at the first 2 min, and the two times intensity cancer and help to quantify the tumor [163].
curves crossed at 8  min, then the peripheral According to the relationship between spicula
enhancement curve continued to decrease while and mass, it is divided into long spicula, short
the central enhancement curve remained as the spicula, and star shadow. There is a significant
platform manifesting as a washout curve. In the difference in histological composition between
dynamic MRI images, the filling phase of con- the star shadow and the former two. The long and
trast medium reflects the transmission rate of short spicula are mainly homogenous in patho-
contrast medium from endovascular to intersti- logical type, and the ratio of cancer cells to inter-
tial. On the clear phase of contrast medium, just stitial can be as follows: simple type (type Ib),
the opposite occurred. The peripheral washout even distribution of cancer nest and collagen
sign is a special indication for malignant lesions fibers; medullary type (type II), with few colla-
in delay-phase dynamic MRI enhancement. This gen fibers in the cancer nest; and the sclerotic
sign also has potential value in the presence of type (type III), mainly composed of collagen
tissue interstitial pressure in malignancy. fibers and a few cancer cells. The star shadow is
mainly heterogeneous, that is, there is a large col-
lagen fiber (type Ia) between the cancer nests,
4.52 Spicular Sign and the attenuation inside the tumor is not inho-
mogeneous on the X-rays. The spicula at the edge
Feature of the mass may be accompanied by calcification,
A sharp-angled, whisker-like, slender or thin-­ on basis of cancer infiltration and diffusion, and
short, flaming, or irregularly shaped shadow is of great significance for suggesting malignant
extending from the breast mass to the s­ urrounding diagnosis. The incidence of spicular sign is
glandular tissue with occasional calcification. affected by many factors, especially the type of
mammary gland development. Other factors
Explanation (such as radiographic conditions, technical equip-
Spicular sign is an imaging manifestation of ment) are also related to the detection rate of
breast cancer infiltrating into surrounding glan- lesions, and the use of CT, MRI, and molybde-
dular tissue. According to the relationship num target enhancement is easier to show spicu-
between spicula and mass, it can be divided into lar sign, and can eliminate the false spicula sign
three types: (1) long spicula: from the edge of the caused by the overlap of mammary trabecula and
mass, the length of the spicula exceeds one half mass.
the maximum diameter of the mass; (2) short The breast mass with spicular sign is the
spicula: from the edge of the mass, the length of highest diagnostic X-ray sign of breast cancer,
the spicula is smaller than one half the maximum with an incidence of more than 60%. For the his-
diameter of the mass; (3) star shadow: spicula tological essence of the edge of the spicular sign
from the center of the mass to surrounding diver- in the breast mass, most scholars formerly
gence, radial or no clear mass, only radial spicula believed that it was mainly collagen fiber hyper-
feature (Fig. 4.52). plasia, especially hard cancer. The reaction of
peripheral fibrous hyperplasia was obvious, and
Discussion most of them had marked spicular sign, which
Spicular sign is an image finding of breast cancer was longer, and sometimes could even cover up
infiltrating into surrounding glands. It is a sharp-­ the mass. Some investigators have found activity
angled, whisker-like, slender or thin-short, flam- of collagen fibers around the breast mass was
ing or irregularly shaped shadow extending from mainly moderate to low, indicating fibroprolif-
the breast mass to the surrounding glandular tis- erative response is unremarkable, but the cancer
sue with occasional calcification. Recently, it has infiltration is correspondingly significant.
been reported that mammography analysis based Therefore, the histological essence of spicular
4 Chest 167

a b

Fig. 4.52  A 64-year-old breast cancer patient. (a, b) A nodular high-density shadow is seen in the central area of the
right breast; the margin was rough and lobulated and spicular sign could be seen

sign is mainly cancer infiltration. Pathology 4.53 Tiny Calcium Sign

showed the root of the spicula is a cancerous bed
belt, the middle part is the inflammatory cell
exudation zone, and the tip is the fibrous tissue
hyperplasia zone. In addition, spicular sign may
also be associated with lymphatic invasion of the
tumor, catheter infiltration, abnormal vascular-
ization, and tumor invasion of the suspensory
ligament. In short, benign tumors generally do
not have spicula, but spicula may also occur in
tuberculosis and postsurgical scars. We should
identify clinically relevant history to improve the
accuracy of diagnosis.
Feature
Microcalcification is a mammography sign of
breast cancer. It shows that many small calcifica-
tion foci in the breast form calcification clusters,
which are in small in size, of various shapes, and
may be accompanied by masses.
Explanation
Calcification can occur in breast cancer cells,
including living cancer cells and necrotic cancer
cells. When the calcification point is more than
168
Fig. 4.53  A right breast cancer patient has dense glands
in the upper outer quadrant of the breast with multiple
microcalcifications
100 μm, fine and dense calcification shadow can
be displayed on mammography (Fig. 4.53).
Discussion
Microcalcifications are defined as localized cal-
cium deposits in the breast tissue that represent
an early diagnostic sign of breast cancer. The
current strategy for evaluating and managing
microcalcifications makes the important
assumption that the microcalcifications are
present within or are closely related to the most
important underlying pathological change in the
breast. Microcalcifications occur as a sequela of
inflammation, progression of fibroadenoma,
intraductal papilloma, and cystic and fibrotic
changes, but may also be actively secreted, as is
the case with malignant lesions.
Microcalcifications are one of the main catego-
ries of abnormalities detectable by mammo-
T. Jiang et al.
grams. Mammography has a sensitivity of
63–95%, and sensitivity increases with the pres-
ence of palpable lumps and is reduced in dense
breasts [164]. The survival rates of breast cancer
have risen significantly in recent decades from a
combination of improved treatment options and
early detection. Although some controversy
exists, most studies have shown the adoption of
mammography programming to confer a signifi-
cant decrease in breast cancer mortality. Breast
cancer can be detected by numberous mammo-
graphic features including density, architectural
distortions, and the presence of
microcalcifications. The clinical relevance of
­
microcalcifications was first identified in 1951
by Leborgne, who recognized they could consti-
tute the sole mammographic indicator of carci-
noma [165]. Microcalcifications also display a
significant association with human epidermal
growth factor receptor 2 (HER2) overexpres-
sion, although their relationship with hormone
receptor (estrogen or progesterone) status is
unclear as various studies have found both posi-
tive and negative associations or no association
at all. Despite their significant contribution to
the detection of breast tumors, the detailed
mechanism by which microcalcifications form
remains unknown [166].
Mammographic detection of microcalcifica-
tions has come to be regarded as a highly useful
marker of breast cancer, with between 30% and
50% of nonpalpable tumors found in screening
identified solely by the presence of microcalcifi-
cations. They are also present in the majority of
ductal carcinoma in situ (DCIS) cases.
Microcalcifications detected by mammography
can be categorized based on their size, shape,
chemical composition, and spatial distribution
within the breast, allowing for assessment as a
benign or suspicious finding. In addition to their
utility as a detection marker, the presence of
microcalcifications within a breast tumor may
also be of prognostic significance, with many
studies highlighting links between calcifications
and poor prognosis, high tumor grade, and
increased risk of recurrence.
4 Chest
4.54 Tattoo Sign
Feature
On mammography, the calcification is character-
ized by relative immobilization at different radio-
graphs or at the same location.
Explanation
Intramammary calcifications lie within a volume
of compressible fat and fibroglandular tissue. The
precise relationship of the individual calcifica-
tions within the cluster can change as the tissue is
compressed. Intramammary calcifications, there-
fore, do not maintain a fixed relationship to one
another on mammograms obtained with the same
view over time. In contrast, dermal calcifications
are fixed within a thin plane of dermal tissue and
do not change with relationship to one other dur-
ing compression. Therefore, in the same way that
pigments are fixed within the dermal layer in a
tattoo, dermal calcifications maintain a fixed ori-
entation to each other on mammograms obtained
at different times (Fig. 4.54).
Discussion
In 1994, the tattoo sign regarding the orientation
of dermal calcifications was recognized [167].
We call this the tattoo sign because it looks like
the fixed pattern of a tattoo on the skin.
Fig. 4.54  The tattoo sign. Calcifications do not change
orientation between the craniocaudal and the mediolateral
oblique projections or from year to year. The tattoo sign is
characteristic of benign skin calcifications [169]
169
Intramammary calcifications are contained
within a volume of breast tissue, and their
arrangement appears different in different projec-
tions. In contradistinction, dermal calcifications
are oriented in a thin plane so that their arrange-
ment should be similar, regardless of the projec-
tion used [167].
A cluster of microcalcifications observed on
mammograms may be an early sign of breast can-
cer. Various characteristics, such as number, size,
shape, and location, are used to judge whether the
calcifications appear benign or malignant and
whether further evaluation is warranted. Dermal
calcifications are benign and require no further
evaluation [168]. The pathognomonic mammo-
graphic feature of skin calcifications is conspicu-
ous, round, solid, or lucent-centered calcifications,
which frequently are grouped. They are com-
monly seen along the inframammary fold, cleav-
age area, overlying the axilla, and around the
areola. If superficial in location, a tangential view
is needed to confirm that they are dermal versus
parenchymal [169]. Tattoo sign is important
because it may be the only clue that suggests the
dermal location of microcalcifications when
other characteristics of dermal calcification are
not present. In addition to the tattoo sign, another
similar unnamed mammographic sign also indi-
cates the presence of dermal calcifications, and it
should be applied in all cases of peripheral calci-
fications. When mammograms are compared
with prior mammograms obtained with the same
projection and the tattoo sign or the afore-­
described unnamed sign is present, the suspected
location of the microcalcifications should be the
dermal layer [168]. Tattoo signs may even appear
bilaterally and are most likely caused by a degen-
erative metaplastic process, including trauma or
even sunburn. Dermal calcifications could sug-
gest other skin-related diseases, including skin
cancer, but dermal calcifications are unrelated to
breast cancer.
Breast calcifications are common findings on
mammography, and their frequency increases
with the age of the patient. Although the majority
of microcalcifications that occur are benign,
some specific grouped patterns can be caused by
malignant disease or high-risk lesions. It is
170
important to differentiate the microcalcifications
of benign origin from those that are suspicious,
because 55% of nonpalpable cancers are diag-
nosed by the presence of microcalcifications, and
because microcalcifications are the main form of
manifestation of ductal carcinoma in situ (DCIS).
Some of these calcifications correspond not only
to pure DCIS but also to the intraductal portion of
infiltrating carcinomas. The density difference
between the benign and malignant calcifications
is mainly given by the various chemical com-
pounds prevailing in each one. Benign calcifica-
tions are composed mainly of calcium oxalate,
but malignant calcifications are composed pre-
dominantly of calcium phosphate. The two types
coexist, and their components cannot be deter-
mined via mammography, so chemical studies
are required for these purposes [170].
Tomosynthesis still exhibits a debatable
usefulness in the detection of microcalcifica-
­ 2014;73(873):930–7.
tions. Some studies show detection rates similar
to or somewhat lower for tomosynthesis com-
pared with digital mammography. A recent
meta-analysis evaluated the usefulness of this
method for classifying microcalcifications
according to the BI-RADS categories, demon-
strating that tomosynthesis classified the find-
ings similarly to digital mammography in most
cases; however, it subclassified some malignant
and premalignant lesions. Therefore, tomosyn-
thesis should still be used with caution in evalu-
ating microcalcifications, and it is possible that
the incorporation of new or complementary
descriptors to the BI-RADS lexicon will be
required in the future [170].
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 Solid Organs of Upper Abdomen
5
Xin Li, Chengkai Zhou, and Jie Zhou

Contents
5.1 Light Bulb Sign  179
5.2 Bright Dot Sign  180
5.3 Mother-in-Law Sign  181
5.4 Rapid Wash-in Followed by Washout  182
5.5 Mosaic Pattern  184
5.6 Bull’s Eye Sign  184
5.7 Pupil-like Sign  185
5.8 Lollipop Sign  186
5.9 Target Sign  187
5.10 Cluster Sign  188
5.11 Peripheral Washout Sign  189
5.12 Halo Sign  191
5.13 Transparent Ring Sign  192
5.14 Wedge-Shaped Sign  193
5.15 Straight Line Sign  194
5.16 Liver Capsule Depressed Sign  195

X. Li (*) · C. Zhou
Department of Radiology Union Hospital,
Tongji Medical College, Huazhong University of
Science and Technology, Wuhan, China
J. Zhou
Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China

© Springer Nature Switzerland AG 2021 177

B. Gao, A. M. McKinney (eds.), Classic Imaging Signs,
https://doi.org/10.1007/978-3-030-56348-6_5
178 X. Li et al.

5.17 Straight Border Sign  196

5.18 Target Sign and Crescent Sign  197
5.19 Pearl Necklace Sign  198
5.20 Garland Sign  200
5.21 Tortoise Shell Sign  201
5.22 Periportal Tracking Sign  202
5.23 Periportal Halo Sign  203
5.24 Focal Hepatic Hot Spot Sign  205
5.25 Cyst-in-Cyst Sign  206
5.26 Floating Membrane Sign  207
5.27 Beaded Sign  208
5.28 Soft Rattan Sign  209
5.29 Double Duct Sign  211
5.30 Teardrop Superior Mesenteric Vein Sign  212
5.31 Duct-Penetrating Sign  213
5.32 Central Dots Sign  214
5.33 Central Arrowhead Sign  215
5.34 Golf Ball-on-Tee Sign  216
5.35 Calyceal Crescent Sign  218
5.36 Cortical Rim Sign  220
5.37 Renal Halo Sign  221
5.38 Perirenal Halo Sign  223
5.39 Perirenal Cobwebs Sign  224
5.40 Pseudo-capsule Sign  225
5.41 Spoke Wheel Sign  226
5.42 Soft-Tissue Rim Sign  227
5.43 Comet-tail Sign  228
5.44 Faceless Kidney  229
5.45 Goblet Sign  230
5.46 Cobra Head Sign  231
5.47 Drooping Lily Sign  233
References  234
5  Solid Organs of Upper Abdomen
Fig. 5.1  A 38-year-old man. (a) A nodule was detected
with low signal intensity on T1WI, with homogeneous sig-
nal intensity on T2WI well defined; the high signal inten-
5.1 Light Bulb Sign
Feature
Hepatic hemangioma presents homogeneous
hyperintensity on T2WI, and its signal intensity
increases with the extension of echo time in a
multi-echo sequence, called the light bulb sign.
Explanation
Hepatic hemangioma is mainly composed of
sinusoids or blood pools. The blood flow is slow.
Because of large amount of water in the blood
and long T2 signal, the signal intensity becomes
higher and higher with the extension of echo
time, forming the light bulb sign (Fig. 5.1).
Discussion
Hepatic hemangioma is one of the most common
benign tumors in the liver. The incidence of
hepatic hemangioma ranges from 0.14% to 7.3%.
Pathologically, hepatic hemangioma can be
divided into cavernous hemangioma, sclerosing
hemangioma, hemangioendothelioma, and capil-
lary hemangioma. Hepatic cavernous hemangi-
oma (HCH) is the most common type of hepatic
hemangioma in the liver, accounting for 95% to
98% of hemangioma. HCH can be classified into
thick-walled hemangioma and thin-walled hem-
angioma; the wall of the former has more colla-
gen fibers and fibroblast, and the vascular lacuna
179
sity resembled cerebrospinal fluid (CSF), and thus is
called the “bulb sign” (b)
is small, even slit like. However, the latter has
only a small number of collagen fibers and fibro-
blasts in the wall and the vascular lacuna is larger.
Hepatic hemangioma is mainly composed of
blood pools or sinusoidal structures with low-­
speed blood flow. Hemangiomas on T2WI are
usually homogeneously hyperintense. Because
the blood contains about 81% water, the T2 signal
intensity is longer, and the lesion is markedly
hyperintense on T2WI. With the extension of echo
time, the signal intensity of the lesion becomes
higher and higher, forming a light bulb sign. The
sensitivity, specificity, and accuracy of magnetic
resonance imaging (MRI) for the diagnosis of
HCH are 100%, 93%, and 95%, respectively.
Most of the lesions were round or oval, with clear
and sharp margins. On T1WI, HCH shows homo-
geneous hypointense signals, and some may show
heterogeneous signals from hemorrhage, necro-
sis, calcification, fibrosis, and thrombosis. In
multi-echo sequences, the signal intensity of the
lesion increases with the extension of echo time,
which is the characteristic MRI feature for hepatic
hemangiomas [1]. The light bulb sign is also com-
monly seen in liver metastases with smooth,
round, or oval image manifestations. On T2WI,
the signal content of the neoplasm resembles that
of the gallbladder, cerebrospinal fluid, cyst, and
hemangioma. However, high signal intensity is
detected in hepatic metastatic lesions because of
180
the complete necrosis of the tumor. Although both
hepatic hemangioma and hepatic metastasis may
show “light bulb” sign, the former is benign,
whereas the latter is malignant [2]. Spectral com-
puted tomography (CT) with fast switching tube
voltage may increase the sensitivity of differenti-
ating small hemangiomas from small hepatic car-
cinomas [3].
5.2 Bright Dot Sign
Feature
In dynamic contrast-enhanced CT or MRI,
hepatic hemangiomas in the hepatic arterial
phase (HAP) or portal venous phase (PVP) are
mainly low density or hypointensity; enhanced
nodules are seen in the periphery of the lesion.
Explanation
Some atypical hepatic hemangiomas show low
density in CT images or hypointensity in MRI
without obvious enhancement in HAP and
PVP. This pathology may be related to thicker ves-
sel wall, smaller lumen, difficult access of contrast
medium, thrombosis, or hyalinization. The lesions
are gradually filled in contrast medium in the
delayed phase. The bright spot is the small nodule
that is enhanced in the lesion, representing a small
blood sinus filled with contrast medium (Fig. 5.2).
Discussion
Hemangiomas are usually small and solitary
hepatic lesions formed of multiple blood-filled
vascular malformations. They are the most com-
mon benign hepatic tumor, with a prevalence of
0.4% to 20% and female preponderance of 3 to
6:1, typically diagnosed in patients between 30
and 50  years of age. Noncontrast CT shows
hypoattenuation in comparison to the adjacent
liver parenchyma. The most striking imaging fea-
ture of a hemangioma is that it always follows the
blood pool. The classic appearance of hemangi-
oma on contrast-enhanced CT is of peripheral
nodular enhancement in the arterial phase with
centripetal progression on the portal venous
phase. Certain variants of this classic CT appear-
ance include the flash-filling hemangioma, a less
X. Li et al.
Fig. 5.2  Postcontrast CT shows a mainly unenhanced
nodule in the right lobe of the liver, with markedly dot-­
like enhancement peripherally in the arterial phase
common manifestation where the entire heman-
gioma opacifies in the arterial phase. In addition,
the giant hemangioma may not demonstrate com-
plete centripetal opacification because of the
internal thrombosis and scarring as a complica-
tion of its size. On serial imaging, an interval
increase in its size should raise suspicion of a
metastatic lesion. MRI exploits the long T2 relax-
ation time of the blood-filled vascular malforma-
tion, yielding a hyperintense signal intensity on
T2WI that is not as bright as that of a simple cyst
or cerebrospinal fluid (CSF). T2WI alone has a
sensitivity of 100% in differentiating hemangi-
oma from a hepatic lesion of malignancy [4].
Small hemangiomas are detected more frequently
with multi-slice CT.  However, they are easily
overlooked on conventional CT because they tend
to be iso-attenuating on late-phase enhanced
images. Because of earlier scanning after admin-
istration of contrast medium, slowly enhancing
hemangiomas have more chance to show persis-
tent hypoattenuation, the incidence being as much
as 8% to 16%. In clinical practice, the incidence
of this enhanced pattern is even greater than previ-
ously reported for hemangioma, especially for
small hemangiomas that may not show the classic
rapid fill-in pattern. Small hypoattenuating hem-
angiomas are particularly problematic in patients
with underlying malignancy. If present, the
“bright-dot” sign, tiny enhancing dots in the hem-
angioma that do not progress to the classic globu-
lar enhancement because of the small size of the
5  Solid Organs of Upper Abdomen 181

a b

Fig. 5.3  A 42-year-old woman with hepatic hemangioma. Nodular enhancement at edge of the lesion in arterial phase
(a) and the enhancement area enlarged in the portal vein phase (b) manifest as mother-in-law sign in the delay phase (c)

lesion and the propensity for very slow fill-in, is Explanation

helpful in diagnosing this type of hemangioma.
One pathological correlative study suggested that
hemangiomas with a slow fill-in pattern have rela-
tively large vascular spaces and that those with
rapid enhancement have small vascular spaces
and a large interstitium. Such a tendency has no
relationship to the size of the tumor. Therefore,
hemangioma should be included in the differen-
tial diagnoses of small hypoattenuating lesions as
well as hypervascular lesions [5].
5.3 Mother-in-Law Sign
Feature
In the delayed phase of enhancement CT, con-
trast agent fills the lesion and stagnates for a long
time, resulting in a loss of attenuation difference
between lesion and surrounding liver tissue.
Mother-in-law sign is a characteristic CT finding
of hepatic cavernous hemangioma (HCH). HCH
consists of a blood-filled vascular sinus cavity
with fibrous tissue spacing between the sinus
cavities. In enhancement CT, the early manifesta-
tions are nodular enhancement around the lesion,
and gradually progress toward the center with
time delay. Finally, the contrast agent fills the
entire lesion and remains for a long time. In
Eastern and Western cultures, there is a custom of
the mother-in-law who likes her son-in-law.
When the daughter brings the son-in-law to her
family, the mother-in-law always persuades him
to stay for a few more days. Therefore, some
scholars have called this phenomenon of contrast
agent filled with cavernous hemangioma that
stays for a long time as the mother-in-law sign
(Fig. 5.3).
182
Discussion
The mother-in-law sign is a characteristic CT find-
ing of hepatic cavernous hemangioma. It is mani-
fested as the contrast agent fills the lesion and
stagnates for a long time, resulting in a loss of
attenuation difference between the lesion and the
surrounding liver tissue in the delayed phase of
liver CT enhancement scan. Hepatic hemangioma
is the most common benign tumor in the liver,
accounting for 84% of these, and is more common
in older women. Pathological classification
includes cavernous hemangioma, capillary heman-
gioma, and hemangioendothelioma, which is more
common in the former. The lesion can be single or
multiple, and the site of the lesion is commonly in
the right lobe. In most cases, there was no obvious
clinical manifestation. Larger lesions could cause
upper abdominal discomfort, and the mass was pal-
pated. Pathologically, the tumor is covered with a
layer of connective tissue membrane, which is
composed of a blood-filled vascular cyst, with
fibrous tissue partitions between the capsules, and
the cyst wall is lined with flat endothelial cells.
Tumors can undergo fibrosis, calcification, and
thrombosis. Slowly growing hemangiomas in liver
tissue can produce a mass effect, resembling a
tumor. However, the microscopic histopathology is
composed of abnormal sinusoids with different
sizes of expansion, and there is no abnormal prolif-
eration of sinusoidal endothelial cells. This finding
indicates that the hemangioma is the result of poor
blood flow and expansion of the sinus cavity caused
by abnormal development of the sinusoidal
embryo. It is a congenital malformation of the por-
tal vein rather than a tumor.
Noncontrast CT shows a low-attenuation
lesion in the liver, with clear outline and uniform
attenuation. Lower-attenuation areas in the cen-
tral area are detected in a few lesions, which rep-
resent pathological changes of thrombotic or
fibrous scar tissue. Further, some lesions may
show calcification. Enhanced scanning is more
characteristic or helpful to evaluate the hemangi-
oma; one specific sign is that the early margin of
typical lesions is significantly nodular or patchy.
The attenuation resembles that of arteries. Over
time, the enhanced area gradually expands and
advances toward the center of the lesion. The
X. Li et al.
attenuation of this specific sign is of equal attenu-
ation or slightly higher attenuation in the delay
phase of enhanced examination. Hypoattenuation
in the center of the lesion can never be enhanced
[6]. Not all cavernous hemangiomas have the
aforementioned classic CT features: some lesions
may not be enhanced, or are not enhanced obvi-
ously, because the sinus wall of the hemangioma
is thick and the cavity is too small. Therefore, the
contrast agent does not enter easily or less may
enter. Dynamic contrast-enhanced CT is an
important method for diagnosing HCH. The diag-
nostic accuracy of hepatic hemangioma is as great
as 90%. MRI T1WI shows low signal intensity,
and T2WI signal is increased abnormally,
expressed as “light bulb sign.” Cavernous heman-
gioma should be differentiated from the following
diseases. (1) Hepatocellular carcinoma (HCC):
CT enhancement of HCC lacks the mother-in-law
sign; the specific sign of HCC is characterized as
contrast medium wash-in in arterial phase, and
washout in portal venous phase or delay phase
[7]. (2) Liver metastasis: early enhancement of
marginal enhancement may occur in some intra-
hepatic metastases, resembling hemangioma, but
can be identified by low-attenuation performance
in delayed scan. (3) Liver abscess: low-attenua-
tion halo can be seen around the abscess, and the
typical lesion shows ring-shaped enhancement.
5.4  apid Wash-in Followed by
R
Washout
Feature
In the three-phase enhanced CT scan of primary
hepatocellular carcinoma (HCC), the carcinoma
is in hyperattenuation in the arterial phase and
hypoattenuation in the portal vein phase or
delayed phase. The enhancement pattern of HCC
is that the contrast agent shows the characteristics
of rapid wash-in followed by washout.
Explanation
In three-phase enhanced CT scan of primary
HCC, within 20–30 s after injection the contrast
agent is in the arterial phase. The blood supply of
the parenchyma is mainly supplied by the portal
5  Solid Organs of Upper Abdomen
a b
Fig. 5.4  Hepatic arterial phase (a) shows patchy enhance-
ment fully occupying the right lobe of the liver; visible
traversing vessels are detected in the tumor. In the portal
vein (75%) whereas HCC is mainly supplied by
the hepatic artery. In the arterial phase, CT value
quickly reaches the peak. In 50–60 s after injec-
tion of contrast agent in the portal vein phase, the
attenuation of the mass decreased rapidly.
Delaying to the equilibrium phase of a 110–120 s
scan, as the attenuation of hepatic parenchyma
continues to rise and the contrast attenuation of
HCC continues to decrease, attenuation in the
tumor returns to the original state of low attenua-
tion. If the CT value is measured on a dynamic
CT and the time-attenuation curve is plotted, the
curve of HCC is rapidly increasing in arterial
phase and decreasing in portal venous phase: this
reflects the characteristics of rapid wash-in fol-
lowed by washout in tumors (Fig. 5.4).
Discussion
“Rapid wash-in followed by washout” is a char-
acteristic sign of the CT three-phase enhanced
scan of primary HCC. Liver spiral CT dual-phase
183
venous phase (b) and delayed phase (c), the enhancement
pattern shows rapid wash-in followed by washout
or triple-phase enhanced scans are important in
the diagnosis of hepatic space-occupying lesions.
Not only can this improve the detection rate of
tumors, but it also shows the blood supply char-
acteristics of tumors to some extent, effectively
carrying out differential diagnosis and guiding
the treatment options. Postcontrast CT scans can
more clearly show the features of tumors. (1)
Abnormal blood vessels in the HCC lesion are
found in the hepatic arterial phase with higher
attenuation. During the subsequent portal and
equilibrium phase scans, these abnormal blood
vessels and tumor areas are rapidly changing,
with the characteristics of contrast agent rapid
wash-in followed by washout, which are different
from hepatic cavernous hemangioma, hepatic
metastases, and intrahepatic cholangiocarci-
noma. (2) The margin of most tumors not only
are enhanced in the hepatic artery phase, but also
persist in the portal vein phase, indicating that
there is a double blood supply from the hepatic
184
artery and portal vein at the margin of such HCC,
which indicates the marginal part grows
vigorously. Single hepatic artery embolization
­
does not completely block tumor blood supply,
which is a very important reference for selecting
a reasonable intervention or other treatment
options [7]. (3) The majority of intrahepatic met-
astatic foci showed significant enhancement of
hepatic artery phase and rapid increasing and
decreasing. The use of MR liver tissue-specific
contrast agents can selectively target hepatocytes
in the hepatobiliary phase, while maintaining
good dynamic enhancement during the arterial
phase, further improving the diagnostic accuracy
of HCC [8].
5.5 Mosaic Pattern
Feature
Heterogeneous signal intensity or linear low sig-
nal intensity structure appeared in the main hepa-
tocellular carcinoma (HCC). The enhanced
inhomogeneity is also known as the mosaic sign.
Explanation
The mosaic appearance is caused by an intratu-
moral septum or histological diversity. The
mosaic pattern is defined as several areas or com-
partments with various intensities, shapes,
enhancements, and sizes. Most overt HCCs pres-
ent with a mosaic pattern. This feature is specific
for HCC and often considered to be a major
ancillary sign (Fig. 5.5).
Discussion
HCC is the most common tumor in the liver. It is
composed of tumor cells with hepatocellular dif-
ferentiation, arranged in a trabecular, acinar, or
compact pattern. HCC often grows in a mosaic
pattern with different cell types arranged in dif-
ferent architectural patterns in a large tumor.
HCC can be occasionally combined with other
cell types with nonhepatocellular differentiation.
Combined hepatocellular-cholangiocarcinoma is
the most common combination [9]. This feature
is specific for HCC and is often considered to be
a major ancillary sign. At the same time, the
X. Li et al.
Fig. 5.5  A 64-year-old man presented with a mass in the
right lobe of the liver with uneven enhancement and
enhancement of the intratumoral septum
mosaic pattern is mainly found in large HCCs,
which are easier to diagnose [10]. HCC has a
wide spectrum of radiologic characteristics
depending on its size and degree of histological
differentiation. HCC can be classified as early or
progressed HCC.  Progressed HCCs are malig-
nant lesions with the ability to invade vascular
planes and metastasize. The radiologic pattern is
variable, but frequently a mosaic pattern is exhib-
ited because nodular areas are interspersed by
areas of hemorrhage, arteriovenous shunting,
fibrosis, and necrosis. The main findings are (1)
high signal intensity on T2-weighted imaging; (2)
hyperenhancement on arterial phase, and wash-
out appearance on delayed phase; and (3) nod-
ules surrounded by a capsule/pseudo-capsule
(more evident in the delayed phase) [11].
5.6 Bull’s Eye Sign
Feature
Hepatic metastases show low density in the center
of lesion, annular enhancement zone around
lesion, low-density zone with no obvious enhance-
ment at the outermost layer on enhanced CT.
Explanation
The pathological basis is that necrosis or cystic
degeneration in the center of the tumor is low
density without enhancement after injection of
5  Solid Organs of Upper Abdomen
Fig. 5.6  A 66-year-old woman presented with an annular
enhancement lesion in the upper right lobe of the liver.
Low-density necrosis was detected in the center of the
lesion, and a low-density zone with no obvious enhance-
ment at the outermost layer
contrast medium, the middle high density is
tumor tissue, and the outer low density is the
compression change of normal liver tissue and
blood vessels (Fig. 5.6).
Discussion
The term bull’s-eye is used in archery and target
shooting to denote the center of the target. The
origin of the word is unclear. However, one theory
is that English archers would often practice using
the skull of a bull, with the most difficult shot
being one that entered an eye socket. Multiple
radiologic signs characterized by concentric cir-
cles are named after this [12]. Most hepatic metas-
tases are hypovascular lesions. Because of the
strong metabolism, insufficient blood supply, and
lack of feeding conditions, necrotic cystic degen-
eration can easily occur, and central necrosis can
also occur in small lesions. CT manifestations of
liver metastases are complex and varied, with
multiple diffuse distributions being common.
Most metastases are revealed as low- or iso-atten-
uating masses on CT. Depending on lesion size,
the margins tend to be irregular, and necrosis may
be present in the tumor. Central low attenuation
may be the result of necrosis or cystic change.
Calcification may be present with metastases
from mucinous gastrointestinal tract tumors, and
primary ovarian, breast, lung, renal, and thyroid
cancer [13]. Enhanced scan showed continuous
annular enhancement at the edge of the lesion in
185
the arteriovenous phase, with more obvious annu-
lar enhancement at the edge of the lesion in portal
venous phase than that in arterial phase. The bull’s
eye sign could also be seen in the portal venous
phase. This sign is a more common sign among
the special signs of hepatic metastases, showing
no enhancement in the central low-density area,
high-density shadows with circumferential
enhancement, and low-density shadows in the
outer layer. The bull’s eye sign is a classic imag-
ing manifestation of hepatic metastases. However,
we should know that this bull’s eye sign can also
occur in other diseases, such as hepatic tuberculo-
sis and metastasis.
5.7 Pupil-like Sign
Feature
The CT signs of hepatic metastasis usually have
multiple circular or quasi-circular shadows of
low density. The lower-density region with clear
boundaries is found in the center of the lesion.
The diameter of the lower lesion is significantly
smaller than that of the surrounding low-density
area formed by tumor tissue, which resembles the
shape of a pupil. The other name for this CT sign
is thick rim sign.
Explanation
Most hepatic metastases are poorly supplied
tumors, characterized by low density, with mild
enhancement. For example, the necrosis in the
center of a tumor shows a lower-density area
without enhancement, forming a pupil-like sign
(Fig. 5.7).
Discussion
When the density in the center of the tumor is
lower during enhanced scanning, the area with a
clear boundary is small and circular, and its diam-
eter is significantly smaller than the surrounding
low-density area formed by tumor tissue. The liver
is the largest substantial organ in the human body,
which has the dual blood supply of hepatic artery
and portal vein. Therefore, many malignant tumors
of organs are prone to liver metastasis, especially
malignant tumors of the gastrointestinal tract.
186
Fig. 5.7 Postcontrast CT reveals lesions with ring
enhancement; the center is without enhancement, which is
the pupil-like sign
Because a liver metastatic tumor is mainly sup-
plied by the portal vein in the early stage and by
the hepatic artery in the middle and late stages, the
nature and type of tumor can be estimated accord-
ing to the degree of enhancement of the tumor and
the change of degree with time [14].
Multiple low-density nodules are common in
liver metastatic tumors, and arterial blood supply
is more common in enhanced scanning, present-
ing as peripheral ring enhancement or uniform
and nonuniform enhancement of the full tumor.
Among these, peripheral ring or low-density
enhancement is typical, whereas the low-density
nonenhancement area is in the tumor, namely, the
bull’s eye sign. This difference is an important
indication that metastatic liver tumors are differ-
ent from primary liver cancer, and pathological
studies have confirmed that the low-density unre-
inforced area is composed of compressed liver
cells or fibrous tissue. The outer layer is a high-­
density enhancement zone, with the main patho-
logical manifestations being compression of liver
parenchyma, hyperemia of liver sinus, hyperpla-
sia of connective tissue, infiltration of inflamma-
tory cells, and hyperplasia of blood vessels. The
clinical diagnosis of metastatic liver cancer is not
difficult, but partial metastatic liver cancer is not
easy to identify with liver abscess, especially cys-
tic metastatic liver cancer. The pathological basis
of the formation of cystic metastatic hepatocel-
lular carcinoma is the severe liquefactive necrosis
of the tumor lesions. The typical CT findings of
X. Li et al.
hepatic abscess are that the density of the lesion
is lower than that of surrounding hepatic paren-
chyma in plain scanning; partial lesions have a
gas body, and the circle-target sign, separation,
and enhancement can be seen in enhanced scan-
ning. MRI and CT are comparable in their ability
to detect metastases, which generally appear
hypointense compared with normal liver paren-
chyma on T1-weighted MR images and hyperin-
tense on T2WI. CT remains the preferred
screening test for hepatic metastases, and MRI is
a useful tool to generally define lesions more
clearly than CT, as well as to detect hepatic
lesions in the liver parenchyma [15].
5.8 Lollipop Sign
Feature
The lollipop sign, which is seen on postcontrast
CT or MRI, manifests as multiple large unen-
hanced or nodular edge-enhanced masses. The
hepatic vein or portal vein tapers toward these
lesions and terminates at the edge of the lesions,
forming a lollipop-like appearance.
Explanation
The lollipop sign is considered a typical manifes-
tation of hepatic epithelioid hemangioendotheli-
oma (HEH). This sign can better identify HEH in
cross-sectional images. The lollipop sign consists
mainly of two structures: (1) a clear mass with a
low-attenuation border on the enhanced image,
representing the candy in the lollipop; and (2) a
histologically occluded vein, including the hepatic
vein and the portal vein, representing the stick in
the lollipop. Masses with unclear boundaries, gas-
filled cavities, or outward-growth masses do not
meet the characteristics of the lollipop sign. If
there is a scar-like enhancement in the center of
the lesion or a significant or irregular enhance-
ment of the mass, it cannot be judged as the lolli-
pop sign. The enhanced vein should terminate at
the edge of the lesion or only extend into the
enhancement ring of the lesion. If the blood vessel
passes through the lesion or is moved by the mass,
and the collateral vessels are formed, the lollipop
sign cannot be considered (Fig. 5.8.)
5  Solid Organs of Upper Abdomen
Fig. 5.8 Postcontrast CT shows multiple hypodense
large parenchymal nodules in both liver lobes and the
nodule in Couinaud’s segment VII, showing a lollipop
sign (arrow)
Discussion
The lollipop sign is a sign of postcontrast CT or
MRI, manifested as multiple large unenhanced or
nodular edge-enhanced masses. The hepatic vein
or portal vein tapers toward these lesions and ter-
minates at the edge of these lesions, forming a
lollipop-like appearance [16]. The lollipop sign is
considered a typical manifestation of HEH. HEH
is a rare vascular endothelium tumor with mild to
moderate malignancy, usually occurring in
adults, in significantly more women than men.
The cause is not known, but may be related to
oral contraceptives, exposure to polyethylene,
trauma, or viral hepatitis [17]. HEH is mostly
asymptomatic. Occasional symptoms are mainly
characterized by frequent episodes of upper right
abdominal pain and weight loss, and some
patients show liver failure, Budd–Chiari syn-
drome, or portal hypertension. The histological
feature of HEH is the infiltration of the hepatic
sinus and intrahepatic venous system, which sur-
rounds the hepatic vein, portal vein, or venule
and causes stenosis or occlusion. There are two
manifestations of the affected vein. One is that
the affected hepatic vein or portal vein is tapered
around the tumor, and the edge is smooth.
Second, the vein is completely occluded or cut
off when it reaches the edge of the tumor.
CT findings of HEH mainly include multifo-
cal low-attenuation nodules of varying sizes.
These nodules can grow and fuse into large
masses, mostly distributed at the edge of the liver.
Enhanced scans show that these nodules are cir-
187
cumferentially enhanced, usually with calcifica-
tion, central low density, and envelope
invagination. Some patients were observed to
have metastases, usually in the lungs, lymph
nodes, spleen, bones, and other substantial
organs. On MRI T1WI, the nodules show a low
signal, and postcontrast T1WI shows marginal
enhancement. The normal liver parenchyma
enhancement is more obvious than enhancement
of the tumor. The central part of the tumor shows
a low signal resembling the findings on CT. The
tumor shows an inhomogeneous high signal on
T2WI. The signal component in the tumor is more
complicated than CT. The decrease of the central
part signal may be related to intratumoral hemor-
rhage, coagulative necrosis, and calcification.
Differential diagnosis of HEH includes hepatic
metastases, intrahepatic cholangiocarcinoma,
and other intrahepatic vascular tumors [18]. The
presentation of lollipop sign raises the specificity
of diagnosing HEH, combined with other imag-
ing findings, which can help differentiate the dis-
ease from other liver tumors.
5.9 Target Sign
Feature
The typical finding of postcontrast CT for
hepatic abscess is named target ring. It is charac-
terized by a cystic-like low-attenuation mass in
the liver; the margins are mostly vague, and a
ring belt of different attenuations often appears
around the abscess. In contrast-enhanced CT, the
wall of the abscess shows different degree of
ring enhancement, single ring or double ring or
tricyclic.
Explanation
Target sign is a typical sign of hepatic abscess.
The abscess liquefaction and necrosis in the for-
mation of abscess cause the wall to be single ring,
double ring, or tricyclic. The appearance of the
target sign in hepatic abscess represents the path-
ological process of a certain stage of the disease,
which is a characteristic finding of hepatic
abscess and has great value for diagnosis
(Fig. 5.9).
188
Fig. 5.9  Patient with hepatic abscess. On postcontrast
CT, the lesion shows target sign
Discussion
Hepatic abscess is a common inflammatory dis-
ease in the liver. The clinical manifestations are
acute and rapid, often accompanied by symp-
toms of inflammatory poisoning, such as high
fever, chills, liver pain, or multiple organ failure.
In a blood test, white blood cell count is signifi-
cantly increased. The formation of hepatic
abscess can be divided into suppurative inflam-
matory, early abscess formation, and abscess
formation stage. The pathological changes in the
stage of suppurative inflammatory stage are local
inflammation, congestion, and edema of hepatic
tissue. In the early abscess formation stage,
hepatic tissue begins to show necrosis and partial
liquefaction. During the abscess formation stage,
the cavity of the abscess has complete necrosis
and liquefaction, and the wall of the abscess is
formed by fibrous granulation tissue or an
inflammatory congestive zone. The liver tissue
around the abscess is often accompanied by con-
gestion and edema. Liver abscess occurs mostly
within the right lobe, can be single or multiple,
and varies in size. The boundaries of lesion are
unclear and the abscesses are thicker. The more
complete the necrosis of the diseased tissue, the
lower the attenuation and the more uniform [19].
Such as in chronic hepatic abscess, the edge is
clear, the CT value is close to the attenuation of
edema, and sometimes a circle of low-attenua-
tion edema ring is visible around, so it is easy to
diagnose. If there is a gas–liquid level in the
X. Li et al.
abscess, it means that the liquefaction is rela-
tively complete and accompanied by gas-borne
infection, which is generally considered to be a
specific sign for the diagnosis of hepatic abscess.
After contrast-enhanced scan, the lesion revealed
the relationship between the internal structure of
the lesion, the margin of the lesion, and the nor-
mal liver tissue is clearer. The portal venous
phase can show typical CT signs of hepatic
abscess, which is the CT finding after the
enhancement of typical three-layer pathological
changes. The central necrosis area is not
enhanced, and the middle layer is the low-den-
sity band between the liquefaction necrosis area
and the normal liver tissue. The boundary of
peripheral layer and normal tissue is vague [20].
Three rings correspond to different pathological
structures for the wall of the abscess: edema,
fibrous granulation tissue, and inflammatory
necrosis tissue, respectively. It is worth noting
target sign is not unique to hepatic abscess, but it
is still important for this diagnosis.
5.10 Cluster Sign
Feature
In precontrast or postcontrast CT, focal or multi-
ple smaller circular enhancements can be seen in
the liver, stacked close to each other into the
shape of clusters or honeycombs.
Explanation
This sign is more common at the early stage of
bacterial liver abscess formation. The lesions are
usually less than 2 cm in diameter, and connected
to each other; the smaller low-density lesions are
clustered together. Infecting bacteria are mostly
Escherichia coli. Fungi or Mycobacterium spp.
are rare in this sign (Fig. 5.10).
Discussion
The presence of the cluster sign usually suggests
that the lesions are pyogenic abscesses [21]. With
the necrosis liquefaction of the liver tissue in the
lesion area, the cluster sign is the multifocal
necrotic areas and the residual normal liver tissue
that coexisted first. “Cluster sign” is only a phase
of the pathogenesis of liver abscess, which can be
5  Solid Organs of Upper Abdomen
a b
Fig. 5.10  On postcontrast CT, arterial phase (a) and portal venous phase (b) solitary or multiple smaller circular
enhancements can be seen in the liver, stacked close to each other into the shape of clusters
dissipated and absorbed with effective treatment
and progression. In the period of inflammation,
lesions do not present necrosis and liquefaction,
and the performance is solid sign. In the early
abscess formation stage, multiple scattered small
abscess cavities begin to form, which then gather
and merge, and dynamic enhanced scan shows
“honey sign,” “cluster sign,” or “petal sign.” In
the abscess formation stage, complete necrosis
and liquefaction of the lesion are observed, the
abscess wall is mature, and enhanced scan shows
typical “ring target sign”; some lesions show
small bubbles or gas level. In the fibrous granulo-
matous stage, the lesions show small petal sign,
or single- or double ring sign.
Pyogenic micro-abscesses may appear as mul-
tiple widely scattered lesions being resembling
the distribution of fungal micro-abscesses in
immunosuppressed patients, or as a cluster of
micro-abscesses that appear to coalesce focally.
The diffuse miliary pattern of pyogenic micro-­
abscesses is caused by staphylococcal infection in
patients with generalized septicemia and usually
involves both liver and spleen. The cluster pattern
is associated with coliform bacteria and enteric
organisms. It is likely that clustering of pyogenic
micro-abscesses represents an early stage in the
evolution of a large pyogenic abscess cavity. At
postcontrast CT, large abscesses are generally
well defined and hypoattenuating; They may be
unilocular with smooth margins or complex with
internal septa and an irregular contour. Rim
189
enhancement is relatively uncommon, as it is in
the presence of gas. Pyogenic abscesses have vari-
able signal intensity on T1WI and T2WI, depend-
ing on their protein content. Perilesional edema,
characterized by subtly increased signal intensity,
can be seen on T2WI [22]. On CT, the small
abscesses showed a miliary pattern characterized
by widely disseminated, hypodense lesions scat-
tered throughout the liver. Probably the cluster
pattern represents an early stage of abscess evolu-
tion. If left untreated, many of these small pyo-
genic abscesses might have coalesced into a larger
abscess cavity with a multiseptated appearance.
In some instances, abscesses could possibly
coalesce into a relatively unilocular-­ appearing
cavity. The diagnosis for liver abscess is that the
appropriate imaging modalities and culture of
causative organisms should be performed.
5.11 Peripheral Washout Sign
Feature
In dynamic postcontrast liver MRI, the signal
intensities of lesions in the peripheral area is
lower than that in central area during delayed
contrast-enhanced phase, forming a low-signal
ring.
Explanation
This sign is mainly caused by the difference of
blood supply between the center and the periph-
190 X. Li et al.

a b

Fig. 5.11  A 55-year-old woman with right lobe hepatocellular carcinoma. (a) T1WI enhancement in the arterial phase.
(b) Portal venous phase. (c) Delay phase. Peripheral washout sign shown by arrow

ery of lesion. The center represents the denatured
and necrotic area with relative ischemia, and the
periphery is the edge of the growing tumors. The
edge with abundant peripheral blood supply in
the delayed phase can be quickly cleared by con-
trast medium (Fig. 5.11).
Discussion
The peripheral washout sign was first reported by
Mahfouz et al. in 1994 [23]. It was considered to
reflect rapid perfusion and clearance of the mar-
gin of malignant liver lesions. The peripheral
washout sign is associated with metastasis, hepa-
tocellular carcinoma, and cholangiocarcinoma in
most cases. In previous studies, this sign was
considered always associated with malignant
lesions, with a specificity of 100%. The dynamic
manifestation of margin enhancement of malig-
nant tumors is rapid enhancement in the early
stage and then continuous decline. In contrast,
the enhancement of central region of malignant
tumors shows a continuous increase, which may
be related to a different proportion of vascular
components and interstitial components between
the two regions. Vascular components in the mar-
ginal region are more numerous than those in the
interstitial region, and the qualitative components
in the central region are more than those in the
vessels, or to the different vascular structures
between the two regions. The structure of blood
vessels in the central area is relatively complete,
and the blood flow is cleared quickly, while the
structure of the central area is incomplete, and
the blood enters and flows slowly. Alessandrino
et al. [24] reported peripheral washout sign in a
rare benign lesion of the liver, namely, hepatic
epithelioid angiomyolipoma (HEA). Therefore, it
is crucial to differentiate benign from malignant
lesions that may have peripheral washout sign.
Generally speaking, patients with HCC are more
5  Solid Organs of Upper Abdomen
a b
Fig. 5.12  A 64-year-old patient with chronic hepatitis
and cirrhosis. On enhanced arterial phase (a), the lesions
show obvious enhancement. Contrast agents were rapidly
introduced in contrast-enhanced delayed lesions (b).
common among middle-aged and elderly men
with a history of hepatitis B and cirrhosis, often
accompanied by elevated alpha-fetoprotein
(AFP); HEA is more common in middle-aged
women, with no history of hepatitis B or cirrho-
sis, and AFP is normal [25]. For HEA lesions, the
surrounding and central veins are enlarged and
convoluted. Drainage veins are visualized in the
early stage. Peripheral and central veins of portal
and delayed lesions are continuously enhanced,
and the enhancement degree of arterial lesions is
lower than that of HCC.  Fatty degeneration in
HCC lesions is intracellular fat showing low sig-
nal T1 out of phase; the fat in HEA is mature fat,
and the signal of fat suppression is decreased.
The abundant blood supply of active and prolif-
erative tumor margin tissue seems to be impor-
tant in the performance of peripheral washout
sign, which has high specificity for the diagnosis
of malignant lesions, but cannot be used as the
only feature to distinguish malignant from
benign. In judging benign and malignant lesions,
it should be considered in combination with other
imaging modalities.
5.12 Halo Sign
Feature
The halo sign is a CT or MRI sign of hepatocel-
lular carcinoma (HCH), which refers to a circle
191
Thin-walled circular enhancement around the lesion could
be seen in delayed phase, which was a pseudo-capsule of
the tumor
of translucent band on the edge of the mass in
precontrast or postcontrast, which can separate
the tumor from the liver tissue.
Explanation
Tumors with swelling growth are slower, com-
pressing liver tissue or causing fibrosis of liver
tissue, forming a thicker pseudo-capsule. Both
the precontrast or postcontrast scan show a lower
attenuation (or low signal) ring shadow or trans-
lucent band around the tumor, which is the halo
sign (Fig. 5.12).
Discussion
The pseudo-capsule of HCC is a sign of qualita-
tive value. The biological characteristics of
tumors determine the performance and develop-
ment of imaging, and the results of imaging
examination are objective reflections of tumor
pathology. If the tumor shows an equal attenua-
tion, this sign is often the only finding to detect
the lesion. A pseudo-capsule can be formed
when the lesion is more than 1.5 cm; the tumors
compress noncancerous liver tissue, with fibrous
tissue components occupying the main body.
Inflammatory cell infiltration and neovascular-
ization can be seen around the capsule and
around the compressed liver tissue. Because the
contrast medium flows in and out slowly in the
fibrous tissue, the tumor pseudo-capsule is
enhanced during portal phase and delay phase.
192
Some studies have suggested that HCC with no
halo sign are poorly differentiated and grow
faster. Kadoya et  al. [26] believed the pseudo-
capsule of small HCC is formed by the com-
pression of tumor expansion, and the reticular
fibers around the liver plate and the liver plate
are formed by a radial arrangement and a paral-
lel arrangement. The pseudo-capsule consists of
two layers: the inner layer is thicker and com-
posed of rich fibrous tissue, and the outer layer
consists of extruded water-rich small blood ves-
sels and new bile ducts; 78% of tumors are
reported to have the pseudo-capsule [27]. As for
MRI finding, the pseudo-capsule shows as a
single-layer hypointensity ring around the tumor
on T1WI and double-­ layered ring on T2WI
(hypointensity in inner layer and hyperintensity
in outer layer).
a b
c d
Fig. 5.13  Physical examination of a 23-year-old woman
revealed decreased attenuation shadow on liver. (a)
Abdominal plain CT scan: round low-attenuation shadow
appears in the right lobe of the liver with unclear bound-
ary is unclear. (b) Arterial phase: lesion shows inhomoge-
X. Li et al.
5.13 Transparent Ring Sign
Feature
The low attenuation ring around hepatocellular
adenoma (HCA) appears on precontrast or post-
contrast CT of the arterial phase; it can be com-
plete or incomplete and located between tumor
and normal liver parenchyma. The attenuation of
this sign is lower than that of the tumor and the
normal liver parenchyma. Other name: low-­
density peripheral ring.
Explanation
Transparent ring sign is a characteristic CT find-
ing of HCA. It may be associated with hepatocel-
lular fat vacuolation caused by tumor expansive
growth and compression of surrounding liver
parenchyma (Fig. 5.13).
neous enhancement with low-attenuation ring seen around
the lesion. (c) Portal phase: lesion is in equal attenuation
with the liver, and circular-like high attenuation is seen
around it. (d) Delay phase: lesion is in equal attenuation
with the liver
5  Solid Organs of Upper Abdomen 193

Discussion 5.14 Wedge-Shaped Sign

Transparent ring sign was first described by
Angres in 1980 [28]. On plain CT, tumor shows Feature
slightly low attenuation, and the peritumoral The wedge-shaped area with increased hyperin-
area was surrounded by a lower-attenuation tensity on T1WI accompanying hepatic tumors is
shadow (3–4  mm thick; CT value 18 HU). On called wedge-shaped sign.
enhanced CT scan, the tumor show slight
enhancement; the low-attenuation ring between Explanation
the tumor and the normal hepatic parenchyma Because of malignant hepatic tumor infiltrating
shows no obvious enhancement, and is called a along bile duct, wedge-shaped signal abnormali-
low-attenuation peripheral ring. Surgical pathol- ties are formed on MRI. The shortened T1 may be
ogy revealed that the peritumoral liver was sur- associated with atrophic hepatocyte lipofuscin
rounded by a yellow margin band, which deposition (Fig. 5.14).
contained numbers of compressed hepatocytes
with fat vacuoles. It was speculated that the fatty Discussion
degeneration of peritumoral hepatocytes might The wedge-shaped signs that appear as hyperinten-
be the basis of the formation of low-attenuation sity on T1WI are rare, which are excepted from
rings. HCA was considered the most rare benign focal fatty infiltration, infarction, and tumor hem-
tumor of the liver. Since the 1970s, with the orrhage. There are two types of wedge-shaped
development of imaging technology, more and areas. One type was seen around the enlarged intra-
more studies have been reported for this tumor. hepatic bile ducts with extension of tumor next to
The disease may be single or multiple; single the lateral portion of the tumor mass. The configu-
cases often occur in women of childbearing age ration of this type of wedge-shaped area was vari-
with a history of oral contraceptives; and 50% to able because of tumor mass effect. The other type
80% of children with type 1 or type 3 glycogen of wedge-shaped area was seen around the tumor
storage disorder can have multiple HCA. HCA is
prone to bleeding and carcinogenesis. Imaging is
of great value in the early diagnosis and differen-
tial diagnosis of HCA [29]. On plain CT, most
show iso- or slightly low attenuation; the attenu-
ation is homogeneous. On postcontrast CT, arte-
rial phase can be enhanced to different degrees;
portal vein phase and delayed phase can show
equal or slightly high attenuation, or low attenu-
ation. On MRI, it can show iso-intensity or
hypointensity and hyperintensity on T2WI.
Differentiation from HCC or focal nodular
hyperplasia (FNH) is sometimes difficult
because the attenuation or signal changes of
tumors are not characteristic. The application of
hepatobiliary specific contrast agent Gd-BOPTA
or Gd-EOB-DTPA is valuable for differential
diagnosis. The hypointensity of HCA in paren-
chymal phase results from the lack of bile duct Fig. 5.14  Liver metastasis from colorectal cancer in a
65-year-old woman. MR T1 opposed-phase shows wedge-­
structure in HCA, which may lead to change in shaped area mild diffuse fatty infiltration with fatty spar-
intracellular transport of contrast agents in HCA ing (arrow) around enlarged intrahepatic bile duct next to
[30]. lateral portion of tumor [31]
194 X. Li et al.

mass. The tip of the wedge-shaped area was sepa-

rate from the tumor mass and located medially next
to the enlarged intrahepatic bile duct; This configu-
ration is useful for recognizing intraductal tumor
spread toward the hepatic portal veins [31].
Lipofuscin consists of polymerized phospholipids
and polymerized unsaturated fatty acids that are
mixed with neutral lipids and protein. Some lipo-
fuscins show positive fat-type reactions; others
show positive reducing reactions [31]. Hepatic iron
deposition is associated with iron overload disor-
ders, such as primary hemochromatosis and hemo-
siderosis. However, iron deposition is commonly
Fig. 5.15  CTAP demonstrates a peripheral perfusion
not segmental but diffuse [32]. Various factors may defect (straight line sign) in the right hepatic lobe caused
contribute to the formation of these wedge-shaped by compression of a portal vein branch [34]
areas. The wedge-shaped areas of increased signal
intensity are indicators of hepatic masses on liver portal vein branches by blood clots, especially
MR images. In patients with hepatic neoplasms, hepatocellular carcinoma. The triangular or
these areas should be seen a possible predictive wedge-shaped low-density areas represent the
sign of disease progression. distal low-perfusion areas of the involved portal
MRI studies have reported the high signal vein branches, and the enhanced liver paren-
intensity of wedge-shaped areas that surround chyma represents the normal perfusion areas of
liver masses. These findings are seen mainly on the portal vein branches (Fig. 5.15).
T2WI and have been attributed to sinusoidal con-
gestion and edema around tumors, bile stasis, Discussion
parenchymal compression, and infiltrating tumor Straight line sign was first described and formally
[31]. Hepatic infarction also appears as the named by Tyrrel et al. in 1989 [34]. CTAP is a sen-
wedge-shaped sign in CT, but there is little refer- sitive and reliable technique for identifying defects
ence to MRI findings of hepatic infarction in the in portal vein perfusion of the liver. Patients with
literature. In general, the infarcted foci are squamous cell carcinoma (SCC) who are candi-
shaped by the partially obstructed vascular sup- dates for transarterial chemoembolization (TACE)
ply that is usually one- or two sided, resulting in often undergo CTAP before TACE to confirm the
irregular shapes such as a wedge or triangle [33]. absence of HCC tumor thrombosis in the main
portal vein, which helps prevent severe liver injury
or liver failure associated with TACE. Portal vein
5.15 Straight Line Sign thrombosis involving the main trunk is usually a
contraindication for TACE as a treatment for HCC
Feature [35]. In most cases, the straight line sign at CTAP
A triangular or wedge-shaped low-density area demarks a low-attenuation area of relative hypo-
appears in the hepatic parenchyma of computed perfusion distal to the obstructing tumor or vessel
tomography arterial portography (CTAP), a line and may appear to resemble vascular infarction.
of varying length dividing both contrast material-­ We believe it is primarily seen when the portal
enhanced and less-enhanced liver, from the focal vein is obstructed by tumor or clot. Its recognition
mass to the peripheral edge of the liver. We have is important when central primary hepatocellular
named this the straight line sign. carcinomas are evaluated, because its appearance
signifies that the tumor is inoperable. In patients
Explanation with metastatic disease, it may not obviate surgery
Straight line sign is a CTAP manifestation of but it does alert the surgeon to the proximity of the
direct invasion of hepatic tumor or blockage of portal vein to the neoplasm [34]. Tyrrel et  al.
5  Solid Organs of Upper Abdomen
described the straight line sign (a line dividing
hepatic contrast material enhancement from less
enhanced liver) at CTAP and discussed its appear-
ance and significance. However, such line border-
ing had been reported earlier at unenhanced and
enhanced CT. We use the term straight border sign
to indicate hepatic attenuation differences bor-
dered by straight lines on any type of CT scan,
regardless of the use or technique of contrast
enhancement [36].
5.16 Liver Capsule
Depressed Sign
Feature
On abdominal CT scan, malignant tumors located
on the surface of the liver leading to liver capsule
invagination, loss of the original radian, and with
its successive liver capsule to form a complete large
radian, are known as the liver capsule depressed
sign (LCD).
Explanation
During the development of hepatic malignant
tumors, small blood vessels and small bile duct
obstructions cause limited hepatic atrophy, cen-
tral necrosis of tumors, proliferation of peritu-
moral fibrous tissue, and invasion of hepatic
envelope and other factors, together leading to
the liver capsule depressed sign (Fig. 5.16).
a b
Fig. 5.16 (a) Woman, 58  years old, with intrahepatic
cholangiocarcinoma, low-density mass in left lobe of
liver, and local hepatic capsule depression in portal phase
enhanced by CT. (b) Man, 48 years old, with hepatocel-
195
Discussion
The liver capsule depressed sign, also known as
retraction sign of hepatic capsule, refers to the flat
or concave hepatic capsule, resembling the pleu-
ral indentation sign [37]. Previous studies have
reported that the liver capsule depressed sign is a
specific sign of hepatic malignant tumors.
However, with the continuous updating of the
examination equipment and the popularization of
the examination, the liver capsule depressed sign
can also be observed in benign liver lesions. The
liver capsule depressed sign can be the result of
focal and diffuse lesions, which are caused by
tumors and nontumorous lesions [38]. Tumors
include primary, secondary malignant tumors,
and atypical hepatic hemangioma before and after
treatment. Especially, some tumors contain or can
induce large amount of fibrous tissue metastases,
such as lung cancer, breast cancer, or colon can-
cer. Malignant tumors adjacent to the liver surface
invade hepatic sinuses, small blood vessels, and
small bile ducts, resulting in cholestatic cirrhosis
and depression of the capsule after local hepatic
atrophy. The center of the tumor necrosis, the pro-
liferation of fibrous tissue traction near the liver
envelope is flattened, retracted, even in the form
of an anti-­arc or umbilical concave, invasion of
the liver envelope when a serrated change. The
retraction of hepatic capsule in cavernous heman-
gioma is related to fibrosis, thromboembolism,
and ischemia. Nonneoplastic factors include cir-
lular carcinoma, heterogeneous enhancement mass in
right lobe of liver, and hepatic capsule depression in portal
phase enhanced by CT
196
rhosis, fibrosis, cholangitis, bile duct necrosis,
and liver injury. The depression of hepatic capsule
caused by posthepatitis cirrhosis is caused by liver
regeneration nodules and fibrous tissue prolifera-
tion, resulting in an uneven liver surface. With the
progress of hepatic fibrosis, the degree of hepatic
capsule depression is more obvious. The liver
capsule depressed sign is related to the size of the
tumors: the larger the tumors, the higher the prob-
ability of the hepatic capsule indentation sign.
With increase of the tumors, width and depth con-
tinue to increase.
The liver capsule depressed sign is common in
malignant tumors, but it is not specific. Benign
tumors and a variety of nonneoplastic lesions can
also occur. There are differences between benign
tumors and malignant tumors with different
degrees of differentiation in the smooth or rough
margin of retraction of the hepatic envelope. The
rough margin of retraction of hepatic envelope of
malignant tumors highly suggests that the tumors
invade the envelope and tend to differentiate
poorly. The width and depth of retraction of
hepatic capsule vary with the amount of fibrous
tissue proliferation. Therefore, careful observa-
tion of this manifestation can preliminarily deter-
mine the benign and malignant lesions, if the
liver capsule is invaded, and the degree of liver
fibrosis. It is very helpful to the clinical staging of
tumors, the formulation of treatment plans, and
prognosis evaluation. However, it is not enough
to observe this manifestation alone, but also to
make a complete diagnosis in combination with
the overall imaging manifestations of the lesions.
5.17 Straight Border Sign
Feature
According to CT plain scan or dynamic enhance-
ment, between different density areas in the liver,
the edge of straight line appearance is called liver
straight border sign.
Explanation
The straight border sign of liver is not a manifes-
tation of liver mass, but is caused by vascular
embolism, arterial–portal shunt, fat deposition,
X. Li et al.
Fig. 5.17  Large patches of diffuse hypodensities are seen
in the liver. Enhanced scan showed a straight border
between a fatty liver lobe and normal liver lobe
aggregated fibrosis, radiation hepatitis, tumor,
enhanced scanning factors, and artifacts
(Fig. 5.17).
Discussion
Attenuation differences bordered by straight
lines within the liver are occasionally encoun-
tered at unenhanced CT.  Entities have been
reported to cause such attenuation differences,
including fatty liver, radiation hepatitis, and vas-
cular abnormalities. The prevalence of this find-
ing increases with the use of contrast material,
especially when administered via the superior
mesenteric and hepatic arteries. Tyrrel et al. [39]
described the straight border sign (a line dividing
hepatic contrast material enhancement from less
enhanced liver) at CT arterial portography
(CTAP) and discussed its appearance and signifi-
cance [36]. The liver is an unusual organ from the
aspect of blood supply; it has dual blood supply
through the hepatic artery and the portal vein.
When vascular compromise occurs, this dual
blood supply system can cause changes in the
volume of blood flow in individual vessels or
even in the direction of blood flow [40]. When
portal venous blood supply is decreased or
stopped by tumor thrombus, thrombo-embolus,
or compression of the portal vein, the corre-
sponding parenchyma appears as a hypoattenuat-
ing area with straight borders at CTAP.
The concept of straight border sign of liver is
different from that of linear sign. The common
5  Solid Organs of Upper Abdomen
reasons are as follows. (1) Vascular anomalies
are the common cause of this sign. (2) There are
many types of fat infiltration in the liver, such as
extensive, lobar, segmental, irregular, and focal.
The anatomical division is determined by the
blood supply, especially the portal vein. Even
with extensive fat infiltration, it is usually dis-
tributed according to the anatomical region. The
area affected by fat infiltration showed low den-
sity on CT plain scan and no enhancement on
postcontrast CT images. There was no displace-
ment of portal vein and hepatic vein during fat
infiltration. (3) On plain CT, the aggregated
fibrosis caused by liver cirrhosis presented as
low density or peripheral low density, and iso-
dense or slightly low density area on CT. In these
areas, portal vein blood supply decreases while
hepatic artery blood supply increases slightly,
which can be detected on CTAP.  Aggregated
fibrosis can show high density on delayed post-
contrast scans, especially when a large amount
of contrast media is injected. (4) Radioactive
hepatitis showed low density on plain CT and
high density on postcontrast CT. The density dif-
ference in the boundary area forms a straight
border sign, but not all of these are distributed
according to anatomical region. (5) Tumors gen-
erally do not have straight border sign unless
secondary vascular abnormalities occur. (6)
Artifacts in plain CT scan may also form a
straight border sign [41].
a b
Fig. 5.18 (a, b) Two patients with choledocholithiasis: red arrow indicates the target sign, and yellow arrow the cres-
cent sign
197
5.18 Target Sign
and Crescent Sign
Feature
In the CT image, the stone in the center of the
dilated common bile duct shows a dense or soft
tissue shadow, surrounded by a water-like density
of bile shadows, called the target sign. The com-
mon bile duct stones are incarcerated and close to
a side wall, and the bile of the water sample den-
sity is crescent shaped on the opposite side,
which is called the crescent sign.
Explanation
Target sign and crescent sign are direct CT signs
of common bile duct stones. The stones showing
the target sign and the crescent sign are mostly
high density, soft tissue density, and mixed den-
sity. The density of the annular water around the
stone is formed by surrounding bile and may also
be related to the inflammatory edema of the inter-
nal wall of the common bile duct (Fig. 5.18).
Discussion
As a common disease, gallstones account for
60% of biliary diseases and have a high inci-
dence. As an imaging method, the CT imaging
principle is relatively simple, mainly depending
on the absorption of material to X-ray. With
image performance of hyperattenuation, isoat-
tenuation, and hypoattenuation shadow, CT is the
198
most effective and sensitive imaging modality for
evaluation of gallstones. (1) High-density stones
are mainly bile pigment stones containing vari-
ous calcium salts; CT value is more than 60 Hu
and higher than surrounding soft tissue density.
(2 Soft tissue density stones are cholesterol
stones containing a small amount of calcium
salts; CT value is 20–60 Hu with soft tissue den-
sity. (3) Low-density stones mainly contain cho-
lesterol; CT value is less than 20 Hu with
translucent shadow below the bile density. (4) CT
images of mixed-density stones show inhomoge-
neous density of stones and are typically layered,
a characteristic manifestation of bile duct stones.
CT value is negatively correlated with cholesterol
content and positively correlated with bile pig-
ment and calcium content. Direct CT signs of
common bile duct stones include these. (1) High-­
density stones in the common bile duct fill the
entire lumen, with no surrounding low-density
bile shadow. (2) The target sign was first pro-
posed by Baron in 1987 and is considered a direct
sign of common bile duct stones [42]. The stones
showing the target signs are mostly high density,
soft tissue density, or mixed density. The density
of the annular water around the stone is formed
by the surrounding bile and may also be related
to the inflammatory edema of the internal wall of
the common bile duct. A typical target sign can
appear as a uniform ring or a wide upper and
lower narrow, a left wide and a right narrow, or a
left upper wide and a lower right narrow sign. (3)
There are some common bile duct stones. The
density of water samples around the stones does
not constitute a complete ring shape, but a cres-
cent shape, called the crescent sign. The crescent-­
shaped water sample density is mostly located at
the upper left or left side of the stone, which may
be related to the gravitational effect of the stone
and the kinetic effect of bile flow from the upper
left to the lower right at the lower end of the com-
mon bile duct.
The target sign and the crescent sign are char-
acteristic signs in the diagnosis of common bile
duct stones, especially on enhanced images. The
indirect CT findings of stones in the common bile
duct follow. (1) Mild or moderate dilatation of
the common bile duct above the obstructive
X. Li et al.
s­ egment. (2) High-density circular thickening of
the wall of the common bile duct, the feature of
choledocholithiasis and choledochitis. The diag-
nostic accuracy of CT in diagnosing common
bile duct stones is 50% to 90%, depending on
stone composition. CT is highly sensitive to pig-
ment stones, that is, high-density stones and
mixed-­density stones, and the diagnostic accu-
racy is more than 90%. In CT, it is difficult to
diagnose cholesterol stones with approximate
bile density. The combination of significant CT
features, such as common bile duct (CBD) diam-
eter of 8 mm or more, pericholecystic fat infiltra-
tion, and papillitis can be translated into a
nomogram allowing a reliable estimation of CBD
stone presence; this may serve as a decision sup-
port tool to determine whether to proceed to fur-
ther diagnostic tests or treatment options [43].
Spectral CT has a high diagnostic value for nega-
tive gallstones or bile duct stones, and material
decomposition CT images and spectral curves
can make an accurate diagnosis [44]. The signal
changes of gallstones on MRI are related to lipid
and macromolecular proteins in gallstones, but
not to the density of gallstones, which effectively
complements the deficiency of CT in the diagno-
sis of gallstones. MR cholangiopancreatography
(MRCP) can show three-dimensional images of
the biliary tract system and has unique advan-
tages in the diagnosis of gallstones.
5.19 Pearl Necklace Sign
Feature
On MRCP or T2WI, the thickened wall in gall-
bladder adenomyomatosis (GA) or diverticular
disease shows multiple tiny, dotted high-signal
cysts, 2–7  mm in size, generally 4  mm, resem-
bling a pearl necklace. Identification of the pearl
necklace sign is useful to distinguish GA from
wall thickening secondary to gallbladder carci-
noma (GC).
Explanation
The myometrium and epithelium of gallbladder
proliferate and hypertrophy, and the mucosa val-
gus in the myometrium forms the Rokitansky–
5  Solid Organs of Upper Abdomen
a b
c d
Fig. 5.19  A 49-year-old man. (a) Nodular thickening at
the bottom of the gallbladder with cystic formation shown
on postcontrast CT. (b–d) Fluid signals in the cystic cavity
Aschoff sinus (RAS). RAS is filled with bile;
significant high signal points can be seen in the
thickened wall on MRCP or T2WI. MRCP depicts
these closely located cystic spaces as tiny bright
foci, all along the wall of gallbladder, resembling
the metaphorical pearl necklace. MRCP is more
useful than the other MRI sequences in identify-
ing GA (Fig. 5.19).
Discussion
The pearl necklace sign indicates the presence of
Rokitansky–Aschoff sinuses within the thick-
ened gallbladder wall, specifically detected on
MRCP for GA.  The sign was initially used in
description of the characteristic appearance of
GA on drip-infusion cholecystography [45].
This specific sign can also be seen on oral chole-
199
were seen on T2WI, T1WI with fat-suppressed, linear
enhancement of cystic septum on post-contrast T1WI
cystography, and now is widely used to describe
the MRI appearance of GA. The finding of GA is
relatively common with a reported incidence of
2% to 5% of specimens at cholecystectomy [46].
The gallbladder wall is composed of four layers:
mucosa, lamina propria, muscularis propria, and
serosa. Adenomyomatosis or diverticular disease
of the gallbladder is characterized by excessive
proliferation of surface epithelium that results in
multiple diverticula or out-pouches, termed
RAS. These diverticula invaginate into the deep
muscular layer and appear as cystic spaces in the
wall, contiguous with the gallbladder lumen.
These diverticula contain bile with cholesterol,
which on precipitation results in cholesterol
crystal formation. In the presence of fluid (bile),
T2WI demonstrates the bright cystic spaces rep-
200
resenting RAS.  MRCP depicts these closely
located cystic spaces as tiny bright foci, all along
the wall of the gallbladder, resembling the (met-
aphorical) pearl necklace. The pearl necklace
sign is useful to distinguish GA from wall thick-
ening secondary to GC [45, 46]. Focal adeno-
myomatosis may sometimes appear as a discrete
mass and can be mistaken for GC.  Surgical
resection is usually not indicated, except in
symptomatic patients and in cases where GC
cannot be completely excluded [47].
MRCP frequently depicted RAS within the
thickened gallbladder wall (the pearl necklace
sign) in the majority of patients with all mor-
phological types of GA.  The pearl necklace
sign of small connected sinuses on MRI, or the
“rosary” sign on CT are additional characteris-
tics that may assist in establishing a diagnosis
of GA. MRCP is more useful than CT and arte-
rial phase MR images in the differentiation
between GC and GA [46]. A combination of
arterial phase MRI T1WI and MRCP may be
helpful for differentiation between GC and GA
when the pearl necklace sign is not identified
on MRCP images or GC coexists with GA, par-
ticularly the segmental type of adenomyomato-
sis [46]. A recent study reported the cotton ball
sign was more sensitive than the pearl necklace
sign for diagnosis of adenomyomatosis diagno-
sis and was also useful in differentiating GA
from GC [48].
a b
Fig. 5.20 (a) Localized gallbladder agenesis (GBA). (b) Diffuse GBA
X. Li et al.
5.20 Garland Sign
Feature
When CT cholecystography is performed with
oral contrast medium, the thickened gallbladder
wall is filled with small dots of contrast medium,
which are connected with the gallbladder and
resemble a garland, thus called the garland sign.
Explanation
The garland sign is a CT feature of adenomyoma-
tosis of the gallbladder on oral contrast cholecys-
tography. It is formed by the filling of contrast
media in the thickened Rokitansky–Aschoff
sinus of the gallbladder wall (Fig. 5.20).
Discussion
Adenomyomatosis of the gallbladder (GA) is a
common benign disease characterized by asymp-
tomatic gallbladder masses or thickening of the
gallbladder wall [49]. The diagnostic rate in all
cholecystectomies is from 2% to 9%. GA was
proposed by Jutras in 1960 [50]. According to the
range of lesions, GA can be divided into three
types. (1) Diffuse type (extensive type): the entire
gallbladder wall shows diffuse thickening and the
thickened wall shows a diverticulum. (2)
Segmental type (ring type) is characterized by
ring-shaped thickening of the gallbladder wall,
ring-shaped thickening of the typical part of the
gallbladder body; the general specimen of the
5  Solid Organs of Upper Abdomen 201

gallbladder showed hourglass-like changes, with

the gallbladder divided into two interconnected
small cavities. (3) The localized type (basal type),
the most common, also known as adenomyoma,
is characterized by a clear border at the bottom of
the gallbladder mass, a semilunar or crescent
(cap sign).
The exposure of Rokitansky–Aschoff sinus
(RAS) is the main basis for diagnosis of this dis-
ease by CT examination. CT shows mainly an
enlarged gallbladder, diffuse or localized thicken-
ing of the gallbladder wall, and uneven distribu-
tion. The small cap sign appearing on the basal
type is highly suggestive of this disease. Because Fig. 5.21  In a 26-year-old man, axial precontrast CT
of the influence of partial volume effect, many shows manifestations characterized by interstitial striated
calcification of the hepatic parenchyma, crisscrossing into
small diverticula connected with a gallbladder the shape of a map
cavity in the gallbladder wall cannot be displayed
by precontrast CT, so are easy to confuse with ized by poor contractile function and no RAS. (3)
gallbladder carcinoma. Dynamic contrast-­Xanthogranulomatous cholecystitis. Enhanced
enhanced or multiphase spiral CT scan showed scan is typically characterized by “sandwich bis-
the thickened gallbladder wall in arterial phase cuit sign,” that is, a thickened gallbladder wall
was markedly enhanced in mucosa and submu- with enhanced inner and outer rings.
cosa, the lesion was enhanced and expanded in
portal vein phase, the gallbladder wall was
enlarged in delayed phase, and the muscular layer 5.21 Tortoise Shell Sign
of mucosa and submucosa was heterogeneously
or homogeneously enhanced. This enhancement Feature
is rare in other lesions of the gallbladder, reflect- CT of liver in schistosomiasis is characterized by
ing the pathological hyperplasia and hypertrophy interstitial striated calcification of the hepatic
of the gallbladder mucosa and muscular layer, parenchyma, crisscrossing into the shape of a
which is the enhancement characteristic of gall- map or tortoise shell pattern.
bladder adenomyosis. In addition, the interface
between liver and gallbladder was clear, the inner Explanation
and outer walls of gallbladder were smooth, and The eggs of schistosomes (trematodes), causing
the boundary between the normal part of gallblad- schistosomiasis, stay in the small branch of the
der and the involved part of gallbladder was clear. portal vein to form nodules of the eggs and a
GA is often differentiated from other gallblad- fibrosis reaction, which leads to hyperplasia of a
der diseases. (1) Gallbladder carcinoma shows large amount of fibrous tissues around the branch
uneven thickening of the cystic wall with of the portal vein. Finally, linear calcification
enhancement, uneven inner wall, unclear bound- forms. When linear calcification is very exten-
ary between the outer wall and the surrounding, sive, the crisscross pattern will become the char-
which can directly invade the liver; the hepatobi- acteristic images of map-like or net-like
liary interface disappears, and sometimes lymph morphology (Fig. 5.21).
node metastasis can be seen surrounding. (2) In
chronic cholecystitis, the fat meal test has differ- Discussion
ential significance. Diffuse cystic adenoidopathy The German physician Theodor Bilharz first
can be manifested as hyperactivity of the gall- described schistosomiasis after he performed an
bladder. Chronic cholecystitis can be character- autopsy in 1851 in Egypt [51]. Schistosomiasis is
202
a trematode infection endemic to various tropical
and subtropical locations. Human infections with
liver involvement are typically caused by the spe-
cies Schistosoma mansoni and Schistosoma
japonicum. After infection, schistosomes migrate
into the mesenteric vasculature and release their
eggs, which then travel to the liver via the portal
circulation, inducing inflammation and sinusoi-
dal hypertension. The smaller eggs of S. japoni-
cum embed more peripherally within the liver.
When the eggs die, they induce inflammation and
fibrous septa formation with eventual calcifica-
tion. The fibrotic septa, oriented perpendicular to
the liver surface, surround normal liver paren-
chyma in a polygonal distribution to produce the
classic “fish scale” appearance by ultrasound. On
CT, the calcified fibrotic septa and thickened cap-
sule result in the classic “tortoise shell” or “turtle
back” appearance of chronic S. japonicum infec-
tion. On MRI, the fibrotic septa appear hypoin-
tense on T1WI and hyperintense on T2WI and
enhance following intravenous contrast adminis-
tration [52].
CT findings in patients with chronic schisto-
somiasis include target organ damage and the
peculiar calcification pattern of eggs in the
lesions. A peculiar type of septal calcification of
eggs in Schistosoma japonica resembling a turtle
shell also indicates the severity of hepatic fibro-
sis. This peculiar septal and capsular calcification
results in a geographic or map-like appearance on
CT [53]. Hepatocellular carcinoma (HCC) is
associated with chronic hepatic schistosomiasis,
a b
Fig. 5.22  Periportal low attenuation. Postcontrast CT (Transverse view a and Sagittal view b) shows low-attenuation
areas around portal vein and its branches (arrowheads). Note laceration in right lobe
X. Li et al.
and most of the nodules appear as masses of
homogeneous low density surrounded by
shell-­
­ like calcification. CT evidence of septal
enhancement in broad fibrous septa is suggestive
of hepatic S. japonica infection. Other suggestive
findings of schistosomiasis such as splenomeg-
aly, ascites, and dilated collateral vessels are well
demonstrated on CT. Both CT and US show char-
acteristic features and are good modalities for
evaluation of hepatic schistosomiasis. The MRI
appearance is less characteristic. MRI has an
inherent disadvantage in evaluation of schistoso-
miasis because it does not allow identification of
the characteristic calcifications [53].
5.22 Periportal Tracking Sign
Feature
Postcontrast CT shows a tubular low-density
shadow around the portal vein and its branches,
with a dendritic orbital shadow on the long-axial
section and a circular shadow on the cross
section.
Explanation
Periportal tracking sign is an important sign of
subtle liver injury. The pathological basis is rup-
ture and hemorrhage of small blood vessels in the
intrahepatic triangle area during hepatic blunt
contusion, and the blood spreads along the con-
nective tissue sheath with low resistance around
portal veins (Fig. 5.22).
5  Solid Organs of Upper Abdomen
Discussion
Macrander et  al. found the “periportal tracking
sign” that may be an important sign of subtle
liver injury in 1989. After blunt abdominal
trauma, the periportal tracking sign (PPT), which
may represent hemorrhage along the portal veins,
has also been described. The periportal region
describes the area around the portal vein and its
branches. Hepatic artery branches, bile duct
branches, autonomic nerves, lymphatics, and a
potential space are found within. A variety of
pathological manifestations can involve any of
these structures with a characteristic finding in
contrast-enhanced CT, best described as peripor-
tal low attenuation, which is called periportal
tracking. The periportal lymphatics and nerves
are not visible in the general population. These
structures can be involved by various diffuse pro-
cesses [54]. PPT has also been seen in patients
with hepatitis, liver transplant, congestive heart
failure, hepatic artery thrombosis, and lymphatic
obstruction [55]. Vigorous intravenous fluid
administration or elevated central venous pres-
sure caused by tension pneumothorax or pericar-
dial tamponade may be further reasons for
PPT.  In inflammatory diseases, PPT seems to
reflect altered hepatic lymphatic dynamics.
However, the pathogenesis is uncertain. It is
obvious from the foregoing that the differential
diagnoses of PPT are numerous [56]. The other
radiologic findings associated with hepatic peri-
portal tracking include a thickened gallbladder
wall, pleural effusion, and a dilated inferior vena
cava. A multifactorial etiology for periportal
edema in acute infectious disease has been sug-
gested, including altered sodium reabsorption as
a result of the infectious process involving the
renal interstitium and increased vascular perme-
ability secondary to systemic sepsis or hypoalbu-
minemia [56]. The PPT has been reported to be
an extrarenal manifestation of acute pyelonephri-
tis. The limited data suggest that PPT may be
associated with a more severe course of acute
pyelonephritis [54]. On occasion, this is the only
sign of hepatic injury. The CT features of blunt
liver trauma include lacerations, subcapsular or
parenchymal hematomas, active hemorrhage,
203
juxta-hepatic venous injuries, and periportal low
attenuation. In addition, CT is a useful tool in the
assessment of delayed complications in blunt
liver trauma, including delayed hemorrhage,
hepatic or perihepatic abscess, posttraumatic
pseudoaneurysm and hemobilia, and biliary com-
plications such as biloma and bile peritonitis. CT
is also needed for follow-up in patients with
high-grade liver injuries to identify potential
complications that require early intervention in
clinical practice [57].
5.23 Periportal Halo Sign
Feature
MRI T2WI and postcontrast T1WI show hypoin-
tensity surroundings around portal vein branches;
CT enhanced scan showed a halo-like low-­
attenuation area around hepatic segments or
peripheral portal vein branches; depending on the
prognosis, development or disappearance of the
disease follows. The branches of the portal vein
in the left lobe of the liver run parallel to the
transverse axis, so the low-attenuation area
around the portal vein extends to a tram track line
appearance; the branch of the portal vein in the
right lobe of the liver runs in the coronal direc-
tion, so the low-attenuation area around the por-
tal vein appears as a ring or circle.
Explanation
About 80% of the hepatic lymph drainage is to the
hilar lymph nodes and into the small omental
lymph nodes. The hilar mass and omental lymph
node cause the intrahepatic lymphatic dilation to
form lymphedema around portal vein. Heart fail-
ure and venule obstruction lead to excessive lym-
phatic production in the liver, lymphatic dilatation,
and periportal edema, edema formed around the
branches of the intrahepatic portal vein during
trauma. All these changes increase the fluid
around the portal vein branches, forming a halo
sign around the portal vein. The low-­attenuation
shadow around the portal vein caused by trauma
is considered to be caused more by bleeding, and
is called the periportal tracking sign (Fig. 5.23).
204
a b
Fig. 5.23 (a) CT postcontrast image shows halos of hypoattenuation around portal veins. (b) T2-weighted MRI also
shows halos of high signal intensity around portal veins
Discussion
Periportal halo sign is a valuable CT sign of
occult liver disease. The pathophysiological basis
of the periportal halo sign or tracking sign has not
been confirmed. Periportal halo sign is likely to
indicate fluid or dilated lymphatic system in the
loose stroma around the portal vein and portal
triple structure. The central hepatic vein of the
hepatic lobule is closely connected with the adja-
cent hepatocytes, and there is no potential gap.
The triple structure of porta hepatica located
around the hepatic lobule includes not only the
segment of portal vein, hepatic artery, and bile
duct, but also lymphatic vessels. There is a poten-
tial space around the triple structure of the hilum
of the liver, which is relatively loose connective
tissue. The branches of lymphatic vessels are
located around the portal vein: 80% of the lym-
phatic fluid is transported from the liver to the
portal area, then drained to the adjacent lesser
omental lymph nodes, and finally into the chy-
lous cistern. A small portion (nearly 20%) of the
hepatic lymphatic drainage system runs along the
hepatic vein and enters the thoracic duct. Hilar
masses can obstruct the lymphatic reflux of the
liver. Lymphatic dilatation in the liver can lead to
lymphedema around the portal vein. In some
patients with severe hepatitis, congestive heart
failure, or venule obstruction, the liver may
become congested or develop edema, resulting in
increased lymphatic production. Increased lym-
phatic volume overloads the lymphatic system
X. Li et al.
and consequently leads to lymphatic dilatation
and edema around the portal vein. In patients
with liver trauma, intrahepatic hemorrhage and
edema occur in the area with the lowest tension,
that is, the porous space around the portal vein.
The similarity of these processes is the accumu-
lation of fluid around the portal vein, which leads
to the enlargement of the potential gap, which is
manifested in the low-attenuation halo around
the portal vein in enhanced CT scan [58].
Biliary dilatation, portal vein thrombosis, and
normal fat around the main portal vein resemble
the periportal halo sign. Periportal halo sign is
common around the portal vein below the seg-
ment, away from the fat around the main portal
vein. Unlike the low-attenuation shadow surround-
ing portal vein branches, the low-­attenuation areas
of bile duct dilatation do not surround portal vein
branches. In some patients, periportal halo and
biliary dilatation may be associated. Portal vein
thrombosis is characterized by focal low-attenua-
tion areas around the hepatic artery after enhanced
contrast. Understanding that complete or partial
thrombosis is common in the main portal vein and
understanding its anatomical relationship cor-
rectly usually leads to correct diagnosis. In conclu-
sion, periportal halo sign and tracking sign may
represent fluid accumulation, either hemorrhage or
edema, or lymphatic dilatation around the portal
vein and portal triple structure. The pathophysio-
logical basis of this sign has not been confirmed.
There is no specificity in this manifestation, but
5  Solid Organs of Upper Abdomen
the hilar and lesser omentum areas should be care-
fully observed when this sign occurs. Periportal
halo sign can occur in different diseases, including
end-stage primary cholestasis cirrhosis, trauma,
congestive heart failure, hepatitis, mass, lymph
node enlargement in portal area, and hepatic vein
obstruction, treated with liver transplantation and
bone marrow transplantation [59].
5.24 Focal Hepatic Hot Spot Sign
Feature
The focal hepatic hot spot sign can be seen in
99m
Tc-sulfur gel scanning of the liver and spleen;
it can be shown as an increase in radiopharma-
ceutical intake of the liver. This sign can also be
seen in postcontrast CT scanning [60].
Explanation
When superior vena cava obstruction occurs, the
left hepatic lobe on the radionuclide scan image
occasionally shows an increase in localized blood
flow in the collateral vein. The general collateral
vein pathway includes an internal mammary vein
that is drained through the paraumbilical vein to
the left branch of the portal vein. Blood flow
through the collateral vein can cause an increase
in blood flow in the focal region of the liver.
Especially when the superior vena cava (SVC) is
obstructed, activity is increased in the fourth seg-
ment of the liver (Fig. 5.24).
Discussion
Other causes of the focal hepatic hot spot sign
include Budd–Chiari syndrome, liver abscess,
liver focal nodular hyperplasia, and hepatocellu-
lar carcinoma. Except for the hepatic hot spot
sign caused by Budd–Chiari syndrome in the
caudate lobe, the focal hepatic hot spot sign
caused by all other diseases can be seen any-
where in the liver. Patients with SVC obstruction
showed increased focal activity or hot spot in the
fourth segment of the liver (S4) on 99mTc-sulfur
gel scanning of liver and spleen. The hot spot is
thought to be caused by the shunt of the superior
vena cava and the portal vein, which leads to an
increase in focal hepatic blood flow. SVC
205
Fig. 5.24 A 51-year-old male patient with systemic
lupus erythematosus and SVC obstruction. Arterial phase
postcontrast CT shows a patchy area with abnormal
enhancement in S4. The boundary is clear, the shape irreg-
ular, and accompanied by formation of collateral veins
(para-umbilical vein) [62]
obstruction is usually caused by extrinsic com-
pression from malignant disease such as bron-
chogenic carcinoma, lymphoma, and metastatic
lymph nodes; occasionally it may result from
benign causes such as aortic aneurysms, chronic/
fibrosing mediastinitis, and retrosternal goiter
[61]. There are many ways to form bypass of col-
lateral vessels and central venous obstruction.
There are three main collateral pathways in the
chest: upper pathway, posterior pathway, and
anterolateral pathway [62]. The upper pathway is
seen in the distal central vein (subclavian) and
includes the anterior jugular vein system that
connects the subclavian and internal jugular vein
system. The posterior pathway includes the venae
azygos-venae azygos minor inferior and the para-
spinal system. The presence of these collateral
pathways on axial image strongly suggests supe-
rior vena cava obstruction. The anterolateral
pathway system drains the anterior intercostal
vein, internal mammary vein, and thoracic long
vein to the inferior vena cava through the pericar-
dial phrenic vein, diaphragmatic vein, lumbar
vein, and hepatic vein. As with patients with SVC
obstruction, patients with inferior vena cava
obstruction can also have the focal hepatic hot
spot sign if the 99mTc-sulfur gel is injected from
the lower extremity.
Collateral veins in patients with SVC obstruc-
tion send blood back to the left lobe of the liver
206 X. Li et al.

through the internal mammary vein and the left Discussion

umbilical vein, thereby forming a localized area Hepatic hydatidosis is divided into two types,
of increased blood flow where the left umbilical echinococcosis caused by infection with
vein and the left main branch of the portal vein Echinococcus granulosus eggs and echinococco-
are inserted. On arterial phase or early portal sis caused by infection with Echinococcus multi-
vein phase of postcontrast CT, focal high attenu- locularis eggs. The cyst-in-cyst sign can be seen
ation enhancement, or on the radionuclide scan in echinococcosis granulosa. Echinococcosis
the accumulation of focal radiopharmaceuticals, granulosus is a parasitic disease caused by human
is manifested by an increase in blood flow from infection with Echinococcus granulosus. The
the collateral vessels of the liver, which is the right lobe of the liver is the predisposing site of
focal hepatic hot spot sign. The focal hepatic hot the disease. According to the literature, the pro-
spot sign strongly suggests SVC obstruction of portion of liver, lung, and other locations is 75%,
the chest. 15%, and 10%, respectively [63]. Hydatid cysts
formed by Echinococcus granulosus mostly par-
asitized in the right lobe of the liver, often single,
5.25 Cyst-in-Cyst Sign a few multiple, with slowly expanding growth,
gradually growing into giant cysts. During the
Feature growth process, the inflammatory reaction around
When hepatic echinococcosis is examined by CT, the hydatid cyst forms a thick fibrous capsule,
there are different sizes and number of ascites in which constitutes the outer cyst of the hydatid
the mother cyst, forming a multiple or honeycomb-­ cyst, and the hydatid cyst itself is the inner cyst.
like, sometimes wheeled, appearance. There are abundant blood vessels between the
external and internal cysts to ensure the blood
Explanation supply of hydatid cysts. The inner capsule is thin
The cyst-in-cyst sign is the characteristic mani- and consists of the outer corneal cortex and the
festation of cystic hepatic hydatidosis. The inner germinal layer. The cortical cortex protects
mother cyst is the hydatid cyst itself. The subcyst the germinal layer and absorbs nutrients; the ger-
is the germinal cyst or ganglion produced by the minal layer has strong reproductive ability, and
germinal layer of the mother cyst. The germinal can produce fine-pedicled germinal vesicles in
cyst falls out into the cyst, forms the ascus, floats the cyst cavity, containing many cephalic nodes.
in the mother cyst, and forms the characteristic The germinal sac falls off into the sac and forms
cyst-in-cyst sign (Fig. 5.25). an ascus, which floats in the mother sac. The sco-
lex also produces ascus. The ascus is the same as
the maternal sac, and can continue to produce
germinal or grandchild sacs, forming three gen-
erations coexisting in one sac. The rupture of cyst
wall is a serious complication. The fluid contain-
ing toxic protein in the cyst can cause an allergic
reaction or even anaphylactic shock. The rup-
tured scolex is planted in the abdominal cavity
and a secondary hydatid cyst occurs. Calcification
can occur in the cyst wall of long-term growth
hydatid cysts.
The CT features of echinococcosis granulosus
are quite characteristic. CT is a major means of
examination in the diagnosis of hepatic echino-
Fig. 5.25  A 48-year-old man. Intrahepatic space occupa- coccosis, the location of echinococcal cysts, and
tion and cyst-in-cyst sign on postcontrast CT the number, size, shape and complications of
5  Solid Organs of Upper Abdomen
cysts. Echinococcosis granulosus can be divided
into four types [64]: (1) unilocular cystic type,
single or multiple cystic low-density shadows,
showing round or oval water samples of uniform
density; (2) child–mother relation cystic type, in
which the number and size of round, lower-­
density cysts filling can be seen, showing multi-
chamber or honeycomb-like “cyst” changes,
namely cyst-in-cyst sign; (3) calcific type, the
wall of the cyst, that is, the contents of the cyst
are calcified in large quantities; and (4) compli-
cated type, manifested by cyst rupture, wherein
the contents of the posterior capsule flow into the
abdominal cavity, causing peritonitis. The cyst
size of hepatic echinococcosis is related to the
time of formation [65], which is generally larger,
mainly because the onset of hepatic echinococ-
cosis is concealed; the early clinical symptoms
are mild, and the development is slow. Hepatic
damage caused by hepatic echinococcosis is
usually a single or multiple cyst in the liver. Its
imaging classification is relative, and it is differ-
ent from the same disease. Imaging examination
can visually display various signs, such as cyst
size, cyst wall shape, cyst wall thickness, cyst
fluid density, combined with high calcification
rate, cyst-in-cyst sign, and other characteristic
imaging manifestations, and pay attention to a
small number of cases may be accompanied by
sensation. Complications such as dyeing and
rupture can be used to diagnose hepatic
echinococcosis.
a b
Fig. 5.26  Postcontrast CT (a, b) shows floating ruptured ascus in the mother sac with floating membrane sign
207
5.26 Floating Membrane Sign
Feature
This sign is one of characteristic CT signs of
hepatic echinococcus cyst; the ascus appears in
the mother cyst of hepatic echinococcosis, the
ascus and the mother cyst are completely sepa-
rated and detached, and the ascus floats in the
mother cyst fluid, showing a floating membrane
sign.
Explanation
Hepatic echinococcosis internal capsule separa-
tion is caused by infection or injury; if completely
separated, then the falling internal capsule scat-
ters in a floating membrane shadow (Fig. 5.26).
Discussion
Hydatidosis is a common zoonotic parasitic dis-
ease in livestock areas, and 70% of hydatidosis
occurs in the liver. Generally, it is caused by acci-
dental ingestion of tapeworm eggs; the larvae
pass through the small intestine and invade the
liver through the portal vein. There are two types
of hepatic echinococcosis: one is hepatic cystic
echinococcosis caused by Echinococcus granu-
losus infection, and the other is hepatic alveolar
echinococcosis caused by Echinococcus multi-
locularis infection [66]. CT has obvious advan-
tages in the diagnosis of hepatic echinococcosis,
and its display of characteristic pathological
manifestations is the key factor in this diagnosis
208
and activity judgment. According to the latest
expert consensus, hepatic Echinococcus granulo-
sus disease can be divided into single cyst type,
multiple cyst type, internal cyst collapse type,
consolidation type, and calcification type. The
internal capsule collapse is caused by external
forces, hydatid cyst degeneration, and infection.
When the internal and external capsules are sepa-
rated or ruptured fluid enters between internal
and external capsules, “bilateral sign” is seen;
when the internal capsule is completely sepa-
rated, collapsed, or suspended from the cystic
fluid, it is called “water lily sign”; when the inter-
nal capsule is completely exfoliated, it can show
“floating membranes sign.” Calcification and
polycystic and endocystic collapse have been
identified as characteristic signs of hepatic hyda-
tidosis. The floating membranes sign is one of the
characteristic signs.
Hepatic echinococcosis should be distin-
guished from simple hepatic cyst, liver abscess,
hepatic hemangioma, and hepatocellular carci-
noma [67]. The mechanism of hepatic alveolar
echinococcosis is unknown and should be differ-
entiated from multiple hepatic cysts. For exam-
Fig. 5.27  MRCP (a, b) in a 58-year-old woman presented with an uneven thickness of intrahepatic bile ducts of the
liver and a slightly less smooth surface, showing the “string of beads” sign
X. Li et al.
ple, hepatic cystic type and hepatic alveolar type
echinococcosis coexist. CT diagnosis is relatively
easy. It is not difficult to differentiate and diag-
nose hepatic hydatidosis from hepatic hemangi-
oma, hepatic abscess and hepatocellular
carcinoma by comparing their CT features and
clinical laboratory tests.
5.27 Beaded Sign
Feature
Endoscopic retrograde cholangiopancreatogra-
phy (ERCP) and MR cholangiography (MRCP)
in patients with primary sclerosing cholangitis
(PSC) show stricture of intrahepatic and extrahe-
patic bile ducts with normal or mildly dilated bile
ducts with beaded changes.
Explanation
In primary sclerosing cholangitis, short (1–2 cm)
circumferential strictures of intrahepatic and
extrahepatic bile ducts are accompanied by nor-
mal or mildly dilated bile ducts, which form the
typical beaded change (Fig. 5.27).
5  Solid Organs of Upper Abdomen
Discussion
PSC, also known as stenotic cholangitis, closed
cholangitis, or fibrotic cholangitis, is a rare dis-
ease caused by immune-mediated cholangiocyte
injury through a complex interaction with envi-
ronmental factors. Although the etiopathogenesis
of PSC is still unclear, it is widely accepted that
the interaction of different autoimmune, genetic,
and environmental factors is responsible for the
changes occurring in PSC [68]. PSC typically
occurs in young and middle-aged men with an
age of onset of 30 to 40 years. It is a chronic cho-
lestatic liver disease characterized by intrahepatic
or extrahepatic bile duct inflammation and fibro-
sis, and eventually develops into cirrhosis. The
intrahepatic bile duct is almost always affected
and tends to be more pronounced than in the
extrahepatic bile duct. Moreover, the long-­
standing PSC is associated with serious compli-
cations such as hepatic osteodystrophy,
development of dominant bile duct strictures,
recurrent cholangitis, and disease-associated
malignancies including cholangiocarcinoma.
Most patients ultimately require liver transplan-
tation, after which the disease may recur [69].
Liver histology changes in most patients are non-
specific, so liver biopsy has little value in the
diagnosis of PSC, but may suggest PSC and his-
tological staging. Histological changes in the dis-
ease include fibrosis around the bile duct,
inflammation in the portal area, varying degrees
of peripheral hepatitis in the portal area, and
changes in liver parenchyma. As the disease pro-
gresses, fibrosis in the portal area increases,
interlobular bile ducts decrease, and interlobular
septal formation and eventually cholestatic cir-
rhosis appear. According to its abnormal degree,
histology can be divided into stages I–IV. Phase
IV is cholestatic cirrhosis.
The characteristic radiologic features of PSC
are irregular multiple local strictures and dilata-
tions of intrahepatic and extrahepatic bile ducts,
and typical beaded changes of stricture and nor-
mal dilated bile ducts. The branches of the intra-
hepatic bile duct are thinner and fewer. Stenosis
of the intrahepatic bile duct is predominant.
ERCP is the gold standard for diagnosing PSC,
but it is an invasive examination and can cause
209
many complications. According to the latest rec-
ommendations of the American Association for
the Study of Liver Diseases (AASLD) and the
European Association of the Study of the Liver
(EASL) guidelines, MRCP is the first-line modal-
ity for investigating bile duct abnormalities in
PSC patients. MRCP is a noninvasive examina-
tion. Moreover, MRCP allows for visualization
of small ducts proximal to tight strictures, which
are often not visualized during ERCP. Comparable
to ERCP, sensitivity and specificity of MRCP are
88% and 99%, respectively [59]. However, when
there is clinical suspicion with negative or nondi-
agnostic MRCP findings, ERCP should be per-
formed. ERCP is also a therapeutic procedure
with balloon dilatation or stenting possibilities,
but with postprocedural complications ranging
from 3% to 8%, and allows for histological
sampling.
5.28 Soft Rattan Sign
Feature
Soft rattan sign refers to intrahepatic bile duct
dilatation; as its course is gentle, on CT, MRI,
MRCP, and ERCP like soft rattan, it is the so-­
called soft rattan sign. The incidence of malig-
nant biliary obstruction is the highest.
Explanation
When a tumor causes complete obstruction of the
bile duct in a short period of time, cholestasis
may cause the bile duct above the obstruction to
be uniformly expanded and may reach hepatic
capsule. Because tube wall is still soft, it shows
the soft rattan shape. The soft rattan sign suggests
more acute obstruction. The cause is generally
more common in fast-growing tumors, such as
pancreatic carcinoma and cholangiocarcinoma,
but other lesions can also cause similar changes
(Fig. 5.28).
Discussion
The normal intrahepatic bile duct cannot be dis-
played. If it can be shown, its diameter is only
1–3  mm; when intrahepatic bile duct diameter
reaches 5  mm, it is considered the bile duct is
210
Fig. 5.28  In a 56-year-old woman with ampullary can-
cer, MRCP shows dilatation of the common bile duct,
common hepatic duct, intrahepatic bile duct, and pancre-
atic duct
slightly dilated; 6–8 mm is moderate expansion;
and up to 9 mm is severe expansion. The normal
common hepatic duct and common bile duct are
more than 1 cm in diameter. Clinically, the site of
biliary obstruction is divided into four segments:
(1) the hepatic portal segment refers to the hepatic
left and right tube and common hepatic duct seg-
ment; (2) the upper pancreatic segment is the
common bile duct before entering the pancreas;
(3) the pancreatic segment is the common bile
duct segment through the pancreatic tissue; and
(4) ampulla segment refers to the bile duct seg-
ment below the pancreatic segment [70].
Common causes of biliary obstruction include
bile duct tumors, stones, and inflammation. The
former are mostly malignant lesions whereas the
latter are benign lesions. With malignant obstruc-
tion in the upper pancreatic segment and the
hepatic portal segment, first consider cholangio-
carcinoma, followed by lymphatic metastasis;
pancreatic carcinomas are common in the head of
the pancreas, and ampullary carcinoma are com-
mon in the ampulla [71]. Malignant signs: (1) the
soft rattan sign refers to the expansion of the
intrahepatic bile duct, which is soft, shaped like
soft rattan, with the highest incidence in malig-
nant biliary obstruction; (2) the emptiness sign,
X. Li et al.
originally proposed in ERCP, but also applying to
MRCP images, is characterized by extreme dila-
tation of the bile duct above the lesion, soft
rattan-­like dilatation of the intrahepatic bile duct,
normal development of the bile duct below the
lesion, and no development of the hepatic portal
bile duct, which causes the hepatic portal bile
duct filling defect to be emptied; and (3) the trun-
cation sign is characterized by a sudden narrow-
ing or disappearance of the dilated bile duct.
When the hepatic portal biliary obstruction is
present, in the higher position, the intrahepatic
bile duct is dilated like arborization, also called
the residual root sign. (4) The double duct sign:
manifested as expansion of common bile duct
and pancreatic duct at the same time, this indi-
cates that the obstruction point is relatively low,
which is more common in pancreatic head carci-
noma, ampullary carcinoma, and duodenal papil-
lary carcinoma; and (5) soft tissue mass shadow:
most data suggest that soft tissue mass and sud-
den interruption of dilated common bile duct are
the definite basis for the diagnosis of malignant
biliary obstruction.
Ultrasound, CT, or MRI are the main imaging
modalities for biliary obstruction, but PTC and
ERCP are still reliable methods. CT shows bile
duct dilatation with accuracy of 98% to 100%.
MRI shows intrahepatic, external bile duct diam-
eter increased, with hypointensity on T1WI and
hyperintensity on T2WI. MRCP can be seen from
the hilar to the periphery of the liver from high to
small hyperintensity dilatation of the bile duct,
and can be observed from multiple aspects of the
dilated biliary obstruction at the lower end of the
biliary obstruction site [72]. The soft rattan sign
is caused by obstruction in a short period of time
of progressive aggravation, progressive increase
in bile duct pressure, which leads to small bile
duct cavity enlargement and small bile duct wall
thinning. The bile duct wall is still soft and elas-
tic, and the bile duct above the obstructive end is
obviously dilated, with flexion and extension,
showing a lotus-root shape. The appearance of
the soft rattan sign highly suggests the existence
of aa malignant tumor in the corresponding site
of obstruction. Although soft rattan sign is an
important sign of malignant obstruction, it is not
5  Solid Organs of Upper Abdomen
a specific sign. A few benign obstructions can
also appear as soft rattan sign.
5.29 Double Duct Sign
Feature
In MR cholangiopancreatography (MRCP), the
common bile duct and pancreatic duct are simul-
taneously dilated, called the double duct sign.
This sign can also be seen in endoscopic retro-
grade cholangiopancreatography (ERCP), CT
with curved multiplanar reformats, and
ultrasonography.
Explanation
This sign is usually caused by the pancreatic head
tumor obstruction and embedding in common
bile duct and main pancreatic duct. Double duct
stenosis of the common bile duct and pancreatic
duct causes simultaneous dilatation of the double
duct (Fig. 5.29).
Discussion
“Double duct sign” was first reported by Freeny
et al. in 1976 [73]. It was characterized by simul-
taneous dilatation of the common bile duct and
pancreatic duct in ERCP. It is usually caused by
the pancreatic head tumor obstruction and
embedding the common bile duct and main pan-
creatic duct. The two most important causes of
double duct sign are pancreatic head cancer and
ampullary carcinoma. Other malignant lesions
Fig. 5.29  A 46-year-old woman with cholangiocarci-
noma. MRCP shows dilatation of common bile duct and
main pancreatic duct with double duct sign
211
include cholangiocarcinoma, lymphoma, or
metastases at the distal end of the common bile
duct. Benign lesions include chronic pancreatitis
and ampullary stenosis; primary retroperitoneal
fibrosis and Kaposi sarcoma are rare causes, only
reported in a few cases [74]. Because early symp-
toms of pancreatic head cancer are more insidi-
ous, early diagnosis of resectable lesions is more
difficult. Its characteristic image manifestation is
the double duct sign caused by the narrowing and
obstruction of the pancreatic duct and common
bile duct. Most pancreatic malignancies are ade-
nocarcinomas and are intraductal growth, usually
manifesting as a local mass of the head of the
pancreas. In pancreatic head cancer, 62% to 77%
of cases have double duct sign, but even though
the pancreatic duct is not expanded, we cannot
exclude the diagnosis of pancreatic head cancer,
because the pancreatic duct diameter is normal in
20% of pancreatic malignant tumors. Smaller
ampullary carcinoma can cause significant bile
duct dilatation, and 52% of cases have double
duct sign. Pancreatic cancer, ampullary carci-
noma, and distal common bile duct cancer some-
times present difficulties in differential diagnosis.
Tumors of ampullary carcinoma have different
enhancement from pancreatic cancer in enhanced
scans, whereas pancreatic head cancer has double
duct sign and truncated changes. In addition,
ampullary carcinoma rarely involves the postpan-
creatic fat gap and the fat layer between the supe-
rior mesenteric artery and the uncinate process.
Pancreatic body atrophy is rare and can be dif-
ferentiated from pancreatic cancer [75].
MRCP has a good shape and localization of
pancreaticobiliary obstruction, and catheter mor-
phology is useful in qualitative assessment. When
obstruction or stenosis is suddenly interrupted,
especially the irregular edge of the wall, 78%
were malignant lesions [76]. Progressive inter-
ruption or stenosis, especially the smooth edge of
the wall, is mostly a benign lesion. In short, the
double duct sign is an important sign. In the clini-
cal view, if there is a double duct sign, it can be
highly suggestive of pancreatic malignant tumor,
but it is not an absolute diagnosis. It is necessary
to make a correct diagnosis by combining rele-
vant medical history and other signs.
212
5.30 Teardrop Superior
Mesenteric Vein Sign
Feature
On postcontrast CT or MRI, the normal round
superior mesenteric vein is compressed by tumor
tissue and becomes teardrop, linear, or oval in
shape.
Explanation
The portal vein is composed of the splenic vein
and superior mesenteric vein, which converge
behind the head of the pancreas. On axial CT,
fatty tissue separation is seen between the normal
pancreatic head or uncinate process and superior
mesenteric vein. When pancreatic head cancer
occurs, it can invade the surrounding area, break
through the fatty layer, and infiltrate the sur-
rounding blood vessels. When the superior mes-
enteric vein is directly infiltrated by cancer tissue
or stretched by surrounding fibrous connective
tissue, the circular section of the normal superior
mesenteric vein can be changed into a teardrop,
linear, or oval shape and the fat gap between
tumor and superior mesenteric vein disappears.
This sign is called the teardrop superior mesen-
teric vein sign (Fig. 5.30).
Discussion
Pancreatic cancer is a solid tumor with poor blood
supply and no envelope. It is characterized by
a b
Fig. 5.30  A 67-year-old woman with pancreatic cancer.
On postcontrast CT venous phase, a decreased attenuation
mass was seen in the pancreatic head (a), with compres-
X. Li et al.
invasive growth, easily spreading and involving
adjacent organs and blood vessels, with lymph
node and distant organ metastasis. Surgical resec-
tion of pancreatic cancer is considered the only
radical treatment. Before the superior mesenteric
artery is involved, pancreatic head cancer invades
the portal vein or superior mesenteric vein. The
invasion of portal vein or superior mesenteric vein
is a contraindication for pancreatoduodenectomy.
The role of the invasive degree of the peripancre-
atic vein structure in evaluating the resectability
of pancreatic head cancer has gradually attracted
more and more attention. Invasion of the portal
vein or superior mesenteric vein is no longer a
contraindication. According to the recent radiol-
ogy reporting guideline for pancreatic ductal ade-
nocarcinoma, venous involvement should be
described in terms of the tumor–vein interface
(TVI); that is, values of 180° or less are defined as
“abutment; resectable,” whereas those greater
than 180° are referred to as “encasement; border-
line or unresectable” [77]. A recent study showed
that TVI and tumor size, determined using preop-
erative CT, were independently associated with
histopathological portal vein–superior mesenteric
vein (PV-SMV) invasion in patients with pancre-
atic head cancer. Histopathological PV-SMV
invasion did not significantly affect overall sur-
vival after surgery [78].
When applying the teardrop superior mesen-
teric vein sign to evaluate the unresectability of
sion of adjacent superior mesenteric vein and meeting
with splenic vein, forming a teardrop superior mesenteric
vein sign (b)
5  Solid Organs of Upper Abdomen 213

pancreatic head cancer, the following points

should be noted. (1) When advanced pancreatic
head cancer has extruded into the superior mes-
enteric vein and presented annular stenosis or
complete occlusion, it could present a false-­
negative, so it must be combined with other unre-
sectable signs to improve sensitivity and accuracy.
(2) The partial volume effect of CT is caused by
vascular alignment for teardrop superior mesen-
teric vein sign, especially at the transition of
superior mesenteric vein and portal vein, where
the superior mesenteric vein transits from the XY
plane to z-axis plane. Superior mesenteric vein
deformation is best demonstrated on T1WI.
Fig. 5.31  Duct-penetrating sign in pancreatic head mass
Superior mesenteric vein deformation is consid- chronic pancreatitis
ered as a useful sign of unresectable pancreatic
head cancer.
is also called mass chronic pancreatitis. It is an
important imaging sign used to differentiate from
5.31 Duct-Penetrating Sign PC. Ichikawa et al. classified the pancreatic duct
into four types according to the shape and dila-
Feature tion of pancreatic duct on MRCP [80]: type I,
On MRCP, there is a smooth perforation of the main pancreatic duct obstruction, with or without
main pancreatic duct in the pancreatic mass, thickening of the upper main pancreatic duct;
which is the duct-penetrating sign. type II a, narrowing of the main pancreatic duct
tumor segment with irregular wall; type II b, nar-
Explanation rowing of the main pancreatic duct tumor seg-
The duct-penetrating sign is a smooth stenosis or ment without irregular duct wall; type III, the
no abnormality in the main pancreatic duct pass- whole main pancreatic duct is dilated without
ing through the inflammatory mass (Fig. 5.31). clarity; and type IV, true stenosis, normal main
pancreatic duct. Type II and type IV are generally
Discussion positive for pancreatic duct penetration sign, sug-
Differential diagnosis of pancreatic carcinoma gesting IPM, whereas type I and type III are
(PC) and inflammatory pancreatic mass (IPM) mostly suggestive of pancreatic malignant
has always been a tough clinical problem. tumors.
Conventional CT, MRI, and ultrasonography Quantitative MRI is of great significance in
have difficulty in distinguishing the two; some- differential diagnosis between IPM and choroid
times diagnosis is difficult with surgical explora- plexus carcinoma. Niu et  al. found DWI had
tion and even pathological biopsy. MRCP can important significance in differentiating PC from
visually display the pancreaticobiliary tree, accu- IPM [81]. Cho et al. found lipid peaks on MRS of
rately display the shape, extent, and extent of IPM patients decreased and other metabolites
obstruction and dilation of pancreaticobiliary peaks increased [82]. MRI is of great value in the
duct, and the shape of the obstruction end, thus diagnosis of IPM: it not only can assess physio-
providing a powerful aid for the differential diag- logical and pathological changes of pancreatic
nosis of pancreaticobiliary duct diseases [79]. It parenchyma, but also detects exocrine function
is the characteristic manifestation of IPM, which and blood perfusion of the pancreas.
214
5.32 Central Dots Sign
Feature
One CT sign of Caroli’s disease is a small round
dot shadow in the cystic dilatation of the bile
duct. Its density is less than or equal to the sur-
rounding liver parenchyma, although higher than
the surrounding liver parenchyma after enhance-
ment; this is called the central dots sign.
Explanation
The pathological basis for the formation of the
central dots sign is the axial projection of portal
venous branch surrounded by dilated intrahepatic
bile duct with congenital abnormal development,
which is then involuted into dilated intrahepatic
bile duct (Fig. 5.32).
Fig. 5.32 Longitudinal hepatic sonogram (a), axial
contrast-­enhanced CT (b), axial contrast-enhanced T1WI
(c), and T2WI reveal multifocal, segmental, cystic dilata-
X. Li et al.
Discussion
Central dot sign is suggested as a pathognomonic
finding of Caroli disease (CD). Caroli disease is a
rare, autosomal recessive disorder characterized
by communicating cavernous biliary ectasia. It
comprises two entities: the pure form, or Caroli
disease, and a form associated with periportal
fibrosis, also known as the Caroli syndrome.
Caroli syndrome is a combination of Caroli dis-
ease with congenital hepatic fibrosis. The clini-
cal course is usually asymptomatic for the first
5 to 20  years of life, and symptoms may sel-
domly occur throughout the patient’s life. Bile
statis leads to recurrent episodes of cholangitis,
stone formation, or liver abscesses, and biliary
cirrhosis usually occurs years later [83]. Cases
of this pure form of Caroli disease are uncom-
tion of the intrahepatic bile ducts with enhancing central
dot sign (arrows) and multiple calculi (asterisks) [85]
5  Solid Organs of Upper Abdomen
mon, and most patients have coexisting hepatic
fibrosis [84].
On imaging, Caroli disease demonstrates
multifocal, segmental, saccular or fusiform cys-
tic intrahepatic biliary dilatation. These dilated
bile ducts can contain calculi or biliary sludge.
The central dot sign, representing a portal vein
branch protruding into the lumen of a dilated
bile duct, can be seen with ultrasound, CT, and
MRI.  On CT scans, pontal radicles seem to be
within the lumina of dilated bile ducts. However,
they are not within the bile ducts but are sur-
rounded by abnormally developed ectatic bile
ducts. The central fibrovascular bundle enhances
after contrast administration. Presence of the
central dot sign is highly suggestive of Carolis
disease, helping to differentiate it from other
causes of intrahepatic biliary dilatation such as
primary sclerosing ­ cholangitis and recurrent
pyogenic cholangitis [85]. Treatment of CD
depends on the clinical symptoms and location
of the biliary abnormalities. Potential curative
treatment of CD is surgical resection, such as
segmentectomy, lobectomy, or hepaticojejunos-
tomy, determined by the range of distribution
[83].
5.33 Central Arrowhead Sign
Feature
Central arrowhead sign is a CT sign of suppura-
tive cholangitis that shows dilatation of the first
and second branches of the intrahepatic bile duct
although the surrounding bile ducts are not
dilated. The dilated intrahepatic bile ducts are
aggregated and the endings can show an arrow-
head shape.
Explanation
In suppurative cholangitis, asymmetrical or
localized dilated bile ducts are often manifested
in the first or second branches of intrahepatic
bile ducts, with gas or pus in the bile ducts,
whereas peripheral bile ducts lose the ability to
dilate, presenting as a central arrowhead sign
(Fig. 5.33).
215
Fig. 5.33  Coronal reformatted CT demonstrates dilata-
tion of first- and second-order ducts (arrows) with relative
sparing of peripheral biliary tree. Multiple intraductal cal-
culi are also seen (arrowhead) [86]
Discussion
Suppurative cholangitis is often caused by bile
duct obstruction and biliary tract infection. The
most common obstruction is bile duct stones.
Biliary inflammatory stenosis is also an impor-
tant factor causing the disease. The main types
of infecting bacteria are gram-negative bacilli,
most commonly Escherichia coli, Proteus spp.,
and Pseudomonas aeruginosa. Most patients
have a history of recurrent episodes. Acute epi-
sodes are characterized by epigastric pain,
chills, fever, jaundice, and even coma and
death [87].
Purulent cholangitis has relatively characteris-
tic CT findings. CT is effective and ideal for
purulent cholangitis. CT can show obstruction
site, etiological lesion range, extent of bile duct
dilatation, bile duct pneumatosis and/or p­ yogenia,
and liver involvement. It can reflect various path-
ological indications of purulent cholangitis.
Suppurative cholangitis has characteristic CT
findings. (1) Hepatobiliary dilatation: intrahe-
patic bile duct dilatation often presents asym-
metrical or localized distribution, with the left
lobe obvious; dilated intrahepatic bile duct is
aggregated, and bile duct dilatation often mani-
fests in the first and second branches of intrahe-
patic bile duct, while peripheral biliary
inflammatory fibers lose the ability to dilate,
manifested as central arrowhead sign.
216
Extrahepatic bile duct dilatation is also common
and varied in degree. The postcontrast enhance-
ment density of the intrahepatic bile duct wall is
higher than that of hepatic parenchyma, which
often indicates acute attack, and diffuse eccentric
thickening of bile duct wall can be seen. (2) Liver
abscess: because of infection of the bile duct, and
infiltration of inflammatory cells around it, a
large number of neutral polynuclear cells in the
hepatic sinus, forming a small abscess, single or
multiple, so single or multiple hepatic abscess is
also one of the common manifestations. After
enhancement, the abscess wall and its septa are
enhanced. (3) Limited hepatic atrophy: as a result
of repeated inflammatory obstruction and
destruction, the volume of hepatic parenchyma is
reduced and the liver segment atrophied locally,
especially in the left liver. Limited hepatic paren-
chyma density decreased from fat infiltration in a
small number of patients, such as homogeneous
or heterogeneous hepatic parenchyma that
enhanced significantly after enhancement, sug-
gesting the development of acute suppurative
inflammation. (4) Gas in the bile duct: diffuse or
limited, more common in the left lobe of liver
and associated with three factors, namely, a his-
tory of choledochojejunostomy, Odd’s sphincter
insufficiency, and pneumonia infection. (5)
Cholangiolithiasis: multiple, predisposing in the
left lobe of the liver, especially the outer part. The
stone is sandy or large pebble like. Most patients
with suppurative cholangitis have intrahepatic
bile duct stones, accompanied by or without
extrahepatic bile duct stones, which indicates
suppurative cholangitis and bile duct stones are
causal and closely related [86].
5.34 Golf Ball-on-Tee Sign
Feature
Golf ball-on-tee sign is seen during excretory
urography and appears as a contrast agent-filled
cavity (the golf ball) that lies adjacent to a blunted
calyx (the tee).
X. Li et al.
Explanation
Collecting tubules within the medullary pyramid
come together to form papillary ducts that pene-
trate the papillary tip and drain into a calyx. In
renal papillary necrosis, however, central necro-
sis and sloughing of papillae create a cavity,
which is occasionally large, filling with contrast
material and communicates with a calyceal con-
cavity. Thus, golf ball-on-tee sign is created, indi-
cating necrosis. The renal papillary tip is still
within the sunken calyces. The calyx is filled
with contrast agent to form a signet sign
(Fig. 5.34).
Discussion
The “golf ball-on-tee” describes imaging find-
ings that signify renal papillary necrosis. Once
opacified with contrast material, the central cal-
yceal cavity (the “golf ball”) appears to rest on
the calyx (the “tee”). Although this sign origi-
nally was described at excretory urography, now
the findings are most often seen on CT.  Other
“classic” imaging patterns of papillary excava-
tion seen in papillary necrosis include the “lob-
ster claw” and “signet ring” appearance [88].
The lobster claw sign is seen in the papillary
form of renal papillary necrosis on excretory
urography or CT urography (CTU). Necrosis of
the papilla causes the fornices of the minor
calyx to elongate, creating the impression of a
lobster claw. Eventually the fornices may even
communicate all the way around the necrotic
papilla, creating a signet ring [89]. The common
etiology of papillary necrosis can be conve-
niently remembered with Dunnick’s mnemonic
NSAID: nonsteroidal antiinflammatory medica-
tions, sickle cell hemoglobinopathies, analgesic
nephropathy (specifically aspirin and phenace-
tin), infection (specifically tuberculosis), and
diabetes. Some less common causes include
renal vein t­ hrombosis, hypotension, and obstruc-
tive uropathy. The papillary necrosis seen in
tuberculosis and severe pyelonephritis is a direct
result of infection. The pathophysiology of pap-
illary necrosis seen in other diverse group of
5  Solid Organs of Upper Abdomen
a b
Fig. 5.34 (a) Golf ball-on-tee sign. Axial CT image dur-
ing excretory phase imaging shows a large lower pole
papillary cavity in the left kidney with the golf balloon-tee
appearance (arrow). (b) Coronally reconstructed image
diseases appears to be ischemia to the papillae.
The medullary papillae are especially suscepti-
ble to ischemic insult because of low oxygen
tension, high blood osmolality, and relatively
poor perfusion in the papillary tips [90]
(Fig. 5.35).
The radiologic appearance of papillary
necrosis depends on the severity and chronicity
of the necrosis [91]. The earliest and most subtle
changes result in papillary swelling (necrosis in
situ) that is often impossible to observe radio-
logically without serial urograms. These papil-
lae often shrink over time and may calcify (as in
medullary nephrocalcinosis); the calcification
217
during the excretory phase in the same patient shows the
classic “golf ball-on-tee” appearance in multiple calyces
(arrows) [88]
may sometimes be detectable on a conventional
radiograph. Progressive necrosis may result in
interruption of the uroepithelial lining of the
calyx. If the cavitation is central, as in the fig-
ure, the contrast agent will fill the medullary
cavity adjacent to the calyceal concavity. As the
necrotizing process proceeds (especially if the
inciting factor is not removed), the cavity may
enlarge, and create a radiographic appearance
that resembles a golf ball on tee. Eccentric
necrosis that originates at the margin of the
papilla will cause irregular cavitation at the
margin of the papilla and make the angle of the
calyx appear elongated, which may result in a
218
a b
Fig. 5.35  A 22-year-old woman with tuberculosis of the
kidney. (a) The golf ball-on-tee sign is seen in the papil-
lary form of renal papillary necrosis on excretory urogra-
phy. Necrosis of the papilla causes the fornices of the
“lobster claw” deformity. If the necrotic papilla
is sloughed or resorbed, the resultant calyx will
be blunted. The entire papilla or portions of it
may be retained, in which case contrast material
will surround the unextruded papillary tip,
resulting in circular or irregular filling defects.
The peripheral portions of these necrotic papil-
lae may calcify. In conclusion, the golf ball-on-
tee sign is part of the spectrum of papillary
necrosis and is distinguished by a papillary cav-
ity that lies adjacent to a blunted calyx.
Diagnosing papillary necrosis by recognizing
the golf ball-on-tee sign is important for pre-
X. Li et al.
minor calyx to elongate, creating the sign. (b, c) Renal
papillary necrosis on CT intravenous pyelogram with
excavation of the calyces gives the appearance of a lobster
claw [89]
serving renal function because many of the
causes of papillary necrosis are treatable.
5.35 Calyceal Crescent Sign
Feature
Calyceal crescent sign is seen in the early stages
of intravenous pyelography (IVP). It appears as a
crescent-shaped contrast agent density, gradually
secretes into the renal pelvis system with the con-
trast agent, and disappears on subsequent con-
trast films.
5  Solid Organs of Upper Abdomen
Explanation
When chronic obstruction and hydronephrosis
occur, the expansion of renal pelvis causes com-
pression and deformation of papilla, and the nip-
ple flattens and eventually turns over, resulting in
a significant change in the direction of the col-
a b
Fig. 5.36 (a) IVP shows calyceal crescent sign (thin
arrow) in the left kidney. (b) The calyceal crescent sign
gradually disappeared at 2  min and the contrast agent
219
lecting tube. An increase in intrarenal pressure
increases the filtration time through tubules,
resulting in an increase in urine content as it
passes through the collection tube. These changes
explain X-ray features of the calyceal crescent
sign (Fig. 5.36).
gradually secreted into the renal pelvis. (c) Contrast agent
was excreted into the whole renal pelvic system at 90 min
220
Discussion
The calyceal crescent sign was proposed and sys-
tematically explained by Khanna in 2005 [92]. In
mild hydronephrosis, the local development of
the renal pelvis is visually called calyceal cres-
cent sign. Its essence is caused by hydronephro-
sis, which causes the valgus of the renal pelvis to
displace the collecting duct of the renal papilla,
dilate and deform, and rearrange it parallelly
around the valgus pelvis. It is the exact indication
of hydronephrosis from the filling of contrast
medium. It is also the exact indication of delayed
development of urinary tract obstructive disease.
The signs appeared earlier. Calyceal crescent
sign can be seen in hydronephrosis caused by
obstruction at the junction of the pelvis and ureter
or at the end of the ureter. Many causes can cause
obstruction of the pelvic–ureteral junction, such
as an abnormal ureter itself, dilatation and abnor-
mal peristalsis caused by defective muscles,
obstruction of the lumen caused by ureteral
valves, and polyps or abnormal renal vessels.
X-ray radiography of hydronephrosis patients
often shows various degrees of pyelomegaly,
accompanied by poor emptying of the renal pel-
vic system. In more severe cases, thin renal
parenchymal bands can be seen during renal
imaging to delineate dilated undetected calyces.
Contrast agents in dilated or rearranged collect-
ing ducts can be distributed along the outer edge
of the calyces and show calyceal crescent sign.
The calyceal crescent sign needs to be differenti-
ated from normal papillary staining of the normal
collecting duct during IVU with hypoosmotic
contrast agent [93]. As a common and frequently
occurring disease of the urinary system, IVP is
often used as the preferred choice for hydrone-
phrosis in clinical practice. IVP has the advan-
tages of simple, low price and many years of
clinical practice. It is a mature examination
method, but its false-positive rate and missed
diagnosis rate are higher. With the development
and application of imaging equipment in clinic,
the advantages of CTU and magnetic resonance
urography (MRU) in urinary hydronephrosis are
becoming more and more obvious. The presence
of calyceal crescent sign is considered a sign of
increased intrapelvic pressure, suggesting that
X. Li et al.
delayed radiography should be performed and
other imaging modalities are needed to better
demonstrate the collective system and to deter-
mine the etiology of an obstruction [93].
5.36 Cortical Rim Sign
Feature
Renal infarction showing low density of infarct
organs and linear high-density shadow around
the cortical edge of infarcted kidney tissue on
postcontrast CT.
Explanation
Cortical rim sign is a characteristic manifestation
of renal infarction and represents the enhance-
ment of the undamaged cortex under the capsule,
which is the part of renal parenchyma that pro-
vides blood supply from perirenal capsule
(Fig. 5.37).
Discussion
In 1974, Frank et al. [94] first described the corti-
cal rim sign with a high-density ring around the
infarcted kidney tissue on CT.  Postcontrast CT
has a higher contrast resolution, and it is easier to
see the cortical rim sign. It is characterized by a
high-density margin 2–4  mm thick under the
renal capsule with a smooth edge. The cortical
rim sign may be continuous or discontinuous,
and the discontinuous sign may be caused by a
Fig. 5.37 Postcontrast CT of a 35-year-old woman
shows low density of the left renal infarction with linear
high-density shadow, which is the cortical rim sign
(arrow)
5  Solid Organs of Upper Abdomen
discontinuous capsule plexus after trauma. The
cortical rim sign, seen in about 50% of acute
renal infarctions, is relatively specific to this con-
dition and believed to result from intact renal col-
lateral circulation following a vascular insult,
such as renal artery thrombosis or embolization,
renal artery dissection or renal trauma. Acute
renal infarction can be cardiogenic or noncardio-
genic in origin. In patients with noncardiogenic
acute renal infarction who have no apparent risk
factors (e.g., thromboembolism, coagulation dys-
function, hematological diseases), the cause
often remains elusive [95].
Studies have shown that the cortical rim sign
does not appear immediately after renal infarc-
tion, but the sign can appear about 1 week later,
become most obvious at 2 weeks, and disappear
after 8 weeks. Yoshiro et al. reported that the cor-
tical rim sign appeared after 7  days of vascular
occlusion, and the sign disappeared after the
involvement of renal parenchyma began to sig-
nificantly scar. The collateral circulation of the
kidney is always present, and blood supply is
provided by the renal capsule system, peripel-
vicular system, and the periureteral system. After
acute renal artery occlusion, the collateral circu-
lation responds immediately, increasing blood
flow through vasodilation. No evidence of the
cortical rim sign was found on CT after trauma
and the infarction could not be ruled out, because
it occurred 8  h to 1  week after trauma. Acute
infarcts typically appear as wedge-shaped areas
of decreased attenuation within an otherwise
normal-­ appearing kidney. The parenchymal
appearance depends on the size of the embolus,
the location of the arterial occlusion, and its age.
When large areas of the kidney are involved, an
increase in the size of the kidney caused by
edema can be seen. In global infarction, the entire
kidney is enlarged and its reniform configuration
remains preserved. The extent and degree of
parenchymal loss reflect the distribution of the
affected artery and revascularization from collat-
eral circulation [96]. Differential diagnosis for
the imaging appearance of renal infarction
includes pyelonephritis. However, in kidney
infection, neither the “cortical rim sign” nor
“flip-flop enhancement” is found on CT [97].
221
5.37 Renal Halo Sign
Feature
Normally, the internal boundary of perirenal fat
is clearly shown on the abdominal X-ray,
although the external boundary is not clear. On
the abdominal X-ray, the inner and outer bound-
aries of the perirenal fat space can be clearly seen
when effusion is accumulated in the anterior
renal, so that the perirenal fat space appears as a
ring-shaped low-density shadow, which resem-
bles a halo.
Explanation
When the retroperitoneal disease causes inflam-
matory exudate to accumulate in the prerenal
space, the external boundary of the perirenal fat
gap can be clearly displayed by the obvious dif-
ference in the absorption rate of X-rays between
inflammatory exudate and perirenal fat. At this
time, the perirenal fat gap appears on the X-rays
as a ring-shaped low-density shadow with a clear
boundary, so it is called the renal halo sign. This
sign is most common in acute pancreatitis
(Fig. 5.38).
Discussion
The retroperitoneal space refers to the gap
between the wall peritoneum and the transverse
fascia and its anatomical structure. The prerenal
fascia, the posterior fascia, and the lateral verte-
bral fascia divide the retroperitoneal space into
three parts: the anterior renal space, the perire-
nal space, and the posterior renal space. The
anterior renal space is located between the prer-
enal fascia and the posterior wall peritoneum,
and the lateral side is located in the lateral verte-
bral fascia, which mainly contains the pancreas.
The perirenal fascia is located between the prer-
enal fascia and the posterior fascia, which
mainly contains the adrenal gland and the kid-
ney. The posterior renal space is located between
the posterior fascia and the transverse fascia,
and contains only adipose tissue. Although the
three posterior retroperitoneal spaces are ana-
tomically intact, there is potential traffic
between them, and one gap lesion can affect the
others.
222
Fig. 5.38  A plain radiograph of the abdomen (a) and cor-
responding radiograph from an excretory urogram (b)
show a radiolucent halo about the left kidney. Contrast
enhancement (b) of the perirenal (Gerota) fascia has
Normally, the internal boundaries of the peri-
renal fat spaces are clearly shown on the abdomi-
nal X-ray because of the different X-ray
absorption rates of the parenchyma and perirenal
fat. The external boundary of the perirenal fat
space is not clearly shown on X-ray because of
the lack of contrast between the perirenal fat and
the pararenal retroperitoneal fat fusion.
Inflammatory exudates caused by retroperitoneal
disease accumulate in the prerenal space, because
inflammatory exudates and perirenal fat absorb
significantly different X-rays, so the perirenal fat
space can be clearly shown outside; at this time
perirenal fat space on the X-ray features of a clear
border ring low-density shadow, known as the
renal halo sign. Susman, through a series of
abdominal X-ray and CT studies of acute pancre-
atitis, proposed a renal halo sign [98]. The
appearance of the renal halo sign suggests that
there is more fluid accumulation in the retroperi-
toneal space, especially in the prerenal space,
thus indirectly suggesting the presence of acute
pancreatitis. This sign is usually seen on the left
X. Li et al.
resulted from acute inflammation. The left psoas shadow
is obliterated. An impression on the bladder from the left
(b) is caused by extension of inflammatory process retro-
peritoneally into the pelvis
side, rarely on the right side [99]. However, the
presence of renal halo sign is not a specific sign
of pancreatitis; retroperitoneal bacterial inflam-
mation, traumatic hematoma, and disseminated
lymphoma completely invading the perirenal fas-
cia can also occur with renal halo sign, so it also
needs to be distinguished from acute pancreatitis.
When the abdominal X-ray shows renal halo
sign, combined with the typical clinical features,
it should be initially diagnosed as acute pancre-
atitis. The renal halo sign is a sign on X-ray that
is manifested as a perirenal halo sign on
CT. Perirenal halo sign indicates that the extent
of retroperitoneal inflammatory expansion has
reached the perirenal adipose layer, and Balthazar
grade can reach grade E [100]. It is a reliable
diagnostic criterion for acute necrotizing pancre-
atitis, suggesting that the perirenal fascia has
been broken through. The perirenal halo sign can
also be seen in renal diseases such as renal lym-
phoma and abscess. Perirenal halo sign is one of
the CT signs of complications of acute necrotiz-
ing pancreatitis (ANP).
5  Solid Organs of Upper Abdomen
5.38 Perirenal Halo Sign
Feature
On CT, the anterior renal fascia thickened, the
anterior pararenal space is exuded, and the peri-
renal space fat density is replaced by halo-like
low-density shadows. The low-density shadows
had a higher CT value, which could exceed 25
Hu.
Explanation
The perirenal halo sign is one of the CT signs of
complications of acute necrotizing pancreatitis.
In ANP, loose connective tissue inflammation is
caused by extravasation of proteinase containing
pancreatic fluid, often occurring in the tail of the
pancreas, presenting as prerenal fascia thicken-
ing, penetrating renal fascia involving the perire-
nal fat layer, forming the perirenal halo sign
(Fig. 5.39).
Discussion
CT findings of acute pancreatitis depend on the
severity and extent of the inflammatory process.
A CT scan that is performed within the first 48 h
of the onset of symptoms may be completely nor-
mal. CT findings of acute pancreatitis include
enlargement of the pancreas (localized or dif-
fuse), poorly defined parenchymal contours, and
decreased density and inhomogeneity of the pan-
Fig. 5.39  In a male patient with acute pancreatitis, the
anterior renal fascia was thickened (left), and the anterior
pararenal space exuded on abdominal CT
223
creatic parenchyma and fluid collections in the
peripancreatic region. The inflammatory reaction
can produce increased attenuation of the peripan-
creatic fat tissue, commonly described as “strand-
ing.” The inflammatory process is usually
diffused and involves all the gland [101].
The inflammatory process in acute pancreati-
tis usually expands toward the left of the pancre-
atic tail and the left pararenal space. A relative
decrease in the density of the perirenal fat tissue
caused by an increase in the density of Gerota
fascia and the pararenal space resulting from the
inflammatory process leads to the “renal halo”
sign [102]. The perirenal halo sign indicates that
the retroperitoneal inflammatory extension has
reached the perirenal adipose tissue; Balthazar
grade can reach grade E. It is a reliable diagnostic
and grading sign of acute necrotizing pancreati-
tis. Renal halo sign is a sign of abdominal plain
film before perirenal fat; the adjacent inflamma-
tion exudation absorption rate is different, result-
ing in plain film that can clearly show the
perirenal fat peripheral edge, the performance of
abdominal plain film on the perirenal light, sug-
gesting acute pancreatitis. The renal halo ring
sign on CT is the loose connective tissue inflam-
mation in the renal anterior space, presenting as
effusion and exudation. The perirenal halo sign is
loose connective tissue inflammation in the peri-
renal adipose tissue, suggesting that the perirenal
fascia has broken through. The perirenal halo
sign can also be seen in renal diseases, such as
renal lymphoma and abscess. The imaging mani-
festations of renal lymphoma depend on the pro-
liferation pattern of the tumor. Because malignant
lymphocytes are easily disseminated through the
bloodstream, they can proliferate in the intersti-
tium and spread to the retroperitoneal cavity or
other adjacent tissues after dissemination to the
renal parenchyma. If the malignant lymphocytes
grow or proliferate infiltratively along the normal
interstitial tissue in the kidney, the normal shape
of the kidney will not change; only the volume of
the kidney will increase. If the malignant lym-
phocytes show focal proliferation, it would
destroy the adjacent renal parenchyma to form
swelling or nodular lesions, which could occur
unilaterally or bilaterally. If a large number of
224
small lesions of the tumor merge, it will destroy
the kidney shape and cause the change of the
wheel.
5.39 Perirenal Cobwebs Sign
Feature
The perirenal cobwebs sign refers to the fibrous
curve high-density shadow of the medial perire-
nal interspace of Gerota’s fascia caused by vari-
ous pathological conditions.
Explanation
The perirenal cobwebs sign originally referred to
the collateral vessels in the perirenal space in
patients with renal vein thrombosis. Perirenal fat
contains peritoneal perforator arteries and veins,
which anastomose with the branches of adrenal
vessels, superior and inferior mesenteric vessels,
and gonadal vessels. When these vessels do not
dilate, they are hard to see on conventional CT
scans; however, they clearly appear to show
enhanced perirenal cobwebs sign (Fig. 5.40).
Discussion
In 1981, Winfield et al. coined the term “perire-
nal cobwebs” to describe vermiform curvilinear
densities observed around the kidney on CT
[103]. Perirenal cobwebs were initially attrib-
uted to collateral vessels seen in the perinephric
Fig. 5.40 (a, b) In a 68-year-old man, noncontrast CT shows the fibrous curve high-density shadow of double kidneys,
which is the perirenal cobwebs sign
X. Li et al.
space in patients with renal vein thrombosis. As
our ­ability to image the perinephric space with
CT improved, it became clear that numbers of
disease processes were manifested by develop-
ment of prominent perinephric structures [91].
The renal interspace is not a simple, undivided
fat interspace, but is composed of multiple
fibrous divisions. Tumors or inflammation within
the anterior renal interspace often extend along
and thicken Gerota’s fascia, and the dense renal
capsule is similarly demarcated. Fluid, inflam-
matory tissue, and invasive neoplasms may all
enter along the blood vessels through the weak-
ness of the perirenal space, giving priority to
dividing the loose lobules that support the perire-
nal vessels. The striated shadows in the spider
web of perineal kidney represent pathological
thickening of fibrous separations that can
envelop or limit the diffusion of inflammatory
exudation or effusion. There are several types of
septa that compartmentalize the perirenal space
and which may confine, or act as a conduit for,
extension of a disease process [91].
Perirenal cobwebs (visualization of perirenal
septa) are most frequently encountered during
the CT evaluation of urinary tract obstruction
from stone disease. Perirenal stranding, occur-
ring in the setting of flank pain from ureteral
colic, is an exaggeration of the visibility of these
septations caused by edema and fluid extravasa-
tion, and is an important secondary sign of acute
5  Solid Organs of Upper Abdomen
ureteral obstruction from stones. Perirenal strand-
ing in the asymptomatic patient is often a nonspe-
cific finding that may be seen in benign and
malignant conditions [91]. Inflammatory and
neoplastic processes, particularly those originat-
ing in the kidney, may produce similar appear-
ances. If no cause for the cobwebs is found in the
kidney, extrarenal pathology should be consid-
ered, acute pancreatitis or aortic aneurysm rup-
ture particularly [103]. This appearance is
nonspecific and often results from fluid within
the septations existing in the perirenal space. The
perirenal cobwebs sign is most common in uri-
nary stones with infection, which also can be
seen in a variety of lesions, including subcapsular
hematoma, abdominal aortic aneurysm rupture,
acute pancreatitis, and pyelonephritis [104].
5.40 Pseudo-capsule Sign
Feature
The pseudo-capsule of renal carcinoma appears
as a complete or intermittent low-signal ring or
band on the edge of the tumor on MRI, showing
better on T2WI, that is, pseudo-capsule sign.
Explanation
The pathological basis of the pseudo-capsule
sign is the peritumoral structure, which is com-
posed of a fibrous capsule and a compacted renal
parenchyma. The fibrous tissue is in close contact
a b
Fig. 5.41  A 62-year-old female patient with renal cell carcinoma. Axial T1WI (a) false capsule sign was not obvious,
and axial T2FS image (b) showed a regular pseudo-capsule surrounding high-signal tumor, the “pseudo-capsule sign”
225
with the tumor tissue of renal carcinoma, and the
compacted renal parenchyma continues to the
outside of the fibrous capsule. The tightly packed
renal parenchyma is uneven in thickness, and
coagulation necrosis, hyaline degeneration, and
fibroblast proliferation can be seen. The appear-
ance of the pseudo-capsule sign has a certain
value for the MRI staging of the tumor. The
occurrence of the pseudo-capsule sign allows
considering that the perirenal fat sac has not been
infiltrated, suggesting that the tumor can be par-
tially removed by surgery (Fig. 5.41).
Discussion
The “pseudo-capsule sign” is an MRI finding of
renal cell carcinoma (RCC) that appears as a
complete or intermittent low-signal ring or band
on the edge of the tumor and is better shown on
T2WI. The appearance of the pseudo-capsule
sign has a certain value for the MRI staging of the
tumor. The occurrence of the pseudo-capsule
sign may consider that the perirenal fat sac has
not been infiltrated, suggesting that the tumor can
be partially removed by surgery. RCC accounts
for 1% to 3% of visceral tumors. Partial nephrec-
tomy can only be performed if the tumor is con-
fined within the renal parenchyma and there is a
clear pseudo-capsule around it. RCC does not
have a true histological capsule, but a surround-
ing pseudo-capsule that is composed of com-
pressed renal parenchyma and fibrous tissue. The
fibrous tissue can be connected to the fibers that
226
extend into the tumor. When the tumor grows, the
fibrous tissue of the renal interstitial is stimulated
to grow around the tumor, which has a certain
limiting effect on the tumor growth. The thick-
ness of the pseudo-capsule varies with different
growth rates and where the tumor is located.
Carcinoma tissues with a lower degree of malig-
nancy grow more slowly. The interstitial fibers
have a longer period of reactive hyperplasia and a
thicker fiber component in the pseudo-capsule.
Carcinoma tissues with a higher degree of malig-
nancy grow faster. Interstitial fibers do not have
enough reactive hyperplasia, and the fiber com-
ponent in the pseudo-capsule is thinner.
In 1985, Hricak et al. first discovered the exis-
tence of the pseudo-capsule with a low signal
band in renal MRI [105]. Scholars have con-
ducted much research. It was reported that T2WI
has a sensitivity of 68%, and specificity up to
91%, for displaying pseudo-capsule; it is consid-
ered characteristic of MRI of renal cell carci-
noma [106]. The pseudo-capsule appears in T1WI
and T2WI as a low-signal ring surrounding the
tumor, separating the tumor from normal renal
parenchyma or peripheral fat, and interruptions
of the pseudo-capsule are associated with perire-
nal fat infiltration and higher staging [107]. On
T2WI, because the renal parenchymal signal is
significantly increased, renal cell carcinoma is
often equal or higher than the renal parenchyma;
therefore, the low-signal pseudo-capsule sign is
easily compared. Tumors with low signal on
T2WI chemical shift artifacts are potential short-
comings in detecting the pseudo-capsule sign on
MRI [107].
5.41 Spoke Wheel Sign
Feature
On noncontrast CT, renal oncocytoma presents as
a low-density mass with clear boundary. The cen-
ter of the tumor is a lower-density area and
extends radially into surrounding tumor paren-
chyma, resembling the spoke of a wheel. On
postcontrast CT, the tumor parenchyma is homo-
geneous in enhancement, but the lower-density
X. Li et al.
area in the center and the spoke shadow of the
wheel are not enhanced.
Explanation
Pathologically, renal oncocytoma originates from
proximal convoluted tubules of the renal cortex.
The cytoplasm of the tumor cells is filled with
eosinophilic granules. The gross specimens are
brown-red or brown-yellow, with complete cap-
sule, rare hemorrhage, and necrosis. The center
of the tumor is a colloidal viscous substance,
which extends radially to the surrounding area.
Radial septation is the essence of the tumor
(Fig. 5.42).
Discussion
Renal oncocytoma (RO) is a benign tumor origi-
nating from distal convoluted tubules and collect-
ing ducts, accounting for 3% to 9% of primary
renal tumors [108]. Because of its low incidence,
it is difficult to diagnose and identify, and is often
misdiagnosed as clear cell renal cell carcinoma
(CCRCC). CT scan showed homogeneous or
low-density lesions with clear boundaries.
Enhanced scan showed homogeneous enhance-
ment, but it was still lower than the density of
kidney. The low-density area without enhance-
ment in the center showed a wheel-spoke distri-
Fig. 5.42  Postcontrast CT shows enhancement of paren-
chymal components, irregular center without enhance-
ment of low-density area, and wheel-like radiation to the
surrounding area
5  Solid Organs of Upper Abdomen
bution to the surrounding tumor parenchyma.
The spoke wheel sign was first proposed by
Quinn in 1984 and is considered to be the charac-
teristic feature of RO [109]. Stellate scar and seg-
mental enhancement inversion are also considered
to be characteristic features of RO, and are often
used in the differential diagnosis of RO and
CCRCC. Kim et al. [110] report that segmental
enhancement inversion is helpful in differentiat-
ing RO and CCRCC less than 4 cm. Segmental
inversion enhancement refers to the enhancement
of cortical and medullary phases in CT enhanced
scan, which shows two different degrees of
enhancement in tumors. In the delayed phase, the
enhancement degree of the two parts is reversed;
that is, the obvious part of corticomedullary
phase was weakened in the delayed phase, and
the weak part of corticomedullary phase was
strengthened obviously in the delayed phase.
However, it should be noted that the spoke wheel
sign, stellate scar, or segmental enhancement
inversion can be reported in renal cell carcinoma,
and the central stellate scar is sometimes difficult
to distinguish from the central necrosis of renal
cell carcinoma [111]. In summary, RO is a rela-
tively rare benign tumor of kidney, and its imag-
ing features have certain characteristics. However,
preoperative CT enhanced examination did not
completely distinguish between RO and
CCRCC. For those cases difficult to differentiate,
it is recommended that puncture biopsy or frozen
section be performed to avoid unnecessary radi-
cal nephrectomy.
5.42 Soft-Tissue Rim Sign
Feature
The soft-tissue rim sign is described on CT
obtained in patients suspected to have ureteral
calculi, an area of soft-tissue attenuation sur-
rounding a suspended ureteral calculus that
appears calcified.
Explanation
The soft-tissue rim sign is caused by edema of
the ureteral wall surrounding a stone at its site of
impaction (Fig. 5.43).
227
Fig. 5.43  CT plain scan shows calcified calculus on right
side of the ureter with soft tissue around it, showing the
soft-tissue rim sign
Discussion
The soft-tissue rim sign has evolved as a useful
sign in the diagnosis of urolithiasis in patients
with renal colic. The sign usually develops within
4 to 24  h after obstruction. The soft-tissue rim
sign has been found to have a sensitivity of 77%
and a specificity reaching 92% [112].
Visualization of the soft-tissue rim sign is depen-
dent on stone size; smaller ureteral calculi are
more likely to exhibit this finding than are larger
calculi. It has been postulated that larger calculi
tend to thin the ureteral wall to a greater degree
than do smaller stones, which makes detection of
the ureteral wall more difficult. Heneghan et al.
[113] determined that the rim sign tends to be
present with smaller stones (mean size, 4.3 mm)
rather than with larger stones (mean size,
6.3 mm). Most ureteral calculi are of sufficiently
high attenuation to be readily apparent on non-
contrast CT. Occasionally, it may be difficult to
differentiate a ureteral calculus from a phlebolith.
This problem typically occurs in patients who are
elderly, who have minimal retroperitoneal fat, or
who have nonobstructing calculi.
CT evaluation of stones has given rise to new
signs. The soft-tissue rim sign is caused by edema
of the ureteral wall surrounding a stone at its site
of impaction. The importance of the sign lies in
the fact that it may help to distinguish a stone in
the ureter from a phlebolith in an adjacent vein,
because the occurrence of a soft-tissue rim
around a phlebolith is uncommon [91]. If the
228 X. Li et al.

soft-tissue rim sign is present, it is useful in dif-

ferentiating ureteral calculi from pelvic phlebo-
liths in patients suspected of having ureteral
colic. The soft-tissue rim sign is visible for 76%
of ureteric calculi but only 2% of phleboliths.
Kawashima et  al. reported that 50% of stones
manifested a rim sign, 34% of stones were inde-
terminate for a rim sign, and 16% of the stones
did not manifest a rim sign [114]. The presence
or absence of this soft-tissue rim sign correlates
with the size of a calculus but not with the degree
of urinary obstruction. When CT reveals an inde-
terminate soft-tissue rim sign, careful inspection
for other findings, such as ipsilateral ureteral dil-
atation, perinephric edema, dilatation of the
intrarenal collecting system, and renal swelling,
is necessary [114]. In evaluation for ureteral
stone, one should focus at the most common
locations; narrowing of the ureter occurs natu-
rally at the uretero-vesicular junction (UVJ), the Fig. 5.44  In 56-year-old man, on CT plain scan, a soft-­
tissue attenuation shadow in front of the high-attenuation
pelvic brim as the ureter crosses iliac vessels, and shadow shows the comet-tail sign
at the uretero-pelvic junction (UPJ). Frequently,
a transition point is visible, with urinary decom-
pression more distally. Secondary CT findings in Explanation
obstructive uropathy include hydroureter, hydro- After the vein wall thrombus is calcified, the
nephrosis, perinephric stranding, and possible phleboliths are formed. Because the phleboliths
enlargement of the unilateral kidney. Periureteral locate in the vein or venous plexus, a vein blood
wall thickening and perinephric/periureteral fat vessel adjacent to phleboliths appears as a linear,
stranding reflect acute inflammation. A positive curved, or crescent-shaped soft-tissue attenuation
soft-tissue rim sign is specific for the diagnosis of shadow of different length or width and con-
ureterolithiasis. However, a negative soft-tissue nected to the phleboliths, thus forming the comet-­
rim sign does not preclude such a diagnosis. tail sign (Fig. 5.44).

5.43 Comet-tail Sign
Feature
Calcification in the abdominal cavity or pelvic
cavity vein or venous plexus appears as a linear,
curved, or crescent-shaped soft-tissue attenuation
shadow of different length or width that is con-
nected to calcification on CT, referred to as the
comet-tail sign. It usually indicates the calcifica-
tion of the abdominal cavity or pelvic cavity are
phleboliths.
Discussion
Phleboliths most often occur in the pelvic veins
near the end of the ureter and in the venous plexus
around the prostate or around the vagina.
Phleboliths can be seen at any age, and the num-
ber of phleboliths tends to increase in middle-­
aged and elderly people. The main factors of
phlebolith formation in adult pelvic vein traffic
include venous hypertension caused by cough,
venous deformation, and residual venous valve
orifice caused by the absence of a normal venous
double valve. In the case of venous blood flow
5  Solid Organs of Upper Abdomen
stagnation, residual valve fragments cause throm-
bosis, and eventually after the thrombus is calci-
fied, the phleboliths are formed [115]. The
“comet tail sign” is thin soft tissue extending
from a focus of calcification in the abdomen or
pelvis; it can also be used to differentiate these
two entities, and typically indicates a phlebolith.
CT is the main method for diagnosing phlebo-
liths. Because thrombosis and ureteral calculi are
similar in location and performance on CT scan
images, sometimes it is difficult to identify these,
especially if there is no sign of secondary obstruc-
tion in ureteral calculi and the fat content in the
retroperitoneal and pelvic cavity is very low
[116]. Although intravenous urography, retro-
grade ureterography, and enhanced CT scan can
show a clear separation of phleboliths from con-
trast medium-filled ureters, thereby distinguish-
ing between phleboliths and ureteral calculi,
however, if the CT scan can show comet tail sign,
this can help identify ureter calculi and phlebo-
liths. In addition, the curved unexpanded ureter
connected to the ureteral calculi may resemble
the soft-tissue image formed by the venous struc-
ture of the phleboliths on the CT plain scan.
Called false tail sign, this is most often located in
the pelvic ureteral bladder junction, where the
ureter often travels in the axial direction. The
existence of the false tail sign indicates that the
diagnostic effect of the comet tail has certain
limitations. However, it is possible to avoid mis-
takes by carefully observing the relationship
between the tail and the ureter, the attenuation of
the center of the tail, and the direction of the tail
associated with suspected calcification. If the
upper ureter and the lower tail traffic or the center
of the tail is liquid attenuation, it is suggested to
be a false tail sign. In many instances, observers
did not agree about whether the rim and comet-­
tail signs were present. The rim sign was observed
in the absence of any secondary signs of urinary
tract obstruction in only 1 (1.5%) of 65 patients
[117]. The comet-tail sign, when accompanied
by secondary signs of obstruction, should indi-
cate that an ipsilateral ureteral stone is present
and not the reverse [117].
229
5.44 Faceless Kidney
Feature
The faceless kidney refers to the renal paren-
chyma lacking vascular or collecting system ele-
ments, which is a characteristic CT sign for
duplication of the renal pelvis and ureter.
Explanation
In kidneys with either bifid renal pelvis or com-
plete duplication of the collecting system, a CT
section obtained at the mid-pole or junction of
the fused upper and lower pole cortical moieties
may reveal a “faceless” renal appearance lacking
vascular or collecting system elements.
Recognition of this finding allows a correct diag-
nosis of partial or complete duplication of the
collecting system and prevents a false impression
of an intrarenal mass lesion (Fig. 5.45).
Discussion
Duplication of renal pelvis and ureter is the most
common congenital disease of the upper urinary
tract, with many complications. The incidence
rate reported in the literature is high, about 0.7%.
In 1986 Hulnick et al. first described the faceless
kidney. This sign was originally reported on CT,
as an indication of a renal duplication anomaly
(either a bifid renal pelvis, or incomplete or com-
plete ureteral duplication) [118]. The sign is
most often seen on axial CT images obtained
between the upper- and lower-pole duplicated
collecting system elements of the kidney. The
image obtained between the separate sinus ele-
ments shows normally enhancing renal paren-
chyma, without the anticipated renal sinus
components, such as fat, blood vessels, and col-
lecting system elements [119]. Recognizing a
“faceless” kidney should then prompt a search
for some form of collecting system duplication
anomaly. It should be noted that the meaning of
a faceless kidney has been expanded to include
conditions that alter the appearance of the renal
sinus, either from edema (pyelonephritis or con-
tusion) or from neoplasia. Fetal genital anoma-
lies are rare as well and among the most difficult
230
Fig. 5.45  A 37-year-old woman with complete duplica-
tion of the collecting system. A CT section obtained at the
mid-pole or junction of the fused upper and lower pole
to diagnose. A combination and pattern of find-
ings allows for specific diagnosis of renal tract
abnormalities [91].
5.45 Goblet Sign
Feature
The goblet sign is a cup-shaped contrast agent at
the distal end of the ureteral lumen defect, which
is best seen in retrograde ureterography. Venous
renal angiography and now CTU or MRU can
X. Li et al.
cortical moieties shows a “faceless” renal appearance
lacking vascular or collecting system elements
also be shown when the ureter is not completely
occluded.
Explanation
The goblet sign suggests that the filling defect in
the ureter is caused by a lump rather than a stone.
The slow growth of the intraluminal mass origi-
nating in the urothelium causes ureteral dilatation
at the distal end of the mass and adjacent sites.
The ureteral peristalsis pushes the distal end of
the ureter to promote the expansion of the distal
ureter of the mass, thus forming a cup-like struc-
5  Solid Organs of Upper Abdomen
Fig. 5.46 Ureteral transitional cell carcinoma in a
65-year-old patient. On retrograde ureterography, arrow
shows a goblet sign and a filling defect formed by the
mass
ture of the contrast agent, and the mechanical
obstruction caused by the stone is the stenosis
caused by the edema of the ureter at the distal end
of the ureter (Fig. 5.46).
Discussion
The goblet sign was first proposed and systemati-
cally described by Daniels in 1999 [120]. That is,
in retrograde ureterography, because of the ure-
teral mass caused by nonmechanical obstruction
of the ureter, the proximal end of the stenosis is a
filling defect, and the distal end expansion is a
goblet change. In the setting of acute obstruction
such as ureterolithiasis, the ureter is unable to
accommodate the obstructing process. Focal
downstream ureteral dilatation does not occur,
and a goblet sign will be absent. In fact, the distal
ureter is often narrowed with an acute obstructive
process by reactive edema and ureteral spasm
[120]. The proximal ureter can be dilated to a
variable degree in both the acute and chronic set-
231
ting, depending on the extent of obstruction, and
therefore is not a helpful discriminator of chro-
nicity [121]. Uroepithelial carcinomas usually
occurs in elderly patients, including transitional
epithelial cell carcinoma, squamous cell carci-
noma, and adenocarcinoma [122]. Urinary tract
carcinoma located in the ureter is relatively rare
compared to other tumors located in the urinary
tract. Transitional epithelial cell carcinoma is the
most common tumor of the ureter, and tends to be
low grade, with slow infiltration and late metasta-
sis. Therefore, transitional epithelial cell carci-
noma is most strongly associated with the goblet
sign, which is caused by the slow growth of the
ureteral mass.
Intravenous urography has been the first
choice of evaluating ureteral tumors. Once a
lesion is found in the ureter, a complete ureteral
examination is required because transitional epi-
thelial cell carcinoma has a multi-lesion ten-
dency. The nonmechanical obstruction caused by
the ureteral mass is manifested by the expansion
of the distal ureter of the mass, which is caused
by ureteral peristalsis propelling to the distal end
of the ureter. Mechanical obstruction caused by
ureteral calculi is characterized by stenosis from
edema of the ureter at its distal end. Intravenous
urography shows a goblet sign of the ureter,
mostly caused by the slow infiltration of transi-
tional epithelial carcinoma. CT and MRI are the
main imaging modalities for ureteral diseases,
especially CTU and MRU, which can detect
lesions early and aid in early treatment.
5.46 Cobra Head Sign
Feature
The cobra head sign was manifested by intrave-
nous urography. In the bladder filled with con-
trast medium, spherical dilatation of the distal
ureter and transparent halo around it were seen,
which resembled a cobra head.
Explanation
Ureteral cysts are filled with contrast medium
and surrounded by high-density urine in the blad-
der during intravenous urography because the
232
Fig. 5.47  Magnetic resonance urography (MRU) dem-
onstrated the hydronephrotic upper pole collecting system
and cobra head appearance of a right ureterocele in a
2-year-old child with duplicated renal collecting systems
bilayer mucosal wall of the ureter cyst forms a
thin light or halo around it. The translucent band
represents the thickness of the ureteral wall and
the prolapsed bladder mucosa. It is supported by
contrast medium in the bladder cavity. The trans-
lucent band is thin and smooth. It delineates the
ureter cyst and forms the cobra head-like appear-
ance [123] (Fig. 5.47).
Discussion
Ureteral cyst (ureterocele) refers to the balloon
dilatation of the distal ureter. Distal ureteral dila-
tation reflects the obstruction of urine flow at the
entrance of the ureter and bladder. The cobra
head sign is common in ureteral orifice cysts in
the bladder. Because it originates in the triangle
of the ureter and bladder, it is also called ortho-
topic ureteral cyst. Ureteral cysts are classified as
intravesical and ectopic [124]. The intravesical
type is considered simple; the ureteral orifice and
ureterocyst are both in the bladder. The ectopic
type is located under the bladder mucosa and
X. Li et al.
may extend into the human bladder neck or ure-
thra. Intravesical ureteroceles can be unilateral or
bilateral. They are usually found in adulthood, so
they are also called adult-type ureteroceles; these
are more common in females than in males. The
ureteral cyst is a congenital disease, and ureteral
orifice stenosis is one of its causes. But there is
reason to believe that not all unilateral ureteral
cysts are congenital, because inflammation and
trauma can lead to fibrosis and develop into ure-
teral cysts. Most intravesical ureterocysts are
occasionally found in asymptomatic adult
patients. When ureterocysts are large, they can
cause bladder neck and unilateral ureteral
obstruction, which leads to an increase in the
incidence of stones and infections. With the
occurrence of obstruction and delayed filling of
the ureter, delayed imaging examination is
required. Ectopic ureteral cysts are almost always
associated with duplicate ureteral deformities
and originate from the upper pole of the ureter.
They are usually found in childhood and are
characterized by filling defects in the bladder
rather than typical cobra head signs [125].
The cobra head sign is a sign of simple ure-
teral cyst, but the snake-head dilatation of the dis-
tal ureter can also be caused by incomplete
obstruction of the distal ureter caused by tumors
and stones. This manifestation is called pseudo-­
ureterocele. The light transmission wall around
the dilated distal ureter is an important distin-
guishing point between ureterocyst and pseudo-­
ureterocyst, pseudo-ureterocele. Swollen
translucent walls or halos are thick and unclear.
In tumors, they can be irregular and have filling
defects in ureteral cysts. Although cobra head
sign is a typical sign of ureteral cyst, about 50%
of ureteral cysts show this sign [125]. Cystoscopy
confirmed that the size and shape of ureteral cyst
vary with the filling degree of contrast medium;
this also explains why some ureteral cysts are
invisible during IVU. Ultrasonography can show
ureteral cysts protruding into the bladder cavity.
In some questionable cases, cystoscopy may help
to determine whether a pseudo-ureteral cyst is
caused by a tumor if the cobra head sign is
atypical.
5  Solid Organs of Upper Abdomen
5.47 Drooping Lily Sign
Feature
The drooping lily sign can be identified at excre-
tory urography in patients with duplicated renal
collecting systems. The sign consists of inferolat-
eral displacement of a functioning lower-pole
moiety, usually by a nonopacified, hydrone-
phrotic upper pole collecting system. The appear-
ance of the lower-pole collecting system is
reminiscent of a lily flower that is wilting or
drooping.
Explanation
In intravenous pyelography, because of the severe
accumulation of water in the upper pole with
duplicated renal collecting systems, the displace-
ment of the renal pelvis and renal calyces is sup-
pressed, and the angle between the renal pelvis
and the ureter becomes smaller (Fig. 5.48).
Discussion
The “drooping lily” has been used as a metaphor
for the urographic appearance of the opacified,
functioning lower-pole moiety in a completely
duplicated collecting system. The mass effect of
a b
Fig. 5.48 (a, b) A 31-year-old male patient with dupli-
cated renal collecting systems. CTU VR and MPR image
shows inferolateral displacement of lower pole moiety by
233
the dilated and often nonopacified upper collect-
ing system elements displaces the lower-pole col-
lecting system inferolaterally, producing the
appearance of a fading flower [126]. An obstruct-
ing ectopic ureterocele or ectopic insertion of the
upper-pole ureter is the usual cause of hydrone-
phrosis of the upper-pole collecting system in a
duplex kidney. The enlarged, obstructed upper-­
pole moiety exerts a mass effect on the remaining
lower portion of the kidney, which results in
inferolateral displacement of the lower-pole moi-
ety and lateral displacement of the most superior
calyces of the lower-pole collecting system.
During excretory urography, a normally func-
tioning, nonobstructed, completely duplicated
collecting system will demonstrate two separate
renal pelvises and two separate ureters. However,
in the setting of an obstructed upper-pole moiety,
which is usually dysplastic and poorly function-
ing, there is often absent or severely delayed con-
trast material excretion into the upper-pole
collecting system. This lack of upper-pole
excretion, combined with visualization of
­
decreased numbers of calyces oriented in an
abnormal axis, are the fundamental components
of the drooping lily sign [127]. Albeit rare, the
a non-opacified, hydronephrotic upper-pole collecting
system, which is the drooping lily sign
234
drooping lily sign can also be identified in a non-
duplicated collecting system in the presence of
an upper-pole renal mass, such as a renal abscess
or Wilms tumor. The drooping lily configuration
would not be expected if the entire kidney is dis-
placed by an extrarenal mass lesion; as such, dis-
placement of only the lower-pole moiety, rather
than displacement of the entire kidney, allows the
radiologist to suggest an intrarenal rather than an
extrarenal process [127]. The drooping lily sign
is often seen in conjunction with an ectopic ure-
terocele, and manifests as an eccentrically placed
round or ovoid filling defect within an opacified
bladder. This filling defect is usually best seen
with a small amount of contrast material in the
bladder, as increasing bladder distention may
efface or evert the ureterocele [127].
Duplex kidneys are a common abnormality of
renal tract development, carrying an incidence of
approximately 1%. This diagnosis is defined as a
renal unit composed of two pelvicalyceal systems
and is the most frequent congenital anomaly of
the urinary tract [128]. The “drooping lily” sign is
identified on intravenous urography or voiding
cystourethrography in patients with a duplicated
renal collecting system and refers to inferolateral
displacement of a functioning lower-­pole moiety
by an obstructed upper-pole collecting system
[129]. A good rule of thumb is to consider the
presence of an obstructed, upper-­pole duplicated
system any time a cystic structure is seen in the
upper pole of the kidney. The obstructed upper
moiety and its draining ureter may also be recog-
nized on ultrasound or MRI [126].
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 Gastrointestinal Tract
6
Jiani Chen, Hengtian Xu, and Gui Quan Shen

Contents
6.1 Double Bubble Sign  240
6.2 Small-Bowel Feces Sign  241
6.3 Bird’s Beak Sign  242
6.4 String of Pearls Sign  243
6.5 Coffee Bean Sign  245
6.6 Spoke Wheel Sign  246
6.7 Whirl Sign  247
6.8 Corkscrew Sign  248
6.9 Target Sign  249
6.10 Target Sign  250
6.11 Double Halo Sign  251
6.12 Comb Sign  252
6.13 Gastrointestinal String Sign  253
6.14 Bowel Wall Fat Halo Sign  254
6.15 Disproportionate Fat Stranding Sign  255
6.16 Misty Mesentery Sign  257
6.17 Fat Ring Sign  258
6.18 Hyperattenuating Ring Sign  259
6.19 Arrowhead Sign  260
6.20 Accordion Sign  261
6.21 Apple Core Sign; Apple Core Lesion  263

J. Chen (*) · H. Xu · G. Q. Shen

Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China

© Springer Nature Switzerland AG 2021 239

B. Gao, A. M. McKinney (eds.), Classic Imaging Signs,
https://doi.org/10.1007/978-3-030-56348-6_6
240
6.22 Duodenal Wind Sock Sign
6.23 Rigler Sign
6.24 Football Sign
6.25 Dependent Viscera Sign
6.26 Northern Exposure Sign
References
6.1 Double Bubble Sign
Feature
On abdominal X-ray radiographs, there are two
air-filled cystic structures in the upper abdomen,
slightly below the left upper abdomen and the
right midline. Gas–liquid level can be seen in the
abdomen. There is no or only a small amount of
gas in the distal intestinal canal.
Explanation
The double bubble sign is a specific manifesta-
tion of duodenal obstruction in neonates or
infants. In duodenal obstruction, the proximal
duodenum and stomach progressively accumu-
late gas, accumulate fluid, and expand, forming
the so-called double bubble sign (Fig. 6.1).
Discussion
The double bubble sign was systematically
described by Traubici in 2001 [1]. It is consid-
ered a classic imaging manifestation of duode-
nal atresia. Typical imaging findings are that
larger gastric bubbles occupy the left upper
abdomen on abdominal X-ray plain film, while
smaller duodenal bubbles are locating in the
right upper abdomen or the right middle abdo-
men. Double bubble dilation reflects postpar-
tum gas swallowing, and atresia of the duodenal
segment does not allow the swallowing gas to
pass through the distal end. If newborns develop
abdominal distension, vomiting, and other
symptoms within the first 24  h after birth, the
possibility of duodenal atresia should be con-
sidered [2]. Vomiting in duodenal atresia is
often biliary, because the atresia is usually
located at the distal end of the duodenum.
J. Chen et al.
 264
 265
 266
 267
 269
 270
Therefore, the possibility of duodenal atresia
should be considered in infants with biliary
vomiting, and an imaging examination should
be performed immediately. In addition to
abdominal X-ray, prenatal diagnosis can now
be made by ultrasound or fetal magnetic reso-
nance imaging (MRI), both of which can
observe fluid-filled dilated stomach and duode-
num. Prenatal double bubble sign is a reliable
predictor of duodenal atresia. In addition to tri-
somy 21, heterotaxy may be encountered [3].
Neonatal malrotation very seldom mimics duo-
denal atresia. The classic double bubble sign is
Fig. 6.1  A 1-year-old female infant. On neonatal abdom-
inal radiograph, upper abdomen has two inflatable struc-
tures. Larger transparent structure of left upper abdomen
(black arrow) is the dilated stomach. Smaller transparent
structure in right mid-abdomen represents the gas that
expands proximally to the duodenum. Note lack of distal
intestinal gas, a typical manifestation of duodenal atresia
6  Gastrointestinal Tract
the only true double bubble sign [1]. Over the
years, the usage of this term has become altered
so that it has become a little unclear. However,
anything other than this sign should be treated
with great suspicion for the presence of malro-
tation and midgut volvulus. Furthermore, if the
patient has bilious vomiting, the diagnosis is
basically secured [4].
Although double bubble sign is a classic
sign of duodenal atresia, differential diagnosis
includes duodenal stenosis, duodenal reticu-
lum, annular pancreas, and malrotation with
midgut volvulus. The degree of obstruction
and the cause of obstruction can be generally
judged according to the double vesicle sign
and its accompanying signs. If the bilateral
vesicles are large and the distal part is not
inflated, this indicates complete duodenal
obstruction (duodenal atresia); if the bilateral
vesicles are small and the distal part has more
or less inflatability, it is mostly incomplete
obstruction (intestinal malrotation, duodenal
stenosis, circular pancreas, etc.). Sometimes
incomplete obstruction is absorbed by the
intestinal wall because the gas does not enter
the distal part of the obstruction or a small
amount of air is absorbed by the distal part of
the obstruction. It can also be manifested as a
simple double vesicle sign. On the other hand,
the possibility of complete obstruction cannot
be ruled out when the distal intestinal tract of
double vesicle sign is inflated, because when
duodenal atresia combined with abnormal bile
duct development, the proximal gas of obstruc-
tion can enter the distal part of the obstruction
through an abnormal bile duct. Therefore, in
judging the degree of duodenal obstruction and
the cause of the obstruction, we should not
depend on whether the distal part of the
obstruction is inflated, but should observe and
analyze comprehensively, with barium or ultra-
sonogram if necessary. It is important to keep
in mind that there is only one true double bub-
ble sign, which need not require immediate
attention or intervention. Anything other than
this sign requires immediate management if
the diagnosis would be malrotation with pos-
sible midgut volvulus [4].
241
6.2 Small-Bowel Feces Sign
Feature
On computed tomography (CT) scans of the
abdomen, colon-like feculent matter mingled
with gas bubbles can be seen in the lumen of
dilated loops of the small intestine.
Explanation
The contents of the dilated small intestine seen in
the small-bowel feces sign are similar to colon-­
like feculent matter on CT scans. It is the result of
delayed intestinal transit and is believed to be
caused by incompletely digested food, bacterial
overgrowth, or increased water absorption of the
distal small-bowel contents because of obstruc-
tion (Fig. 6.2).
Discussion
The small-bowel feces sign was first described in
1995 by Mayo-Smith et al. [5]. The presence of
the small-bowel feces sign indicates small-bowel
obstruction or other acute small-bowel lesions
(such as metabolic or infectious diseases). Bowel
obstruction accounts for approximately 20% of
acute abdominal surgical interventions in
60–80% of cases of intestinal obstruction. The
clinical performance of small-bowel obstruction
includes abdominal tenderness, distention, and
increased high-pitched bowel sounds. However,
in complete obstruction with predominantly
fluid-filled bowel loops, there may be less disten-
tion and diminished sounds. Similar clinical pre-
sentations can be found in paralytic ileus,
intraabdominal abscess, malignant tumor, pan-
creatitis, peptic ulcer disease, or gastroenteritis.
Thus, an early and accurate radiologic diagnosis
of small-bowel obstruction is very important
clinically. The small-bowel feces sign is most
often present in the distal small intestine at length
of 4–200 cm. The reported prevalence of the sign
is low (7–8%), but the diagnostic reliability is
high. The small-bowel feces sign has shown a
high specificity for subacute or low-grade small
bowel obstruction [6], because in the process of
progressive small intestinal obstruction, the
intestinal contents pass slowly, resulting in
increased water absorption and subsequent for-
242
a b
Fig. 6.2 A 59-year-old male patient with intestinal
obstruction, on coronal and sagittal abdominal CT plain
scan. Adhesions of small intestine on the abdominal wall
mation of colon-like feculent matter. It is impor-
tant to recognize the sign as early as possible in
the clinic so that early surgical treatment can be
carried out; as the sign often appears in the proxi-
mal part of the obstruction it may be helpful in
recognition of the exact site and cause. The pri-
mary reason for this sign is classic mechanical
small-bowel obstruction caused by adhesions,
hernias, and tumors. Other causes are inflamma-
tory stenoses and infectious, metabolic, and isch-
emic disorders [7]. Other conditions may include
heterogeneous patchy substances with gas accu-
mulation in the small intestinal cavity, such as
cystic fibrosis, infectious or metabolic bowel dis-
ease, rapid jejunostomy tube feedings, or, rarely,
bezoars. However, according to the definition of
this sign, the diameter of intestinal dilatation
more than 2.5 cm is also a necessary diagnostic
criterion. In a few cases, fecal residues can be
seen in normal nondilated distal ileum, presum-
ably from fecal reflux in the cecum. The small-­
bowel feces sign is a useful auxiliary sign for the
diagnosis of small-bowel obstruction based on
other traditional obstructive signs, particularly in
patients with low-grade or intermittent obstruc-
tion. Most patients with this sign need to be hos-
pitalized and often require surgical treatment.
Radiologists should master this sign to make an
J. Chen et al.
after operation. Narrowing of small bowel and feculent
matter mingled with gas bubbles in the proximal dilated
small bowel is called the small-bowel feces sign
accurate diagnosis of small-bowel obstruction as
soon as possible.
6.3 Bird’s Beak Sign
Feature
This is a CT sign of closed loop intestinal obstruc-
tion. The dilated intestinal loop gradually
becomes sharp at the obstructive site, and the
intestinal loop contracts, resembling slightly a
bird’s mouth.
Explanation
When intestinal obstruction occurs, a transitional
zone is formed between the atrophic bowel and
the dilated bowel, and the dilated bowel extends
to the protruding part of the atrophic bowel,
which resembles the beak of a bird (Fig. 6.3).
Discussion
The causes of intestinal obstruction are com-
plex and varied, including intestinal adhesion,
primary or secondary tumors, Crohn’s dis-
ease, vascular lesions, parasites, gallstones,
feces, abdominal hernia, chronic colonic
diverticulitis, intussusception, and volvulus
[8]. When intestinal obstruction occurs, the
6  Gastrointestinal Tract
a b
Fig. 6.3  In a 19-year-old girl, multi-planner reformation (MPR) shows small intestinal obstruction and bird’s beak sign
intestinal cavity widens with the accumula-
tion of fluid and gas. The lower the obstruc-
tion site and the longer the obstruction time,
the more obvious the dilatation of the intesti-
nal cavity. The intestinal cavity below the
obstruction is atrophic, empty, or with only a
small amount of feces.
CT features are intestinal dilatation, signifi-
cantly enlarged diameter, intestinal dilatation in
general visible gas–liquid level, also filled with
liquid, and intestinal wall thinning. Obstruction
distal bowel collapse, with obstruction distal
and proximal bowel diameter significantly dif-
ferent, is a very valuable sign to judge the loca-
tion of intestinal obstruction [9]. Closed loop
intestinal obstruction is mostly caused by intes-
tinal volvulus resulting from the rotation of the
loop along the long axis of mesentery. It can
also be formed by the contraction and conver-
gence of the two ends of a bowel by the adhe-
sion of fibrous bands [10]. When the scan plane
passes through the closed loop, there are two
dilated intestinal rings, and the distance
between the two adjacent intestinal rings is
gradually closer as the plane approaches the
root of the closed loop. When the scan plane
passes through the root of the closed loop, the
intestinal tube is deformed and the soft tissue
density is triangular when the intestinal volvu-
lus occurs. When the closed loop is parallel to
the scanning plane, it appears as U-shaped
closed loops. At the scanning level, the two
adjacent collapsing intestinal rings are seen
243
through the input and output terminals of the
closed loop. When the long axis of the input or
output segment of the volvulus closure loop is
parallel to the CT scan, the input segment
becomes thinner and the output segment
becomes thicker because of volvulus. On the
CT image, the beak sign appears [11].
6.4 String of Pearls Sign
Feature
The string of pearls sign can be seen on
abdominal radiographs obtained with the
patient in the upright position or on decubitus
abdominal radiographs. The sign consists of a
row or line of several small air bubbles
obliquely or horizontally oriented in the abdo-
men. It is also commonly referred to as the
“string of beads sign.” Other name: the string
of beads sign.
Explanation
The obliquely oriented row of air bubbles repre-
sents small amounts of air trapped between the
valvulae conniventes along the superior wall of
predominantly fluid-filled, dilated small bowel
loops. The meniscal effect of the surrounding
fluid gives the trapped air an ovoid or rounded
appearance. The appearance of the string of
pearls sign depends on the combination of air,
fluid-filled bowel loops, and peristaltic hyperac-
tivity (Fig. 6.4).
244
Fig. 6.4  In a 72-year-old woman, the string of pearls sign
can be seen on abdominal radiographs obtained with the
patient in the upright position. The sign consists of a row
or line of several small air bubbles obliquely or horizon-
tally oriented in the abdomen
Discussion
The string of pearls sign metaphorically describes
a radiographic finding highly suggestive of
mechanical small bowel obstruction (SBO). SBO
is a common clinical syndrome for which effec-
tive treatment depends on a rapid and accurate
diagnosis. The importance of recognizing the
string of pearls sign is often related to the clinical
findings of SBO.  As the small bowel becomes
distended, intraluminal fluid traps gas along the
valvulae conniventes. Upright radiographs depict
a row of elliptical lucency produced by the menis-
cal surface of fluid on one side and the bowel
wall on the other, evocative of a string of pearls
[11]. SBO typically produces gaseous distention
of the bowel loops proximal to the obstructing
lesion. The dilatation of the small bowel stimu-
lates the mucosa to secrete fluid. Thus, the dis-
tended bowel contains varying amounts of air
and fluid, which accounts for the air–fluid inter-
faces seen on horizontal beam radiographs. As
the small bowel dilates, the valvulae conniventes
widen, causing the small bubbles of air to become
trapped [12]. Although the string of pearls sign is
rarely seen in adynamic ileus, acute gastroenteri-
J. Chen et al.
tis, and saline catharsis, when present in the right
clinical setting, it is considered to be virtually
diagnostic of SBO.  The classic signs of SBO
include abdominal tenderness, distention, and
increased high-pitched bowel sounds. However,
in cases of complete obstruction with predomi-
nantly fluid-filled loops of bowel, there may be
much less distention, and the bowel sounds may
be normal or diminished because there is little or
no air to cause the typical high-pitched gurgling
sounds.
Knowledge of the radiographic findings of
fluid-filled obstructions, including the string of
pearls sign, can help diagnosis of SBO when the
clinical picture is somewhat confusing [12]. SBO
is often difficult to diagnose on the single con-
ventional radiograph. Horizontal beam radio-
graph and radiographs obtained in the supine
position are the second choice when SBO is sus-
pected. Often, sequential views obtained within a
12–24  h timeframe help establish an evolving
obstructive gas pattern. Successive abdominal
radiographs obtained in 5-min intervals are a reli-
able tool for differentiating mechanical obstruc-
tion from a dynamic ileus [12]. When an SBO is
accompanied by signs of strangulation, emergent
surgical treatment is advised. If surgery cannot be
performed immediately or if a partial obstruction
is suspected, then a more detailed radiologic
workup is needed.
The imaging sign can also be observed on
computed tomography. In the absence of indica-
tions for urgent operative intervention, a CT scan
with and without IV contrast should be obtained
in most patients to identify the location, grade,
and etiology of the obstruction. The sensitivity
and specificity of MRI to diagnose and character-
ize SBO resemble CT scanning; however, it is
more expensive and less available. MRI is most
appropriate for children, younger patients with
multiple prior CT examinations, and pregnant
women. Despite advances in imaging and a better
understanding of small-bowel pathophysiology,
SBO is often diagnosed late or is misdiagnosed,
resulting in significant morbidity and mortality. If
a low-grade partial obstruction is suspected,
enteroclysis and CT enteroclysis are preferred. If
a complete or high-grade obstruction is sus-
6  Gastrointestinal Tract
pected, ultrasonography or CT are preferred to
exclude strangulation. The imaging techniques
used subsequently vary according to the initial
findings. An algorithmic approach to imaging is
proposed for the management of SBO to deter-
mine its severity, site, and cause and to assess the
presence of strangulation. Radiologists have a
pivotal role in clinical decision making in cases
of SBO. A comprehensive approach that includes
clinical findings, patient history, and triage exam-
inations such as plain abdominal radiography
will help the clinician develop an individualized
treatment plan. Confounding conditions include
age greater than 65 years, post Roux-en-Y gastric
bypass, inflammatory bowel disease, malignancy,
virgin abdomen, pregnancy, hernia, and early
postoperative state [13].
6.5 Coffee Bean Sign
Feature
The coffee bean sign is seen on abdominal radio-
graphs obtained in a supine patient as an area of
hyperlucency that resembles the shape of a coffee
bean.
Explanation
The coffee bean sign is a classic conventional
radiographic finding of sigmoid volvulus. As the
closed loop of the sigmoid colon distends with
gas, apposition of the medial walls of the dilated
bowel form the cleft of the coffee bean, and the
lateral walls of the dilated bowel form the outer
walls of the bean (Fig. 6.5).
Discussion
The coffee bean sign has been described as an
indication of a closed-loop obstruction of the
small bowel but commonly applies to the appear-
ance of a closed-loop obstruction of the sigmoid
colon [14]. The coffee bean sign is a metaphor
describing the classic radiographic appearance of
a closed loop obstruction, most notably associ-
ated with sigmoid volvulus. Twisting of the sig-
moid colon about its mesenteric axis creates an
inverted, U-shaped, and gas-filled segment of
dilated bowel originating in the pelvis and
245
Fig. 6.5  Abdominal radiographs of a patient with sig-
moid volvulus show the “coffee bean sign”
extending cephalad. A central linear opacity
bisects the dilated loop, mimicking the cleft of a
coffee bean. Failure to recognize this finding may
lead to delayed diagnosis with increased risk of
ischemia, infarction, and perforation [15].
Routinely, the diagnosis of acute sigmoid vol-
vulus is established by clinical and radiologic
findings. From a clinical point of view, sudden
abdominal pain, abdominal tenderness, asym-
metrical abdominal distension, constipation,
abdominal tympany, abnormal bowel sounds,
and a palpable abdominal mass are among the
most prevalent initial symptoms and signs. CT
scans are often unnecessary because since a plain
X-ray is diagnostic in 57–90% of patients. The
classical sign of an acute sigmoid volvulus in
plain X-rays is the coffee bean sign; in an abdom-
inal CT scan, the characteristic “whirl sign” as
well as dilated colon with air–fluid levels can be
detected. Those radiologic findings are the result
of the torsion of the often long and redundant sig-
moid colon around its elongated mesenteric axis,
which ultimately leads to intestinal obstruction
[16]. In as many as 80% of the occurrences, sig-
moid volvulus can be diagnosed only by supine
abdominal radiograph. The absence of rectal gas
may help with diagnosis. If the supine abdominal
radiograph cannot be clearly diagnosed, a single-­
contrast barium enema examination should be
246
performed. In the distorted position, the barium
column will abruptly terminate at a point that
typically has the appearance of a bird’s beak.
Barium that is forced beyond the twist may result
in perforation or convert a partial obstruction into
a complete blockage. A barium enema examina-
tion should be avoided altogether, and if there is
evidence of bowel ischemia or perforation, sur-
gery should be performed immediately [17].
6.6 Spoke Wheel Sign
Feature
During an abdominal CT plain scan, the mesen-
teric vessels are thickened, prolonged, and gath-
ered. The fluid-filled enlarged intestinal loop is
radially aligned along the mesenteric vessels.
Explanation
When small intestinal volvulus occurs, mesen-
teric root volvulus occurs correspondingly, the
mesentery shortens and tightens, and a funnel
shape is displayed along the axis of rotation,
causing the intestinal tube connected with the
mesentery to show a concentric circle around the
mesenteric vessels. The distorted mesenteric ves-
sels become thicker, occupying the center, and
the intestines are dilated and filled with fluid. The
vessels distributed on the mesentery are arranged
in a radial direction from the intestinal wall to the
reversed mesenteric root, forming plica of soft-­
tissue attenuation. The shape resembles connec-
tion of the spoked wheel to the central axle, and
thus is called the spoke wheel sign (Fig. 6.6).
Discussion
Small intestinal volvulus is a rare but life-­
threatening surgical emergency. It has been
reported that the incidence of intestinal ischemia
is as high as 46%, and the total fatality rate is 9%.
Intestinal volvulus combined with various factors
makes the damage of the intestinal tube more
serious than the simple mechanical intestinal
obstruction. No matter in which segment of the
intestine obstruction occurs, intestinal fluid accu-
mulates rapidly, and the proliferation of bacteria
will cause a large amount of gas to be produced;
J. Chen et al.
intestinal pressure will increase, intestinal tube
dilatation will be further aggravated, and the
intestinal wall blood supply will be obstructed,
eventually leading to hemorrhagic infarction,
necrosis, and perforation [17]. The most common
cause of small intestinal volvulus is intestinal
adhesion and internal and external hernia. The
squeezing effect caused by the adhesion of two
adjacent intestinal tubes causes a long-moving
obstructed intestinal tube to have only a relatively
narrow base. This anatomical structure makes the
closed loop rotate along its long axis and then
forms an intestinal volvulus [18].
There are some signs on CT scans to diagnose
simple or closed loop intestinal obstruction. (1)
The two adjacent collapsed loops represent the
intestinal tube adhesions with limited dilatation,
and between them is a closed loop of obstruction.
(2) The dilated fluid-filled small intestine has a
U-shaped structure, resulting from the obstructed
liquid-filled dilated intestinal loops that are
arranged radially around the tightly twisted mes-
entery; the CT findings are seen after longitudi-
nal section scanning. (3) The least common CT
findings are triangle sign (or beak sign) and (4)
Fig. 6.6  On abdominal plain CT, the attenuation of mes-
entery increases and gathers around the mesenteric ves-
sels, which show radial arrangement. The shape resembles
the wheel of spokes connected to the central axle, called
spoke wheel sign
6  Gastrointestinal Tract 247

whirl sign. The triangle sign appears in the longi-

tudinal section at the distorted collapse of the
intestine, and the intestinal loop gradually thins
into a sharp triangular shape. The whirl sign is
formed by a twisted mesentery [19]. (5) Spoke
wheel sign: in addition to diagnosing closed loop
intestinal obstruction, the spoke wheel sign can
also predict strangulated small intestinal obstruc-
tion, because it can evaluate the intestinal loop,
mesentery, and mesenteric vessels, and the afore-
mentioned structures can show characteristic
changes during intestinal ischemia and necrosis. Fig. 6.7  In 42-year-old woman with abdominal pain, vis-
ible twisted mesenteric vessels and collapsed intestinal
These signs have been suggested to help distin- canals form a whirl sign (arrow)
guish necrotic and nonnecrotic intestinal seg-
ments in closed loop intestinal obstruction. The
CT findings of small intestinal obstruction vary. ribbon-shaped shadows of soft tissue density in
Despite the importance of diagnosing complex the whirlpool sign. The background is a low-­
obstacles, there are still some difficulties. density shadow formed by mesenteric fat, thus
Experienced physicians can detect volvulus and forming a whirlpool image resembling a meteo-
ischemia caused by internal hernia in closed loop rological map. The appearance of the sample is
intestinal obstruction, but the detection rate is called the whirl sign. When the CT scan axis is
less than 50%. The appearance of spoke wheel perpendicular to the torsional axis of the small
sign strongly suggests small intestinal volvulus: intestine, the spiral sign is more clearly displayed
it provides diagnostic information on both the (Fig. 6.7).
mesentery and the intestine at the same time, thus
helping to detect closed loop intestinal obstruc- Discussion
tion. Other signs of ischemia and necrosis should Intestinal volvulus has symptoms of intestinal
also be observed in the presence of this sign to obstruction and intestinal ischemia. It is an emer-
further confirm the presence or absence of intes- gency surgical disease. Early detection and
tinal stenosis. timely operation are of great value to the progno-
sis of patients. Intestinal volvulus can cause
intestinal blood flow disorders, leading to intesti-
6.7 Whirl Sign nal wall ischemia, edema, and necrosis. The
diameter of the mesenteric artery is small, and its
Feature wall is relatively thick. The mesenteric vein is
On CT, the whirl sign is a circular or quasi-­ large in diameter with a thin wall. It is easily
circular soft tissue mass whose internal structure compressed, narrowed, and occluded under
is formed by the spacing between the soft band external force. The pathological changes of small
density shadow of the turbine ribbon and the fat intestinal volvulus are submucosal edema and
density shadow. intestinal wall congestion. The location of the
whirl sign may provide the cause of the whirl. If
Explanation the upper abdomen shows swirling sign and the
The whirl sign is a sign of volvulus. As the input intestinal tube is fixed in a fixed position, we
and output loops of the twisted small intestine should consider whether it is complicated with
rotate around the fixed obstruction point, the intraabdominal hernia, such as small omentum
mesentery is twisted around the rotation axis and hernia or para-duodenal hernia. The whirl sign
wraps tightly around the loops. These twisted that appears in mid-abdomen mostly suggests
loops and branches of mesenteric vessels form small intestine volvulus, whereas a whirl sign
248
appearing in lower abdomen may be related to
sigmoid colon volvulus. The manifestations of
whirl sign can be as follows: (1) intestinal swirl,
often accompanied by edema of mesentery; (2)
mesenteric swirl, often accompanied by expan-
sion of mesenteric vessels between edema of
mesentery, accompanied by formation of swirl;
(3) swirl mainly composed of mesenteric vessels,
mostly veins.
The whirl sign has specific value for the diag-
nosis of small-bowel volvulus. The whirl sign is
found on CT of volvulus and described as a rota-
tional arrangement centered on the volvulus mes-
enteric artery [20]. In acute abdomen, bowel
volvulus and intestinal adhesion occur simultane-
ously in the mesentery and are vascularly related
in many cases. Whenever there is a whirl change
in CT images, it can be called a whirl sign.
Although the whirl sign as a specific sign of CT
diagnosis of small intestinal volvulus, Yang et al.
believe that the whirl sign is more sensitive to the
diagnosis of small intestinal volvulus [21].
­Blake  et  al. pointed out that this manifestation
can also occur in patients with malrotation of the
midgut, intestinal adhesion, intestinal tumors,
and abdominal and pelvic surgery [22]. Gollub
et al. also reported that whirl signs on CT did not
always indicate small-bowel volvulus [23]. Whirl
sign has important diagnostic value for CT diag-
nosis of small intestinal volvulus, but some non-­
small intestinal volvulus factors should be
excluded. Close reference to other signs of intes-
tinal obstruction, such as intestinal wall thicken-
ing, edema, enhancement weakening, ascites,
and pneumatocele dilatation, especially to
actively find the causes of obstruction, are helpful
to the correct diagnosis of intestinal volvulus
before operation.
6.8 Corkscrew Sign
Feature
Upper gastrointestinal radiography of neonates
with midgut volvulus revealed spiral movement
of the ascending duodenum and adjacent jejunum
on both lateral and positive radiographs. It resem-
bles a corkscrew.
J. Chen et al.
Explanation
The mesentery is a large retrograde peritoneum
attached to the posterior abdominal wall. The
jejunum and ileum are connected by the mesen-
tery to the posterior abdominal wall. Midgut vol-
vulus mainly occurs in the neonatal period.
Because mesentery is relatively free in neonatal
period, especially in middle jejunum and upper
ileum. During the neonatal period, the abdominal
cavity volume is small. If intestinal malrotation
occurs, sometimes it cannot be self-repositioned,
thus aggravating the formation of intestinal vol-
vulus. The horizontal part of the duodenum, the
ascending part and the adjacent jejunum do not
cross the midline, but go downward, resulting in
the spiral of the intestinal loop, forming a
corkscrew-­like appearance.
Discussion
In 2007, Ortizneira named and described the
corkscrew sign; that is, when performing upper
gastrointestinal radiography, the ascending part
of the duodenum and its adjacent jejunum were
spiral shaped, resembling the corkscrew [24].
The corkscrew sign often indicates that neonates
have malrotation of intestine combined with mid-
gut volvulus, which requires close clinical obser-
vation and active treatment. When the intestine
rotates poorly, the mesenteric root becomes thin-
ner, and the duodenal jejunal flexure (Treitz liga-
ment) almost always is ectopic. The most typical
part is that the duodenal jejunal flexure descends
and is ectopic to the right front of the midline.
The most serious complication of intestinal
­malrotation is volvulus. Because the mesentery is
only narrowly attached to the root of superior
mesenteric artery, midgut volvulus occurs when
the mal-fixed duodenum and upper jejunum twist
clockwise around the root of mesentery. Intestinal
volvulus often occurs in newborns, infants, and
children. The typical clinical manifestation of
intestinal malrotation is biliary vomiting.
Therefore, infants and young children with bili-
ary vomiting should be considered for the possi-
bility of intestinal malrotation, and should
undergo immediate imaging examination. When
neonatal intestinal malrotation is combined with
midgut volvulus, the early manifestations of neo-
6  Gastrointestinal Tract
natal intestinal malrotation are mainly biliary
vomiting, oliguria, or incontinence, and even
hematochezia in the late stage.
The preferred method of examination for
intestinal malrotation is usually abdominal
X-ray plain film. Positive and lateral X-ray
examination is the key to display the connection
between duodenum and jejunum. Projection in
the front and back direction is the clearest.
Patients can use the supine left anterior oblique
position to fill the stomach cavity with contrast
agent. Then, patients rotate to prone right ante-
rior oblique position to make the contrast agent
flow into the duodenum. Lateral X-ray radio-
graph can accurately observe the direction of
duodenum. When intestinal malrotation occurs,
anterior and posterior X-ray radiograph can
show that duodenal jejunal curvature descends
to the right or midline of the spine while the lat-
eral X-ray radiograph is anterior to the spine. If
combined with midgut volvulus, the corkscrew
sign may be shown; if there are peritoneal cords,
the duodenum will expand. With the degree of
proximal duodenal obstruction further aggra-
vated, the corkscrew sign will disappear. The
emergence of corkscrew sign requires long-­term
observation, because in some cases of severe
obstruction, the passage of barium is not smooth,
and often requires continuous observation for
several hours; if necessary, the patient takes the
right lateral decubitus position until the upper
jejunum shows. Doppler ultrasound has been
more and more used in the diagnosis of intesti-
nal malrotation. The “whirlpool sign” of color
Doppler ultrasound is considered as the charac-
teristic manifestation of intestinal malrotation
[25]. In a word, the corkscrew sign often indi-
cates midgut volvulus [26].
6.9 Target Sign
Feature
On a CT scan of the abdomen, this sign appears
as a round or rounded mass, with the structure
arranged in the target ring layers, from the inside
to the outside density showing high–low–high
layered changes, like the target ring name. Other
249
names: concentric circle sign, layering target
mass.
Explanation
Target sign is the most common characteristic CT
sign of intussusception. It is the feature of intus-
susception when the long axis is perpendicular to
the CT scan plane. It reflects the anatomical rela-
tionship among the intestinal wall, intestinal cav-
ity, and mesentery of intussusception. Typically
arranged from the outside to the inside are the
sheath of the outer intestinal wall, sheath of the
intestinal cavity contrast agent, sheath of the inner
intestine, eccentric intussusception of the mesen-
tery, intussusception of the intestinal wall, and
intussusception of the intestinal cavity contrast
agent (Fig. 6.8).
Discussion
Intussusception is the most common cause of
intestinal obstruction in infancy and early child-
hood. Intussusception occurs when a more proxi-
mal portion of bowel invaginates into more distal
bowel. These patients often present with a wide
range of nonspecific symptoms. The classic pre-
sentations are intermittent abdominal pain, vom-
iting, and red currant jelly-like stool. The
mechanism of intussusception is generally
believed to be caused by intestinal peristalsis
rhythm disorder, local circular muscle spasm,
severe intestinal peristalsis with spastic bowel
and its adjacent mesentery in the adjacent intesti-
nal cavity and formed mostly in the direction of
Fig. 6.8  An 11-year-old girl with right colon intussus-
ception, showing visible target sign (arrow)
250
intestinal peristalsis anterograde intussusception
[27]. A high rate of bowel resection is a
­consequence of delayed presentation, and efforts
should be made for an early diagnosis of intus-
susception and prompt referral to improve out-
come [28].
The most common CT manifestation of intus-
susception is the target sign, which reflects the
anatomical relationship among the intestinal
wall, intestinal cavity, and mesentery of the vari-
ous layers of the body of intussusception, and is
the most common characteristic CT sign of intus-
susception [29]. The target blocks are circular or
round, and can be in concentric circles. Because
of intestinal fissure, irregular alignment and
direction, when CT scan is parallel to the long
axis of intussusception, the transverse section can
show comet tail sign or renal sign, that is, mesen-
teric fat and vascular involvement. Comet tail
sign is a sign of pull-up and coalescence of proxi-
mal mesenteric intussusception vessels, and its
composition includes intussusception of the
proximal mesenteric tube. Nephroid sign or renal
mass is the oblique CT image of the free margin
of the sheath and the proximal intestine and mes-
entery of the intussusception. Comet tail sign
accompanied with renal sign is another common
characteristic CT sign besides target sign in
intussusception. Target sign can be seen in all
types of intussusception. Comet tail sign and kid-
ney sign are most common in small-bowel intus-
susception. CT features of intussusception have
certain characteristics, the diagnosis is relatively
easy, but the etiology is sometimes difficult to
determine, and examination should focus on the
head of intussusception, to find hidden primary
lesions.
6.10 Target Sign
Feature
Target sign can be seen on postcontrast CT of the
abdomen. The thickened intestinal wall shows
three-layer structures; the inner and outer layers
are high attenuation enhancement layers with a
low attenuation middle layer between them.
J. Chen et al.
Explanation
Target sign is a variety of intestinal lesions that
can cause intestinal edema, inflammation, or
both. The inner layer represents the mucosa layer,
the outer layer represents the muscular coat and
serous layer, showing high attenuation after
injecting contrast medium. The low attenuation
in the middle layer is thought to be mainly caused
by submucosa edema. The presence of target sign
suggests congestion of the mucosa or muscular
coat and serous layer with submucosa edema and
inflammation (Fig. 6.9).
Discussion
On CT, a benign intestinal tube lesion usually
manifest as a circular or homogeneous thicken-
ing of the intestinal wall, which usually does not
exceed 1 cm from the mucosa layer to the serous
layer. According to the etiology and severity of
the disease, this thickening may be slightly more
than 1  cm but is generally less than 2  cm. The
target is caused by the circumferential thickening
of the intestinal wall. The earliest report was in
the CT finding of Crohn’s disease, but this sign
can be found in a variety of benign intestinal tube
lesions. These lesions include ischemic enteropa-
thy (ischemic enterocolitis), small intestinal wall
hemorrhage, idiopathic inflammatory intestinal
disease (Crohn’s disease and colitis gravis), vas-
cular diseases (Henoch–Schonlein purpura),
infectious disease (infectious enteritis and pseu-
domembranous colitis), radiation injury, and
intestinal edema from portal hypertension. The
target sign is not a specific diagnosis, but because
there is usually no target sign in a malignant
Fig. 6.9  In patient with Crohn’s disease, CT shows thick-
ened intestinal wall at the end of ileum with target sign
6  Gastrointestinal Tract
lesion, the appearance of the target usually indi-
cates that the thickening of the intestinal wall is
caused by inflammatory disease rather than a
tumor. One exception should be noted: infiltrat-
ing sclerosing carcinoma seen in the rectum can
also appear as target sign [30].
Wall ischemia is thickening of the intestinal
wall, sometimes with target sign. This sign is an
early nonspecific sign of intestinal ischemia.
Ischemic colitis is usually seen in the elderly and
is a nonobstructive ischemic bowel disease with
no gender differences. When thickening of the
intestinal wall is observed on CT in patients
receiving anticoagulant therapy or with a poten-
tial bleeding tendency, bleeding in the intestinal
wall should be considered at this time [31]. The
most common finding of Crohn’s disease and
colitis gravis on CT is thickening of the intestinal
wall. In the acute phase, the small intestine and
colon of Crohn’s disease show mucosa stratifica-
tion when no scar has been formed, which usu-
ally also appears as the target sign. When
injecting contrast medium, the inflamed mucosa
and serosa can be enhanced, and the degree of
enhancement is related to the activity of the clini-
cal disease. Intestinal fibrosis in patients with
chronic Crohn’s disease does not show target
sign [31]. The target sign can appear in postcon-
trast CT; although there is no specificity, it can be
predicted that the thickened intestinal wall is gen-
erally caused by inflammatory enteropathy when
the target sign is found [32].
6.11 Double Halo Sign
Feature
Resembling the target sign, the thickened intesti-
nal wall shows a double-layer structure; the outer
layer is a high-density enhancement layer, and
the inner layer is weaker or not as enhanced as
the outer layer, showing soft-tissue density.
Explanation
The double halo sign is also seen in a variety of
inflammatory bowel diseases. The meaning of
each layer resembles the target sign, but because
the inner layer represents the mucosal layer and
251
the inherent muscular layer of mucosa is not
strengthened or weakened, there is no difference
in density between the middle layer and the low-­
density submucosa caused by inflammation and
edema. Some researchers believe that the weak-
ness of the inner layer of the intestinal canal indi-
cates that intestinal blood perfusion is poor and
will soon develop into irreversible ischemic
necrosis, suggesting that surgery is needed as
soon as possible (Fig. 6.10).
Discussion
The double halo sign was first proposed on CT in
Crohn’s disease of the small intestine.
Pathologically, small-bowel ischemia may be
divided into several types: mucosal necrosis in
which the lesion is limited to the mucosa; mural
necrosis in which the lesion extends to the sub-
mucosa or even into, but not through, the muscu-
laris propria; and transmural necrosis in which
the lesion extends through the muscularis propria
[33]. It cannot solely attribute a high small-bowel
necrosis or mortality rate to different enhance-
ment patterns of bowel [34]. The mucosa is the
most vascularized part of the intestines, followed
by the submucosa and the muscularis propria. A
normally perfused mucosa should be the most
intensely, or at least iso-intensely, enhancing
layer of a thickened small-bowel wall. The sub-
mucosa is composed of connective tissue with
nerves, vessels, and lymphatics traversing it.
Fig. 6.10  A 61-year-old woman presented with abdomi-
nal pain for 1 month. Computed tomography angiography
(CTA) showed the wall of the distal ascending colon was
thickened, and the enhancement manifested as a double-­
layer structure
252
However, its microvascular network is less abun-
dant than that of the mucosa. The normal submu-
cosa is uncommonly seen as a separate structure
on CT scans unless it is edematous, hemor-
rhagic, or infiltrated by tumor, or has fat deposits.
Contrast enhancement of the thickened
­submucosa rarely if ever approaches that of the
normally perfused mucosa. Homogeneous
­ ies that are arched together in the mesentery. Its
enhancement of a thickened wall might be attrib-
uted to a hyperemic mucosa. Although poor
inner-layer enhancement does not necessarily
mean the absence of perfusion, it may represent a
severe compromise of the blood supply to the
mucosa or sloughing of the mucosa [33].
The diagnostic value of CT in intestinal wall
thickening diseases and differential diagnosis has
been discussed widely [34]. The small bowel is
associated with a group of acute disorders that
are distinct from those that affect the colon, in
part because of its unique vascular supply and
physiological functions, which differ from those
of the colon. Nonlocalized acute abdominal pain
is often the first clinical presentation of disease,
which leads to an initial imaging examination,
usually performed with postcontrast CT in the
emergency department. Diffuse or regional acute
disorders of the small bowel often manifest with
nonspecific findings on CT, most commonly
mural stratification and circumferential bowel
wall thickening. On postcontrast CT images of
the abdomen and pelvis, the “target” or “double
halo” sign represents mural stratification caused
by hyperenhancement of both the inner mucosa
and the outer muscularis propria/serosa, with a
middle layer of low-attenuating submucosal
edema. In the absence of contrast enhancement,
stratified hyperenhancement is not depicted; the
only indications of underlying disease may be
bowel wall thickening (with or without associ-
ated edema), peri-enteric inflammatory change,
or ascites [35].
6.12 Comb Sign
Feature
In the abdominal pelvic postcontrast CT, a num-
ber of straight tubular, twisted shadows arranged
J. Chen et al.
in a comb-like shape can be seen on the mesan-
gial side of the ileum.
Explanation
The arteries supplying the small intestine are
emitted from the superior and inferior mesenteric
arteries, forming a series of small intestine arter-
terminal branch (straight arteriole) is longer in
the jejunum and greater in distance from each
other, whereas it is shorter and relatively close in
the ileum. Therefore, when the small arterioles in
the ileum are enlarged, distorted, and expanded,
and the distance between them increases, it
appears as a comb-like shape in the CT enhanced
scan, thus called the comb sign. This sign results
from the increase of blood flow in the affected
intestine when the inflammatory bowel disease
occurs, and the corresponding mesentery is
caused by the proliferation of fibrous fat, which is
more common in Crohn’s disease (Fig. 6.11).
Discussion
Crohn’s disease is a chronic granulomatous
inflammatory disease involving the entire layer
of the intestinal wall [36]. The digestive tract can
be affected throughout the course, but the termi-
nal ileum and proximal colon are the most com-
mon. The earliest microscopic manifestations
Fig. 6.11  A 56-year-old woman with small intestinal
lesions with “comb sign.” Crohn’s disease was
considered
6  Gastrointestinal Tract
were enlarged lymphoid follicles and small ulcers
of thrush, which are often seen in double contrast
barium angiography and are often difficult to
resolve because of low spatial resolution.
Thickening of the intestinal wall is the most
common features of Crohn’s disease, seen in
­ plications are abscess, fistula, sinus, or perianal
more than 82% of patients. It is usually thickened
by 5–10 mm or even 20 mm [37]. The thickened
intestinal wall is more common in the terminal
ileum and can also be seen in digestion. The clin-
ical history, the distribution of the disease, and
other related tests are helpful for differential
diagnosis of the disease.
In the acute phase, the intestinal wall is strati-
fied, and there is a target or double halo on CT,
which may be caused by submucosal edema or
intestinal wall fat infiltration. Thickening of the
intestinal wall is not a unique manifestation of
Crohn’s disease. In fact, more than 60% of
patients have inactive ulcerative colitis, and only
about 8% of patients have Crohn’s disease [38]. It
can also be found in radiation enteropathy, graft-­
versus-­host disease, and chronic ischemia of the
intestinal wall. Inflamed mucosal and serosal lay-
ers can be intensified during postcontrast CT
scanning, and the degree of enhancement is
related to the clinical activity of the disease. In
patients with longer course of disease, intestinal
wall fibrosis, stratification loss, and intestinal
wall density were uniform on CT [38]. In patients
known to have Crohn’s disease, if the aforemen-
tioned mesenteric vascular proliferation, distor-
tion, dilatation, and comb signs caused by
protrusion of the small blood vessels occur, it
indicates a tendency for the disease to deteriorate
acutely. Patients with clinical symptoms for the
first time can have a CT scan that reveals the pos-
sibility of Crohn’s disease diagnosis, but this is
not an absolute specificity because it can also
occur in patients with lupus mesangial
vasculitis.
Other diseases can develop vasodilatation dur-
ing development, such as vasculitis (including
nodular polyarteritis, Henoch–Schonlein syn-
drome, microscopic polyangiitis, Bechet’s syn-
drome), mesenteric thrombosis, strangulated
intestinal obstruction, or ulcerative colitis. The
appearance of comb signs is of great help in iden-
253
tifying lymphomas and metastases, as these two
diseases usually show less blood supply. About
28% of patients with Crohn’s disease can also
show complications on CT, which is very helpful
for the treatment of the disease. The main com-
disease, which can be well shown on CT. In addi-
tion, patients with Crohn’s disease should also be
carefully examined for other signs of the disease
on CT, including liver fatty infiltration, kidney
stones, gallstones, ankle arthritis, and hydrone-
phrosis [37].
6.13 Gastrointestinal String Sign
Feature
In small intestinal barium examination, fine bar-
ium lines resembling rough cotton threads are
formed in the small intestine.
Explanation
The gastrointestinal tract is severely narrowed,
leading to linear changes in the internal cavity.
Gastrointestinal stricture is generally termed as
endoluminal stenosis, but the term was originally
used to describe reversible stenosis in Crohn’s
disease. The cause of stenosis is incomplete
obstruction from irritability and spasm caused by
severe ulcer, and alternation of stenosis and dila-
tion can be found. When stenosis is mainly
caused by edema and spasm, the degree of steno-
sis is not the same. If the small intestinal wall is
thickened by fibrosis, the internal diameter of the
cavity will be narrowed uniformly. Mucosa is
replaced with fibrous necrotic tissue; islands of
mucosa can be found occasionally.
Discussion
The gastrointestinal string sign has been identi-
fied as a characteristic manifestation of Crohn’s
disease, most commonly in the terminal ileum
[39]. Intestinal abnormalities in stage Crohn’s
disease include coarse villus sign, fold thicken-
ing, and aphthous ulcer. These signs are not spe-
cific and can be found in other diseases, but their
presence provides solid evidence for Crohn’s
disease. Linear ulcers along the mesenteric mar-
254 J. Chen et al.

gin are one of the most important diagnostic fea- 6.14 Bowel Wall Fat Halo Sign
tures of Crohn’s disease of the small intestine,
parallel to shortened, concave, or rigid mesen- Feature
teric margins. Adjacent mesentery thickens and In the CT scan the thickened middle layer of the
retracts, especially at the junction with the intestinal wall or the submucosa forms low den-
invaded intestinal segment. The rigid mesenteric sity from fat infiltration, thereby forming a three-­
margin is caused by transmural inflammation layer structure throughout the intestinal wall.
that spreads from a linear ulcer into the mesen- Other names: fat halo sign.
tery. As the ulcer progresses, spasms and irrita-
bility increase, folds become coarser and thicker, Explanation
and gastrointestinal strings can appear. The appearance of the bowel wall fat halo sign on
According to the different stages of development CT is usually seen in Crohn’s disease in the small
of the lesion, the proximal intestinal tract may or intestine or idiopathic inflammatory bowel dis-
may not be dilated. Spasms are often change- ease in the colon, and can also occur in normal
able. Repeated observation of photographs con- people without inflammatory bowel disease. The
firms that dilation sometimes occurs in the lesion black density formed by the infiltration of fat in
intestinal segment. However, when the spasm the middle layer of the intestinal wall is different
persists, temporary proximal intestinal dilatation from the gray density formed by edema of the fat
may occur with symptoms of intestinal obstruc- wall. The CT value of the infiltrated tissue of the
tion. In the stenosis stage, spasms secondary to annular fat is mostly less than 10 Hu, but its den-
ulcers lead to sustained proximal dilation, sity is different from pure mesenteric fat or retro-
although stenosis and complete intestinal peritoneal fat, which may be caused by partial
obstruction are rare. volume effect or simultaneous edema of the
Barium fluoroscopy remains a valuable diag- intestinal wall. The outer margin of the lamina
nostic technique for evaluating structural and propria of the mucosa may be more clearly visi-
functional disorders of the small bowel in the ble or may be unclear from dispersion in the infil-
sophisticated imaging modalities. Conventional trated fat (Fig. 6.12).
small-bowel follow-through studies can be per-
formed in most patients, in which periodic imag-
ing of the entire small bowel is examined using
fluoroscopic guidance. Some patients may bene-
fit from enteroclysis, in which barium is instilled
into the small bowel via a catheter placed in the
proximal jejunum for optimal distention and bet-
ter depiction of individual small-bowel loops. A
pattern approach for the wide spectrum of abnor-
malities found on barium studies would contrib-
ute to the diagnostic clues [40]. In addition to
Crohn’s disease, other diseases can also show
similar signs. In cases of pyloric stenosis, the nar-
row elongated pyloric canal shows a single bar-
ium line. If the intestinal tract narrows and some
obstructions occur, carcinoid tumors can also
lead to radiologic manifestations of gastrointesti-
nal linear signs. In conclusion, the presence of
gastrointestinal string sign is highly suggestive of
Crohn’s disease, but it can also occur in other dis- Fig. 6.12  A 43-year-old woman presented with bowel
eases [41]. wall fat halo sign in the terminal ileum
6  Gastrointestinal Tract
Discussion
The presence of fat in the intestinal wall is usu-
ally considered to be the evidence of prior inflam-
matory bowel disease (IBD). Essentially, fat in
the intestinal wall is a pathological change of
chronic inflammation [42]. When fat halo sign is
visible in the small intestine and colon, it is often
considered as a specific sign of Crohn’s disease.
Only when there is colon involvement are the
extent of involvement and the extent and distribu-
tion of thickened intestinal wall the main basis
for distinguishing between ulcerative colitis and
Crohn’s disease. The fat halo sign of the intesti-
nal wall is different from edema. The pathologi-
cal basis of the fat halo sign is the accumulation
of submucosal fat, and the edema is the increase
of the water in the interstitial space of the intesti-
nal wall. Therefore, edema is mainly caused by
thickening of the intestinal wall, whereas fat halo
sign is mainly separated by mucosa and intestinal
wall. In addition, edema is often an acute reaction
to a disease, and it generally has corresponding
clinical symptoms, but patients with fat halo
signs do not necessarily have gastrointestinal
symptoms [43]. Some studies have found that
scattered fat halos can be seen in the distal ileum
or colon on CT in some patients with kidney
stones. In the absence of a history of IBD or other
supporting signs of IBD, intestinal fat halo is
thought to be a normal feature, especially in
obese patients [44].
Fat halo sign is best seen when the intestinal
cavity is moderately dilated, but is less seen when
the intestinal cavity is dilated significantly, pre-
sumably the result of intestinal wall tension and
compression of the adipose layer when the intes-
tinal cavity was dilated excessively. If the intesti-
nal cavity is clean and full of gas, the mucosal
layer between the intestinal cavity and the fat
halo can be shown. If the intestinal cavity is
unclean, the mucosal layer and intestinal contents
may be mixed. In general, fat in normal intestinal
wall is thinner than that seen in idiopathic
IBD.  The mucosa propria muscle layer is also
uniform in thickness structure; the thickness is
generally less than 1 mm, the surrounding mes-
entery is rarely abnormal, and normal intestinal
wall fat in the intestinal cavity generally is not
255
dilated or is slightly dilated. It is difficult to dis-
tinguish between normal fat and Crohn’s disease
when fat layers are found in the wall of the termi-
nal ileum. Fat halo syndrome in Crohn’s disease
is often accompanied by mucosal disorders,
intestinal wall thickening, intestinal stenosis, and
other changes, but the simple “fat halo syndrome”
is not [44]. It is necessary to inquire about the
detailed medical history and other tests for fur-
ther diagnosis. In summary, intestinal fat halo is
one of the manifestations of inflammatory bowel
disease, but it can also occur in the absence of
inflammatory bowel disease; the sign is normal
or only represents obesity.
6.15 Disproportionate Fat
Stranding Sign
Feature
The fat stranding adjacent to thickened bowel
wall suggests the cause of abdominal pain com-
ing from gastrointestinal tract on CT. It is a CT
sign of abdominal inflammatory diseases. The
key point of disproportionate fat stranding is the
degree of fat stranding is significantly heavier
than the degree of bowel wall thickened and out
of proportion.
Explanation
In a few acute diseases of the gastrointestinal
tract, the pathological process is c­ haracteristically
centered in the mesentery adjacent to the bowel
wall rather than in bowel wall itself. In these dis-
eases, the fat stranding is often disproportion-
ately greater than the degree of wall thickening.
Because the duration of diseases typically mani-
festing disproportionate fat stranding is short,
this sign may help narrow the scope of differen-
tial diagnosis (Fig. 6.13).
Discussion
The disproportionate fat stranding sign is a CT
sign proposed by Pereira et  al. [45] that shows
that the fat stranding adjacent to thickened bowel
wall on CT scan and the degree of fat stranding is
significantly heavier than the degree of bowel
wall thickened and out of proportion. Most acute
256
2. Appendices epiploicae are pedunculated adi-
Fig. 6.13  Noncontrast CT of a male patient with right-­
sided diverticulitis shows severe peri-colonic fat
stranding
inflammatory diseases of the gastrointestinal
tract are centered in the bowel wall; the degree of
bowel wall thickening typically exceeds the
degree of associated fat stranding. In a few acute
diseases of the gastrointestinal tract, the patho-
logical process is characteristically centered in
the mesentery adjacent to the bowel wall rather
than in the bowel wall itself. In these diseases, the
fat stranding is often disproportionately greater
than the degree of wall thickening, then the dis-
proportionate fat stranding sign are formed. On
CT this sign often suggests the cause of abdomi-
nal pain coming from the gastrointestinal tract, 3. The omentum is formed by the overlapping of
mainly including four diseases: diverticulitis,
epiploic appendagitis, omental infarction, and
appendicitis.
1. Diverticulitis is a mucosal and submucosal
capsular bag that passes through the muscular
layer of the colon wall. The muscle layer
between the colonic zone and the mesentery
undergoes perforation involving the nerves
and blood vessels. Diverticula can be found
anywhere in the colon, but they occur pre-
dominantly in the descending and sigmoid
colon. The appearance of acute diverticulitis
on CT scans parallels the pathological fea-
tures. The most common CT finding is para-
colic fat stranding, which characteristically is
disproportionately more severe than the rela- 4. Appendicitis is the most common cause of
tively mild, focal colonic wall thickening.
J. Chen et al.
Diverticula are typically present. The inflam-
matory process can result in accumulation of
fluid in the root of the sigmoid mesentery, and
engorgement of the mesenteric vessels [46].
pose structures protruding from the external
surface of the colon into the peritoneal cavity,
typically 1–2  cm thick and 2–5  cm long.
Epiploic appendagitis often occurs in the left
and right lower abdomen, because sigmoid
colon and cecum have numbers of large appen-
dices epiploicae. An epiploic appendagitis is a
lesion caused by torsion of the omental fat sag
or spontaneous venous embolization, resulting
in ischemia or embolism of intestinal lipids,
and concurrent infection. The patient’s clinical
manifestations are sudden, with severe abdom-
inal pain resembling appendicitis. Generally,
only conservative treatment is needed. On CT,
the main manifestation is oval fat attenuation
lesions of 1–4 cm, and the surrounding mesen-
tery may have an inflammatory exudation ring
surrounded by an obvious high-attenuating
crescent sign [47]. A small number of patients
have a point-like high attenuation (embolized
blood vessels or bleeding) in the center of the
lesion. Adjacent bowel walls may be thickened
and compressed, with disproportionate fat
stranding around them.
the peritoneum between the transverse colon
and the stomach, which contains a large
amount of fat and hangs in front of the intes-
tine. Omental infarction involves a segment of
the omentum that often occurs on the right
side. Because the blood supply route on the
right side is long and fragile, it easily caused
venous embolism, which eventually leads to
omental infarction. The specific CT signs of
omental infarction are a large pie-shaped
high-attenuation fatty mass in the omentum,
which can be adjacent to the colon or at a cer-
tain distance. The bowel wall can be thickened
nearby, but fat stranding is more pronounced.
Omental infarction and epiploic appendagitis
are benign and self-limiting diseases.
acute abdominal pain that requires surgical
6  Gastrointestinal Tract
intervention. The most characteristic CT
manifestation of appendicitis is the direct
­
visualization of a dilated (>6 mm in diameter)
and fluid-filled appendix. Other direct signs
include an abnormally thickened appendix,
increased attenuation of the appendix after
contrast material administration, and peri-­
appendicular fat stranding. Secondary signs
include the appearance of appendicolith or
thickening of the cecal apex. Peri-­appendicular
fat stranding is typically mild to moderate, but
it can be severe. The diagnosis of appendicitis
from CT findings is straightforward if the
appendix is easily visualized. However, in
cases of perforated appendicitis with peritoni-
tis or abscess formation, the appendix may be
difficult to see. The finding of severe fat
stranding in the right lower quadrant without
substantial cecal or ileal thickening may sug-
gest the possibility of appendicitis. A careful
search for a thickened or focally perforated
appendix will yield the diagnosis.
The disproportionate fat stranding sign sug-
gests the causes of abdominal pain coming from
the gastrointestinal tract, including diverticulitis,
epiploic appendagitis, omental infarction, and
appendicitis. It was reported that fat stranding
sign is one of the most frequent findings in isch-
emic colitis regardless of severity of involvement
[48]. It is necessary to make a correct diagnosis,
as epiploic appendagitis and omental infarction
are typically self-limited conditions, whereas
appendicitis and many cases of diverticulitis
require surgery or other intervention.
6.16 Misty Mesentery Sign
Feature
Abdominal CT scan shows an increase in mesen-
teric fat density, which may be homogeneous or
heterogeneous, diffuse or focal, depending on the
nature of the lesion.
Explanation
The term “misty mesentery” indicates a patho-
logical increase in mesenteric fat attenuation on
257
Fig. 6.14  A 64-year-old woman presented with upper
abdominal pain for 1 day. Abdominal CT shows uneven
increased attenuation of the mesenteric fat
CT. On abdominal CT scans, normal mesenteric
fat showed uniform low density, similar in den-
sity to the fat in subcutaneous and retroperitoneal
spaces. CT sensitively shows the changes of mes-
enteric fat density caused by abdominal lesions.
Mindelzun et al. [49] used mesenteric turbidity to
describe the infiltration of mesenteric fat by
inflammatory cells, fluid (edema, lymph, blood),
tumor, and the increase of mesenteric fat density
during fibrosis. The main causes include edema,
inflammation, hemorrhage, neoplasm, and mes-
enteritis (Fig. 6.14).
Discussion
A misty mesentery is a sign of mesenteric infil-
tration, showing increased attenuation of the
mesenteric fat-called misty mesentery, with some
soft tissue nodules on CT. It was first described
by Mindelzun in 1996 [49]. This sign is seen in
mesenteric panniculitis, a nonspecific inflamma-
tory disorder of the mesenteric fat, which can be
either acute or chronic. Mesenteric panniculitis
can lead to fat necrosis, fibrosis, and retraction of
the mesentery. The normal small bowel mesen-
tery is rich in fat, which has the same attenuation
as subcutaneous fat on CT (−100 to −160 HU).
However, if there is cellular or acellular infiltra-
tion of the mesentery, the attenuation value
increases (−40 to −60 HU). This increased atten-
uation of the fat is referred to as the misty mesen-
tery sign. In such cases, the mesenteric vessels,
258
which normally appear distinct from the fat, may
sometimes become indistinct or effaced like a
tree in the mist. The sign is nonspecific and has
been ascribed to various factors such as edema,
inflammation, malignancy, lymphatic obstruc-
tion, hemorrhage, or idiopathic (mesenteric pan-
niculitis). There are no specific presenting
complaints and it is usually diagnosed inciden-
tally, with an incidence of about 0.6% [50]. The
treatment usually involves treating the underly-
ing condition. Atypically, mesenteric lymphoma
can present with imaging findings that overlap
with sclerosing mesenteritis. Calcification is not
typically seen in lymphoma before treatment, and
its presence in a mesenteric mass suggests an
alternate etiology such as sclerosing mesenteritis or
carcinoid tumor. In the absence of a known history
of malignancy, the presence of a “misty mesentery”
with small nodal masses incur diagnostic dilemma.
More specifically, differentiating lymphoma from
asymptomatic sclerosing mesenteritis can present a
challenge [51]. A wide spectrum of diseases can
result in the misty mesentery. Although on occa-
sion the cause of this misty mesentery may prove
elusive, in most situations the cause can be deter-
mined by analysis of the patient’s history and asso-
ciated CT findings [52]. In patients suffering from
acute abdominal disease, misty mesentery may be
considered a feature of the underlying disease.
Otherwise, it may represent an incidental finding
Fig. 6.15  Two cases with mesenteric panniculitis. (a)
The fat density of the mesentery had increased unevenly,
which appeared foggy or like ground glass, and sur-
rounded the mesentery vessels on postcontrast
J. Chen et al.
for other reasons [53]. The development of malig-
nancy in patients with incidentally detected misty
mesentery is reported to correlate with mesenteric
lymph node size. Patients with misty mesentery
and largest mesenteric lymph node less than 10 mm
without lymphadenopathy in other areas demon-
strate a benign course, and no further follow-­up
may be necessary [54].
6.17 Fat Ring Sign
Feature
CT findings of mesenteric panniculitis. The den-
sity of mesenteric adipose tissue increased (−40
to −60 HU), showing a single or multiple soft tis-
sue density masses with clear boundary and
uneven density. The masses surround the mesen-
teric macrovascular but do not involve the vascu-
lar, and fat may exist around the mesenteric
vascular, forming a fat ring sign.
Explanation
Mesenteric panniculitis is characterized by
chronic inflammatory cell infiltration, fat necro-
sis, and fibrous tissue forming a “pseudo-tumor
nodule.” It surrounds but does not invade mesen-
teric vessels. Mesenteric arteriovenous vessels
are growing in the lesion and adjacent vessels
have normal fat density (Fig. 6.15).
CT. Multiple lymph nodes at the root of mesentery with
“fat ring sign.” (b) Postcontrast CT of another case indi-
cated the pseudo-capsule of the mesenteric panniculitis
6  Gastrointestinal Tract
Discussion
Sclerosing mesenteritis (SM) is a rare idiopathic
and complex inflammatory and fibrotic disorder
primarily affecting the small-bowel mesentery.
Its exact cause is unknown. The spectrum of this
disease has included mesenteric lipodystrophy,
mesenteric panniculitis, mesenteric sclerosis, and
retractile mesenteritis [55]. The integrity of mes-
enteric vessels and gastrointestinal lumen is com-
promised by mass effect, leading to the clinical
symptoms. The most common symptoms include
abdominal pain, nausea, vomiting, diarrhea,
weight loss, and rarely ascites and small-bowel
obstruction. In physical examination, abdominal
tenderness, palpable abdominal mass in the left
upper quadrant or epigastrium, are noted. The
mass is often deep and poorly defined. Surgical
resection is sometimes attempted for definitive
therapy, although the surgical approach is often
limited by vascular involvement. The most com-
mon complications of SM include bowel obstruc-
tion, ileus or ischemia, and obstructive uropathy
or renal failure; 85.7% of deaths are secondary to
SM-related complications [56].
The CT appearance of SM may vary depend-
ing on the predominant tissue component (fat,
inflammation, or fibrosis). CT has an important
function in suggesting the diagnosis in the proper
clinical setting and is useful in distinguishing SM
from other mesenteric diseases with similar CT
features such as carcinomatosis, carcinoid tumor,
lymphoma, desmoid tumor, and mesenteric
edema. The most common finding on CT is a
soft-tissue mass within the small bowel mesen-
tery. Two signs seen on CT, that is, “fat ring” and
“tumor pseudo-capsule,” are considered some-
what specific for mesenteric panniculitis [57].
The fat ring sign is caused by preservation of the
fat nearest the mesenteric vessels; the tumor
pseudo-capsule represents separation of the unin-
volved mesentery from the inflamed fat by a band
of tissue [58]. The CT appearance of sclerosing
mesenteritis can vary from subtle increased atten-
uation in the mesentery to a solid soft-tissue
mass. Sclerosing mesenteritis most commonly
appears as a soft-tissue mass in the small-bowel
mesentery, although infiltration of the region of
the pancreas or porta hepatis is also possible. The
259
mass may envelop the mesenteric vessels, and,
over time, collateral vessels may develop.
Sclerosing mesenteritis is a benign chronic
inflammatory condition often confused with neo-
plastic process. There may be preservation of fat
around the mesenteric vessels, a phenomenon
that is referred to as the “fat ring sign.” This find-
ing may help distinguish sclerosing mesenteritis
from other mesenteric processes such as lym-
phoma, carcinoid tumor, or carcinomatosis [59].
CT angiography is especially helpful in delineat-
ing the relationship of the mass to the mesenteric
vasculature, significant involvement of which can
compromise blood supply to the bowel and result
in bowel wall ischemia.
6.18 Hyperattenuating Ring Sign
Feature
The hyperattenuating ring sign is found in
abdominal CT scan, which consists of a thin cir-
cular or oval soft tissue high-density ring around
the colon surrounding the low-density fat.
Explanation
The hyperattenuating ring sign is the characteris-
tic finding of primary epiploic appendagitis
(PEA). The hyperattenuating ring represents the
thickened peritoneum, the fat density in it repre-
sents inflamed epiploic appendages.
Histologically, white blood cells exudate around
the inflammatory epiploic appendages [60]
(Fig. 6.16).
Discussion
Primary epiploic appendagitis (PEA) is a rare
cause of acute abdominal pain determined by a
benign self-limiting inflammation of the epiploic
appendages, and ischemia is the main pathophys-
iological mechanism [61]. The possible reasons
are related to the spontaneous torsion of intesti-
nal fat lobe and spontaneous venous thrombosis,
which result in aseptic fat necrosis and aseptic
inflammatory reaction. It may manifest with het-
erogeneous clinical presentations, mimicking
other more severe entities responsible for acute
abdominal pain, such as acute diverticulitis or
260
Fig. 6.16  A 34-year-old woman presented with abdomi-
nal pain and visible paracolonic fat density lesions sur-
rounded by hyperattenuating rings (arrows).
Hyperattenuating rings represent the thickened perito-
neum around the lesion
appendicitis. PEA is a benign self-limiting dis-
ease and spontaneously resolves without surgery
within 5–7 days [62]. Imaging is crucial to avoid
inaccurate diagnosis that may lead to appropriate
therapy, and it is imperative that radiologists be
familiar with this entity. The hyperattenuating
ring sign is a characteristic manifestation of PEA,
although the negative sign cannot exclude the
diagnosis of PEA. CT is currently the most effec-
tive means to diagnose PEA. The CT findings of
PEA change with time. The size, extent, size of
high-density ring, and exudation around the
lesion will change, but the change is irregular,
and the lesion may persist for several months
before disappearing. Correct understanding of
the sign and definite imaging diagnosis of the
disease can avoid unnecessary clinical
­ tion. Similar manifestations can also be seen in
overtreatment.
The imaging features of PEA have certain
characteristics, most of which can provide a defi-
nite diagnosis. The most common CT findings of
PEA are round-like fat-density lesions on the
opposite side of the mesocolon adjacent to the
colon. Soft tissue density rings (the hyperattenu-
ating ring sign) can be seen around them, repre-
senting inflammatory reaction of the peritoneum
covering the mesocolon. Punctate or small
patches of high-density shadow can be seen in
the center of the lesion, suggesting necrosis or
thrombosis of the central vein of epiploic append-
age [61], slight enhancement of the thin wall on
J. Chen et al.
postcontrast CT scanning, high-density shadow
of cords and strips in the fat space around the
lesion, rare involvement of the adjacent intestinal
wall, and no obvious signs of fluid accumulation
around the lesion. CT represents the gold stan-
dard technique for the evaluation of patients with
indeterminate acute abdominal pain [63].
Imaging findings include the presence of an oval
lesion with fat-attenuation surrounded by a thin
hyperdense rim on CT (“hyperattenuating ring
sign”) abutting the large bowel, usually associ-
ated with inflammation of the mesentery. A cen-
tral high-attenuation focus within the fatty lesion
(“central dot sign”) can be observed and indicates
a central thrombosed vein within the inflamed
epiploic appendage. PEA may be located within
a hernia sac or attached to the vermiform appen-
dix. Chronically infarcted epiploic appendage
may detach, appearing as an intraperitoneal loose
calcified body in the abdominal cavity [63].
6.19 Arrowhead Sign
Feature
The arrowhead sign, which is obtained after the
administration of oral or rectal contrast material,
is seen on CT images as an arrowhead-shaped
collection of contrast medium localized to the
upper part of the cecum near the orifice of the
appendix. An air-arrowhead sign has also been
described, which refers to a collection of air
rather than of contrast medium at the same loca-
the diverticulum mouth of the colon, also known
as arrow sign.
Explanation
Inflammatory changes associated with acute
appendicitis can cause focal, symmetrical thick-
ening and coaptation of the upper cecal wall,
which allows contrast material to assume the
configuration of an arrowhead as it funnels to
the  level of the obstructed appendiceal orifice.
The amount of contrast medium collected at the
cecal–appendiceal junction can vary and depends
on the presence or absence of cecal air, the degree
of cecal distention, and the cecal wall swells in
6  Gastrointestinal Tract
the particular manner. Hence, the resulting arrow-
head sign also assumes a variety of appearances
ranging from short and fat to long and thin.
Although the arrowhead sign is generally most
conspicuous on transverse CT images, it may
occasionally be difficult to see. In these cases,
additional images reformatted in the sagittal or
coronal plane will occasionally show a more
expected arrowhead shape. The arrowhead sign
formed by inflammatory changes occurring in
colonic diverticula resembles the arrowhead sign
formation mechanism of acute appendicitis. The
pathophysiology of diverticulitis mirrors that of
appendicitis, with an obstructive fecalith initiat-
ing the inflammatory process.
Discussion
Appendicitis is the most common cause of acute
abdominal pain that requires surgical interven-
tion. Primary diagnostic criteria for acute
appendicitis have been defined as visualization
of an enlarged appendix greater than 6  mm in
diameter. Secondary criteria were wall thicken-
ing and enhancement, appendicolith, peri-
appendiceal fat stranding, free fluid in right
lower quadrant or pelvis, peri-appendiceal
abscess, small bowel obstruction, and mural
thickening of cecum [64]. However, because the
position of the appendix varies, the diagnosis of
appendicitis in a patient with abdominal pain
can be a challenge. It is reported that up to one
third of patients with appendicitis have atypical
findings at presentation. The use of clinical cri-
teria alone to diagnose appendicitis results in
removal of a normal appendix in approximately
20% of patients undergoing diagnostic laparot-
omy and causes approximately 20% of patients
with appendicitis to be discharged without
undergoing surgery. As a result, many imaging
modalities, including CT examination of the
abdomen or of the right lower quadrant, have
been employed to balance the false-positive lap-
arotomy rate with the rate of perforation and
peritonitis at the time of surgery. When nonvisu-
alization of the appendix is a problem, the radi-
ologist must rely on the presence or absence of
so-called secondary signs of appendicitis to
help make or exclude the diagnosis [65].
261
The CT arrowhead sign is another of these
secondary signs of appendicitis. Rao et  al. [66]
performed a study with 100 patients suspected of
having appendicitis. The CT arrowhead sign was
present in 17 of the 56 patients with appendicitis
(sensitivity, 30%). The sign was absent in all 43
of the patients without appendicitis (specificity,
100%). This sign is, therefore, helpful in the eval-
uation of patients with appendicitis whose stud-
ies otherwise reveal (i.e., in addition to the
arrowhead sign) only mild, nonspecific inflam-
matory findings in the right lower quadrant.
Because the sign is formed by the extension of
inflammation from the appendix to the cecum,
the arrowhead sign may allow for placement of
patients with appendicitis into two surgical
groups: those who likely will do well with stan-
dard ligation (arrowhead sign not present) and
those who may require partial cecectomy (arrow-
head sign present) [65]. The pathophysiological
process of colonic diverticulitis mirrors appendi-
citis; that is, a diverticulum is obstructed by a
fecalith and becomes inflamed. Contiguous
spread of inflammation at the site of diverticular
perforation through the colonic wall results in
focal inflammation of the colonic wall. On occa-
sion, as the inflammation spreads through the
colonic wall, an arrowhead-shaped collection of
contrast material becomes evident in the adjacent
colonic lumen. The appearance and frequency of
occurrence of the arrowhead sign at CT are
dependent on the degree of colonic luminal dis-
tention, the orientation of the affected bowel rela-
tive to the axial scanning plane, and the amount
of potentially obscurant adjacent inflammation.
In addition to contrast material, luminal air may
also collect at the site of focal wall thickening,
resulting in an “air-arrowhead” sign [67].
6.20 Accordion Sign
Feature
The accordion sign is a finding on CT scans in
patients who have received oral contrast material.
It constitutes alternating bands of lower soft tis-
sue attenuation and higher contrast material
attenuation within the large bowel.
262
a b
Fig. 6.17 (a, b) Accordion sign in a patient with pseudo-membranous colitis. Contiguous CT sections show marked
wall thickening of the colon with contrast material (arrows) in crevices between the folds
Explanation
A small amount of contrast agent that reaches the
colon after oral contrast is filled in the fissure
between the thickened colon folds. This low
attenuation and high attenuation strip-like
appearance is very similar to an accordion. The
pattern varies depending on the degree of colonic
edema and the amount of contrast agent depos-
ited between the folds of the colon (Fig. 6.17).
Discussion
The low-attenuation soft tissue shadow of the
accordion sign represents a significant thickening
of the colon fold from edema of the intestinal
wall. This sign is considered a characteristic CT
manifestation of pseudo-membranous colitis
(PMC) [68]. Pathologically, low-attenuation soft
tissue shadow represents a markedly thickened
colon fold caused by intestinal wall edema, and
the high-attenuation shadow is a small amount of
contrast agent that reaches the colon after oral
contrast and is filled into the fissure between the
thickened colon folds [69]. PMC is an intestinal
disease caused by gram-positive anaerobic bacte-
ria, primarily Clostridium difficile in the colon,
also known as C. difficile overgrowth of intracta-
ble Clostridium spp. This reaction causes a
decrease in the normal flora in the intestine from
heavy use of antibiotics, and some oncology
drugs can also produce the same effect. It is a
series of diseases that are clinically capable of
producing fulminant colitis from mild diarrhea to
life-threatening colitis. The diagnosis of PMC
J. Chen et al.
relied on the positive detection of toxins in the
feces and the detection of pseudo-membranous
plaques under colonoscopy.
This pathological change can be manifested in
imaging. Plain radiography, contrast enema stud-
ies, and CT are useful in the evaluation of
PMC. Conventional radiography can show non-
specific changes such as thickening of colon
folds, colon expansion, and peritoneal effusion.
Plain film can demonstrate polypoid mucosal
thickening, “thumb printing” (wide transverse
bands associated with haustral fold thickening),
or gaseous distention of the colon. Small nodular
filling defects representing mucosal plaques is
the primary finding in mild cases of PMC on con-
trast enema. Contrast enema study is contraindi-
cated in patients with severe PMC by the potential
danger of perforation. CT is mainly used in
patients with advanced PMC who have no spe-
cific symptoms and are difficult to diagnose.
Common CT findings include wall thickening,
low-attenuation mural thickening corresponding
to mucosal and submucosal edema, the accordion
sign, the target sign (double halo sign), perico-
lonic stranding, and ascites [70]. Macari et  al.
[71] believed that the accordion sign was a mani-
festation of a high degree of edema in the colon
and was unspecific for the cause. Intestinal wall
thickening and nodules can also be seen in other
colitis, but mainly in patients with PMC. In gen-
eral, except for Crohn’s disease, the degree of
colon wall thickening of pseudo-membranous
colitis is usually greater than other causes [69].
6  Gastrointestinal Tract
Fishman et  al. reported that the accordion sign
occurred in 5 of 26 patients with confirmed PMC
[72]. Since then, there have been further reports
that the positive rate of accordion signs in
advanced PMC patients accounted for 51% to
67%. Familiarity with these imaging features
may help make the diagnosis and prevent pro-
gression to deterioration.
6.21 A
 pple Core Sign; Apple Core
Lesion
Feature
The apple core sign refers to the local stenosis of
the colorectal during the barium enema examina-
tion. This stenosis is characterized by the shape
of the shoulder at both ends, and the central
lumen is narrow, the mucosa is destroyed, and the
edges are irregular, which shape resembles a left-
over apple core.
Explanation
This sign is observed when the cancer infiltrates
around the intestinal wall more than two thirds of
a b
Fig. 6.18  In this 66-year-old man, the apple core sign refers to the local stenosis of the sigmoid colon during barium
enema study
263
the circumference of the intestinal lumen. The
two ends of the sign are the bulging boundary
formed by the round mount, and the central nar-
row segment of the lumen is the cancer canal of
ulcer (Fig. 6.18).
Discussion
An apple core lesion is the radiologic manifesta-
tion of a focal stricture of the bowel at a contrast
material enema study [73]. The apple core sign
was originally described on barium enemas as an
abrupt, irregular, and segmental stenosis with
“shouldered margins” in the colonic wall. This
sign represents a nondistensible narrowing of the
intestinal lumen by a stenosing circumferential
colorectal mass that allows passage of only a
small amount of contrast media. The appearance
resembles an apple core, the remnant of a par-
tially eaten apple. The apple core sign is also
known as “napkin ring sign” [74]. From the path-
ological point of view, when the diameter of the
cancer exceeds 4–5 cm, the incidence of “apple
core sign” is significantly increased, indicating
that as the volume of the cancer increases, infil-
tration along the circumference of the intestine
264
also increases. When the infiltration exceeds two
thirds of the circumference of the lumen, it can
cause narrowing of the lumen, which is mani-
fested as apple core sign. When the cancer has
infiltrated along the intestine, the two sides of the
ring are merged and disappear, and a cancerous
ulcer tunnel is formed in the center. The two ends
of the mass retain the ring embankment, forming
a bulge boundary at both ends of the lesion [75].
Imaging studies are a major component in the
evaluation of patients for the screening, staging,
and surveillance of colorectal cancer. CT colonog-
raphy provides important information for the pre-
operative assessment of T stage as an option for
colorectal cancer screening. Three-­ dimensional
CT to image the vascular anatomy facilitates lapa-
roscopic surgery. MRI is more accurate than CT in
evaluating liver metastases. Positron emission
tomography (PET)/CT is valuable in the evalua-
tion of extracolonic and hepatic disease. The clas-
sic apple core sign is not specific for colorectal
cancer and has also been described in other dis-
eases of the colon, such as diverticulitis, inflam-
matory colitis, ischemic colitis, radiation-­induced
colitis, including Crohn’s ­disease, and intestinal
tuberculosis, and even in colonic amyloidosis [74].
6.22 Duodenal Wind Sock Sign
Feature
The duodenal wind sock sign is a finding that
may be seen on an upper gastrointestinal series.
This sign consists of a barium-filled sac that lies
entirely within the duodenum and is surrounded
by a narrow radiolucent line that is well demon-
strated as the barium in the duodenum passes dis-
tal to the diverticulum.
Explanation
The duodenal wind sock sign has been described
as a typical appearance of an intraluminal duode-
nal diverticulum. The narrow radiolucent line
represents an intraluminal mucosal diaphragm or
web caused by failure of normal recanalization of
the duodenum after epithelial cell occlusion of
the foregut lumen in the 7-week human embryo.
Over time, the diaphragm passively elongates as
J. Chen et al.
Fig. 6.19 Upper gastrointestinal series shows orally
administered barium filling a sac-like structure extending
from the distal second to the proximal third portion of the
duodenum, surrounded by a narrow radiolucent line [78]
a result of continual peristalsis to form the wind
sock configuration of an intraluminal duodenal
diverticulum. Because of the thin radiolucent
stripe surrounding the diverticulum, the appear-
ance on an upper gastrointestinal series has also
been described as the halo sign (Fig. 6.19).
Discussion  The “wind sock” sign refers to the
pathognomonic appearance of an intraluminal
duodenal diverticulum [76]. An intraluminal duo-
denal diverticulum is a rare developmental anom-
aly usually within the second portion of
duodenum. Most cases originate near the ampulla
of Vater and lie in an isoperistaltic direction.
Attachment of the diverticulum to the duodenum
usually involves less than one half of the wall cir-
cumference, although in a few cases to the entire
circumference also has been reported. When the
diverticulum is attached to the entire circumfer-
ence of the duodenal wall, an aperture or fenestra
located either centrally or peripherally may allow
the distal passage of duodenal contents. It has a
characteristic radiographic appearance on con-
trast studies, resembling a “wind sock web” or
“thumb of a glove” [77]. Intraluminal duodenal
diverticula are rare congenital abnormalities,
thought to arise from improper recanalization of
the foregut lumen during the seventh week of
6  Gastrointestinal Tract 265

embryogenesis. This anomaly results in an intra- shows the inner wall, the pneumoperitoneum can
luminal mucosal web which, with repetitive peri- display the outer wall of the gastrointestinal tract.
stalsis, can elongate over time to form a The Rigler sign is an indication of free air
featureless intraluminal cul de sac. These struc- enclosed within the peritoneal cavity (pneumo-
tures typically reach 2 to 4 cm in length and arise peritoneum), imprinting a visible pattern on
from the second portion of the duodenum near abdominal plain radiograph in supine. Other
Vater’s ampulla. On upper gastrointestinal series, name: double-wall sign.
administered barium fills the sac-like diverticu-
lum, which appears “blown” into the duodenal Explanation
lumen, mimicking the configuration of a wind Gas normally outlines only the luminal surface of
sock. A radiolucent stripe, representing the the bowel wall and not the serosal surface, which
mucosal web, separates contrast within the diver- has a degree of opacity resembling that of adja-
ticulum from contrast in the true duodenal lumen, cent peritoneal contents. However, when there is
an appearance described as the “halo” sign [78]. appropriate amount of free gas in the abdominal
cavity, this free air is more likely to accumulate
Although the “wind sock” description is derived between bowel loops, thus permitting visualiza-
from the findings on upper gastrointestinal series, tion of the outer walls of the bowel: this is the
intraluminal duodenal diverticula have also been classic appearance of Rigler sign. When the
diagnosed by ultrasound and CT. Findings similar intestinal cavity is filled with fluid, the inner wall
to those observed on upper gastrointestinal series is invisible, and only the lateral wall is visible, it
can be seen on CT with oral contrast material or shows an atypical double-wall sign (Fig. 6.20).
when the diverticulum is distended with debris. A
collapsed diverticulum on CT can mimic an intra-
luminal mass or appear as a subtle low-density flap
[78]. Patients with an intraluminal duodenal diver-
ticulum can present in childhood, but more typi-
cally in the ages of 30 to 40 years. There is wide
variation in clinical presentation, ranging from dull
postprandial epigastric pain to diverticular ulcer-
ation and hemorrhage. The close relationship of the
diverticulum to the ampulla of Vater has been asso-
ciated with an increased incidence of pancreatitis.
Treatment traditionally consists of surgical exci-
sion, with endoscopic incision advocated by some.
Given the nonspecific clinical presentation of this
entity, radiologists should be familiar with the
imaging appearance of this congenital abnormality,
as they could be the first to suggest the diagnosis
[78]. It is quite important to know the duodenal
wind sock sign, the characteristic manifestation of
intraluminal duodenal diverticulum.

6.23 Rigler Sign

Fig. 6.20  Abdominal supine radiograph shows air in
Feature both sides of the bowel wall (Rigler sign) (white arrows).
On the supine position abdominal radiography, Both sides of the bowel wall are visualized; the wall
although the gas in the gastrointestinal tract appears as a white linear stripe
266
Discussion
The double-wall sign was first proposed and
described by Rigler in 1941 [79]. At present,
most literature reports are named after the Rigler
sign [80]. The emergence of pneumoperitoneum
often indicates the severity of the lesion, which
should be receive attention in emergency surgical
observation. Therefore, it is very important to
recognize its regular abdominal X-ray finding.
There are four etiological categories of pneumo-
peritoneum: iatrogenic, spontaneous, traumatic,
and miscellaneous, and these may also be female
genital tract related (douching, sexual inter-
course, insufflation). A wide range of clinical
symptoms of pneumoperitoneum are possible, or
there may be no symptoms at all, or there may be
marked peritoneal signs. Often, a careful history
can elucidate the cause [80]. This sign presents
because of the separation between free air and
intraluminal by the intestinal wall, marking the
air radiolucency and radiopacity of the wall; both
serosal and luminal surfaces of bowel are then
visible [81].
Orthostatic chest radiography is the best
choice to detect a small amount of free gas in
peritoneal cavity, on which the free gas in the
lower diaphragm can be shown. For patients who
cannot stand, an alternative is to lie on the left
side. The results showed that the free gas in peri-
toneal cavity less than 1 ml could be found in the
quality lateral position radiography as the ortho-
static chest radiography. CT can detect 1 ml free
gas and help confirm suspicious pneumoperito-
neum on plain film. However, infants or ICU
patients often can only undergo supine position
abdominal radiography. In this case, it is impor-
tant to recognize the Rigler sign. It is not uncom-
mon to have performance similar to the
double-wall sign. It is necessary to distinguish
the true positive Rigler sign from the false-­
positive Rigler sign without pneumoperitoneum
sign. The double-wall sign can sometimes be dis-
turbed by the adjacent intestinal loops. Therefore,
the contour of adjacent intestinal loops can also
appear inside the loops, leading to misdiagnosis
as free gas. A few residual contrast media cover-
ing the inner surface of the intestinal cavity can
also increase the density of the intestinal wall and
J. Chen et al.
form false Rigler sign. Equivocal appearance of
Rigler sign may be clarified using erect or lateral
decubitus radiograph and CT [82]. In conclusion,
pneumoperitoneum often indicates potential seri-
ous intraperitoneal diseases. Critical patients
often only can take decubitus position abdominal
radiography. Discovering free gas in decubitus
position abdominal radiography can provide
important treatment information by recognizing
the Rigler sign [83].
6.24 Football Sign
Feature
On supine abdominal X-ray plain film, a large
oval translucent image resembling a football can
be seen. Other name: rugby sign.
Explanation
Football sign is more common in infants with
pneumoperitoneum caused by spontaneous or
iatrogenic gastrointestinal perforation. The long
axis of the ball is from the head to the tail. The
diaphragm and the bottom of the pelvis form two
ends of the ball, which are obtuse and circular.
The oval translucent shadow represents a large
amount of gas in the peritoneal cavity, which
expands and expands the peritoneal cavity. In
supine position, these free gases accumulate
between the front of the abdominal viscera and
the peritoneum of the wall of the anterior abdom-
inal wall, creating a football-like appearance.
Some believed that the structure of the anterior
abdominal wall is a necessary part of the football
sign and have described it as the suture or ribbon
of the football [84] (Fig. 6.21).
Discussion
Pneumoperitoneum is caused by the rupture of
the hollow viscus including stomach, small
bowel, and large bowel, except those portions
that are retroperitoneal in the duodenum and
colon. When enough free gas is gathered in the
abdominal cavity, the football sign can appear on
supine abdominal plain film. Pneumoperitoneum
with enough free gas is more common in infants
or newborns than in adults or adolescents, which
6  Gastrointestinal Tract
Fig. 6.21  Anteroposterior radiograph of a neonate shows
a large radiolucency resembling the shape of an American
football. This sign represents an extensive pneumoperito-
neum, which is demarcated by the parietal peritoneal
reflections
may be caused by the timely and conscious
­consultation of adults with gastrointestinal perfo-
ration symptoms and early treatment. In adults,
pneumoperitoneum may not be enough to show
football sign sometimes, but the same amount of
gas can be shown in infants. Only 2% of adult
patients with pneumoperitoneum found by X-ray
have football sign, but there are no exact statistics
in the literature about football sign in infants. The
causes of pneumoperitoneum are numerous,
ranging from iatrogenic and benign causes to
more life-threatening conditions [85]. Other
causes include necrotizing enterocolitis, colonic
obstruction (such as intestinal malrotation, meco-
nium intestinal obstruction, digestive tract atre-
sia, etc.), and inflammation caused by gastric and
duodenal ulcers. In the absence of a benign cause
of pneumoperitoneum, the identification of free
intraperitoneal gas usually indicates the need for
emergency surgery to repair a perforated bowel.
The large oval translucent area seen on the
supine abdominal X-ray film resembles rugby
and represents a large amount of gas accumulated
in the peritoneal cavity, which is called football
sign. In most cases, infants with rugby syndrome
267
can be diagnosed as gastrointestinal perforation
without further imaging. In a few cases, when
only a small amount of gas is located outside the
intestinal cavity, there is no football sign. It may
only be seen on both sides of the intestinal wall or
in a local light transmission area. The lateral
position or lateral projection is needed for further
diagnosis. The appearance of falciform ligament
sign may be delineated by the presence of these
gases, which shows a long blurred linear shadow
located longitudinally in the right upper abdomen
[86]. Similarly, the shape of the umbilical liga-
ment or lateral umbilical ligament can also be
foiled by a large amount of gas, which shows a
blurred longitudinal linear shadow in the mid- or
mid-lower abdomen. The plain film is the pri-
mary diagnostic tool for detecting pneumoperito-
neum: multiple signs of free intraperitoneal air
can be found especially on supine abdominal
radiographs. CT has been shown to be more sen-
sitive than radiographs for the detection of free
intraperitoneal air. It is quite important for the
radiologist be familiar with the signs of pneumo-
peritoneum on radiographs and CT [87].
6.25 Dependent Viscera Sign
Feature
The dependent viscera sign is seen at supine CT
in the thoracoabdominal area. The viscera (i.e.,
the bowel or solid organs) are positioned against
the posterior ribs, with obliteration of the poste-
rior costophrenic recess.
Explanation
The dependent viscera sign is seen with dia-
phragmatic rupture. The absence of posterior
support by the diaphragm allows viscera to “fall”
against the posterior ribs to a dependent position.
On the right side, the upper one third of the liver
typically does not abut the posterior chest wall
(i.e., the right ribs) when the diaphragm is intact.
On the left side, the stomach and bowel lie ante-
rior to the spleen and generally do not abut the
left ribs when the diaphragm is intact. Therefore,
the dependent viscera sign is said to be present on
the right side if the upper one third of the liver
268
a b
Fig. 6.22 (a) Axial abdominal CT scan demonstrates dependent viscera sign in a patient with proven diaphragmatic
rupture. (b, c) MPR demonstrates the collar sign (or hourglass sign)
abuts the posterior ribs and on the left side if the
stomach or bowel abuts the posterior ribs or lies
posterior to the spleen (Fig. 6.22).
Discussion
Bergin et  al. [88] first described the dependent
viscera sign in diaphragmatic rupture in 2001.
The dependent viscera sign on CT scan refers to
hollow and solid organs lying in a dependent
position against the posterior thoracic wall, with
obliteration of the posterior costophrenic recess,
in patients with diaphragmatic rupture. Blunt
abdominal trauma usually is the cause, and it can
involve either hemidiaphragm [89]. Most dia-
phragmatic ruptures are longer than 10  cm and
occur in the posterolateral aspect of the hemidia-
phragm; this site is structurally weak because of
its embryologic origin from the pleuroperitoneal
membrane. In healthy patients, CT images
obtained at the level of the right hemidiaphragm
show the liver suspended anteriorly in the right
hemithorax. The position of the liver in the ante-
rior hemithorax creates a deep posterior costo-
phrenic sulcus, and the lung separates the upper
one third or more of the liver from the posterior
chest wall. In patients with right-sided diaphrag-
matic rupture, the deep posterior costophrenic
sulcus is obliterated, and the upper one third or
more of the liver lies dependent on the posterior
chest wall. In patients with rupture of the left
hemidiaphragm, the left costophrenic sulcus is
obliterated, and the bowel, spleen, or kidneys lie
dependent on the posterior ribs [88].
Although visceral herniation was detected at
CT in 60% of patients with diaphragmatic rup-
ture, the dependent viscera sign was observed on
J. Chen et al.
c
the scans in 90% of patients. This result suggests
that the dependent viscera sign may be an early
indicator of diaphragmatic tear before visceral
herniation can be confidently diagnosed using
cross-sectional imaging, likely reflecting the fact
that the sign is dependent on the absence of pos-
terior diaphragmatic support rather than on frank
visceral herniation [88]. CT often allows the
direct depiction of diaphragmatic lesions as seg-
mental defects; other direct signs of blunt dia-
phragmatic lesions (BDL) are diaphragm
nonvisualization, dangling diaphragm sign, and
diaphragm thickening. Many different indirect
signs have also been associated with BDL, such
as intrathoracic viscera herniation, dependent
viscera sign, collar sign, and hump and band sign
[90]. The dependent viscera sign is up to 100%
sensitivity as a sign of diaphragmatic rupture and
83% sensitivity for right-sided injury.
Intrathoracic herniation of the abdominal con-
tents is 32–64% sensitive for diaphragmatic rup-
ture and represents a late feature of this condition.
Also, diaphragmatic discontinuity is 71–80%
sensitive for rupture. In 6% of the general popu-
lation, discontinuity is a normal variant and is
seen more commonly in older patients, in women,
and in those with emphysema. The collar sign is
seen when the diaphragm constricts the herniated
bowel or solid organs in a waist-like manner. The
collar sign is 67% sensitivity for left-sided rup-
ture and 50% sensitivity for right-sided rupture
when sagittal and coronal reformats are used
[91]. Various imaging modalities including chest
radiograph, ultrasonography, CT, and MRI have
been used in the diagnosis of diaphragmatic rup-
ture. CT is the first-choice modality in detecting
6  Gastrointestinal Tract 269

diaphragmatic injury, as well as in detecting the
associated injuries of chest, abdomen, ribs, and
bones in these polytrauma patients [92].
6.26 Northern Exposure Sign
Feature
In supine position, the sigmoid colon, which was
obviously dilated on abdominal X-ray, rose to the
upper edge of the abdomen and was located
above the transverse colon.
Explanation
When the patient is supine, intraluminal gas tends
to accumulate in the transverse colon, the most
ventral segment of the large intestine. The trans-
verse colon crosses the midline, with its suspend-
ing mesentery separating the greater peritoneal
cavity into supra- and infra-mesocolic hemi-
spheres. Thus, the transverse colon may be con-
sidered the “equator” of the abdomen. Under
normal circumstances, the sigmoid colon is nor-
mally confined to the “southern hemisphere,”
caudad to the transverse colon (infra-mesocolic).
When the apex of the sigmoid colon has migrated
cephalad or “north” of the equator (supra-­
mesocolic), in cases of sigmoid volvulus, we
term this sign the “northern exposure” sign [93]
(Fig. 6.23).
tention (ileus) or simple obstruction of the left
colon, the dilatation of the colon is more diffuse.
In these circumstances, the pressure that devel-
ops within the sigmoid lumen is probably inade-
quate to force the sigmoid colon to relocate
anterior to the less markedly distended transverse
colon. Hence, there is an underlying anatomic
and physiological basis for the northern exposure
sign [94].
A small-bowel volvulus or other closed-loop
obstruction of the small bowel can often be dif-
ferentiated from a sigmoid volvulus by the large
amounts of retained fluid within the involved
jejunum or ileum. A cecal volvulus is distin-
guished by its origin and position outside the pel-
vis, the retention of one or two plicae in the
distended lumen, and the usual absence of gas-
eous dilatation in both the small bowel proximal
to the twist and the large bowel distal to the point
of obstruction. In the absence of concomitant
gas-filled dilatation of the small bowel, a diffuse
dynamic distention of the colon (11  cm) can
sometimes be mistaken for sigmoid volvulus.

Discussion
Javors et al. first described this finding in sigmoid
volvulus in 1999, noting that this feature indi-
cated sigmoid volvulus with 86% sensitivity and
100% specificity. Several reports have corrobo-
rated this hypothesis. Currently, suspected sig-
moid volvulus often is evaluated with computed
tomography (CT). The northern exposure sign is
detectable on the CT scout view, also on CT cor-
onal reformations [93]. Sigmoid volvulus, a form
of closed-loop obstruction, results in dilatation of
the involved colonic segment. In the occluded
loop, the haustra are effaced as the sigmoid colon
balloons upward and out from the pelvis. In doing
so, the sigmoid colon ascends in the anterior Fig. 6.23  CT scout view of a patient with sigmoid volvu-
abdomen to become situated ventral and rostral lus shows the apex of the sigmoid colon (arrowheads)
to the transverse colon. In either a dynamic dis- cephalad to the transverse colon (star) [93]
270
Atony of the sigmoid loop results in a wide tubu-
lar lucency emanating from the pelvis.
Nevertheless, no matter how dilated the unob-
structed sigmoid colon may become, it does not
extend above the transverse colon. Therefore, the
northern exposure sign would not be present in
an atonic large bowel [94]. CT of patients with
sigmoid volvulus shows a spectrum of findings
that can be approached with the use of estab-
lished and novel imaging signs but also shows
that indeterminate features can be present in one
fourth of patients. The need to assess for multiple
imaging signs is supported by the relatively low
sensitivity of several findings that have been gen-
erally assumed to be sensitive (e.g., the whirl sign
and the northern exposure sign). CT signs are
ineffective for prediction of the presence of
pathologically proven ischemia until there is
frank bowel necrosis [95].
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 Peritoneum and Pelvis
7
Pinggui Lei, Bin Huang, and Hui Yu

Contents
7.1 Sentinel Clot Sign  273
7.2 Concentric Ring Sign  275
7.3 Onion Skin Appearance  276
7.4 Hyperintense Rim Sign  277
7.5 Floating Aorta Sign  278
7.6 Sandwich Sign  279
7.7 Spongiform Gas Bubbles  280
7.8 Floating Ball Sign  281
7.9 Shading Sign  282
7.10 Ovarian Vascular Pedicle Sign  283
7.11 Bridging Vascular Sign  284
7.12 Double Peak Sign  286
7.13 Spur Sign  287
References  288

7.1 Sentinel Clot Sign
Feature
This sign is a computed tomography (CT) sign of
acute injury from an abdominal organ, which
manifests as a high-attenuation blood clot near
P. Lei (*) · B. Huang · H. Yu
Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China
the abdominal organs such as liver, spleen, intes-
tine, and mesentery with postcontrast CT value
greater than 60 HU.
Explanation
In the early stage of injury, change of the solid
organ attenuation may not be obvious. The senti-
nel clot sign is formed by the blood flowing into
the subcapsular or extracapsular region through
the site of the leakage. Intraabdominal

© Springer Nature Switzerland AG 2021 273

B. Gao, A. M. McKinney (eds.), Classic Imaging Signs,
https://doi.org/10.1007/978-3-030-56348-6_7
274
a b
Fig. 7.1 (a) Plain CT shows hyperattenuation surrounding the spleen, called the sentinel clot sign. (b) Another trauma
patient with this sign on noncontrast CT
h­ emorrhage is more commonly detected in the
adjacent region of the injured organ, which is
related to local coagulation when the blood over-
flows the vessel (Fig. 7.1).
Discussion
Orwig et al. first reported the sentinel clot sign in
1989 [1]. On noncontrast CT, the high-­attenuation
hematoma appears at the position closest to the
bleeding organ, and the CT value is greater than
60 HU, which is a reliable sign of the adjacent
organ injury. This sign suggests severe damage to
the abdominal organs. In the early stage of the
abdominal organ injury, the attenuation change
of the solid organ usually is not obvious. It is only
manifested as a hematoma formed by the blood
flowing into the subcapsular or extracapsular
region through the site of the breakage. The
intraabdominal hemorrhage is more common in
the adjacent part of the injured organ, as is related
to local coagulation after the blood overflows the
blood vessel. Hematoperitoneum often occurs in
patients with severe abdominal injuries and is a
common sign of abdominal visceral injury. There
is a characteristic distribution of hemorrhage in
the abdomen, depending on the amount of blood
and the location and time of bleeding. Peritoneal
hemorrhage is often located near the source of
bleeding and flows into the pelvis along the com-
mon peritoneal effusion pathway.
CT is widely accepted as the first-line choice
for assessing visceral injuries and determining
P. Lei et al.
treatment options, which has been approved to be
most accurate for the diagnosis of abdominal vis-
ceral injuries. The value of CT attenuation helps
for the identification of simple ascites, nonclot-
ting blood, hematoma, bile, urine, chylorrhea,
and active bleeding caused by recent bleeding.
The sentinel clot sign is a reliable sign of adja-
cent organ damage. Especially for spleen, intes-
tine, and mesentery damage, 9% of spleen injury,
and 32% of intestinal and mesenteric injuries, the
sentinel clot sign is the only positive sign.
Because the direct CT signs of damage to the
mesentery and hollow organs (intestines, blad-
der) are uncommon or are nonspecific, the senti-
nel clot sign is more valuable [2]. Spleen injury is
the most common; the incidence of sentinel clots
is 85.8%, and the incidence is relatively low in
liver injury. For cases of spleen, intestine, and
mesenteric injury, the sentinel clot sign can
improve the diagnostic accuracy rate, and this
sign is the only sign of diagnosis in 14 cases,
accounting for 14.3% of the total number of
cases. Sentinel clot sign is a reliable CT sign indi-
cating the damage of adjacent abdominal organs
and has important guiding significance for the
clinic. However, not all patients with acute
abdominal blunt trauma have sentinel clots.
Because some of the damaged areas are small,
the degree is light, no fluid or blood appeared in
the liquid. Therefore, even if the sentinel clot sign
is not observed, organ damage should not be
ruled out.
7  Peritoneum and Pelvis
7.2 Concentric Ring Sign
Feature
Abdominal hematoma with a period of more than
3 weeks can clearly show concentric ring sign on
T1WI, showing iso-intensity in the center of the
lesion and two concentric ring structures with
distinct signal intensity around it. The inner ring
is obviously the high signal and the outer ring is
the low signal.
Explanation
Concentric ring sign can be seen in chronic
hematoma of the abdomen caused by different
causes. The center of the hematoma is a gelati-
nous blood clot surrounded by liquid, in which
short T1 has been attributed to paramagnetic
Fig. 7.2  A 49-year-old man had history of left upper
abdomen with an adrenal hematoma with partial rupture
for more than 20 days. Iso-signal intensity was observed
on T1WI, and concentric ring appearance with a dark
275
effects of hemoglobin degradation to methemo-
globin. The short T1-weighted image from cells
can form a high signal loop, but macrophage cells
around the hematoma devour the hemosiderin to
cause the edge ring of the hematoma (Fig. 7.2).
Discussion
Hahn et al. first proposed the concentric ring sign
in 1986, in which two cases of duodenal chronic
hematomas showing three concentric rings on
T1WI, T2WI were described [3]. The outer layer
is a regular and thin low signal ring, the middle
layer is a very high signal ring, and the center is a
relatively uniform equal signal region. CT has
become the preferred imaging technique for eval-
uation of hemorrhage. The ring sign appears in
abdominal hematomas at the time when the CT
peripheral rim (a, white arrow) surrounding a bright ring
(a, black arrow) was detected in the hematoma. The adre-
nal hematoma was without enhancement in arterial phase
(b), portal venous phase (c), and delay phase (d)
276
appearance often becomes nonspecific. Acutely
hyperdense hematomas become iso-dense or
hypodense as sedimented blood and fibrinous
clot are reabsorbed; after 2 to 3 weeks a specific
diagnosis of abdominal hematoma by CT may be
impossible. In magnetic resonance imaging
(MRI) diagnosis of hematoma, both the internal
architecture and the temporal evolution of the
lesion are important. Concentric ring sign is best
recognized on T1WI. Surrounding a central core
of intermediate signal are two discrete concentric
rings. The inner ring is bright, indicating short T1
signal. The outer rim is dark on all pulse
sequences, consistent with a short T2 signal. Our
findings are consistent with studies of intracra-
nial hematoma, in which the short T1 has been
attributed to paramagnetic effects of hemoglobin
degradation products such as methemoglobin.
Hemosiderin digested by phagocytic cells sur-
rounding the hematoma may account for the dark
rim of short T2. The concentric ring sign in our
series was a sensitive indicator of the maturing
abdominal hematoma. The sign developed reli-
ably about 3 weeks after hemorrhage and was not
present earlier [3]. The ring sign on T1WI may
prove to be a “tissue-specific” MR feature, aris-
ing in hematomas of more than 2 to 3 weeks of
age. The ring sign may be valuable in distin-
guishing hematomas from other abdominal
masses on fluid collections. The ring sign is com-
mon in abdominal hematomas of varying cause
[4].
Some pitfalls and limitations exist in using
MRI to detect and diagnose abdominal hemato-
mas. Early in the acute period, hematomas may
be iso-intense with adjacent tissue on T1WI. The
differential diagnosis of abdominal chronic
hematoma mainly includes a solid abdominal
mass and a liquid accumulation area (e.g., pan-
creatic pseudocyst around); the latter two often
have fat and a bag around, so that is characterized
by a high signal on T1WI. But the high signal of
the ring is the same in strength as the s­ ubcutaneous
fat and the lack of peripheral low signal rings.
Chronic abdominal hematoma on T1WI, like the
bright high signal, is higher than fat tissue, which
is formed more easily to identify with peripheral
low signal loop. Hemorrhage in the tumor necro-
P. Lei et al.
sis area and internal hemorrhage after tumor
biopsy can also present as a bright spherical or
strip-like high signal in a T1WI image. It is easy
to distinguish that neither presents as ring sign. In
the diagnosis of adrenal tumors, the concentric
ring sign is an important differential finding to
confirm adrenal hemorrhage or hematoma. One
should be aware that short-term MRI follow-up is
needed [5].
7.3 Onion Skin Appearance
Feature
On abdomen CT scan, the spleen, kidney, and
other visceral organs increased significantly.
Under the subcapsular, there are slit-like high-
and low-density shadows, blurred interspaces
with the surrounding tissues, with an onion skin
appearance.
Explanation
Onion skin appearance is a CT sign of abdominal
parenchymal organ contusion and subcapsular
hemorrhage, which is generally chronic repeated
hemorrhage after blunt contusion, resulting in
blood deposition and stratification (Fig. 7.3).
Discussion
Spleen is the most common organ to be injured
and the most common surgery performed is sple-
Fig. 7.3  A 53-year-old male patient underwent routine
examination after an accident. Abdominal CT showed an
enlarged spleen with uneven density and slit-like high-
and low-density shadows
7  Peritoneum and Pelvis
nectomy. The most common extraabdominal
injury is rib fracture, with mortality rate of 4%.
Wound sepsis was the most common complica-
tion [6]. Owing to the current trend toward a more
conservative approach to injury, there has been an
increased emphasis on identifying, staging, and
follow-up in imaging of splenic trauma. Dynamic
contrast-enhanced CT scanning is very sensitive
(95%) for the detection of splenic injuries. The
subcapsular hematoma is a peripheral, well-
defined, lenticular, relatively low-­ attenuation
mass that displaces the splenic parenchyma
inwardly. Rarely, an intrasplenic contusion or
hematoma can be a small, irregular, low-­
attenuation mass within the splenic parenchyma.
The splenic laceration is seen as a cleft, usually
with irregular borders, extending through the cap-
sule into the parenchyma. It is associated with
peri-splenic or intraabdominal fluid. The lacera-
tion traversing two capsular surfaces is designated
a fracture. Repeated episodes of bleeding may
lead to a peri-splenic clot with an onion-skin
appearance [7]. In addition, the presence of active
hemorrhage and/or contained vascular injuries
(pseudoaneurysms and arteriovenous fistulae)
increases the risk of failed nonsurgical manage-
ment. Active hemorrhage is identified as a contrast
material blush or focal area of hyperattenuation in
or emanating from the injured splenic paren-
chyma. In contradistinction to a contained vascu-
lar injury in which the initially identified contrast
material blush is seen to wash out on subsequent
a b
Fig. 7.4 (a) T1WI shows left adrenal mass with signal intensity consistent with the liver. (b) Enhanced scan shows high
signal edge sign
277
delayed-phase images, the hyperattenuation of
active hemorrhage persists and grows larger with
time on a delayed-phase study. Thus, delayed-
phase image acquisition is useful for definitive
characterization of vascular splenic injury as
active hemorrhage or contained vascular injury.
Recently, a CT-based scale system that includes
vascular injuries and active bleeding as part of the
grading criteria has been proposed to improve the
accuracy of predicting the need for intervention,
as compared with the traditional AAST scale. Not
all vascular injuries of the spleen are identified on
the combination of portal venous and delayed-
phase images; some advocate routine acquisition
of an additional arterial phase series during
abdominal CT. Arterial phase imaging in abdomi-
nal trauma warrants further study [8].
7.4 Hyperintense Rim Sign
Feature
On fat suppression of MRI, ring-like hyperinten-
sity appears at the edge of an adrenal mass.
Explanation
Hyperintense rim sign is a characteristic sign of
adrenal adenoma. Hyperintense rim sign is help-
ful to distinguish adrenal adenoma from metasta-
sis. This sign may be related to the envelope of
the tumor or the squeezing of normal adrenal tis-
sue (Fig. 7.4).
278 P. Lei et al.

Discussion slightly and moderately enhanced in the early

An adrenal adenoma is the most common benign
adrenal tumor. With the development of imaging
technology, the detection rate of adrenal lesions
is becoming higher and higher, but the qualitative
diagnosis is still difficult. The adrenal gland itself
is significantly contrasted with the surrounding
high-signal fat capsule and is clearly visualized
on MRI.  An adrenal adenoma is rich in lipids.
The section of adrenal adenoma is golden yellow;
it consists of clear cells and granular cells, mainly
clear cells. Adrenal nodules or masses appear on
MR images. The signal on T1WI is similar to that
on the liver. Most of the signals on T2WI are
equal to that of the liver, and a few are higher
than that of liver or even high signal [9]. Chemical
shift imaging is important in the diagnosis of
adrenal adenoma. This difference increases with
the increase of field strength. The in-phase image
is normal T1WI, and the anti-phase image is char-
acterized by obvious attenuation of tissue signals
mixed with water and fat, whereas the signals of
pure adipose tissue and pure water tissue are not
attenuated significantly. An adrenal adenoma
contains a certain amount of fat, and there is a
characteristic signal reduction on the antiphase
image. Hyperintense rim sign is a characteristic
sign of adrenal adenoma. If this sign is found in
adrenal lesions and the signal of tumors is
decreased on out-of-phase images, the lesions are
stage. Dynamic contrast enhancement is helpful
in the diagnosis of adrenal adenomas. Most of the
adenomas show early mild or moderate enhance-
ment and rapid clearance, which has a certain
significance in differentiating adenomas from
nonadenomas. However, a recent meta-analysis
demonstrated that, despite routine use of imaging
assessment for adrenal masses, there was insuf-
ficient evidence of diagnostic value in distin-
guishing a benign mass from malignancy [10].
7.5 Floating Aorta Sign
Feature
On abdominal CT, the abdominal aorta is embed-
ded in the lymph nodes, which fuse together to
form a mass that is better shown on contrast
CT. When lymph nodes are enlarged to a consid-
erable extent, the large vessels can move forward,
and the large blood vessels are floating in the
mass, which is called a floating aorta sign.
Explanation
The retroperitoneal enlarged lymph nodes often
fuse into masses at a later stage. The abdominal
aorta, celiac trunk, inferior vena cava, or superior
mesenteric artery are obviously removed and
embedded (Fig. 7.5).

a b

Fig. 7.5 (a) A 61-year-old female patient with non-­ aorta and involving the right renal and ureter, leading to
Hodgkin’s lymphoma. On abdominal contrast CT, a soft hydronephrosis. (b) Another patient with malignancy
attenuation mass is seen in the paraaortic space. The atten- shows floating aorta sign on postcontrast CT
uation is homogeneous, slightly enhanced, enclosing the
7  Peritoneum and Pelvis
Discussion
Retroperitoneal lymphoma is a rare retroperito-
neal malignant tumor. It can be either primary or
part of lymphoma disease. Histologically, it is
divided into two categories: Hodgkin’s lym-
phoma and non-Hodgkin’s lymphoma. It is more
common in young and middle-aged patients and
more common in women. The Hodgkin’s lym-
phomas rarely occur in children younger than
5  years, but the non-Hodgkin’s lymphomas fre-
quently affect children younger than 5  years.
Patients may complain of abdominal discomfort,
pain, palpable mass, and other symptoms [11].
Retroperitoneal lymphoma is most likely to
invade the anterior aortic lymph node and left
aortic lymph node, followed by right aortic
lymph node and posterior aortic lymph node.
Lymphomas rarely invade a single group of
lymph nodes.
CT findings. (1) Solitary enlarged lymph
nodes can be seen beside the aorta. The plain
scan can clearly show enlarged lymph nodes,
which are nodular or irregular, with irregular
edges and inhomogeneous attenuation. The
diameter of lymph node larger than 1.5 cm indi-
cates enlargement, and more than 2 cm can con-
firm enlargement. Lymphoma is characterized by
huge masses, most lymphomas being larger than
5  cm. After contrast enhancement, the lesion
shows mild to middle enhancement. (2) The
lymph nodes fuse into a mass with a large soft
tissue attenuation mass, with necrosis in the cen-
ter, and the fat angle of the blood vessels disap-
pears after the aorta and vena cava. The abdominal
aorta, celiac trunk, inferior vena cava, or superior
mesenteric artery are obviously removed and
embedded. The enlarged lymph nodes cross the
midline and fuse into a mass, showing a typical
abdominal aortic inundation sign or vascular
embedding sign [12]. When lymph nodes are
enlarged to a considerable extent, the large ves-
sels can move forward, and the floating aorta sign
appears. (3) Adjacent organs such as liver and
pancreas are displaced and metastasized. On
magnetic resonance imaging (MRI), lymph
nodes are typically iso-intense to muscle on
T1WI, iso- or hyperintense on T2WI with moder-
ately homogeneous or patchy enhancement [13].
279
The floating aorta sign is an important sign for
the identification of retroperitoneal lymphoma
and other lymph node diseases.
7.6 Sandwich Sign
Feature
On abdominal CT, mesenteric fat and blood ves-
sels are the “sandwich filling.” The “bread” on
the upper and lower sides is made up of a soft
tissue shadow of homogeneous attenuation,
which is shaped like a sandwich.
Explanation
On CT, mesenteric fat and blood vessels resem-
ble fillings in the middle of a sandwich, and the
enlargement of the mesenteric lymph nodes is
similar to the two slices of bread. After injecting
the contrast medium, the structure of mesenteric
vessels is significantly enhanced more than the
fat, thus making the “sandwich filling” more
prominent (Fig. 7.6).
Discussion
Sandwich sign refers to a sandwich-like image of a
giant hyperplastic mesenteric lymph node that sur-
rounds the mesenteric fat and blood vessels [14].
There are many causes of mesenteric lymph node
enlargement. In addition to lymphoma, cancer, sar-
Fig. 7.6  Patient with mesenteric lymphoma. On postcon-
trast CT, an oval and long strip increased attenuation
shadow can be seen on the left side, but the boundary is
not clear. Visible mesenteric vessels and fat were encapsu-
lated in both lesions, forming the sandwich sign
280 P. Lei et al.

coma, carcinoid, acquired immunodeficiency-­

associated lymph node hyperplasia syndrome,
tuberculosis, intestinal fat metabolism disorder
(Whipple disease), and inflammatory bowel disease
are also the most common causes. Carcinomas, sar-
comas, and carcinoid can originate from the small
intestine and then spread to the mesenteric lymph
nodes. These tumors invade the intestinal wall and
cause perforation, hemorrhage, and lesions that dif-
fuse rapidly. Infectious and inflammatory lesions
usually do not cause massive lymph node enlarge-
ment. It usually manifested as central necrosis, sur-
rounded by ring enhancement, which is similar to
tuberculosis. Therefore, these tumors, or infectious Fig. 7.7  CT imaging of gossypiboma misdiagnosed as
and inflammatory lesions, do not present the sand- intraabdominal mass
wich sign. The sandwich sign is more common in
mesenteric lymphoma, because only in the mesen- Explanation
teric lymphoma can the lymph nodes grow very The remaining intraperitoneal mass is covered
large and surround the fat, intestines, and blood ves- and adhered by the omentum and adjacent intes-
sels without any clinical symptoms [14]. The mes- tinal tubes. At the early stage, there were more
enteric lymphoma occasionally invades the serous bubbles inside without the surrounding envelope.
and muscle layer; sometimes it causes small intesti- With time, the bubbles inside the mass gradually
nal bleeding but it rarely causes free perforation. decreased, then disappeared, and the surrounding
The mesenteric lymphoma can also cause retroperi- envelope gradually changed from incomplete to
toneal lymph node enlargement. Most mesenteric complete (Fig. 7.7).
lymphomas are non-Hodgkin’s lymphoma (NHL),
and approximately 30% to 50% of patients with Discussion
NHL have the mesenteric nodal disease [15]. Numerous reports about gossypiboma have been
Immune dysfunction is a risk factor for NHL. The published since it was described by Wilson in
sandwich sign also can be seen in posttransplant 1884 [16]. The term gossypiboma is derived from
lymphoproliferative disorders (PTLD). NHL can- the Latin word gossypium, meaning cotton, and
not be distinguished from the PTLD on morpho- the Kiswahili word boma, meaning place of con-
logical grounds, as both conditions are caused by cealment. Gossypiboma is an uncommon surgi-
the Epstein–Barr virus. For patients without a his- cal complication with an estimated incidence of
tory of transplantation, NHL is the main cause of 1  in 1500. Gossypibomas are most frequently
sandwich signs; in patients with a history of trans- discovered in the abdomen. However, occur-
plantation, the cause of the sandwich sign may be rences in the thorax, extremities, central nervous
PTLD.  As an increasing number of patients are system, and breast have also been reported.
undergoing transplantation, the sandwich sign may Pathologically, there are two types of foreign-­
become more common in clinical practice. body reactions in gossypibomas. One is an asep-
tic fibrous response resulting in adhesion,
encapsulation, and granuloma, and the other is an
7.7 Spongiform Gas Bubbles exudative reaction leading to cyst or abscess for-
mation [17].
Feature Imaging methods such as plain X-ray, medi-
There are many different sizes of bubble gas density cal sonography (USG), CT, MRI, and endoscopy
shadows in the abdominal gossypiboma on CT scans, are usually helpful in the diagnosis. Basically, a
which show the modifications of honeycombs. “whorl-like” mass imaging on plain X-ray,
7  Peritoneum and Pelvis
imaging of a hyperechogenic mass with the
hypoechoic rim on USG, or a rounded mass with
a dense central part and enhancing wall on CT
are the basic signs of gossypiboma. CT seems to
be the first diagnostic modality to rule out other
conditions. MRI can be confusing because the
radiopaque marker is not magnetic or paramag-
netic [16]. CT is the best method to detect gos-
sypiboma and its complications. CT findings
have certain features. (1) Morphology and size
of lesions: almost all foci are round or oval,
3–20  cm in diameter; average diameter is
approximately 9 cm. (2) Periphery: the envelope
is complete, composed mostly of the thin walls
and a few thick walls with regular boundary. The
mass may adhere to the adjacent abdominal wall
and surrounding intestinal tube. The envelope
can be continuously strengthened by the contrast
agent. (3) Internal density: multiple bubble gas
density shadows of different sizes can be seen in
the mass at the early stage of a case, showing
modification of a honeycomb shape, and thus
called spongiform gas bubbles. “Spongiform gas
bubbles” are usually observed 3 years after sur-
gery, the characteristic CT sign of early abdomi-
nal gossypiboma.
Clinical symptoms may appear in the immedi-
ate postoperative period or even after weeks,
months, or years. The interval of time from the
causative operation to clinical presentation has
been reported to range from the first postopera-
tive day to 43  years. Clinical presentation is
strongly associated with the type of foreign-body
reaction, which may manifest in various clinical
a b
Fig. 7.8 (a, b) A cystic mass with fat and calcification (arrow) in the right adnexal area of the uterus forms the so-called
floating ball sign
281
presentations ranging from mild abdominal pain
to major surgical complications including bowel
or visceral perforation, obstruction, fistula forma-
tion, or sepsis, although it may remain asymp-
tomatic for many years [16].
7.8 Floating Ball Sign
Feature
Mature teratoma of the ovary can be seen on CT
images as many lipoid globules floating in the
cyst fluid, forming the so-called floating ball
sign.
Explanation
Mature cystic teratoma is characterized by a cys-
tic or cystic solid mass. Cholesterol, fat, fatty
acids, and other substances in the tumors may be
liquid when they are above 34° C. Many movable
lipid-like globules float in the cystic fluid, form-
ing the so-called floating ball sign (Fig. 7.8).
Discussion
Ovarian teratoma is a common gynecological
ovarian germ cell neoplasm that originates from
abnormal proliferation of multifunctional embry-
onic cells. It consists of two or three embryonic
layers of multiple mature tissues, including skin,
sebaceous glands, hair, some teeth, and nerve tis-
sues. Mesodermal tissues such as fat can also be
seen. Fatty acids and cartilage rarely have endo-
dermal tissue. The main incidence group is women
of childbearing age, 20 to 40 years old [18].
282
Most of the cases have some specificity on
CT, so diagnosis is not difficult. On CT, mature
teratomas are mostly cystic. Adipose-dense tis-
sues are characteristic CT findings. Cholesterol,
fat, fatty acids, and other substances in tumors
form many movable lipid-like globules floating
in the cystic fluid, forming the floating ball sign.
On MRI most of the tumors were cystic or cys-
tic solid masses with fat components. Both
T1WI and T2WI showed high signal intensity,
and the signal intensity of the fat suppression
sequence decreased. The latter could be differ-
entiated from hemorrhage but still showed high
signal intensity in the fat suppression sequence.
Teratomas should be differentiated from other
fatty tumors. Uterine fatty leiomyoma, pelvic
lipoma, and retroperitoneal teratoma, all con-
taining fat components, need to be differenti-
ated from ovarian teratoma. The former
originates from the uterus; the latter two are
rare and mostly located in the retroperitoneum.
Careful observation of the location of the lesion
and its relationship with the uterus and ovary
can avoid misdiagnosis. CT is more sensitive
than MRI in displaying microadipose tissue and
calcification, especially in thin-slice CT and
three-dimensional reconstruction. The possibil-
ity of ovarian teratoma should be considered
first if the floating ball sign is found in the uter-
ine appendage area on CT [19].
Fig. 7.9 (a) Axial T1WI demonstrates left adnexal endometriomas with high signal intensity (white arrows). (b) Axial
T2WI with the “T2 shading sign” visible (white arrow)
P. Lei et al.
7.9 Shading Sign
Feature
Shading sign is the MRI finding of T2 shortening
in an adnexal cyst that is hyperintense on T1WI.
The hypointensity was initially described as
either focal or diffuse; however, the most com-
mon manifestation is a complete loss of signal
intensity or dependent layering with a hypoin-
tense fluid level.
Explanation
The precise mechanism of the shading sign is
complex. Endometriotic cysts are highly viscous
and have a high concentration of protein and iron
from recurrent hemorrhage. All these compo-
nents can shorten T2 and may contribute to signal
intensity loss, described as shading. In addition,
intracellular and extracellular methemoglobin
markedly shorten the T1 of fluids, resulting in
hyperintensity on T1WI and hypointensity (shad-
ing) on T2WI (Fig. 7.9).
Discussion
Historically, shading sign has been considered a
distinguishing feature of endometriomas on MR
imaging. First described in 1987 by Nishimura
and his team, the shading sign was confirmed to
be associated with endometriomas by the work of
Togashi et  al. in 1991, which evaluated 374
7  Peritoneum and Pelvis
female patients and concluded that a definitive
diagnosis of endometrioma could be made when
a cyst that was hyperintense on T1WI exhibited
hypointense signal on T2WI (shading), reporting
a sensitivity of 90% and a specificity of 98%
[20]. The shading sign has been considered a dis-
tinguishing feature of endometriomas on
MRI. However, our daily practice showed us that
the same signal loss is seen in other cysts and
even in cystic portions of mixed masses. To the
best of our knowledge, some studies have been
published regarding the diagnostic accuracy of
the shading sign for endometriomas, but data in
the literature are scarce concerning its patterns
and false positives. During this retrospective
analysis, the authors found five different shading
patterns: layering, liquid–liquid level, homoge-
neous, heterogeneous, and focal/multifocal shad-
ing within a complex mass. First, homogeneous
shading was the most prevalent pattern in endo-
metriomas, followed by heterogeneous, layering,
and liquid–liquid level. Second, all lesions with
heterogeneous shading sign were endometrio-
mas, as well as most lesions with homogeneous
shading and layering shading. Third, none of the
endometriomas presented with focal/multifocal
shading within a complex mass. Fourth, half the
cases with focal/multifocal shading within a
complex mass corresponded to endometrioid car-
cinomas [20].
Endometriosis is an important gynecological
disorder that can impact significantly on an
individual’s quality of life and has major impli-
cations for fertility. Deep infiltrating endome-
triosis is a severe form of endometriosis that can
cause obliteration of anatomical compartments.
Laparoscopy remains the gold standard for
diagnosis of endometriosis, although it is an
invasive procedure that has the potential to be
hindered by obliterative disease. Ultrasound is
often the first-­ line imaging modality when
endometriosis is suspected; however, MRI is
more accurate in the assessment of complex dis-
ease. Preoperative MRI is highly specific in the
diagnosis of endometriosis and characterization
of disease extent and has a key role in guiding
surgical management [21]. Patients with endo-
metriosis usually present with one of three com-
283
plaints: pelvic pain, adnexal mass, or infertility.
Because endometriosis is a benign process that
becomes quiescent with pregnancy or meno-
pause, consideration of the natural history and
severity of the disease, as well as age and repro-
ductive status, is necessary when deciding on
treatment. There are many treatment options
such as observation, hormonal therapy, and con-
servative or radical surgery. Relief of symptoms
may be the goal of treatment in all the protean
manifestations of endometriosis [22].
7.10 Ovarian Vascular
Pedicle Sign
Feature
Ovarian vascular pedicle sign is the direct con-
nection of ovarian vein and pelvic mass. It is the
spiral CT sign of a pelvic mass originating from
the ovary.
Explanation
The ovary is mainly supplied by the ovarian
artery and drains to the ovarian vein, which forms
a vascular plexus in the broad ligament of the
uterus. The broad ligament of the uterus commu-
nicates with the uterine venous plexus through
the double blood supply. The ovarian vascular
pedicle anatomically includes blood vessels that
enter and exit the ovary and communicate with
the branches of the uterine blood vessels. When
the ovary appears to be occupying space, the ipsi-
lateral ovarian blood vessels may expand.
Because the gonadal vein is always in front of the
psoas muscle and the common iliac vessels, a spi-
ral CT scan can show the reflux of the ovarian
vein to the ovary (Fig. 7.10).
Discussion
Distinguishing the pelvic mass of ovarian and
nonovarian origins may help to determine the
relationship between the mass and the pelvic
anatomy. The location of the uterus relative to the
pelvic mass may be the most helpful clue to the
origin of the ovarian mass. Tumors originating
from ovaries are usually located in the ovarian
bed, which is usually in the anterior or anterome-
284
Fig. 7.10  A 56-year-old woman with right ovarian neo-
plasm. CT image shows a large solid mass in venous
phase (a) and delay phase (b), which is located in the pel-
dial part of the uterus. When the mass is large, the
uterus is pushed backward or posterolateral.
However, if CT shows that the lumps originating
from the ovary, uterus, intestines, and retroperito-
neum are large, it may be difficult to distinguish
the origin of the organ from the mass. Studies
have shown that multidetector computed tomog-
raphy (MDCT) is highly consistent with the dis-
play of gonadal veins, and MDCT can also
provide important information for determining
the origin of larger pelvic masses (>8  cm) in
women [23].
The ovarian suspensory ligament is an inac-
curate term; here a pelvic mass can be highly
suggestive of ovarian origin. The suspensory
ligament is not continuous with the ovarian large
blood vessels, but it is also difficult to display as
a separate structure on CT so that it can be dis-
tinguished from the ovarian blood vessels that
drain into it. Therefore, the ovarian vein is traced
down the ventral side of the psoas muscle to the
pelvic cavity, and the suspensory ligament may
be found attached to the ovary or an ovarian
mass, or the ovarian vein may be draining
directly to the ovary or ovarian mass without
visualization of the ligament. The suspensory
ligaments are difficult to identify, especially
when there is a very large pelvic mass. Moreover,
because the fallopian tube is close to the attach-
P. Lei et al.
vis. (b) Right ovarian vein was observed in axial CT
enhanced images (white arrow)
ment point of the ovary and ovarian ligament, a
mass originating from the fallopian tube is diffi-
cult to distinguish from an ovarian mass [24]. If
the uterine suspensory ligament cannot be dis-
tinguished, the pelvic mass that is directly con-
nected to the ovarian vein is most likely to
originate in the ovary, or in the f­ allopian tube, or
uterus, or occasionally a nongynecological mass.
It was found that separation of the mass from the
ipsilateral ovary suggests a nonovarian origin,
but often the ovary is unclear or inconspicuous.
Ultrasound (US) is the preferred method for pel-
vic examination in women; it is also an alterna-
tive method of examination for the uterus and
attachments that cannot be evaluated well in
CT. It is especially helpful to find the ipsilateral
ovaries that are distinct from the pelvic mass,
showing morphological changes such as hydro-
salpinx, and to further evaluate the internal com-
position of ovarian cystic masses.
7.11 Bridging Vascular Sign
Feature
On color and power Doppler ultrasound and MRI
of the pelvic cavity, multiple blood vessels can be
seen at the interface between the uterus and the
peri-uterine mass. This finding is called the
7  Peritoneum and Pelvis 285

Fig. 7.11  MRI features of subserous leiomyoma: axial T2WI (a) and axial T1WI (b). The signal of the myoma was
uneven and slightly heterogeneous. A curved vascular empty structure (white arrow), the “bridge vascular sign,” is seen

bridging vascular sign. On color and power relationship. In addition, the mass associated
Doppler ultrasound, blood vessels appear as flow with the uterine round ligament is likely to be a
signals. On MRI, blood vessels appear as curvi- uterine myoma rather than an accessory tumor.
linear tortuous signal voids. Solid ovarian masses, such as fibroids, granulosa
cell tumors, germ cell tumors, metastases, and
Explanation lymphomas, are similar to subserosal uterine
Bridging vascular sign suggests that the peri-­ myomas and are easily confused [27]. The pres-
uterine mass, such as subserosal uterine myomas, ence of normal ovaries is usually a clue to the
originates in the uterus. The bridging vascular evaluation of the source of pelvic masses, but in
sign is formed by nourishing blood vessels that postmenopausal women, normal ovaries may not
originate in the uterine arteries, which supply be seen. In addition, ovarian tumors can originate
large exogenous myomas (>3  cm) through the in the periphery, and normal ovaries are observed
muscular layer (Fig. 7.11). in the vicinity of the tumor, so the possibility that
the tumor originates from the ovary cannot be
Discussion completely ruled out.
The “bridging vascular sign” is a finding of color The bridging vascular sign is very important
and power Doppler ultrasound and MRI of the for the diagnosis of exogenous uterine myomas
pelvic cavity, which shows that multiple blood and identification of the mass of the attachment.
vessels can be seen at the interface between the The nourishing blood vessels originating from
uterus and the peri-uterine mass. On color and the branch of the uterine artery are located at the
power Doppler ultrasound, blood vessels appear junction of the uterus and subserosal myomas
as flow signals. On MRI, blood vessels appear as and can be classified according to their morphol-
curvilinear tortuous signal voids [25, 26], sug- ogy and the direction of the interface. A blood
gesting that the peri-uterine mass originates in vessel parallel to the interface is defined as an
the uterus. Pathologically, the bridging vascular inserted blood vessel, a blood vessel crossing the
sign is formed by nourishing blood vessels that interface is referred to as a crossed blood vessel,
originate in the uterine arteries, which supply and a blood vessel having both these expressions
large exogenous myomas (>3  cm in diameter) is defined as a mixed-blood vessel. These vessels
through the muscular layer. Peri-uterine masses are seen in subserosal uterine myomas more than
include subserosal myomas, accessory masses, 3  cm in diameter. The ovarian mass is directly
intestinal masses, and other pelvic lesions. In supplied by the ovarian artery or the ovarian
imaging, differential diagnosis depends on under- branch of the uterine artery. Therefore, these
standing of the characteristics of these tumors, interfacial blood vessels are also seen when ovar-
including content, structure, and uterine serosa ian malignant tumors invade the uterus.
286
7.12 Double Peak Sign
Feature
The enlarged prostate protrudes into the bladder,
sometimes showing symmetrical, smooth-edged
masses on both sides, called the double peak
sign.
Explanation
Benign prostate hyperplasia originates from the
middle lobe. When the hypertrophic middle
lobe protrudes into the bladder cavity, because
the central part of the prostate is restricted
by  the urethra, it usually goes up or forward
from the central part of the lower wall of the
bladder, showing a bimodal shape with smooth
edges (Fig. 7.12).
Discussion
The prostate is located below the bladder and
behind the pubic symphysis. The parenchymal
adnexal gland enclosing the root of the urethra, it
is flat behind and has a longitudinal shallow sul-
cus in the middle. The main body of the prostate
is divided into left and right lobes, through which
the urethra passes. Benign prostate hyperplasia
(BPH) begins in the glands surrounding the ure-
thral seminal position, which are called transi-
tional zones, accounting for about 5% of the
prostate tissue. The remaining 95% of glands is
composed of peripheral zones (three of four) and
central zones (one in four). BPH is a typical clini-
cal manifestation of glandular tissue, smooth
muscle tissue, and connective tissue prolifera-
a b
Fig. 7.12 (a) In a 61-year-old man, plain pelvic CT scan showed enlarged prostatic gland with bimodal protrusion into
the back of the bladder to form a bimodal sign. (b) Another patient with double peak sign seen on noncontrast CT
P. Lei et al.
tion, wrapping and squeezing the posterior ure-
thra in the central and transitional areas [28].
The CT diagnosis of BPH is based on the
diameter measurement. The standard for the
maximum diameter of the upper and lower diam-
eter, anteroposterior diameter, and left and right
diameter of the prostate of men 60 to 70 years old
is listed as 50 mm, 43 mm, and 48 mm, respec-
tively, with the upper boundary not more than
10 mm of the upper edge of the pubic symphysis.
Only when the prostate as seen in the upper edge
of the pubic symphysis is 20–30  mm can it be
diagnosed as enlarged. Because the hyperplasia
of the central region of the prostate differs from
the degree of atrophy in the peripheral region,
prostate volume may or may not increase.
Therefore, it is generally believed that the diam-
eter measurements have limited diagnostic value
for BPH, especially for older patients. BPH
shows no density difference between the central
zone and the peripheral zone during the CT scan,
and sand-like or short curved calcification is
observed at the junction of the two zones. The
central area of the enhanced scan is strengthened
around the urethra or slightly off the side, and the
nonenhanced area with a crescent-shaped or
eccentric ring surrounds the central area. The
unreinforced area is thin or disappears, and
the ratio of the diameter of the thickest part of the
central area to the surrounding area is greater
than 1. Prostate cancer or BPH can form a soft
tissue mass that protrudes into the bladder cavity.
Prostate cancer on CT is a mass mostly from the
two sides of the posterior wall of the bladder that
7  Peritoneum and Pelvis
is spherical and protrudes into the bladder cavity;
The change of bladder wall caused by BPH is
mainly caused by the migration. When the hyper-
plastic nodule is larger, it can protrude into the
bladder, and the edge is smoother. The prominent
part is from the central area of the lower wall of
the bladder upward or forward, showing a double
peak protrusion.
BPH needs to be differentiated from prostate
cancer. The invasion of the bladder wall by pros-
tate cancer and the change of BPH to the bladder
wall reflect the pathological basis; 75% of pros-
tate cancer originates from the posterior lobe
envelope. In the lower area, BPH originates in the
middle lobe, and the hypertrophic middle lobe
protrudes into the bladder cavity, showed a dou-
ble peak change because the central part is
restricted by the urethra. It is generally believed
that the morphology and location of the mass in
the bladder are important for identification.
Cone-beam CT may be a useful adjunctive tech-
nique to identify the anatomy of the prostatic
arteries and ais treatment planning [29]. BPH
should also be differentiated from bladder cancer.
When BPH occurs, sometimes the mass shadow
can be seen in the bladder, which is caused by
partial volume effect. The upper and lower diam-
eters of the mass shadow are smaller than the
transverse diameters, indicating that the mass
shadow is located outside the bladder, which is
different from that of bladder cancer, which is
manifested as a mass protruding into the bladder
cavity.
7.13 Spur Sign
Feature
The spur sign is seen on transverse CT images or
conventional obturator oblique (45° internal rota-
tion and 15° cephalic tilt) radiographs of the pel-
vis. The fracture fragments that appear as
triangles resemble a spur-like shape with the tip-
ping point downward.
Explanation
The spur sign is produced by a triangular frag-
ment of iliac bone that remains attached to the
287
Fig. 7.13  Axial CT scan shows fracture fragments (white
arrows) medially displaced
sacroiliac joint but is separated from the fractured
acetabulum. The spur sign is indicative of frac-
ture in both the anterior and posterior acetabular
columns (both-column fracture). Not all acetabu-
lar double-column fractures have the spur sign;
the spur sign is exposed when the fractured ace-
tabular columns are medially displaced
(Fig. 7.13).
Discussion
The acetabulum is composed of two columns and
two walls. The columns represent a condensation
of trabecular bone along lines of stress and trans-
fer weight-bearing force from the hip joints to
the axial skeleton. The effect of the walls is to
stabilize the hip joint. The two columns are
unequal in size and, together, form an inverted
Y. The anterior column is composed of the ante-
rior portion of the ilium, including the iliac crest;
the anterior superior portion of the acetabular
roof; and the pubic symphysis. The posterior col-
umn ­(squatting column) is shorter; it provides
the major support for the hip joint and includes
the weight-bearing dome of the acetabulum and
posterior portion of the ischium [30]. The type of
fracture is determined by the damage mechanism
and force of fracture. Fractures of the anterior
column are often the result of force applied in
external rotation, whereas fractures of the poste-
rior column are the result of force applied in
internal rotation. Transverse fractures may occur
as the result of force applied to the adducted
(high transverse) or abducted (low transverse)
hip [31]. The both-column and transverse frac-
ture are among the more common acetabular
288
fractures and account for 18.8–29.0% and 10.4–
11.3% of fractures, respectively. The spur sign
seen on CT and conventional obturator oblique
radiograph is encountered only in both-column
fractures.
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 Signs in Musculoskeletal
Radiology
8
Haitao Yang, Lingling Song, and Zhaoshu Huang

Contents
8.1 Introduction  292
8.2 Flipped Meniscus Sign  292
8.3 Absent Bow Tie Sign  293
8.4 Fragment-in-Notch Sign  294
8.5 Cyclops Lesion  295
8.6 Anterior Tibial Translocation Sign  297
8.7 Celery Stalk Sign  298
8.8 Double Posterior Cruciate Ligament Sign  299
8.9 Double-Line Sign  300
8.10 Crescent Sign  301
8.11 Yo-Yo on String Sign  302
8.12 Arcuate Sign  303
8.13 Double Oreo Cookie Sign  304
8.14 J Sign  305
8.15 Secondary Cleft Sign  306
8.16 Lateral Capsular Sign  307
8.17 Fallen Fragment Sign  308
8.18 Iliac Hyperdense Line  309

H. Yang (*)
Department of Radiology, The First Affiliated
Hospital of Chongqing Medical University,
Chongqing, China
e-mail: frankyang119@126.com
L. Song · Z. Huang
Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China

© Springer Nature Switzerland AG 2021 291

B. Gao, A. M. McKinney (eds.), Classic Imaging Signs,
https://doi.org/10.1007/978-3-030-56348-6_8
292 H. Yang et al.

8.19 Terry Thomas Sign  311

8.20 Lateral Femoral Notch Sign  312
8.21 Elephant Trunk Sign  313
8.22 Fat–Blood Interface Sign  314
8.23 Elbow Fat Pad Sign  315
8.24 C Sign  317
8.25 Target Sign  318
8.26 Swirl Sign  320
8.27 Flow Void Sign  321
8.28 Button Sequestrum Sign  322
References  323

8.1 Introduction 8.2 Flipped Meniscus Sign

In this chapter we describe a number of easily Feature

recognizable signs in musculoskeletal radiology
such as bone and joint trauma, sports medicine,
bone and soft tissue tumors. These signs are dem-
onstrated with imaging to help understand direct
or indirect evidence of the pathology and mecha-
nism of injury. Familiarity with these signs allows
the radiologist and the clinician to toward an
accurate diagnosis or make a brief differential
diagnosis.
On magnetic resonance imaging (MRI) in sagit-
tal plane, the posterior horn of the meniscus is
torn or has disappeared, and the maximum height
of the anterior horn of ipsilateral meniscus
reaches 6 mm or higher. It is also possible that a
well-defined meniscus structure (double anterior
horn sign) may appear behind the anterior horn of
the meniscus, and the posterior horn may become
shorter or even disappear, which is defined as the
flipped meniscus sign.

a b c

Fig. 8.1  A 40-year-old man with flipped-over lateral meniscus structure in the expected location. (b, c) Sagittal
menisci of the left knee. (a) Coronal T2WI with fat-­ T1WI and T2WI with fat-saturated MRI show a bizarre-­
saturated MRI shows a main meniscus body located in the shaped posterior horn (arrow) protruding relative to the
intercondylar notch (arrow) and absence of a lateral edge of the tibial plateau and the small anterior horn
8  Signs in Musculoskeletal Radiology
Explanation
Flipped meniscus sign may occur in a bucket-­
handle tear of the meniscus. The meniscus frag-
ments are usually displaced to the intercondylar
fossa under pressure. If the meniscus fragment
does not move toward the intercondylar fossa but
directly forward to the anterior horn of the ipsi-
lateral meniscus, this is called flipped meniscus
sign [1] (Fig. 8.1).
Discussion
The meniscus of the knee is a kind of fibrous car-
tilage. The common tears of the meniscus can be
divided into four types: (1) the longitudinal tear
is called a bucket-handle tear (BHT) when both
ends are connected, and the cleft can catch the
femoral condyle like a noose; (2) the transverse
tear (radial tear) is rarely completely broken; (3)
the horizontal tear is a tear parallel to the menis-
cus plane; and (4) a marginal tear is along the
joint capsule attachment. BHT of the meniscus is
a special type of meniscus injury, which refers to
the displacement of the combined meniscus frag-
ments to the central area of the joint in longitudi-
nal and vertical tears or oblique tears, named
after its bucket-handle shape [2].
It is important to determine whether there is
BHT because this type of tear usually requires the
removal of displaced fragments. BHT usually
involves the medial meniscus. The torn meniscus
fragments usually move to the intercondylar fossa
and then forward to the patellar tendon. It has been
reported that the transposed bucket-­handle frag-
ments in the intercondylar fossa are often located
in front of the posterior cruciate ligament, which
can result in false “double posterior cruciate liga-
ment,” which is called the double posterior cruci-
ate ligament sign. If the meniscus fragment does
not move toward the intercondylar fossa but
directly forward to the anterior horn of the ipsilat-
eral meniscus, this is called flipped meniscus sign.
The diagnostic criteria of flipped meniscus sign
include (1) tear of posterior horn or not developed;
(2) the maximum height of anterior horn in the
same side meniscus reaches 6 mm or higher, and
the torn meniscus fragments are reversed and
superimposed with anterior horn of meniscus,
resulting in abnormal hypertrophy of anterior
293
horn; (3) a well-defined meniscus structure appears
behind the anterior horn of meniscus, also called
double anterior horn sign, which is caused by torn
meniscus fragments displaced behind the anterior
horn of the meniscus [3].
8.3 Absent Bow Tie Sign
Feature
On sagittal MRI, anterior and posterior horns of the
medial or lateral meniscus are connected through
the body, and the cross section of the normal knee
joint resembles a bow tie (the tie sign). On an MR
image 4–5 mm thick, with 0–0.5 mm spacing, there
are at least two bow ties connected by the body.
When bucket-handle tear occurs, there is only one
or no bow tie, called the absent bow tie sign.
Explanation
The average width of the normal meniscus body
is 9–12  mm, and the body of the meniscus can
appear as a bow tie on two consecutive sagittal
MRI images with a thickness of 4–5  mm. The
absent bow tie sign indicates a meniscus bucket-­
handle tear. The bucket-handle tear is a special
longitudinal rupture of the meniscus; the medial
segment is displaced, the displaced segment is
similar to a bucket handle, and the nondisplaced
lateral segment resembles a bucket, so it is called
a bucket-handle tear (Fig. 8.2).
Discussion
Bucket-handle tear is a special type of longitudi-
nal tear of meniscus, which occurs most fre-
quently in the middle of the meniscus.
Bucket-handle tear is common in young patients
with severe trauma, often involving the entire
meniscus, but may also involve the anterior, pos-
terior, or body of the meniscus alone. Because the
displaced segments are often located between the
intercondylar fossa or parallel to the posterior
cruciate ligament, or in the anterior or posterior
part of the posterior cruciate ligament, bucket-­
handle tear often causes joint stiffness, limited
extension, or joint instability. Therefore, it is very
important to confirm the displaced fragments for
arthroscopic segmentectomy or replacement [4].
294
a b
Fig. 8.2  A 71-year-old woman with knee trauma. Sagittal T1WI (a–c) shows absent bow tie sign (arrow); the normal
tie-like meniscus body is not shown on consecutive slices
A normal meniscus shows hypointensity in
each sequence of MRI.  On sagittal MR images
with slice thickness of 5 mm, the anterior and pos-
terior horns of the normal meniscus show a trian-
gle uniform hypointensity at the level of the
meniscus body. The two triangles are connected
by the body to form two bow-shaped changes
looking like a bow tie sign. When the bow-shaped
meniscus cannot be seen on one or two consecu-
tive layers of sagittal MRI images, it is called
absent bow tie sign. However, bucket-handle tear
may be difficult to diagnose on sagittal MRI, such
as longitudinal tear without displacement and dis-
coid meniscus with bucket handle tear. In discoid
meniscus, part or all of the meniscus tissue can
cover the tibial plateau, so the tie-like meniscus
displayed can be seen in the upper two levels. At
this time, it may not show the absent bow tie sign.
Helms et al. described necktie disappearance as a
sign of tearing of the barrel-­handle meniscus in
1998 [5]. Some normal structures of the knee joint,
including transverse meniscal ligament, accessory
meniscal ligament, and carmine tendon, can be
similar to the displaced segments in meniscus
bucket-handle tear, which can easily lead to misdi-
agnosis. In addition, in some cases, such as menis-
cal free margin resection, osteoarthritis with
meniscal free margin softening, long-term wear of
meniscal free margin in elderly patients, and nar-
row meniscus in children, because there are fewer
than two layers of the tie-like meniscus on sagittal
MRI, it may be mistaken for the absent bow tie
sign and misdiagnosed as bucket-handle tear,
which needs to be differentiated [6].
H. Yang et al.
c
8.4 Fragment-in-Notch Sign
Feature
Coronal MRI shows abnormal band- or clump-­
like hypointensity in intercondylar notch and
around the cruciate ligament, which is similar to
the signals of meniscus on T1WI and T2WI.
Another name: internal displaced fragment sign.
Explanation
The free edge of a bucket-handle tear is shifted to
the intercondylar notch and around the cruciate
ligament, forming a bucket handle-like structure,
and the low signal is the shape of a strip or mass
on the coronal MRI image (Fig. 8.3).
Discussion
Fragment-in-notch sign appears to serve as a reli-
able indicator of the displaced bucket-handle com-
ponent of medial meniscal tears. A bucket-­handle
tear commences as a vertical or oblique tear at the
posterior horn of the meniscus. Longitudinal
extension toward the anterior horn often allows the
inner segment to undergo varying degrees of dis-
placement into the intercondylar notch. The term
bucket handle is derived from the appearance of
the tear in which the inner displaced fragment of
the meniscus resembles a handle and the periph-
eral nondisplaced portion has the appearance of a
bucket. The medial meniscus is usually involved
[7]. Terezidis et al. [7] confirmed two thirds of iso-
lated meniscal tears in young athletes ranging
from 16 to 32 years of age (mean, 22 years) were
in the medial meniscus, presumably related to its
8  Signs in Musculoskeletal Radiology
a b
Fig. 8.3 (a–c) A 42-year-old man with a bucket-handle
tear in the posterior horn of the medial meniscus of the left
knee. Coronal T1WI shows abnormal clump-like hypoin-
tensity in the intercondylar notch and around the posterior
cruciate ligament. Sagittal fat-suppressed T1WI reveals an
firm attachment to the tibia, especially posteriorly
when compared to the more mobile lateral menis-
cus. Vertical tears, including bucket-handle tears,
are more common than horizontal tears both in
children with concomitant anterior cruciate liga-
ment (ACL) tears and in young athletes with iso-
lated tears; in adults, horizontal degenerative tears
are frequently seen. Meniscal injuries in children
younger than 10 years of age usually relate to an
abnormal discoid morphology.
According to the literature, there are five kinds
of signs of bucket-handle tears: (1) internal dis-
placed fragment sign: striated or clustered low-­
signal meniscal fragments of knee intercondylar
notch is positive on coronal or sagittal images; (2)
abnormal circumferential meniscus sign: the
meniscus and joint capsule on coronal image are
obviously smaller, in which the signal of abnormal
or no abnormal is positive; (3) double posterior
cruciate ligament sign (the sign of double PCL):
on sagittal image, if there is a parallel low-­signal
shadow in front of the posterior cruciate ligament,
it is positive; (4) absent bow tie (ABT) sign: nor-
mal meniscus body can be seen in at least two con-
secutive layers on sagittal images, likely a bow tie.
If the complete shape of the meniscus body is less
than two layers or none, it is positive. (5) Double
meniscus forefoot sign: if a clearly demarcated
meniscus structure is seen behind the anterior horn
of meniscus on sagittal image, the posterior horn
becomes obviously smaller. Internal displaced
fragment sign has the highest sensitivity, accuracy,
and negative predictive value, whereas a double
295
c
enlarged appearance of the posterior horn (vertical solid
arrow) and reduced appearance of the anterior horn (hori-
zontal solid arrow); axial fat-suppressed T2WI shows a
bucket handle-like structure (dashed arrow) that tore from
the post horn of the meniscus
PCL sign has the highest specificity and positive
predictive value. The reported sensitivity of ABT
sign is 88% in MRI when compared with
arthroscopic findings. Similarly, the free fragment
sign has a sensitivity of 90.7% with arthroscopic
correlation [8]. The diagnosis of meniscal tears is
usually based on MRI, which is now considered
the gold standard for meniscal pathologies [9].
8.5 Cyclops Lesion
Feature
On MRI, cyclops lesion manifests as a prolifera-
tive fibrous tissue nodule at the leading edge of
the reconstructed anterior cruciate ligament. The
pedicle is connected to the anterior cruciate liga-
ment. In all sequences, it is usually equal signals,
and sometimes low or high signal.
Explanation
Cyclops lesion is one of the major complications
after anterior cruciate ligament reconstruction.
Pathologically, it is mainly localized fibrous connec-
tive tissue hyperplasia, located at the leading edge of
the reconstructed anterior cruciate ligament. The
pedicle is connected to the anterior cruciate liga-
ment. Because the lesion resembles an eyeball dur-
ing arthroscopy, it is called cyclops lesion (Fig. 8.4).
Discussion
The cyclops lesion is mainly characterized by
localized fibrous tissue nodules, located in front of
296 H. Yang et al.

a b c

d e f

Fig. 8.4  (a–c) A 26-year-old man at 6 months after ACL T1WI with fat-saturated MRI. (d–f) A 16-year-old boy at
reconstruction. The cyclops lesion shows a circular iso-­ 3 months after ACL reconstruction for 3  months. The
intensity nodule (arrow) in front of the reconstructed ACL cyclops lesion is also shown
of the intercondylar fossa on sagittal, coronal, and axial

the anterior cruciate ligament of the intercondylar
fossa. It is similar to an eyeball under arthroscopy.
Because the lesion is located in the anterior part of
the joint, it is also called localized anterior joint
fibrosis. The cyclops lesion is one of the complica-
tions of anterior cruciate ligament reconstruction.
The total incidence is 1–9.8% and the incidence of
symptomatic cases is 0–2% [10]. The mechanism
of formation of cyclops lesion is not yet clear, and
there are currently two main explanations. First,
the debris generated by the tibial borehole during
the establishment of the anterior cruciate ligament
graft tunnel causes fibrous tissue hyperplasia; sec-
ond, the long-term impact damage of the intercon-
dylar anterior cruciate ligament graft during joint
movement leads to the formation of local fibropro-
liferative nodules [11]. The boundary between the
cyclops lesion and the anterior cruciate ligament is
unclear, and the pedicle is connected to it, which
supports the latter theory. Once the cyclops lesion
is formed, the hyperplastic fibrous tissue nodules
insert between the femur and the tibia during the
movement of the knee joint, resulting in the knee
joint not being fully extended.
The cyclops lesion shows moderate signal on
MRI. However, a few cases show high signals on
PDWI and low or high signals on T1WI. The
lesions are mostly in front of the anterior cruciate
ligament, and a few are located inside or outside.
The sensitivity of MRI in the diagnosis of cyclops
lesion is 85%, the specificity is 84.6%, and the
accuracy is 84.8%. In lesions with a diameter
greater than 10 mm, the sensitivity, specificity, and
accuracy of MRI diagnosis are higher [12]. When
a cyclops lesion occurs, the probability of the graft
appearing as hyperintensity on PDWI is increased,
and it is often arched, presumably by the compres-
sion stimulation of the fibrous hyperplastic nodule.
It is worth mentioning that not all cyclops lesions
have clinical manifestations, and in a few cases,
8  Signs in Musculoskeletal Radiology
symptoms may appear and progressively worsen
as the lesions gradually increase.
8.6 Anterior Tibial
Translocation Sign
Feature
The anterior tibial translocation sign is seen on
sagittal images of the lateral femoral condyle.
Parallel lines are drawn through the posterior cor-
tex of femoral condyle and the posterior cortex of
tibial plateau, and the vertical distance between the
two is 7 mm or greater anterior translocation.
Explanation
An anterior cruciate ligament (ACL) tear causes
the tibia to shift forward to different degrees rela-
tive to the femur, which is one of the indirect signs
of the anterior cruciate ligament tear (Fig. 8.5).
Discussion
The primary role of the ACL is to provide stability
to the knee joint. It resists anterior translocation
and internal rotation of the tibia over the femur.
The ACL also limits hyperextension and both val-
gus and varus forces on the knee. ACL injury is
a b
Fig. 8.5  Sagittal T1WI (a) and PDWI with fat saturated
(b) MRI of the left knee in a 22-year-old male patient with
anterior cruciate ligament (ACL) tear show abnormal
297
associated with anterolateral instability of the
knee. Deficiency of the ACL allows the tibia to
undergo anterior subluxation relative to the femur,
thus producing the anterior tibial translocation
sign. The degree of anterior subluxation of the
tibia can be measured directly at MRI; this is anal-
ogous to the anterior drawer test elicited during
physical examination, in which the tibia moves
anteriorly as the leg is pulled forward. Along the
midsagittal plane of the lateral compartment of the
knee, the distance between two lines drawn tan-
gent to the posterior of the lateral femoral condyle
and the proximal tibia indicates the degree of ante-
rior tibial translocation. Two methods of drawing
the tangent lines were described by Vahey et  al.
[13]. In the first method, the tangents were drawn
perpendicular to the tibial plateau. In the second
method, the tangents were vertical and parallel to
the image frame. The measured tibial displace-
ment would be greater for the second method [14].
MRI studies of the sagittal section of the lat-
eral femoral condyle are described as an indirect
finding if there was an anterior translocation
7 mm or greater of the tibia relative to the femur.
The mean anterior translocation amount in
chronic ACL tears is 8.7 mm on average; in acute
ACL tears, it is 5.4 mm on average. The anterior
anterior tibial translocation of 7.5 mm. A kissing contu-
sion in the lateral tibial and femoral subchondral bone and
posterior horn tear of the lateral meniscus also can be seen
298
a b
Fig. 8.6 (a, b) In a 72-year-old man, the celery stalk sign can be seen on sagittal T1WI and PDWI with fat-saturated
MRI, indicating ACL degeneration (arrow)
tibial translocation has been shown to increase
with time. According to Vahey et  al. [13], the
tibial anterior translocation was a specific finding
for the ACL tear. It is accepted that subluxation
of at least 5  mm has 58% sensitivity and 93%
specificity for an ACL tear [15]. Exposure (or
posterior displacement) of the posterior horn of
the lateral meniscus has also been described as a
sign of anterior tibial displacement; the tangent to
the posterior edge of the lateral tibial plateau cuts
the posterior horn of the lateral meniscus [16].
8.7 Celery Stalk Sign
Feature
This sign is characterized by an enlarged anterior
cruciate ligament (ACL) and unclear boundary. It
shows high signal intensity on T2WI and there are
strips of low-signal fibers in the ACL. It is named
for its shape, similar to a celery stalk.
Explanation
Celery stalk sign is a characteristic feature of
mucoid degeneration of the ACL. Under arthros-
copy, mucoid degeneration is a pale yellow scle-
rosing substance. The enlargement and swelling of
H. Yang et al.
ACL appear spherical with a certain degree of ten-
sion. MRI shows hyperintensity with blurred
boundary; ACL fiber bundles are scattered in a
hyperintensity area with hypointensity strips,
forming the celery stalk-like appearance (Fig. 8.6).
Discussion
Celery stalk sign is a rare MRI sign of the knee
joint. It shows enlargement of the ACL with an
unclear boundary. It shows high signal on T2WI,
with strips of low-signal fibers. It is named for its
shape, resembling a celery stalk. Mcintyre et al.
[17] first described this sign and considered it to
be a characteristic sign of mucoid degeneration
of ACL. The etiology and pathogenesis of ACL
myxoid degeneration are not yet clear, but may
be related to trauma, tenosynovial cyst, or degen-
eration, often occurring in middle-aged patients,
without gender difference. The main clinical
symptoms include knee pain, and inadequate
knee extension or flexion; most patients have no
definite history of trauma. The knee dyskinesia
may be caused by the compression of the mass-­
like degeneration lesion in the ACL between
femur and tibia. Therefore, even partial excision
of the mucoid degeneration lesion can relieve or
eliminate the clinical symptoms and signs.
8  Signs in Musculoskeletal Radiology
MRI is of great significance in the diagnosis
and differential diagnosis of mucoid degenera-
tion of ACL.  The normal ACL shows a regular
low signal at the edge. When mucoid degenera-
tion occurs, the ACL is enlarged locally and
shows mass-like changes with unclear boundar-
ies. On both T1WI and T2WI, a high signal is
seen, and low signal fibers are visible, forming
the so-­called celery stalk-like changes. Mucous
degeneration of the ACL is often misdiagnosed
by radiologists as partial or complete laceration
of ACL [18]. Mcintyre et  al. [17] reported 10
cases of mucinous degeneration of ACL of which
6 cases were misdiagnosed as ACL laceration
before arthroscopy. ACL mucinous degeneration
often has no definite history of knee trauma. MRI
shows diffuse thickening of ACL on the affected
side, continuous and normal orientation of upper
ligament bundles on T2WI, parallel to the high
signal shadows of degenerated tissues, showing a
typical celery stalk sign. The ACL laceration usu-
ally has a clear history of acute or chronic knee
trauma. Most of the injuries are located in the
middle part of the ligament, with a few located in
the prone point of the femur or tibia. In addition,
tenosynovial cysts and mucinous degeneration
occurring in ACL have similar MRI findings, and
sometimes they coexist. However, tenosynovial
cysts are low and medium signal on T1WI and
hyperintensity on T2WI [19]. The long axis of
a b
Fig. 8.7  A 19-year-old male patient with medial menis-
cus bucket-handle tear of the right knee. Sagittal T1WI (a),
T2WI (b), and PDWI with fat saturated (c) MRI show a
299
tenosynovial cysts can be parallel to the liga-
ment fibers, but the fibers bundles are arranged
in an abnormal direction, so they can be
differentiated.
8.8  ouble Posterior Cruciate
D
Ligament Sign
Feature
On sagittal MRI of the knee, arcuate hypointen-
sity is seen anterior to the posterior cruciate liga-
ment (PCL) and parallel to it, resembling a
double PCL, and hence this is called the double
posterior cruciate ligament sign. The appearance
of this sign often suggests a bucket-handle tear
(BHT) of the meniscus of the knee joint.
Explanation
In BHT of the meniscus, the avulsed portion is
displaced anteriorly and inferiorly of PCL, both
of which have hypointensities on all sequences;
the avulsion-shifted fragments resemble a second
PCL (Fig. 8.7).
Discussion
A double PCL is caused by an ACL located slightly
outside the midline that prevents the torn frag-
ments from continuing to shift outward. Therefore,
the ACL is important in the formation of PCL sign
c
parallel arc-shaped hypointensity in PCL (white solid
arrow), with torn and displaced meniscus fragments
(white hollow arrow)
300
after BHT of the meniscus [20]. BHT of the menis-
cus is a common condition in the knee joint and is
a common cause of knee pain and dysfunction.
The clinical symptoms caused by BHT are more
typical, such as joint lock or limited joint exten-
sion; the degree of meniscus tear is different, and
the clinical symptoms are also different. If the torn
fragments cannot be reset soon enough, the frag-
ments will soften over time.
MRI is an effective method to diagnose BHT of
knee joint, and its sensitivity and specificity to
BHT of the medial meniscus are higher than those
of the lateral meniscus. BHT is a special form of
longitudinal tear, a full-length longitudinal tear.
Some of the fragments of a medial meniscus tear
are connected to the meniscus. The stress can dis-
place the torn part between the PCL and the medial
intercondylar femoral and parallel to PCL. When
the torn part of the meniscus is large, displacement
may occur, forming more characteristic secondary
signs, including double PCL sign, intercondylar
debris sign, meniscus jump sign, and bow tie dis-
appearance sign [21]. In the secondary signs of the
meniscus BHT, the sensitivity of the bow tie disap-
pearance sign is the highest, followed by intercon-
dylar debris sign, meniscus jump sign, and double
a b
Fig. 8.8  A 75-year-old man with avascular necrosis of femoral head on both sides shows double-line sign on coronal
(a, right femoral head) and axial (b, left femoral head) T2WI with fat-saturated MRI (arrow)
H. Yang et al.
PCL sign. If combined with the coronal image, the
sensitivity of secondary signs to the diagnosis of
BHT can be further improved. Torn meniscus frag-
ments can sometimes be confused with Humphry
ligaments and oblique slab ligaments. ACL and
PCL travel between each other. This movement
can form an illusion resembling the double
PCL. To avoid this illusion, the starting and ending
points of the ligament should be found and differ-
entiated [22].
8.9 Double-Line Sign
Feature
The double-line sign is seen on T2WI of medul-
lary bone as hyperintensity line within a parallel
rim of decreased signal intensity surrounding
osteonecrosis foci.
Explanation
Double-line sign is seen with avascular necrosis
(AVN) on MRI.  The hyperintensity inner zone
represents hyperemic granulation tissue, and the
hypointensity outer zone represents adjacent
sclerotic bone (Fig. 8.8).
8  Signs in Musculoskeletal Radiology
Discussion
This sign is considered pathognomonic for avas-
cular necrosis (AVN) because the outer rim rep-
resents the reactive bone and the inner rim
represents the vascular and repair tissue at the
necrotic–viable osseous interface [23]. Trauma is
the most common cause of AVN; other causes
include hemoglobinopathies, Cushing syndrome,
exogenous steroid use, alcoholism, pancreatitis,
and human immunodeficiency virus. The epiphy-
sis and metaphysis of long tubular bones are sus-
ceptible because of their limited arterial supply
and limited venous drainage. Therefore, AVN
may also be idiopathic. The hip is the most com-
mon site, but the knee, shoulder, and carpal and
tarsal bones can also be affected. The location of
AVN may be influenced by the underlying dis-
ease (e.g., the shoulder in sickle cell disease)
[24]. AVN may be initiated by a traumatic disrup-
tion of a vessel or by other factors that cause isch-
emia, such as thromboembolism or venous stasis.
After an initial traumatic insult, hematopoietic
cells die within 6–12  h; fat marrow cells die in
2–5  days. Ischemic bone eventually undergoes
repair from its periphery to its infarcted center.
Healing begins with hyperemia at the ischemic
periphery; the hyperemia is subsequently
replaced by reactive tissue and sclerosis.
Microfractures and bony collapse may occur as
trabeculae are reabsorbed [24].
MRI has been reported to have a sensitivity of
97% and specificity of 98% in the diagnosis of
AVN of the hip when a variety of findings are used
to aid in the diagnosis. MRI is more sensitive than
computed tomography (CT), scintigraphy, or con-
ventional radiography [25]. MRI has become the
first-choice imaging modality for AVN of the fem-
oral head because of its high soft-­tissue resolution
and multiplanar ability. T1WI show serpiginous
band-like lesions with low signal intensity in the
anterosuperior femoral head. The double-line sign
is seen on T2WI and consists of a low signal inten-
sity outer rim and a high signal intensity inner rim.
With or without treatment, AVN may progress to
cystic degeneration, intraarticular osseous bodies,
and collapse of articular surfaces with subsequent
secondary osteoarthritis. Patients may ultimately
require joint replacement [25].
301
8.10 Crescent Sign
Feature
Crescent sign is characterized by a subchondral
arc-shaped transparent area, which can be seen
on plain film and MRI showing arc-like hyperin-
tensity on T2WI. It is common in the proximal
anterolateral femoral head.
Explanation
Crescent sign is a sign of bone avascular necro-
sis. Poor perfusion at the articular end of bone
leads to progressive necrosis and repair. When
the repair reaction begins, a reaction band of
fibrosis, congestion, inflammation, and bone
resorption extends into the dead bone band,
which is the interface. Repair occurs at the inter-
face between dead bone and living bone.
Reactive new bone grows on the necrotic bone
trabecula and produces a sclerotic margin. The
decrease of bone trabecular bearing capacity
leads to progressive microfracture of subchon-
dral bone trabecula and articular surface col-
lapse, forming a translucent zone along the
fracture line under the cartilage, that is, crescent
sign (Fig. 8.9).
Discussion
AVN occurs most frequently in the proximal
femur, followed by proximal humerus, distal
femur, and talus, occasionally in lunate, metatar-
sal head, and tarsal scaphoid. Regardless of the
location of avascular necrosis, the appearance of
crescent sign is helpful for clinical staging and
treatment options. In many cases, bone resorp-
tion causes destruction of the subchondral sup-
port structure, which leads to subchondral
trabecular microfracture and joint collapse. At
this time, articular cartilage can remain active
because it absorbs nutrients from synovial fluid.
As the disease progresses, articular cartilage is
destroyed, joint space is narrowed, and then artic-
ular cartilage collapse occurs. Crescent sign is
considered as an early indication of articular car-
tilage collapse. AVN is the most common type of
osteonecrosis, which often leads to articular car-
tilage collapse of the femoral head and severe
secondary osteoarthritis. The collapse of the
302
a b
Fig. 8.9  A 48-year-old woman with a year of pain in
right hip joint. X-ray plain film (a), CT coronal recon-
struction (b), and coronal T2WI (c) with fat saturated
articular cartilage of the femoral head is the result
of the loss of mechanical support [26].
The appearance of crescent sign can help
clinical staging. According to the findings of
MRI, AVN can be divided into four stages [27]:
stage I, complete femoral head, continuous
articular cartilage and simple fat-like signal in
necrotic area; stage II, complete femoral head,
continuous articular cartilage and mixed signal
of fat granulation tissue in necrotic area; stage
III, collapse of femoral head, no fracture of
articular cartilage of hip; stage IV, collapse of
femoral head, fracture of articular cartilage of
hip. Although crescent sign can also be seen
occasionally in other osteopathy, such as osteo-
chondral shear fracture of the femoral head,
which can be easily identified by clinical his-
tory, it is most common in avascular necrosis of
the femoral head and occurs at a later stage. The
appearance of crescent sign indicates the col-
lapse of the articular surface.
8.11 Yo-Yo on String Sign
Feature
Coronal MRI shows rupture and retract of pha-
langeal ulnar collateral ligament (UCL). The
H. Yang et al.
c
show crescent-shaped transparent area/hyperintensity
under right femoral head
retracted ligament moves to the surface of the
adductor aponeurosis, showing hypointense cir-
cular structure on all sequences. The adductor
aponeurosis shows thin hypointensity line adja-
cent to folded UCL on coronal plane, and the
shape resembles a yo-yo on a string.
Explanation
Yo-yo on a string sign is an MRI sign of a ulnar
collateral ligament that is completely ruptured
(Fig. 8.10).
Discussion
UCL injury is caused by external force in the
radialis. Historically, such injuries have often
occurred in Scottish gamekeepers and are now
often associated with skiing and other sports,
so it is also known as skier’s thumb [28].
Anatomically, the UCL is located deep in the
adductor aponeurosis. The adductor aponeuro-
sis consists of transverse fibers and oblique
fibers from the adductor pollicis tendon and the
extensor pollicis tendon [29]. UCL tear often
occurs at the distal and near the junction of the
phalanx. On MRI, the normal UCL shows a
hypointensity band inside the metacarpopha-
langeal joint, and the adductor aponeurosis
shows as a thin paper-­like hypo-intensity band
8  Signs in Musculoskeletal Radiology
a b
Fig. 8.10  A 36-year-old male patient with right thumb
trauma. MRI T2WI (a) and T1WI (b) show rupture and
retraction of the UCL as a waved string appearance (white
on the surface of the UCL, which covers from
the distal half of the UCL to the base of the
proximal phalanx. MRI can show UCL rup-
tures at the base of the proximal phalanx; the
ligament retracts, and the retracted ligament
moves to the surface of the adductor aponeuro-
sis and shows a circular or a residual root-like
structure with hypointensity in all sequences.
The adductor aponeurosis shows a thin hypoin-
tense line adjacent to the folded UCL on the
coronal MRI, which is called the yo-yo on a
string sign. MRI is sensitive to a displaced
UCL tear, with sensitivity of 100% and speci-
ficity of 94% [30].
303
hollow arrow); tear of the proximal radial collateral liga-
ment is also seen (black arrow)
8.12 Arcuate Sign
Feature
On X-ray the bone fragments avulsed from the
fibula head moved upward. The size of bone
­fragments can range from blurred spots to centi-
meters in diameter, called arcuate sign.
Explanation
Avulsion fractures involving arcuate complex usually
occur at the junction of the ligament and the fibula
head. Arcuate sign indicates the rupture of the arcuate
complex and the presence of acute posterolateral
rotational instability of the knee joint (Fig. 8.11).
304
a b
Fig. 8.11  A 46-year-old male patient with right knee
trauma. Radiography (a) shows an avulsion fracture of the
fibular head (arrow). (b, c) Coronal T1WI and PDWI with
fat saturation show avulsion fracture of fibular head with
Discussion
Arcuate sign was first described as an avulsion
fracture of the fibula head indicating posterolateral
knee instability. The arcuate sign is believed to be
pathognomonic for an injury to one or more of the
structures of the posterolateral structure of the
knee, and an associated posterior cruciate ligament
injury is frequently found. The posterolateral struc-
ture of the knee joint is a complex that includes the
fibular collateral ligament, the ligament of sural
head and fibula, the popliteal fibular ligament, the
arcuate ligament, the popliteal tendon, and the ten-
don of the biceps femoris muscle [31]. The arcuate
sign is described as a small bone fragment of the
fibular head avulsion because of the trauma, and
the bone fragments were torn off from the arcuate
complex. However, the ligaments attached to the
fibular head have different attachment points, so
several different types of avulsion fractures may
occur. Avulsion injuries of the popliteal fibular liga-
ment, the arcuate ligament, and the ligament of
sural head and fibula involve the tip of the fibular
head (fibular styloid process) [32].
This avulsion injury is characterized by an
oval bone fragment on X-ray radiography. On
MRI, edema in the medullary cavity of the
avulsed bone or fibular head can be observed.
The avulsion fracture of the fibular head may be
related to other ligament or tendon injuries in the
posterolateral knee joint. In this case, the fibular
H. Yang et al.
c
edema near the attachment of the fibular collateral liga-
ment combined with injuries of the posterolateral com-
plex of the knee (arrow)
collateral ligament, the tendon of the biceps fem-
oris muscle, and the popliteal tendon may be
damaged. MRI can be used to evaluate the integ-
rity of the posterolateral angle of the knee joint.
The fibular collateral ligament, the tendon of the
biceps femoris muscle, and the popliteal tendon
are the larger structures; conventional MRI can
accurately evaluate their injuries. However, the
popliteal fibular ligament, the arcuate ligament,
and the ligament of the sural head and fibula are
the smaller structures, and they are oblique struc-
tures; it is difficult to identify and evaluate in con-
ventional MRI.  An oblique coronal position is
the best orientation to show these structures.
8.13 Double Oreo Cookie Sign
Feature
In coronal MRI arthrography, two hyperintensity
lines appear on the superior labrum, which are
sandwiched by three hypointensity lines, resem-
bling a double Oreo cookie, and known as the
double Oreo cookie sign.
Explanation
The contrast agent enters between the superior
labrum and glenoid cartilage, indicating the rup-
ture of the superior labrum. One of the two hyper-
intensity lines represents the lower crypt of the
8  Signs in Musculoskeletal Radiology
Fig. 8.12 A 36-year-old man with superior labrum
anteroposterior (SLAP) tear. Oblique coronal T2WI with
fat saturated shows two hyperintensity lines in the supe-
rior labrum, displaying the “double Oreo cookie sign”
labrum and one represents the rupture of the
labrum. The three hypointensity lines represent
the superior labrum and glenoid cartilage. The
appearance of double Oreo cookie sign often
suggests superior labrum anterior and posterior
(SLAP) tear (Fig. 8.12).
Discussion
The appearance of double Oreo cookie sign often
suggests superior labrum anterior and posterior
(SLAP) tear, which is an important cause of
shoulder pain and instability. Snyder et al. classi-
fied SLAP tears into four types under arthros-
copy: type I is the wear and degeneration of the
superior labrum, with no tear of the labrum, and
the biceps tendon is normal; type II refers to the
superior labrum peeling from the supracondylar
nodules; type III is the superior labrum with a
barrel-like tear that shifts into the joint, but the
biceps tendon attachment is not involved. Type
IV has the same handle-like tear as the type III
and involves the biceps tendon. Type II lesions
are the most common, and the incidence of types
I–IV is 9.5–21%, 41–55%, 6–33%, and 3–15%,
respectively [33].
The MRI coronal plane is most sensitive to
superior labrum lesions. MRI diagnosis of SLAP
305
tear is based on changes in signal and morphol-
ogy. On MRI it manifests as an increase in the
labrum signal, with or without the attachment of
the biceps tendon to the tear of the superior labrum
[34]. Several signs are useful for diagnosing
SLAP tear: one is the upper one third of the supe-
rior labrum in the high signal and the other is the
superior labrum is irregular or curved outward
with high signal [35]. In addition, the normal
lower labrum of the labial sac appears on the MRI
as a high signal that curves inwardly. If it shows a
hyperintensity that curves outward, it clearly indi-
cates the tear of the superior labrum. MRI arthrog-
raphy can better display the structure in the joint
cavity and improve the accuracy of the diagnosis.
In the MRI coronal position, if the contrast agent
enters between the glenoid cartilage and the supe-
rior labrum, a hyperintensity band is formed,
sandwiched by two hypointensity bands. That is a
single Oreo cookie sign, which is common in the
crypt under the labrums or type II lesions. The
contrast agent enters between the superior labrum
and the glenoid cartilage (the crypt of the labrum)
and the cleft of the superior labrum. Two hyperin-
tensity lines appear, one for the crypt of the
labrum and one for the rupture of superior labrum.
It is sandwiched by three hypointensity lines (rep-
resenting the upper labrum and the glenoid carti-
lage), which resembles a double cookie sign, and
known as the double Oreo cookie sign. A recent
meta-analysis showed the sensitivity of MR
arthrography in the diagnosis of labrum tear (80%
vs. 63%) was superior to standard MRI with the
similar specificity (91% vs. 87%) [36].
8.14 J Sign
Feature
On conventional MRI and MR arthrography, the
continuous interruption of the right glenohumeral
ligament, which looks like the shape of a “J,” and
hyperintensity liquid accumulation can be seen
around the broken structures.
Explanation
The J sign indicates humeral avulsion of the
glenohumeral ligament (HAGL) lesion of the
­
306
Fig. 8.13  A 23-year-old male patient with left shoulder
trauma. Oblique coronal fat-saturated T2WI shows dis-
continuous inferior glenohumeral ligament (arrow) with
surrounding edema and fluid
shoulder joint. The glenohumeral ligament origi-
nates from the anterior and posterior lip of the
glenoid and ends around the anatomical neck of
the humerus, located just at the edge of the
humeral head and below the joint. The glenohu-
meral ligament is composed of anterior fascicle,
posterior fascicle, and axillary sac. Shoulder
effusion or MR arthrography may reveal a nor-
mal U-shaped glenohumeral ligament. The
humerus anatomical neck attachment of the gle-
nohumeral ligament was torn and the anterior or
posterior fascicles were separated and pendulous,
and the normal U shape was transformed into the
J shape. The left shoulder joint HAGL lesion
forms the reverse J sign. Continuous interruption
of the glenohumeral ligament causes exudation
around the free end of the isolated ligament and
contrast agent accumulation after MRI arthrogra-
phy (Fig. 8.13).
Discussion
HAGL is a rare but important cause of instability
in the front of the shoulder joint. When the arm is
abducted by 90°, the glenohumeral ligament lip
complex is the main stable structure in front of
H. Yang et al.
the shoulder joint [37]. It can prevent anterior
dislocation of the shoulder joint with external
rotation. The pathological mechanism of shoul-
der HAGL is traumatic excessive abduction and
excessive external rotation of the arm. HAGL
lesions are most common in anterior shoulder
joint dislocation. HAGL lesions can occur in dif-
ferent sports, such as football, skiing or water
skiing, surfing, football, basketball, volleyball,
ice hockey, diving, wrestling, or boxing.
Clinically, HAGL often occurs after reduction of
acute anterior dislocation of shoulder or when
traumatic dislocation occurs for the first time in
patients with anterior unstable of shoulder joint.
Then signs and symptoms include tenderness and
pain in the front of the shoulder joint, fear of
abduction and lateral rotation, external rotation,
sensory loss of the shoulder joint, twisting pro-
nunciation, and ligament relaxation [38].
MR arthrography and conventional MRI are
effective in finding HAGL. Oblique coronal fat-­
saturated T2WI is the best method for showing
HAGL [39]. MRI can also directly show discon-
tinuity of the ligament and extravasation of con-
trast material in the region of capsular avulsion
that results in an abnormal distribution of fluid
within the articulation, the conversion of a
U-shaped recess to a J-shaped recess, which can
be used to diagnose HAGL.
8.15 Secondary Cleft Sign
Feature
The hyper-intensity along or below the median
line of pubic symphysis joint and physiological
cleft in the center of the pubic symphysis fibro-
cartilage disc, which is called secondary cleft
sign, is best displayed on coronal T2WI or short-­
TI inversion recovery (STIR) images.
Explanation
There is a liquid cleft in the center of the pubic
symphysis fibrocartilage disc, called the physio-
logical cleft. On coronal T2WI and STIR images,
the pubic symphysis fibrocartilage disc shows a
linear hyperintensity in the center of the pubic
symphysis fibrocartilage disc. The middle part of
8  Signs in Musculoskeletal Radiology
a b
Fig. 8.14  A 32-year-old woman with chronic left groin
pain. (a) Axial and (b) coronal T2WI with fat saturation
MRI show significant marrow edema in the pubic bodies,
the pubis is the attachment of adductor
­aponeurosis, gracilis muscle, and inguinal falx.
Injury of these ligaments can cause abnormal ten-
sion of pelvic ring and lead to rupture of the
pubic symphysis fibrocartilage disc, forming a
secondary cleft connecting with the physiologi-
cal cleft or communicating with each other. This
secondary cleft often extends beyond the edge of
the fibrocartilage disc or between the adductor
and gracilis muscle attachments. Therefore, the
secondary cleft also shows linear hyperintensity
with different lengths on coronal T2WI or STIR
images (Fig. 8.14).
Discussion
Groin strain is more common in sports that
expose the symphysis pubis to repeated shear
and distraction, which is created by the pivoting
and twisting that occurs when kicking, stretch-
ing a limb, or rapidly transferring weight from
one limb to the other. Repeated shear and dis-
traction occur in soccer, rugby, and Australian
football players and have also been noted in
professional football running backs. In matu-
rity, the fibrocartilage of the symphysis pubis,
which serves to buttress impaction and dissi-
pate shear forces, develops a small central
fluid-filled cavity or cleft. This cleft is identi-
fied clearly at symphyseal injection and mani-
307
more marked on the left side. A subtle crescentric hyper-
intensity line along the anteroinferior margin of the left
pubic body suggests a secondary cleft sign (arrow)
fests as a central focus of hyperintensity on
fat-saturated T2WI or STIR [40]. The secondary
cleft sign, which represents micro-tearing of
the short adductor attachment, was described
on MRI by Brennan et  al. [40]. A secondary
cleft could develop as a result of chronic mac-
eration of the central fibrocartilage by abnor-
mal stress in the pelvic ring. Because secondary
cleft is related to many factors, although some
patients with pubic osteitis do not have second-
ary cleft sign on MRI, the display of secondary
cleft sign on MRI can help explain the cause of
inguinal pain, so other unnecessary examina-
tions can be avoided [41].
8.16 Lateral Capsular Sign
Feature
X-ray of the knee joint shows a small bone
shadow on the lateral side of the tibial plateau.
Explanation
Lateral capsular sign is a sign on knee X-ray sug-
gesting Segond fracture. The small bone piece
suggests a partial tear of the middle one third of
the lateral capsular ligament, usually suggesting
tearing of the lateral capsular ligament and ante-
rior cruciate ligament (Fig. 8.15).
308
Fig. 8.15  A 22-year-old woman presented with a free
small bone patch on the lateral margin of the right tibial
plateau on X-ray of the right knee joint (arrow)
Discussion
Segond fracture refers to the avulsion fracture of
the lateral edge of the tibial plateau, which occurs
mainly in acute injury of the knee joint, and may
be associated with structural damage of the joint
[42]. The ACL is damaged after an internal rota-
tion and varus force is applied to the knee flexion
of 10° to 90°. Segond fractures occur after the
violence continues to transmit to the outer joint
capsule ligament. Therefore, Segond fractures
are closely related to ACL injury. One study
reported the incidence of Segond fracture com-
bined with ACL rupture was 75% to 100%. ACL
rupture is best developed in the middle part of the
ligament, and second in the adjacent femoral
attachment, at least in the tibia attachment [43].
ACL includes anterior internal bundle (AMB)
and posterior external bundle (PLB). The adipose
tissue inlay between the two bundles or the side,
under the influence of volume effect, causes the
MRI signal of ACL to be not uniform and higher
than other ligaments. When ligament rupture
occurs, the MRI manifestations include complete
H. Yang et al.
discontinuity of ligament fibers, abnormal signal,
and abnormal morphology. In acute injuries, the
high signal line of T2WI crosses the ligament;
blurred anterior cruciate ligament and abnormal
tilt are observed. Acute ACL tear can also be
accompanied by joint effusion and infrapatellar fat
pad edema (especially infrapatellar fissure effu-
sion). Because ACL rupture is often associated
with rotational displacement injury, this type of
injury usually occurs in the movement of sudden
deceleration and simultaneous change of direc-
tion, which results in ACL stress and ligament tear.
In the process of an ACL tear, tibial anterior move-
ment and femoral condyle compression can cause
meniscus degeneration or tear; the medial inci-
dence is slightly higher than the lateral. Bone con-
tusion and avulsion fracture (i.e., Segond fracture)
are prone to occur at the attachment of the medial
lateral capsular ligament of the tibial plateau,
resulting in the formation of lateral capsular sign
[44]. If radiography of the knee joint reveals free
small bone patches on the lateral tibial plateau,
Segond fracture is often suggested. If not handled
in time, this will lead to instability of knee joint
and osteoarthritis. Timely MRI can not only reduce
missed diagnosis, but also aid treatment and
patient rehabilitation.
8.17 Fallen Fragment Sign
Feature
This sign refers to the appearance of a patchy
bone density shadow at the bottom of the bone
cyst cavity on X-ray as it moves with the change
of body position.
Explanation
Fallen fragment sign is an X-ray sign of bone cyst
complicated with pathological fracture. The
pathological fracture fragment falls into the cyst
cavity, sinks to the lowest part of the cyst cavity,
and can move with the change of body position
(Fig. 8.16).
Discussion
Fallen fragment sign was first reported in simple
bone cyst (SBC) with pathological fracture. The
8  Signs in Musculoskeletal Radiology
Fig. 8.16  A 12-year-old male patient with a simple bone
cyst and pathological fracture of left humerus. X-ray plain
film shows a cystic transparent shadow in the upper
humerus and a patchy density fragment that has fallen
within it (arrow)
fallen fragment sign has been demonstrated in
20% of cases of SBC. Minor trauma to the thin
cortical wall results in a fracture that is bound by
the outer intact periosteum and surrounding soft
tissues. Complete detachment of the fragment
from the periosteum allows it to sink to the bot-
tom of the fluid contained within the cyst. Several
authors have identified this sign in larger series of
simple bone cyst, confirming the suggestion that
it is a pathognomonic sign for SBC [45]; this
occurs if the specific gravity of the fluid is less
than that of the bony fragment. A variation of this
sign occurs if the fragment fails to detach com-
pletely from the periosteum. Pathological frac-
tures are reportedly present in approximately
65% of cases of simple bone cyst. Fragmentation
of the inner bony wall of the cyst can occur after
relatively minor trauma. Fragment migration
cannot occur after the cortical fracture of a solid
lesion such as fibrous dysplasia or nonossifying
309
fibroma. Therefore, cystic bone lesions can be
differentiated from solid bone lesions when the
fallen fragment sign is present [46].
This sign can be demonstrated with radio-
graphs or CT. Multiple views may be necessary
to confirm the intramedullary location of the
fragment, as a fracture through a solid lesion may
produce a fragment that appears to be in the
lesion but may actually be in the extraosseous
soft tissues. Alternatively, CT may be helpful in
identification of the intramedullary location of
the bone fragment [46]. Some authors have sug-
gested this sign does not occur in other benign
lesions, but may be considered in the differential
diagnosis of the later stages of eosinophilic gran-
uloma (EG). One case of chondromyxoid fibroma
has been reported as showing a pseudo-fallen
fragment sign that is thought to be related to a
fortuitous pattern of chondroid calcification [47].
Chondromyxoid fibroma typically causes corti-
cal thinning but no periosteal breach.
Theoretically, other focal fluid-containing lesions
that cause expansion with cortical thinning and
intact periosteum may predispose to fallen frag-
ment sign after trauma. Although SBC is by far
the most common cause for a central well-­
defined, lucent lesion with a fallen fragment,
other lesions should be considered.
8.18 Iliac Hyperdense Line
Feature
On the radiography AP view of pelvis, the verti-
cal hyperdense line shadow near the sacroiliac
joint of the ilium wing is called the ilium hyper-
dense line.
Explanation
The iliac hyperdense sign is a relatively charac-
teristic manifestation of gluteal muscle contrac-
ture (GMC) on X-ray plain film [48]. Normally,
the outer cortex of the sacroiliac joint of the ilium
is smooth and inclined from inside to outside.
When the gluteus maximus muscle contracts, the
muscles of the contraction and their fascia pull
the posterior part of the femur. This long-term
and  continuous pulling force leads to bone
­
310
a b
Fig. 8.17  A 16-year-old girl with right GMC. (a) Pelvic
plain film shows a hyperdense line on the right ilium. The
line runs roughly parallel to the sacroiliac joint (arrow).
(b) Axial T1WI and (c) T2WI with fat saturation show con-
d­ eformation and thickening at the attachment of
the gluteus maximus, and gradually changes the
bone cortex of the external margin of the iliac
sacroiliac joint into nearly forward and backward
walking. The outer cortex of the iliac sacroiliac
joint running forward and backward is consistent
with the X-ray direction (Fig. 8.17).
Discussion
Gluteal muscle contracture (GMC) is a clinical
syndrome caused by degeneration and contrac-
ture of muscle and fascia fibers, which results in
functional limitation of hip joint and shows spe-
cial symptoms and signs. Its etiology is complex
and varied, including intramuscular injection of
gluteus, genetic factors, and scar constitution,
gluteal muscle infection, gluteal compartment
syndrome, and postoperative treatment of con-
genital dislocation of hip. At present, most schol-
ars believe that repeated intramuscular injection
is the main cause of gluteal muscle contracture,
especially for benzyl alcohol solvent penicillin
injection, and the younger the age at injection,
the more injection times, and the greater the
injection frequency, the more likely to cause dis-
ease. Because the opportunity of bilateral gluteal
intramuscular injection is often equal, most of the
cases are bilateral. However, the degree of bilat-
eral contracture is different, and the scope also
differs. Gluteus maximus was the most frequently
involved, gluteus medius was the second, gluteus
minimus was less involved, and severe cases
H. Yang et al.
c
tracted right gluteal muscle with irregular margin (arrow)
and deformity of the posterior ilium with part of the lateral
cortex (arrow)
involved piriformis muscle and hip joint capsule.
The skeletal development of children has not yet
been completed. After the formation of fibrous
contracture bands, the balance of muscle strength
attached to the pelvis and the upper femur is
changed. The development of fibrotic muscle tis-
sue is asymmetrical with the pelvis and femur
attached to it, that is, the pelvis and femur develop
rapidly, while the development of fibrotic gluteal
muscle lags relatively slower, so it can gradually
cause secondary changes of pelvis and hip joint.
The slight cases only show hip joint abduction,
external rotation, and pelvic rotation. The heavier
cases may cause pelvic tilt, unequal length of
lower limbs, even dislocation of hip joint, or
compensatory scoliosis of lumbar spine [49].
Previous studies on X-ray manifestations of
gluteal muscle contracture were mainly aimed at
understanding the effects of gluteal muscle con-
tracture on the growth and development of the
pelvis in children, rather than as a means of diag-
nosing the disease. According to the literature,
these studies included the increase of central
margin angle (CE angle) and neck–shaft angle,
the decrease of femoral head index, the decrease
of iliac height–width ratio and acetabular angle,
and pelvic tilt. The foregoing signs mainly reflect
the morphological changes of the anterior exter-
nal iliac bone and hip affected by gluteal muscle
contracture, and to some extent reflect the extent
of the disease. The study found that the occur-
rence rate of iliac hyperdense line in patients
8  Signs in Musculoskeletal Radiology 311

more than 5  years old was significantly higher

than that in patients under 5  years old, and the
difference was significant. This conclusion indi-
cates the appearance of iliac hyperdense line is
directly related to the course of gluteal muscle
contracture. The hyperdense line of iliac bone
varies in length. The distances of the sacroiliac
joint are different, which may be related to the
degree, extent, and course of gluteal muscle
­contracture. The longer the course of disease, the
wider the scope of contracture and the more
severe the degree of contracture, and the more
obvious, longer, and farther away from the sacro-
iliac joint of the iliac hyperdense line. On the
contrary, the shorter the line of iliac hyperdense
line is, the closer it is to the sacroiliac joint [50].
CT and MRI can directly display the shape of
gluteal muscle, and determine the location,
extent, and severity of the lesion, thus providing
direct signs for the diagnosis of gluteal muscle
Fig. 8.18  A 39-year-old man with chronic trauma of the
contracture. CT has high-density resolution and
right wrist. Radiograph shows scapholunate dissociation,
can show the calcification of sand grains above with the space between the scaphoid and lunate widened
and outside the gluteus maximus muscle, which (Terry Thomas sign) (arrow)
is characteristic. MRI can clearly show morpho-
logical structure and signal changes of the mus-
cles and fascia. Untimely treatment often leads to chronic wrist
pain and weakness (Fig. 8.18).

8.19 Terry Thomas Sign Discussion

Feature  Positive X-ray plain film of wrist shows
the space between scaphoid and lunate joint is
more than 4 mm or twice as wide as that between
the healthy side of (or around) joint. The mid-
point of scaphoid and lunate relative to articular
surface was taken as the measuring point.
Explanation
The carpal bone consists of eight bones, which
have a certain range of motion and maintain a
certain degree of stability. Terry Thomas sign is
an X-ray manifestation of instability of the
scaphoid and lunate joint, named for its resem-
blance to the characteristic anterior teeth of
Terry Thomas, a famous British comedian. The
common reason is that the gap between scaph-
oid and lunate is widened by a tear of the liga-
ment connecting the scaphoid and lunate.
Scapholunate dissociation results from a rup-
ture of the scapholunate interosseous ligament
following forceful extension of the wrist. The
resulting instability allows widening of the
scapholunate joint. Although scapholunate dis-
sociation often occurs as part of a peri-lunate
or lunate dislocation, it may occur as an iso-
lated injury. Patients with scapholunate disso-
ciation usually present with wrist swelling and
pain, especially at extremes of motion. The
resulting decreased strength and limitation of
motion can significantly impair normal func-
tion. There is usually a history of a fall or force
applied to the extended hand. Physical exami-
nation may reveal a palpable clunk in the wrist,
in addition to mild swelling and tenderness
over the dorsal wrist [51].
In scapholunate dissociation, the radiograph
will reveal widening of the scapholunate joint.
312
­   gap between the lunate and scaphoid greater
A fracture. A localized chondral or transchondral
than 4 mm, which has been called “Terry Thomas
sign,” is pathognomonic. The width of these gaps
should not change significantly with radial or
ulnar deviation. However, in dynamic scapholu-
nate instability, the scapholunate interval may not
appear widened on normal view. A clenched fist
increases the force across the wrist because of the
extrinsic ligaments, loading the capitate into the
proximal carpal row and producing increased
widening. Contralateral wrist radiographs may
be necessary to detect or determine a significant
amount of widening. Ulnar and radial deviation
may also aid in diagnosis of dynamic scapholu-
nate ligament injury, increasing gapping at the
scapholunate or lunotriquetral joints, respec-
tively. Physical examination and radiographs
remain essential in the primary workup for carpal
instability. Positive findings suggest the presence
of carpal instability. However, in the diagnosing
of scapholunate dissociation, because of the low
sensitivity of the scaphoid shift test and radio-
graphs, cine radiography is recommended in
suspicion of carpal instability dissociation.
­ as a suitable cutoff for a reliable sign for an ACL
Cineradiography is a qualitative rather than a
quantitative tool, so its exact role in diagnosing
carpal instability is to be determined [52].
8.20 Lateral Femoral Notch Sign
Feature
An impaction fracture of the lateral femoral con-
dyle with abnormal deepening could be apparent
on the lateral radiograph of the knee as the lateral
femoral notch sign, whose significance is that a
sulcus is deeper than 1.5  mm. Another name:
notch sign.
Explanation
Lateral condylopatellar sulcus, also known as lat-
eral femoral notch (LFN), usually forms a shal-
low groove in the middle of the lateral femoral
condyle. It represents the junction zone on the
lateral femoral condyle where the tibiofemoral
and patellofemoral radii of curvature meet. An
abnormally deep lateral condylopatellar sulcus
has been attributed to an impacted osteochondral
H. Yang et al.
abnormality overlying the lateral condylopatellar
sulcus has been observed with a torn ACL during
surgical reconstruction. The most common
mechanism of an ACL tear is rotation and valgus
stress. Disruption of the ACL with valgus stress
causes the posterior aspect of the lateral tibial
plateau and the middle to anterior portion of the
lateral femoral condyle to forcefully impact
against one another. This stress causes a pattern
of injuries known as “kissing contusions,” which
are usually occult injuries to the cartilage and
bone demonstrated as bone contusions On MRI
study (Fig. 8.19).
Discussion
In 1992, Cobby et al. [53] sought to quantify and
associate the depth of the condylopatellar sulcus
with the likelihood of ACL tear. In normal sub-
jects, the mean lateral sulcus depth was 0.45 mm,
whereas 0.89  mm was found with confirmed
ACL tears. No normal subjects had a sulcus depth
greater than 1.2 mm, and 1.5 mm was suggested
tear [54]. The lateral femoral notch (LFN) signi-
fies the junction zone where the tibiofemoral and
patellofemoral radii of curvature meet. Normally,
the lateral femoral notch represents a shallow
groove in the middle of the lateral femoral epi-
condyle. An abnormally deep lateral condylopa-
tellar sulcus has been associated with underlying
pathologies, most notably an underlying ACL
tear. Disruption of ACL may result in abnormal
translation of the tibia onto the femur, causing
forceful impaction onto one another. In some
instances, such forceful impaction may lead to an
osteochondral impaction fracture. Ultimately, an
abnormally deep lateral notch sign may also be a
harbinger for long-term pathology, including
early-onset osteoarthritis. ACL is one of the most
important stabilizers of the knee, providing pri-
mary restraint to anterior tibial translation and
secondary stabilization in regard to rotational
forces and varus or valgus stresses to the knee.
There are few findings suggestive of an ACL
tear on radiographs of the knee. Lateral femo-
ral notch sign and posterior fracture of the
lateral tibial plateau are infrequently seen
8  Signs in Musculoskeletal Radiology 313

a b

Fig. 8.19 (a, b) A 26-year-old male patient with ACL tear of left knee. Lateral X-ray and sagittal PDWI show an
impaction fracture of the lateral femoral condyle as the lateral femoral notch sign (arrow)

radiographic signs corresponding to the kiss-
ing contusions seen on MRI [54]. MRI is the
imaging modality of choice to diagnose ACL
injury, which can manifest as discontinuity,
abnormal slope, or signal intensity of fibers.
There is no statistically significant correlation
between LFN depth on radiographs or MRI
with preoperative lateral compartment transla-
tion or tibial acceleration during quantitative
pivot shift analysis. LFN depth should not be
used as an indicator of high-­ grade rotatory
knee instability. A deepened LFN, either on
imaging or during operation, however, may be
used as an indicator in patients more likely to
have a lateral meniscus tear [55].
8.21 Elephant Trunk Sign
Feature
This sign is a characteristic X-ray feature of cal-
caneonavicular coalition (CNC), and the conven-
tional oblique position of the foot is the best
observing position. Its appearance is that the
anterior and superior processes of the calcaneus
protrude like a nose and form a pseudo-joint or
bony fusion with the scaphoid bone of the foot.
Some literature also refers to this feature of CNC
as the anteater nose sign.
Explanation
Elephant nose sign is an X-ray feature of calca-
neonavicular coalition (CNC), which is the most
common type of syndesmosis. Radiograph shows
abnormal connection between calcaneus and
scaphoid bone, which is the clearest in 45°
oblique positioning. Lateral radiographs show
typical elephant nose (trunk) signs (Fig. 8.20).
Discussion
Elephant nose sign is an X-ray feature of calca-
neonavicular coalition (CNC). The incidence of
tarsal coalition is about 1% to 2%. CNC is the
most common type of syndesmosis. The main
clinical symptoms include pain, limited move-
ment, and stiffness. Radiography shows abnor-
mal connection between calcaneus and scaphoid
bone, which is the clearest in the 45°oblique
position. Lateral radiographs show typical ele-
phant nose signs. Lysak systematically
314 H. Yang et al.

8.22 Fat–Blood Interface Sign

Feature
Fractures in the joint capsule can cause blood in
the joint capsule. The fat in the bone marrow
overflows into the joint capsule through the frac-
ture. Because fat is relatively light, it floats on the
blood level, forming a so-called fat–blood inter-
face (FBI). X-ray, CT, and MRI can all show this
sign.

Explanation
FBI sign has a certain significance in the interpre-
tation of joint trauma. FBI sign is quite common
in practice and its occurrence is related to the fol-
lowing factors: positioning of the patient, amount
Fig. 8.20  Lateral radiograph of the foot shows the union of bleeding, amount of fat spilled, and the restric-
of calcaneus and scaphoid, presenting as elephant nose tion of the joint capsule (Figs. 8.21 and 8.22).
sign (arrow)
Discussion
Fat–blood interface sign (FBI) is caused by an
described the morphological changes of CNC intracapsular fracture resulting in articular cap-
and divided the relationship between sule hemorrhage. Bone marrow fat spills into the
­calcaneoascaphoid syndesmosis into four types articular capsule through the fracture site.
[56]: type 1 is a wide calcaneoascaphoid space Because the fat is relatively light, it floats on the
with smooth and clear bones; type 2 is a narrow blood, forming the so-called fat–blood interface.
calcaneoascaphoid space with flat and widened This sign is found in severe bone and joint inju-
anterior calcaneal space with smooth, regular, ries, especially in the major joints of the limbs,
and clear bones; type 3 is a narrow calcaneo- especially in the knee joint. Most of the injuries
ascaphoid space with a flat and widened ante- are accompanied by tibial plateau fractures, as
rior calcaneal space with rough and irregular well as shoulder, elbow, ankle (talus and calf),
and unclear bones; and type 4 is calcaneo- and hip joints; this will affect or delay the healing
ascaphoid fusion. of trauma. Lipidemia of the joints is associated
Radiography is currently the most com- with intraarticular fractures [58]. Therefore,
monly used imaging method for the diagnosis accurate imaging diagnosis of traumatic arthro-
of the CNC. X-ray diagnosis of CNC relies on plasty is helpful to guide clinical treatment. The
elephant nose sign, which shows that the abrupt pathological basis of this disease is generally
increase of anterior and superior calcaneus is believed to be the compression of blood and adi-
blunt protrusion resembling the elephant nose. pose tissue into the articular capsule after intra-
Crim et  al. reported with simple training the capsular fracture. When joint trauma occurs, both
sensitivity of diagnosis is 80–100% and the articular cartilage and synovium release enzymes
specificity is 98% in diagnosing the X-ray that prevent blood coagulation. Blood is still in a
signs of CNC [57]. CNC needs to be a differen- liquid state. Because of the low density of fat and
tial diagnosis from degenerative joint disease. the high density of blood, a stratification of fat in
CT and MRI are superior to X-ray in the diag- the upper and blood in the lower levels is formed,
nosis of CNC and can detect abnormal fine that is, the lipid–liquid level.
morphological changes in the calcaneal-­ X-ray radiography can show this sign, but
navicular space. special positioning must be applied. It is possi-
8  Signs in Musculoskeletal Radiology
a b
Fig. 8.21 (a–c) A 28-year-old male patient with left knee
trauma caused by traffic accident. Sagittal T1WI, T2WI,
and axial T2WI with fat-saturated MRI present the “fat–
blood interface” sign in superior patellar bursa. Fat shows
a b
Fig. 8.22 (a–c) A 23 year-old man with left knee trauma. “Fat–blood interface” sign is noted in the superior patellar
bursa, fat showing hypointensities on fat-saturated T2WI
ble to observe this sign only in horizontal pro-
jection, whereas in shoulder joint projection, it
can only be shown in anteroposterior or postero-
anterior position. CT and MRI are sensitive to
FBI signs. The knee joint has 5 ml fat and 15 ml
blood, and both CT and MRI can show the lev-
els of fat and liquid. The effusion signals of
various components are obviously contrasted,
which can better show this sign. Because of the
different components of blood in different peri-
ods, the signal intensities are different, and there
even may be multiple fluid levels, and different
degrees of signal changes after the mixture of
blood and intracapsular fluid, so the signal
changes above and below the fluid level vary.
However, the display of small fractures and a
315
c
high signal on T1WI and T2WI, located above the inter-
face, and low signal on T2WI with fat-saturated image;
blood shows low signal on T1WI, located below the inter-
face, and a high signal on T2WI
c
nondisplaced fracture line on MRI are not so
good as that on CT or X-ray, which requires
comprehensive analysis. FBI sign is a character-
istic imaging manifestation of traumatic lipohe-
matosis of the joint and a reliable sign of
intracapsular fracture of the joint [59].
8.23 Elbow Fat Pad Sign
Feature
Normally, on a lateral radiograph of the elbow
held in 90° of flexion, lucency that represents fat
is present along the anterior surface of the distal
humerus, and no lucency is visualized along its
posterior surface. An elevated anterior lucency or
316
a visible posterior lucency on a true lateral radio-
graph of an elbow flexed at 90° is described as a
positive fat pad sign. The presence of intracapsu-
lar fracture of the elbow is usually indicated.
Explanation
The synovium of the elbow joint is located in the
deep part of the fibrous sac. Three small masses of
fat rest in the radial, coronoid, and olecranon fos-
sae and are separated by the fibrous sac and form
fat pads. The anterior fat pad is a summation of
radial and coronoid fat pads. The anterior part is
strengthened by brachial muscle. On a lateral
radiograph of the elbow, the anterior fat pad is usu-
ally seen as a faint line that is more radiolucent
than adjacent muscle and is parallel to the anterior
distal humerus. The posterior fat pad is strength-
ened by triceps brachii tendon and elbow muscle
and is invisible under normal circumstances. When
there is joint distention, the anterior fat pad is dis-
placed further anteriorly and superiorly, and the
posterior fat pad is displaced posteriorly and supe-
riorly. The previously invisible posterior fat pad
then becomes visible (Fig. 8.23).
Fig. 8.23  Lateral radiograph shows a positive fat pad sign
in a 6-year-old girl. The anterior lucency (arrow) represents
the elevated anterior fat pad, and the posterior lucency
(arrowhead) represents the elevated posterior fat pad
H. Yang et al.
Discussion
Elbow effusions are seen on lateral radiograph in
the presence of fat pad sign. The elbow is fre-
quently involved in trauma and is one of the most
frequently radiographed joints in emergency
departments. Although commonly emphasized as
a sign of trauma, the fat pad sign frequently
occurs in nontraumatic elbow disease. Fat pad
displacement is a response to distention of the
joint capsule and occurs irrespective of the cause.
It has been described in a variety of disorders,
such as hemophilia, rheumatoid arthritis, gout,
osteoarthritis, and acute pyarthrosis, and can be
expected to occur whenever there is distention of
the joint capsule. It may be the manifestation of
an occult fracture as a result of trauma, or may
herald the onset of an inflammatory or other
synovial process that occurs in a clinical setting.
Elbow fat pads are best shown on lateral view
radiography with the elbow in 90° of flexion, as
any obliquity may obscure visualization. A false-­
negative fat pad sign may occur if there is poor
positioning, extracapsular abnormality, or capsu-
lar rupture. Normal displacement of the posterior
fat pad with the elbow in extension should not be
mistaken for a sign of joint disease [60]. Rarely,
properly performed conventional radiography
may fail to demonstrate the fat pad sign in patients
with joint effusion or capsular rupture (from
severe trauma) or when there is massive soft-­
tissue swelling around the joint. Ultrasonography
may be useful when conventional radiographs
fail to show the fat pads or when spurious eleva-
tion of the fat pads is suspected. The value of the
fat pad sign is greatest as a predictor of an intraar-
ticular disease process at the elbow in the absence
of any radiographically visible bone abnormality.
Fat pad displacement is independent of fracture
displacement and comminution, particularly in
elbow examination in children, who often have
very slight structural changes at presentation
[61]. In properly performed radiography of the
elbow, the fat pad sign is a highly sensitive indi-
cator of disease processes involving the elbow
joint. When present, the sign is easily demonstra-
ble on conventional radiographs, which are often
the first images obtained to study the elbow. Most
important, being aware of the limitations of this
sign and remembering that the sign is not specific
8  Signs in Musculoskeletal Radiology
to trauma alone will help provide more effective
treatment for patients suspected of involvement
of the elbow joint [62]. In short, when there is no
sign of skeletal abnormality, the fat pad sign is of
great value in indicating intraarticular lesions,
especially in the diagnosis of occult elbow frac-
ture in children.
8.24 C Sign
Feature
The talocalcaneal C sign is a continuous,
C-shaped line that extends from the talus to the
sustentaculum tali and can be seen on lateral
radiographs of the ankle.
Explanation
The talocalcaneal C sign can be seen in patients
with subtalar coalition on lateral ankle radio-
graphs. The anatomic-pathological basis for a
talocalcaneal C sign on lateral ankle radiographs
is the bony bridge that extends from talar dome to
sustentaculum tali, in combination with a promi-
nent inferior outline of sustentaculum tali. The
talocalcaneal C sign can also be seen in the
absence of synostosis of the posterior subtalar
joint in patients with a subtalar syndesmosis or
synchondrosis, which lies in a plane that is not
parallel with the X-ray beam. A posterior inter-
a b
Fig. 8.24  In this 37-year-old man, ankle CT reconstruction images show the talocalcaneal C sign
317
ruption of the talocalcaneal C sign occurs in
patients with radiolucent syndesmosis or syn-
chondrosis of the medial part of the posterior
subtalar joint that is parallel with the X-ray beam,
or in patients with coalition of the middle subta-
lar joint without involvement of the posterior
subtalar joint. The C sign may frequently be pos-
teriorly interrupted in the absence of synostosis
of the posterior facet; therefore, the sign has
lower specificity. Subtalar coalition is frequently
accompanied by a dysplastic sustentaculum tali,
which may not cast a well-defined lower inter-
face to contribute to the inferior aspect of the C
sign (Fig. 8.24).
Discussion
Lateur and colleagues described the “C” sign on
a lateral foot radiograph, which they believed
was indicative of a talocalcaneal coalition [63].
Tarsal coalition is a common cause of rigid flat-
foot deformity in adolescent patients. Patients
with tarsal coalition may present with limited
subtalar motion and pain in the area of the sinus
tarsi or dorsum of the foot. Clinical diagnosis can
be difficult, as most patients do not have peroneal
spasm or flat feet. Numerous radiographic find-
ings have been associated with talocalcaneal
(TC) coalition, including talar beaking, a ball-­
and-­socket ankle joint, failure to see the “middle”
subtalar joint, rounding of the lateral process of
318
the talus, narrowing of the posterior subtalar joint
space, and flattening or concavity of the under-
surface of the talar neck. These observations have
proven to be useful indicators of abnormal subta-
lar motion but are not specific for TC coalition. C
sign noted on non-weight-bearing lateral ankle
radiographs has been described as a feature of TC
coalition. C sign is created by the medial outline
of the talar dome and a bony bridge between the
talar dome and the sustentaculum tali, in
­combination with a prominent inferior outline of
the sustentaculum tali [64].
On standard radiographs, primary signs of
subtalar coalition (i.e., narrowing and subchon-
dral sclerosis of the posterior subtalar joint and
absence of the middle subtalar joint and sinus
tarsi) may be subtle or even absent in up to 50%
of patients. Its secondary signs (e.g., talar
beaking, ball-and-socket deformity of the tibiota-
lar joint, broadening of the talar lateral process,
and concave undersurface of the talar neck),
which are nonspecific, may be absent. Therefore,
subtalar coalition can easily be missed on con-
ventional radiographs. Lateur et al. [65] reported
that in a study of 33 patients with subtalar coali-
tion, only C sign was positive in 32 of 32 true-­
positive cases; the sensitivity and specificity were
86.6% and 93.3%, respectively, with 32 true-­
positive cases, 1 true-negative case, 0 false-­
positive cases, and 2 false-negative cases. The
talocalcaneal C sign is subtle in cases of subtalar
coalition with dysplastic or rounded sustentacu-
lum tali, because the lower part of the talocalca-
neal C is less prominent on lateral ankle
radiographs as the X-ray beam strikes the inferior
surface of the dysplastic or rounded sustentacu-
lum tali tangentially over a shorter distance.
Aplastic sustentaculum tali in patients with
achondroplasia may render C sign absent. A posi-
tional artifact of the foot may cause a false-­
positive C sign in patients without subtalar
coalition. The interrupted C sign may sometimes
be seen with a valgus hindfoot or with inexact
lateral X-ray beam angulation. CT is helpful in
confirming subtalar coalition and establishing its
extent, especially in patients with an interrupted
C sign. MRI is ideally suited for differentiating
syndesmosis and synchondrosis [66].
H. Yang et al.
8.25 Target Sign
Feature
Target sign is a hypo-intensity area in the center
surrounded by hyperintensity on T2WI. Target
sign is seen in peripheral nerve sheath tumor
(PNST), which is related to the composition of
tumors.
Explanation
Pathologically, hypointensity in the central region
of the tumor represents fibro-collagen tissue,
whereas hyperintensity in the periphery corre-
sponds to mucus-rich tissue. When target sign of
peripheral schwannoma occurs, the central area
is usually composed of an Antoni A region with
richer cells, and the peripheral area is composed
of an Antoni B region with poorer cells (Figs. 8.25
and 8.26).
Discussion
Target sign is the specific sign of PNST. The tar-
get signs were first proposed by Banks et al. [67].
PNST is a tumor originating from Schwann cells
in the sheath of the nerve tract. PNST accounts
for about 5% of benign soft tissue tumors. Most
of the lesions are single, slow-growing painless
masses with few symptoms, unless the lesions
increase and cause compression symptoms [68].
Typical PNST is an isolated mass with clear mar-
gins and capsules. The general diameter is less
than 5 cm. Tumor sections show various shapes,
such as a solid gray-white homogeneous mass,
beaded irregular nodules, multilocular cystic
lesions of different sizes, or hemorrhagic and
necrotic areas.
MRI can clearly show the relationship
between tumors and surrounding structures.
Neurilemmomas are usually homogeneous or
heterogeneous low and moderate signal intensity
on T1WI, which is resembling adjacent muscle
tissue, high signal intensity on T2WI, and most
lesions showed heterogeneous high signal inten-
sity. There is a low signal area in the center of the
tumor and a high signal area around it. The target
sign is the characteristic feature of extracranial
neurogenic tumors. Target signs are correlated
with histological features of the tumors; that is,
8  Signs in Musculoskeletal Radiology 319

a b

Fig. 8.25 A 35-year-old man with peripheral nerve hypointensity in the center of the tumor and surrounding
sheath tumor of the left forearm. Axial (a) and sagittal (b) hyperintensity
T2WI with fat saturation show target sign (arrow), with

Fig. 8.26 (a, b) A 64-year-old woman with multiple (arrow), with hypointensity in the center of the tumor and
peripheral nerve sheath tumors on the ischiadic nerve of surrounding hyperintensity
the right thigh. T2WI with fat saturation shows target sign
320 H. Yang et al.

the low signal area in the center of the lesion is The low density on CT and the high signal on
fibrous collagen tissue, and the high signal area MR T2WI are the result of the myxoid element
around the lesion is myxoma-like tissue. Target and presence of water in the lesion (Fig. 8.27).
signs are not unique to schwannomas, and neuro-
fibromas have similar features. Neurilemmoma Discussion
needs to be differentiated from neurofibroma and Aggressive angiomyxoma is relatively rare and
malignant neurilemmoma [69]. Typical MRI fea- has been sporadically reported. It most com-
tures of PNST are elliptical masses with clear monly occurs in the lower pelvis, perineum, or
boundaries consistent with nerve course. The tar- genital area of females, usually in the third to
get sign is helpful in the diagnosis of PNST. fifth decade; these are six times more common in
females. The predominant location of the mass in
the pelvis and the female predilection suggest
8.26 Swirl Sign that hormonal factors are important. It is not a
malignant tumor, but it is locally aggressive and
Feature tends to infiltrate adjacent structures [70].
Swirl sign is the CT or MRI feature of an aggres- The CT features are variable and include a
sive angiomyxoma (AAM) manifested as soft-­ hypoattenuating or iso-attenuating mass
tissue masses locating in pelvic cavity, perineum, involving the pelvis and perineum with
and vulva. The signal or density of the lesion enhancement in the contrast-enhanced scan,
resembles or is slightly lower than that of the which may show the classical swirled appear-
muscle. There are strips of lower-density shadow ance. MRI is the modality of choice in char-
in the center of the lesion, with “swirled” or strat- acterization of the mass as well as for
ified enhancement after enhancing. assessing the extent of the mass. The mass is
usually iso-intense to muscle on T1WI and
Explanation hyperintense on T2WI with “swirled” areas of
The swirled appearance is likely caused by fibro- low signal areas within. This morphology is
vascular stroma of AAM, which are stretched as characteristic of this tumor. The hyperintense
they extend and involve the pelvic diaphragm. signal in T2WI is caused by the myxoid ele-

a b

Fig. 8.27 (a, b) A 42-year-old woman presented with mass in the pelvic with “swirled” areas of low signal areas
lower abdominal and pelvis pain for more than 8 months. within (arrow)
Sagittal and axial T2WI show a hyperintense well-defined
8  Signs in Musculoskeletal Radiology
ment and presence of water. The swirled
appearance is likely from the fibrovascular
stroma, which are stretched as they extend
and involve the pelvic diaphragm. On post-
contrast T1WI, the mass shows significant
enhancement from vascular component of the
neoplasm. The characteristic swirled appear-
ance can also be seen in postcontrast T1WI
[71]. The distinctive imaging appearance is
characterized by very high signal intensity on
T2WI and swirled or layered internal architec-
ture in most patients.
8.27 Flow Void Sign
Feature
On MRI T1WI, T2WI images, multiple punctate
or tubular low-signal areas can be seen in or
around the lesion, representing dilated vessels,
called the flow void sign.
Explanation
Because there are multiple dilated and distorted
blood vessels in or around the lesion, which mani-
fest as multiple dots or tubular low-signal flow
voids on MRI, the flow void sign is common in
bone metastasis of renal cell carcinoma (Fig. 8.28).
a b
Fig. 8.28  A 38-year-old male patient with spinal metastases from right renal cell carcinoma. Sagittal T1WI (a), T2WI
(b), and STIR (c) show a mass with moderate signal intensity and hypointensity (arrow) at multiple points
321
Discussion
Flow void sign is a common sign on MRI in
renal cell carcinoma with bone metastasis. It
was first reported by Choi et  al. in 2003 [72].
Renal cell carcinoma (RCC) is a group of malig-
nant tumors originating from renal tubular epi-
thelial cells that must be considered in the
differential diagnosis of any metastatic tumors.
In patients with RCC, bone is the second most
common site of metastasis after lung. A large
number of low-signal punctate or tubular struc-
tures, namely flow void sign, are often observed
on MRI of renal cell carcinoma bone metasta-
ses, which represent the dilated blood vessels
that supply or drain the tumor [73, 74]. However,
other musculoskeletal lesions with rich blood
supply, such as arteriovenous malformation,
hemangioma, synovial sarcoma, fibrosarcoma,
osteochondroblastoma, giant cell tumor, osteoid
osteoma, and aneurysmal bone cyst, may also
show flow void sign on MRI. Although the spec-
ificity of flow void sign is not high, when meta-
static lesions are confined to the skeletal system,
it is still helpful to establish the diagnosis and
treatment of RCC bone metastasis. Although the
diagnostic sensitivity and specificity of flow
void sign have yet to be determined, the signifi-
cance of this sign lies in its correlation with
c
322
blood vessels, which is still helpful to the diag-
nosis and treatment, especially in patients with
occult primary renal tumors.
8.28 Button Sequestrum Sign
Feature
Button sequestrum sign refers to a lesion locating
in the bone and consists of bone opacity sur-
rounded by a relatively well-defined lucent area.
Initially described on radiographs, this sign can
also be observed on CT scans.
Explanation
Button sequestrum sign is not specific for a single
disease. A lucent area may result from numbers
of processes. In cases of osteomyelitis, the lucent
area is caused by infectious organisms that
destroy the bone, which is then replaced by puru-
lent material and granulation tissue. In cases of
eosinophilic granuloma, the bone is replaced by
an erosive accumulation of histiocytes that make
a b
Fig. 8.29 (a) A 22-year-old man. Lesion in lower seg-
ment of left femur consists of a lucent area with a central
sclerotic focus, which is referred to as “button sequestrum
sign” (arrow). (b) A 12-year-old boy with chronic pyo-
H. Yang et al.
the area appear lucent. The central opacity repre-
sents an island of dead bone (Fig. 8.29).
Discussion
This sign was first described as a radiologic man-
ifestation of eosinophilic granuloma, a localized
form of Langerhans cell histiocytosis [75].
Langerhans cell histiocytosis (LCH) is a systemic
disease of unknown etiology, of which eosino-
philic granuloma (EG) is the most common and
mild form. Sometimes a remnant of bone is seen
centrally, known as a button sequestrum [76].
The exact cause of EG has not yet been deter-
mined, although neoplastic, viral, and immuno-
logical origins have been implicated. The disease
affects children and young adults and has a male
predilection. Pain, tenderness, and soft-tissue
swelling at the affected site are the most common
symptoms. EG most commonly affects the skull,
followed by the long bones, pelvis, ribs, spine,
and mandible [77].
The button sequestrum sign is most often
identified at radiography. In cases in which the
genic osteomyelitis of right tibia. The lesion in the upper
part of the right tibia consists of a lucent area with a cen-
tral sclerotic focus, which is referred to as the “button
sequestrum sign” (arrow)
8  Signs in Musculoskeletal Radiology
presence of the sequestrum within a lytic lesion is
questionable or not apparent, CT can help
increase visualization of central density [77].
Studies reserve this appearance for four entities:
osteomyelitis, eosinophilic granuloma, fibrosar-
coma, and lymphoma. In osteomyelitis, an infec-
tious organism destroys the bone, which is then
replaced by purulent material and granulation tis-
sue, thereby producing the lucent area. The cen-
tral opacity represents an island of dead bone,
and identification of such sequestrum can be an
important indication for surgery in chronic osteo-
myelitis [78]. Other entities can demonstrate the
button sequestrum sign on radiographs. Partially
calcified intraosseous lipoma can also appear as a
bone opacity surrounded by an area of relative
lucency. Case reports of other conditions with a
similar appearance include tuberculous osteitis,
radiation necrosis, metastatic carcinoma, fibrous
dysplasia, epidermoid and dermoid cyst, heman-
gioma, and meningioma. In most cases, lesions
have only a lytic area without a bone opacity. It
should be mentioned that the button sequestrum
sign is an uncommon appearance of all these dis-
orders, including EG. The absence of the seques-
trum broadens the differential diagnoses even
further.
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Suggested Readings for this Chapter
Guglielmi G, Nasuto M.  Emergency and trauma in
MSK radiology. Semin Musculoskelet Radiol.
2017;21(3):165–6.
Lefevre N, Naouri JF, Herman S, Gerometta A, Klouche
S, Bohu Y. A current review of the meniscus imaging:
proposition of a useful tool for its radiologic analysis.
Radiol Res Pract. 2016;2016:8329296.
Leggit JC, McLeod G.  MSK injury? Make splint-
ing choices based on the evidence. J Fam Pract.
2018;67(11):678–83.
Marinković S, Stošić-Opinćal T, Tomić O. Radiology and
fine art. AJR Am J Roentgenol. 2012;199(1):W24–6.
Math KR, Berkowitz JL, Paget SA, Endo Y. Imaging of
musculoskeletal infection. Rheum Dis Clin N Am.
2016;42(4):769–84.
Tagliafico AS, Isaac A, Bignotti B, Rossi F, Zaottini F,
Martinoli C.  Nerve tumors: what the MSK radi-
ologist should know. Semin Musculoskelet Radiol.
2019;23(1):76–84.
 Spine
9
Lingling Song, Wen Wang, Muxi Wu,
and Alexander M. McKinney

Contents
9.1 Peripheral Spinal Cord Hypointensity Sign  327
9.2 The Sugarcoating Sign  329
9.3 The Polka-Dot Sign  330
9.4 The Rugger Jersey Spine Sign  332
9.5 The Ivory Vertebra Sign  333
9.6 The Posterior Vertebral Scalloping Sign  334
9.7 MRI Fluid Sign  336
9.8 The Intravertebral Vacuum Cleft Sign  337
9.9 The Inverted Napoleon’s Hat Sign  339
9.10 The Scotty Dog Collar Sign  340
9.11 The Incomplete Vertebral Ring Sign  342
9.12 Wide Canal Sign  343
9.13 The Naked Facet Sign  345
9.14 The Fat C2 Sign  346
References  347

L. Song (*) · M. Wu 9.1  eripheral Spinal Cord

Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China
W. Wang
Department of Radiology, Tangdu Hospital, Fourth
Military Medial University, Xi’an, China
A. M. McKinney
Miller School of Medicine, University of Miami,
Miami, FL, USA
P
Hypointensity Sign
Feature
On T2WI in the setting of venous hypertensive
myelopathy (VHM), hypointensity can be noted
subjacent to the peripheral pia mater spinalis,
which is particularly evident on gradient echo

© Springer Nature Switzerland AG 2021 327

B. Gao, A. M. McKinney (eds.), Classic Imaging Signs,
https://doi.org/10.1007/978-3-030-56348-6_9
328
a b
Fig. 9.1  The peripheral spinal cord hypointensity sign.
(a) On sagittal postcontrast CT, there are many intensified
and tortuous blood vessels surrounding the spinal cord.
(b) On sagittal T2WI, there is abnormal spinal cord
hypointensity, as well as serpentine and dilated perimed-
T2*WI and spin-echo T2WI sequences, without
significant signal abnormality on the T1WI
sequence. This manifestation is called the
“peripheral spinal cord hypointensity sign.”
Explanation
Peripheral spinal cord hypointensity sign is an
MRI finding that is specific for VHM. It occurs
most commonly in the setting of a spinal dural
arteriovenous fistula (SDAVF). As blood flow is
slow within the capillary and venous system, the
deoxygenated hemoglobin leads to T2 shortening,
thus causing hypointensity under the pia mater
spinalis around the spinal cord (Fig. 9.1).
Discussion
Hurst and Grossman [1] first posited peripheral
hypointensity of the spinal cord on T2WI, sug-
gesting the presence of a venous hypertensive
myelopathy (VHM). With this “sign” one should
consider the possibility of an underlying spinal
dural arteriovenous fistula (SDAVF). The VHM
is a group of syndromes caused by a variety of
vascular diseases in the spinal cord, spine, and
surrounding structures. Obstruction of spinal
cord venous drainage or accessory veins of the
spinal canal leads to increased vein system pres-
L. Song et al.
c d
ullary venous plexi as flow voids. (c) Sagittal short TI
inversion recovery (STIR) shows the same sign as in (b).
(d) Postcontrast T1WI demonstrates gadolinium enhance-
ment with tortuous and dilated perimedullary venous
plexi
sure; as a consequence, the resulting impeded
circulation damages spinal cord function.
However, whether the finding of peripheral cord
hypointensity represents a real pathological alter-
ation or what this peripheral hypointensity repre-
sents is still undetermined [2]. Some investigators
opined that the disease is related to the phenom-
enon of spinal canal veins with reversed flow
with obstruction and caval reversed flow caused
by vascular disease in the spinal canal (such as
SDAVF, perimedullary arteriovenous fistula),
dural arteriovenous fistula, vertebral arteriove-
nous fistula, or paravertebral venous system
abnormalities (such as left renal vein, azygos
vein, hemiazygos vein, accessory azygos vein).
SDAVF, the most common cause for VHM,
refers to the existence of a small arteriovenous
shunt of blood from the radicular arteries, drain-
ing into the pial veins of the spinal cord. Because
there is no venous valve in the spinal veins, when
one or more supplying arteries direct flow into
the spinal dural vein and through the dura mater,
a special channel is formed. Under pathological
conditions, once this channel is opened, it can
become the fistula of a SDAVF. The arterial blood
is drained through a normal vein on the surface of
the spinal cord, leading to the arteriovenous
9 Spine
p­ ressure gradient disorder in the spinal cord, thus
expanding the lumen, causing obstruction of the
reverse flow of the spinal cord vein, edema of the
cord, and subsequent stagnation of blood within
capillaries; as a result, obstructions of the small
arteries induce ischemia and interstitial edema
within the cord, and ischemic necrosis may
develop. The histopathological changes include
pia mater spinal venous congestion, spinal paren-
chymal edema, and ischemia, as well as ulti-
mately venous infarction of the spinal cord. The
MRI findings of VHM related to the foregoing
pathological changes mainly include spinal cord
swelling and circuitous tubular vascular flow
voids surrounding the spinal cord. T2WI depicts
hyperintensity within the center of the cord, with
parenchymal enhancement [3]. SDAVF have
imaging features that are frequently missed or
misinterpreted, which results in a significant
delay to definitive diagnosis and therefore treat-
ment [4]. Notably, the hyperintensity within the
central cord is not specific for this diagnosis, as
cord edema can also be seen in infectious, inflam-
matory, demyelinating, and vasculitic disorders
of the spinal cord [3].
9.2 The Sugarcoating Sign
Feature
The sugarcoating sign is a manifestation on post-
contrast T1WI, with diffuse linear and nodular
enhancements along the surface of the spinal
cord or the nerve roots. Another name: the frost-
ing sign.
Explanation
The blood–brain barrier (BBB) extends around
the spinal cord and the intrathecal portion of the
nerve roots. As a result, these structures usually
do not enhance after the administration of con-
trast material. On the other hand, intradural (lep-
tomeningeal) metastases, which adhere to the
surface of the spinal cord and nerve roots, typi-
cally demonstrate enhancement on T1WI. Thus,
there is a striking contrast between nonenhancing
neural tissue, sheet-like enhancing tumor
implants, and dark cerebrospinal fluid (CSF),
329
producing the sugarcoating sign in patients with
leptomeningeal carcinomatosis (Fig. 9.2).
Discussion
Holz first reported the sugarcoating sign in 1998
[5]. This sugarcoating appearance is nonspecific
on postcontrast T1WI, and may be noted with any
process that affects the meninges and disrupts the
BBB. A nodular enhancement pattern is said to
be more specific for tumors than for infection,
which usually demonstrates more linear enhance-
ment. However, nonneoplastic conditions such as
granulomatous disease (e.g., sarcoidosis), arach-
noiditis, atypical infectious lesions (e.g., fungal
or tuberculous), and neurofibromatosis also may
occasionally produce nodular enhancement [5].
Leptomeningeal metastases of solid cancers usu-
ally result from hematogenous spreading to the
subarachnoid space, direct infiltration from solid
brain lesions, endoneural/perineural and perivas-
cular spread, or iatrogenic spread following neu-
rosurgery. Leptomeningeal metastases occur in
approximately 5% to 10% of cancer patients,
with breast cancer, lung cancer, and melanoma
representing the three most common primary
tumors. The diagnosis of leptomeningeal carci-
nomatosis is typically made in patients in
advanced stages of cancer, where their prognosis
remains poor, usually with only months of
expected survival, even if multimodality treat-
ment is promptly initiated [6].
Although postcontrast imaging is preferred,
fluid-attenuated inversion recovery (FLAIR)
images can be utilized to depict the presence of
meningeal carcinomatosis without using gado-
linium. When the sulci or cisterns show areas of
hyperintensity on unenhanced FLAIR images in
patients with cancer, meningeal carcinomatosis
can be strongly suspected, and contrast-enhanced
images should be obtained. In particular, post-
contrast FLAIR has been shown to be as sensitive
as, and perhaps even more sensitive than, post-
contrast T1WI in detecting leptomeningeal dis-
ease. It is speculated that the appearance on
noncontrast FLAIR is related to the fact that
tumor cells in meningeal carcinomatosis induce
an increase in CSF proteins, which is a typical
laboratory finding; the increase in CSF proteins
330 L. Song et al.

a b

Fig. 9.2 (a, b) A patient with bronchogenic lung carcinoma. Sagittal T1-CE images of the cervical spine show linear,
nodular, peri-medullar contrast enhancement, indicating the sugarcoating sign of leptomeningeal metastases

produces a change similar to that seen in sub-
arachnoid hemorrhage on FLAIR images. Hence,
unenhanced FLAIR images are more sensitive
than T2WI in detecting this disorder. T2 elonga-
tion is difficult to discern on spin-echo T2WI as
the CSF is normally hyperintense on that
sequence [7]. Although the sugarcoating sign is
highly suggestive of leptomeningeal tumor, its
absence does not exclude neoplastic dissemina-
tion in the CSF.  Because of its microscopic
nature, only approximately 20% to 25% of con-
firmed leptomeningeal carcinomatosis cases are
positive for imaging findings. Thus, CSF
cytological analysis is the most definitive test,
sometimes necessitating flow cytometry via a
higher-volume lumbar tap. CSF analyses yields
positive results in approximately 45% to 55% of
leptomeningeal carcinomatosis cases. The yield
may also be further increased using serial lumbar
punctures [5].
9.3 The Polka-Dot Sign
Feature
Parallel bands of osteosclerotic shadow can
be seen in the longitudinal arrangement of the
affected vertebral body contour when verte-
bral hemangioma (VH) involves vertebral
bone, accompanied with strips of alternating
increased and reduced density, which resem-
ble a polka-dot sign (i.e., a defensive enclo-
sure of vertical stakes). Other name: the
corduroy sign [8].
9 Spine
Fig. 9.3  A hemangioma of T9 vertebra in a 62-year-old woman. Sagittal (a) and coronal (b) nonenhanced computed
tomography (NECT) reformats show the “palisades sign”; axial CT (c) shows the typical polka-dot sign
Explanation
The polka-dot sign is a typical X-ray sign of
VH.  The low-density area represents bone ero-
sion and displacement by the vascular lesion,
wherein most of the bone structure in these verti-
cally hypodense regions is absorbed and the nor-
mal bone trabeculae disappear. The parallel
strip-shaped bone hardening shadow is the tumor
interspersed between the trabecular bone, and the
residual trabecular bone is arranged in slightly
more hyperdense longitudinal rows, thought to
arise from compensation and adaptation, induced
by weight on the vertebrae [9] (Fig. 9.3).
Discussion
X-ray radiography showed that the damaged ver-
tebra usually exhibits the typical “palisade” or
“corduroy” morphology in VH, including
decreased bone mineral density, cortical thin-
ning, and residual trabecular thickening [9]. VHs
represent only 2% to 3% of all spinal tumors,
with an incidence of 10% to 12% in the general
population; only 0.9% to 1.2% of these are symp-
tomatic, with the most common complaint (in the
rare instance when they are symptomatic) of back
pain. Asymptomatic patients with VHs are usu-
ally detected incidentally during imaging studies
obtained for other diseases or symptoms. The
physical examination shows pain in the spinous
processes upon direct percussion [10].
Histologically, hemangiomas are divided into
four categories: capillary, cavernous, arteriove-
nous, or venous, with the first two being the most
prevalent. The pathological basis of the polka-dot
sign is that the hemangioma parenchyma is com-
331
posed of pathological vessels with varied diame-
ters, substituting for the normal parenchyma, and
composed of fatty bone marrow. Most of the
bone tissue at the lesion site is absorbed, thus
exhibiting the stripe-shaped regions of reduced
density. The interspersed stripes of thickened tra-
becular bone are caused by the residual compen-
satory reaction of the trabecular bone. When the
remaining trabecular bones are arranged in longi-
tudinal orientation, they form the palisade shape,
or corduroy appearance. When they are irregu-
larly intersected, they form the shape of trabecu-
lae or mesh.
Based on radiographic analysis, aggressive VH
can be classified as typical or atypical. More than
one third of aggressive VH lesions may have at
least one atypical feature [11]. Another appearance
is on CT images, where a typical sign of small
punctate foci of high attenuation represents
sparsely thickened hyperdense trabeculae, sur-
rounded by hypodense stroma, thus forming the
pathognomonic “spotted” or “polka-dot” appear-
ance (polka-dot sign) as well; this mimics the
polka dot clothing pattern [9]. Again, on the recon-
structed sagittal and coronal CT images, such typi-
cal VHs demonstrate the classical vertically
oriented thickened trabeculae that represent the
“palisade” or “corduroy” sign [8]. MRI show high
signals on both T1WI and T2WI. Intralesional fat
causes the hyperintensity on T1WI whereas the
hyperintensity on T2WI is the result of increased
water content. Aggressive VHs contain less fat and
more vascular stroma [11]. Such “atypical heman-
giomas” may appear as bright on STIR or fat-sup-
pressed FLAIR imaging, may have enhancement
332 L. Song et al.

on post-contrast T1WI, and may even lose their T1

hyperintensity over time, thus simulating malig-
nancy such as vertebral metastases.
The polka-dot sign can be easily identified
based on a single imaging modality. CT has a piv-
otal role in the workup of VHs with an atypical
MRI appearance. When a VH is suspected to be
aggressive based on one imaging technique, both
CT and MRI (occasionally catheter angiography)
can be performed to further delineate the lesion
and etiology. CT-guided biopsies are indicated
for these atypical cases [8, 11].

9.4  he Rugger Jersey

T
Spine Sign

Feature
On X-ray radiograph (AP or lateral views), the
upper and lower edge endplates of the thoracolum-
bar vertebral body form a sclerotic zone, with a
clear band in the center of each vertebral body. The
combination of alternating parallel sclerotic zones
and clear bands resemble the stripes on rugby
sweaters; hence, most scholars refer to this as the
“rugger jersey spine” appearance. This appearance
of a clear band between two sclerotic zones also
resembles that of a sandwich cake; thus, this is
sometimes called the “sandwich cake sign.”

Explanation
The sclerotic zones at the lower and upper edges
of the vertebral endplate represent excessive
deposition of bone-like material, often caused by
chronic renal failure. Although their ossification
is insufficient for functional purposes, these
bone-like tissues are denser than normal verte-
brae, causing opacity of the sclerotic zones on
X-ray radiograph [12] (Fig. 9.4).
Discussion
The “rugger jersey spine sign” is most common in
secondary hyperparathyroidism associated with
osteosclerosis and is caused by chronic renal fail-
ure (renal osteodystrophy). X-ray findings of renal
osteodystrophy include osteomalacia, osteosclero-
sis, and soft-tissue calcifications; of note, osteo-
sclerosis caused by renal ­osteodystrophy tends to
Fig. 9.4 A 50-year-old woman with chronic renal failure
for 10  years. Reconstructed sagittal CT image shows
increased opacity of the thoracic vertebral bodies, consis-
tent with chronic osteosclerosis from renal osteodystrophy
occur in the axial skeleton, especially in the pelvis,
ribs, and spine. About 20% of patients with chronic
uremia and renal osteodystrophy develop osteo-
sclerosis [13]. The mechanism in the setting of
chronic renal failure is reduced intestinal absorp-
tion of calcium, calcium- and phosphorus-related
metabolism disorders, changes in the metabolism
of vitamin D, and serum calcium reduction; that
reduction stimulates parathyroid hyperplasia,
thereby resulting in secondary hyperparathyroid-
ism. The increased activity of osteoclasts leads to
9 Spine
increased release of calcium from bone and reac-
tive osteogenesis resulting from the loss of bone
minerals. The result is an overproduction of “bone-
like tissue” (excluding hydroxyapatite), which
appears hyperopaque on radiography, resulting in
the appearance of the rugger jersey spine sign [14].
Other diseases can produce image features simi-
lar to the rugger jersey spine sign, such as Paget’s
disease, osteoporosis, metastatic osteomas, or
osteomalacia [14, 15]. The rugger jersey spine sign
often affects multiple vertebral bodies, which are
multi-segmental. The increased density along the
upper and lower endplates of the vertebral body
differs from Paget’s disease, bone metastasis, or
lymphoma. The vertebral changes caused by bone
metastases and lymphoma are also called the “ivory
vertebral body” (see the following discussion), and
these diseases usually invade only an individual
vertebral body. Regarding Paget’s disease, which
can have the appearance of a “picture frame” verte-
bra, the rugger jersey spine is significantly differ-
ent; in Paget’s, the cortex of the vertebral body
becomes thicker (result of excessive osteogenesis
disrupting cortical formation), leading to the hyper-
density of bony cortex on radiography. Other sys-
temic diseases can produce X-ray features
resembling the rugger jersey spine sign, including
skeletal fluorosis and myelofibrosis. Both diseases
involve the axial bone, leading to increased bony
a b
Fig. 9.5 Lateral (a) and posteroanterior (PA) (b) plain
film X-ray views of the thoracic spine. Note the multilevel
sclerosis of at least four vertebral bodies (arrows) with the
ivory vertebra sign, in the setting of metastasis from lung
333
density of the vertebrae, pelvis, and chest. Fluorosis
can be distinguished from renal osteodystrophy by
such conditions as extensive ligament calcification,
periostitis, and vertebral osteophytes. Bone mar-
row fibrosis can be distinguished, as it produces
megalosplenia and cortical thinning in the long
bones. Hence, detailed clinical and laboratory data
can help identify these disorders.
9.5 The Ivory Vertebra Sign
Feature
On X-ray or axial CT, the vertebral body shows
patchy or diffusely increased attenuation, but the
structure of trabecular bone and cortical bone
cannot be distinguished clearly, together causing
an appearance of “ivory,” thus being called the
ivory vertebra sign.
Explanation
Bony lesions may stimulate the mesenchymal
cells of vertebrae to differentiate into osteoblasts.
The ensuing osteogenesis of the trabecular and
cortical bone results in thickening and fusion,
creating either patchy increased attenuation, or
alternatively increased attenuation of the entire
vertebral body, resulting in the “ivory vertebra
sign” (Fig. 9.5).
c d
cancer. (c) Another patient, a 75-year man with skeletal
fluorosis. (d) Sagittal CT shows sclerosis of multiple ver-
tebral bodies and appendices of a 79-year-old woman with
bronchogenic carcinoma
334
Discussion
The ivory vertebra sign is found in different
lesions in adults and children, being mainly
observed in osteogenic metastasis, Paget’s dis-
ease, or lymphoma. In adults, osteogenic metas-
tases are predominantly from prostate carcinoma
and breast cancer [16]. The ivory vertebra sign is
relatively rare in children, and is even less fre-
quent in malignancies such as osteosarcoma,
neuroblastoma, medulloblastoma, and osteoblas-
toma, which directly invade the vertebral body or
cause osteogenic bone metastases in the vertebra.
When osteogenic bone metastases occur in the
vertebral body, mesenchymal cells in the bone
tissue are transformed into osteoblasts, and bony
proliferation occurs (tumoral bone). Thus, tra-
becular and cortical bone are simultaneously
involved, leading to the blurred interface between
these two types of bone. The resulting tumoral
bone occupies part or the whole vertebral body,
showing homogeneously increased ivory-like
attenuation. Of note, osteogenic metastases of
prostate carcinoma, being quite common in
elderly male patients, involve multiple vertebral
bodies, whereas those of breast cancer, being
quite common in elderly women, usually involve
a single vertebral body [17].
As just described, several types of lesions can
cause an osteogenic appearance of a vertebra.
Osteogenic lesions are characterized by osteo-
blast proliferation within the vertebral body. The
cotton flocculent-like lesions occupy part of or
the whole vertebral body with homogeneously
high-attenuation shadow, forming the ivory ver-
tebra sign. Osteolysis and osteogenesis may exist
together, but osteogenesis can cover the osteo-
lytic destruction to form this sign. Such osteo-
lytic destruction leads to scallop-shaped changes
in the vertebral body, which is the characteristic
manifestation of lymphoma; of note, lymphoma
can invade the vertebral body, producing osteo-
lytic, osteogenic, or mixed lesions. Also, lym-
phoma can directly invade the vertebral body,
more commonly via hematogenous pathways,
rather than through proximate lymph nodes.
Paget’s disease with vertebral involvement can
also manifest as the ivory vertebra sign, which
can involve single or multiple vertebral bodies, or
L. Song et al.
even all the vertebrae; in Paget’s, the lesion is
initially dominated by osteoclast activity. As
the osteoclastic activity gradually decreases, the
osteoblastic activity gradually increases as the
lesion becomes chronic. The osteogenic activity
is more obvious within the periphery of the verte-
bral body than centrally, causing the thickened
bony trabeculae to align in the vertical direction.
On X-rays or axial CT images, this phenomenon
can form the “picture frame vertebra,” which is
characteristic of Paget’s disease [18].
9.6 The Posterior Vertebral
Scalloping Sign
Feature
The posterior vertebral scalloping sign is most
evident on lateral spine radiographs. It is the
enlargement of the concave shape of the normal
cortices of the posterior edge of one or more ver-
tebral bodies, similar to the edge of the scallop
shell. This sign can also be seen in sagittal or
axial images of CT or MRI.
Explanation
A slight depression of the posterior edge of the
vertebral body is considered a variation of the
normal body. If the depression of the posterior
edge of the vertebral body increases to form sin-
gle or multiple levels of scalloping, this pattern
indicates pathological changes of the vertebral
body (Fig. 9.6)
Discussion
The posterior vertebral scalloping sign was
first proposed and described by Wakely et  al.
[19] in 2006. It is characterized by the enlarge-
ment of the central depression on the posterior
cortex of the vertebral body, which resembles
the edge of a scallop shell. The posterior mar-
gin of the vertebral body can appear slightly
depressed under normal conditions, but single
or multiple scallop-­like depressions are mainly
visualized with intraspinal lesions or abnormal
vertebral bodies, whether from direct erosion
or disorders of the spinal canal. The most com-
mon cause of a single scallop depression is
9 Spine
a b
d e
Fig. 9.6 (a–c) CT shows the lumbar spinal canal
expanded irregularly around the lumbar spine at L5 level.
(d, e) On sagittal T1WI and STIR, hypointensity and
increased intraspinal pressure caused by intra-
spinal tumors, with local forward indentation
of the posterior edge of the vertebral body,
such as from ependymoma or schwannoma.
Causes of multi-level scalloped depressions
include dural ectasia (e.g., from neurofibroma-
tosis), increased intraspinal pressure caused by
communicating hydrocephalus, achondropla-
sia, meningocele, and cartilage dysplasia, or
hereditary connective tissue disorders (e.g.,
Marfan syndrome, Ehler–Danlos syndrome,
Loeys–Dietz syndrome, or homocysteinuria).
In the setting of posterior vertebral scalloping,
the etiology of a single level of scalloped indenta-
tion is easy to diagnose, although multiple-level
scalloping may lead to a differential diagnosis
because of the varied mechanisms. However, the
335
c
f
hyperintensity are found in the spinal canal at L5. (f) On
axil T2WI, heterogenous high-signal intensity is found in
the spinal canal at L5
specific cause is usually readily identified on
physical or laboratory tests. The scallop-like
depressions caused by neurofibromatosis (often
having cutaneous skin lesions as well) often
involve several vertebral bodies to varied extents,
whereas those caused by communicating hydro-
cephalus and meningocele mostly involve the
lumbar vertebral bodies [20, 21]. The typical ste-
nosis of facet joints, pedicle shortening, and osse-
ous spinal canal can be seen in patients with
achondroplasia; the scallop-like depression on
the posterior edge of the vertebral body is a com-
pensatory change secondary to spinal canal ste-
nosis. Hereditary connective tissue disorders
usually have a clinically identifiable phenotype
characteristic of the disorder, or are seen on dedi-
cated labs in some cases. If the indentation of the
336
posterior edge is at multiple levels with posterior
vertebral scalloping, further diagnostic tests may
be needed to identify the causes.
9.7 MRI Fluid Sign
Feature
MRI fluid sign is a sign of vertebral compression
fracture on MRI, which is characterized by a
focal, linear, or triangular high signal superim-
posed on the diffusive high signal background of
the collapsed vertebral body, best visualized on
STIR MRI. The signal of the lesion is akin to that
of CSF.
Explanation
If the MRI fluid sign is visible within the com-
pressed vertebral body, it nearly always suggests
that the vertebral body is showing insufficiency
(osteoporosis), and typically represents a benign
lesion (Figs. 9.7 and 9.8).
Discussion
Baur et al. first proposed the “MRI fluid sign” in
2002, as an MRI sign indicating a benign osteo-
porotic vertebral compression/insufficiency frac-
Fig. 9.7 A 54-year-old woman with T12 vertebral com-
pression fracture. (a) T1WI demonstrates that the T12 verte-
bral body has mostly lower signal within the midportion.
(b) On T2WI, it is difficult to discern that there is high sig-
L. Song et al.
ture [22]. On STIR sequence, the fluid sign
appears as a focal, linear, or triangular high signal
superimposed on the diffuse high-signal back-
ground of the collapsed vertebral body. The lin-
ear/triangular fluid signal is equivalent to that of
the CSF, thus giving it the name MRI fluid sign.
If a fluid signal is visible in the compressed ver-
tebral body on the MRI examination, it suggests
that there is vertebral body osteoporosis, and
typically a benign, nonneoplastic lesion. Of note,
vertebral compression fractures can be caused by
trauma, osteoporosis, or tumoral invasion; in the
elderly, osteoporosis and tumor-induced ­vertebral
compression fractures are the most common
causes. Thus, in routine, everyday imaging inter-
pretation, the need to differentiate the cause of a
collapsed vertebra from a benign nonneoplastic
etiology (e.g., osteoporosis), or benign neoplastic
etiology, versus a malignant neoplasm, is very
important. As such, Baker et al. found that benign
lesions causing vertebral body fractures are asso-
ciated with an inhomogeneous MRI fluid sign,
whereas vertebral body fractures caused by
malignant etiologies are associated with a rela-
tively homogeneous MRI fluid sign, indicating
that the tumor cells have replaced the bone
marrow throughout the vertebral body [23].
­
nal (edema) within the midportion. (c) STIR shows the ver-
tebral body has a diffusely high signal, but the higher linear
signal is observed within the midportion (arrows), typical
of the linear signal from a benign insufficiency fracture
9 Spine
a b
Fig. 9.8  A 50-year-old man with L1 vertebral compres-
sion fracture and L2 linear fracture. (a) T1WI demon-
strates L1 and L2 vertebral bodies. (b) On T2WI, it is
difficult to discern that there is high signal (edema). (c)
I­ n addition, this sign suggests a malignant lesion
when a paravertebral soft-tissue mass is also
observed. In the study by Baur et al., 23 (26%) of
87 vertebral compression fractures showed the
fluid sign. Among them, 52 cases (40%) with
fractures caused by osteoporosis had a fluid sign.
In 35 cases of vertebral compression fractures
caused by metastatic tumors, only 2 cases (6%)
had a fluid sign. Of note, 16 fluid signs were
located near the upper endplate, 5 were adjacent
to the lower endplate, 20 were in the anterior ver-
tebral body, and 2 were in the middle of the ver-
tebral body. It is believed the MRI fluid sign is
more common in acute vertebral fractures, and
most of them are benign and nonneoplastic
lesions. There is usually no or minimal liquid sig-
nal in the malignant lesions of the vertebral body.
Histopathological examinations have confirmed
that the liquid signal is caused by edema within
the part of the vertebral body not invaded by
tumor in those cases with neoplasms [24].
The appearance of the MRI fluid sign can help
differentiate benign compression fractures from
malignant lesions. Frederic et al. found that the
mean T2* relaxation time constants of acute
benign and malignant vertebral compression
fractures were significantly different; the accu-
racy of differentiating acute benign from
337
c
STIR shows the vertebral body was diffusely high in sig-
nal, but low linear signal is observed within the upper por-
tion, typical of linear signal from a benign insufficiency
fracture
­ alignant vertebral compression fractures was
m
73% and 89%, respectively [25]. The MRI fluid
sign can be an important sign for vertebral com-
pression fracture. If MRI reveals linear or trian-
gular fluid signal within the vertebral body, it
usually indicates the acute/subacute vertebral
body compression fracture is related to benign
osteoporosis.
9.8 The Intravertebral Vacuum
Cleft Sign
Feature
An X-ray plain film shows a thin linear or semi-
lunar clear area located in the center, or subjacent
to, the endplate of the collapsed vertebral body.
On noncontrast CT there is an irregular lucent
(hypoattenuating) region, which is hypointense
on all MRI sequences.
Explanation
A linear or semilunar translucent shadow repre-
sents the cleft formed by vertebral compression
fractures, which is caused by a secondary com-
pression fracture of the vertebral body with isch-
emic necrosis, resulting in the intervertebral cleft.
The gas is released when the pressure within the
338
Fig. 9.9  The intravertebral vacuum cleft sign of a frac-
ture appears as a transverse, linear, or semilunar radiolu-
cent shadow on plain radiographs and on coronal (a) and
cleft becomes negative, and the dissolved gas
within the fluid within the vertebral body and
serum escapes, ultimately forming a vacuum
phenomenon with gas density within the verte-
bral body (Fig. 9.9).
Discussion
The intravertebral vacuum cleft sign, also known
as a vacuum phenomenon in the vertebral body,
was first proposed by Maldague in 1978 [26].
This sign refers to the presence of gas shadows
within the vertebral body fracture. The majority
of osteoporotic fractures occur within the verte-
bral body (including primary and secondary
osteoporosis). A vacuum phenomenon within a
vertebral body is most common in the thoraco-
lumbar segments. A vertebral body with an
obvious compression deformity, situated pre-
dominately near the endplate, is usually easy to
recognize [27]. The vertebral body vacuum phe-
nomenon is a characteristic manifestation of ver-
tebral ischemic necrosis, also known as vertebral
osteonecrosis, but the etiology is as yet unclear
[28]. It may arise from the injury itself, or alter-
L. Song et al.
sagittal (b) NECT reformats. The intravertebral vacuum
cleft sign appears more heterogeneous and irregular on
CT axial view (c)
natively arise from compression or embolization
of the adjacent vertebral blood vessels, subse-
quently resulting in the decrease or even interrup-
tion of the vertebral blood supply. Ultimately,
compression fractures occurring in vertebral bod-
ies develop ischemic necrosis, resulting in the
vertebral body cleft. The change to a negative
pressure within the cleft subsequently forms a
vacuum within the vertebral body. This sign can
also occur in the setting of a vertebral body insuf-
ficiency osteoporotic fracture. Of note, the verte-
bral arteries of osteoporotic patients may be
narrowed by atherosclerosis, fat embolism, prior/
chronic compression, or v­arious other causes,
resulting in decreased vertebral blood supply.
Osteoporosis can also lead to chronic vertebral
fracture, vascular injury, and further reduction of
the blood supply of a vertebra, making the osteo-
porotic vertebral body susceptible to ischemic
necrosis [27].
On X-ray radiograph, the cleft is located in the
central portion/midportion of the vertebral body,
or alternatively inferior to the edge of the supe-
rior endplate, which is manifested as a thin linear
9 Spine
or semilunar translucent shadow with a regular
contour/shape, 1–3 mm thick, and usually having
sclerotic edges; occasionally, the cleft may
appear slightly rounded. When the vertebra is
stretched or extended, the gas shadow increases
in size or thickness. With flexion, the gas shadow/
cleft becomes smaller and even disappears; it
may reappear when the vertebral body is extended
or stretched. Both AP and lateral radiographs can
depict this sign, but the lateral view may help
determine the location of the vacuum cleft.
Noncontrast CT can show an irregular translu-
cent area within the vertebral body; on all MRI
sequences, a vacuum cleft is hypointense from
the gas signal with surrounding magnetic suscep-
tibility artifact. Occasionally, the cleft can be
confused with gas in the adjacent intervertebral
space, such as most commonly from degenerative
disease, which is more common than the intraver-
tebral vacuum cleft that occurs within the verte-
bral body. The intravertebral vacuum cleft sign is
highly suggestive of osteonecrosis, although not
specific. Overall, most vertebral body vacuum
phenomena occur following benign compression
fractures, the majority of which are osteoporotic
fractures, whereas this only rarely occurs within
the vertebral bodies affected by malignant
tumors. This sign signifies a benign lesion of the
vertebral body, essentially excluding malignant
tumors of the vertebral body, and avoiding fur-
ther unnecessary imaging studies [29].
9.9  he Inverted Napoleon’s
T causes are the most common types (of note, the
Hat Sign
Feature
The inverted Napoleon’s hat sign is visualized on
the spine radiographs at the lumbosacral junction
level, typically being L5–S1. The bone that over-
laps the sacral vertebrae resembles the dome of
an inverted “Napoleon’s cap,” where the trans-
verse process of the superior vertebra (typically
L5) forms the receding rim of a hat.
Explanation
In the standing position, gravity from the upper
body passes through the lumbosacral joint, caus-
339
ing the vertebra to slide forward/anteriorly.
Because of stable restriction from the anterior
longitudinal ligament and the iliolumbar and pos-
terior ligaments, the lumbosacral joint can resist
anterior dislocation. Additionally, the lower joint
surface of L5 can move forward and form a joint
with the posterior joint surface of S1; the anat-
omy of the facet articulation is also usually help-
ful to prevent the lumbosacral joint from slipping
forward and downward to the sacral promontory.
The angle between the L5 and S1 axis is about
140°, whereas the angle between the S1 vertebral
body and horizontal line is 40°; therefore, most
of the external forces act on the superior articular
process of S1. Any significant decrease of these
stabilizing forces will lead to the “inverted
Napoleon’s hat sign” (Fig. 9.10).
Discussion
Anterior displacement of the lumbosacral joint
usually results from a lack of bone stability,
which is most commonly secondary to either
congenital defects of the L5 lamina, pedicle
defects of the L5 inferior facet, or lamina defects
of the superior sacral facet. According to the
Newman classification system, a spondylolisthe-
sis is classified into one of five categories: I: con-
genital or developmental abnormalities; II:
spondylolysis; III: degenerative; IV: traumatic;
V: pathology [30], with an addition to the original
Newman classification of a sixth category, VI:
post surgery. Overall, isthmus disconnection/dis-
articulation, degeneration, and postoperative
interarticular region is often referred to as the
isthmus or pars interarticularis). An isthmic frac-
ture or excessive stretching/lengthening can
cause subluxation of the vertebral body, such as
nonunion of the isthmus and anterior displace-
ment of the vertebral body. The spondylolysis
had often been mistakenly referred as isthmic
defects, particularly of the L5 vertebra. However,
the term spondylolysis is now most commonly
used to refer to degenerative diseases or partial
incomplete development of vertebral joints [31].
Bilateral vertebral detachments lead to a greater
degree of spondylolysis, and degenerative facet
arthropathy often causes less displacement.
340
a b
Fig. 9.10 (a) Posteroanterior radiograph of the lumbosa-
cral joint demonstrates the L5 vertebral body edge proj-
ects over the sacrum. The overlapped parts and the
Degenerative anterior displacement of the spine
is most common at the L4–L5 level, usually
accompanied by back pain or sciatica, indicating
nerve root compression. The postoperative ante-
rior displacement of the spine is usually second-
ary to joint instability caused by facet joint
removal (more than 50%) or secondary to adja-
cent horizontal facet arthrodesis and ligamen-
tum flavum hypertrophy several years post
surgery [32].
In the setting of severe spondylolisthesis or
severe lumbar lordosis, an inverted Napoleon’s
hat sign can be quite evident, where, in general,
spondylolisthesis is most easily assessed on lat-
eral radiographs of the spine, and helps to quan-
tify the extent of vertebral displacement. Hence,
the presence of an inverted Napoleon’s hat sign
can be quite helpful for radiologists when only a
lumbar posteroanterior (PA) radiograph, or a PA
abdominal or pelvic radiograph, is available as a
starting point; subsequently, CT or MRI can help
L. Song et al.
transverse process form the inverted Napoleon’s hat sign.
(b) A lateral lumbosacral joint radiograph shows grade 1
anteriolisthesis of the L5 vertebral body on the sacrum
further evaluate the lumbosacral joints in com-
plex cases.
9.10 The Scotty Dog Collar Sign
Feature
This sign is a feature that is characteristic of lum-
bar spondylolysis on oblique plain film X-ray
views, where the collar of the scotty appears as a
translucent line shadow along the vertebral isth-
mus (pars interarticularis), which represents the
spondylolytic defect. It passes through the isth-
mus from the back of the upper oblique down-
ward, just like a scotty dog wearing a collar,
giving it the name of the scotty dog collar sign.
Explanation
The projection of the normal vertebral arch is
similar to the hunting dog on oblique plain film
radiographs. The projection of the transverse pro-
9 Spine
a b
Fig. 9.11 (a, b) Bilateral pars interarticularis defect (arrows) of L5 on right and left oblique radiographs of the lumbar
spine
cess represents the dog’s nose and mouth, the
pedicle is projected as the dog’s eye, the superior
articular process/facet represents the dog’s ear,
the inferior articular process is the dog’s front
leg, the isthmus/pars interarticularis is the dog’s
neck, the lamina is the dog’s body, the contralat-
eral inferior articular process is the dog’s hind
leg, and the contralateral transverse process is the
dog’s tail. When vertebral spondylolysis occurs,
a transparent fissure is visible along the dog’s
neck (the isthmus), which appears akin to a dog
wearing a collar (Fig. 9.11).
Discussion
The scotty dog collar sign is a characteristic sign
of lumbar spondylolysis in the oblique lumbar
X-ray image, where the mostly linear defect
appears as a transparent line/shadow through the
vertebral isthmus [33]. On oblique lumbar X-ray
images, the transparent line passes through the
isthmus from superiorly to inferiorly, akin to a
dog wearing a collar. With vertebral arch col-
lapse, there is a lesion referred to as a vertebral
arch isthmic defect, which is thought to lead to
341
the spondylolisthesis. The cause of the disease is
unknown, but the mechanism is thought related
to congenital defects and trauma, where congeni-
tal developmental defects or potentially weak
areas make the vertebra susceptible to injury.
Additionally, trauma itself can also induce isth-
mic defects. Overall, spondylolyses of L5 account
for 90% of spondylolytic defects, followed by L4
and other segments for the remaining 10%. The
spondylolysis can be unilateral or bilateral, and is
more common in men aged 20–40  years. The
typical clinical symptoms are lower back pain
that radiates to the hip or lower limb.
The lucent defect/crack in the vertebral isth-
mus is a direct X-ray sign of spondylolysis. On a
posteroanterior (PA) film, the spondylolysis
above L4 is often clearly depicted as a transpar-
ent crevice below the annular pedicular shadow
(the isthmus). The following signs may indicate
the presence of spondylolysis: (1) the lateral edge
of the vertebral plate may have an irregular, bro-
ken border; (2) the lateral superior edge or the
inferior edge of the vertebral plate may have a
crescent-shaped depression; (3) attenuation of
342
the pedicle area is uneven, suggesting disrupted
bone structure [34]. On lateral films, especially
on flexion lateral films, the defect from the break
is often clearly indicated, with a positive detec-
tion rate of about 40%; however, it is difficult to
tell whether the lesion is unilateral or bilateral.
The defect extends between the posterior aspect
of the pedicle and the articulation between supe-
rior and inferior articular processes, traveling
obliquely anterior and inferior from the posterior
aspect, often with a hardened edge. In the unilat-
eral case, sometimes only an incomplete crack or
no crack is visible. The width of the crack is
related to the weight of the slip: the more overt
the shift, the more evident the defect on PA
images. The extent of L5 slippage is better deter-
mined on a lateral film [35]; an oblique film is the
best projection position for diagnosing spondy-
lolysis. The normal vertebral arches resemble
scotty dogs (as mentioned previously on such
oblique plain film images). When the pars is dis-
rupted, a transparent band can be seen in the
dog’s neck, like a dog wearing a neck collar (the
scotty dog collar). If the vertebra has slipped for-
ward (anterolisthesis), the dog’s head is slipped
off because the transverse process and the upper
articular process move forward. Of note, spondy-
lolysis may be most clearly seen on CT images:
a b
Fig. 9.12 (a, b) A 67-year-old woman presented with defects within the bilateral isthmus/pars of the L5 vertebral body
on lumbar spine CT. “Double joint sign” can be observed on axial imaging
L. Song et al.
irregular fissures can be seen within the isthmus
of the vertebral arch with irregular, hardened
edges, mostly bilateral, and occasionally being
unilateral (a “cracked ring sign”). The scotty dog
collar sign is a characteristic of spondylolysis. If
the X-ray oblique film depicts a transparent, lin-
ear shadow through the vertebral isthmus/pars,
this suggests that the vertebral isthmus is cracked,
which can aid the clinical diagnosis.
9.11 The Incomplete Vertebral
Ring Sign
Feature
On CT images through the isthmus of the verte-
bral arch, the integrity of the cortical ring of the
osseous spinal canal is interrupted by unilateral
or bilateral rupture of the isthmus, which is called
incomplete ring sign [36]. Other name: annular
fissure sign.
Explanation
Congenital dysplasia of, or stress on, the verte-
bral isthmus (i.e., the pars), causes the continuity
of the isthmus to be interrupted. On a CT image
of the isthmus, the integrity of the cortical ring
around the spinal canal is interrupted (Fig. 9.12).
9 Spine
Discussion
The isthmus of the vertebral arch (also called the
“pars” or pars interarticularis) refers to the seg-
ment between the superior and inferior facets of
the vertebral arch. The bony vertebral canal
forms a complete circular structure (cortical
ring), consisting of the posterior aspect of the
vertebral body, the medial wall of the pedicle, the
anterior surface of the isthmus, the lamina, and
the anterior portion of the spinous process. A
bilateral vertebral arch fracture is more likely to
cause lumbar spondylolisthesis than a unilateral
fracture. When a bilateral isthmic fissure/defect
and the intervertebral joint appear at the same
level, the “double joint sign” can be observed. In
that situation, the “pseudo-joint” is located on the
medial side, whereas the “true joint” is situated
posterior to the lateral side. There are two major
causes for a vertebral arch fracture: one is a con-
genital development abnormality and the other is
stress-related injury. A fracture or crack of the
vertebral arch can sometimes exist in tandem
with other malformations, such as spina bifida
(spinal dysraphism). Also, although the degree of
lumbar spondylolisthesis is mild in adolescents,
the degree of slippage gradually increases with
increasing age.
Most lesions can be clearly diagnosed on plain
film X-ray images. On an oblique plain film, the
normal appearance is that of a dog shape (the
“scotty dog” discussed in the prior topic), where
the isthmus/pars of the vertebral arch resembles a
dog’s neck. When the isthmus is disrupted, the
scotty dog’s neck can have a longitudinally strip-­
like translucent fracture; if accompanied by lum-
bar spondylolisthesis, the transverse process and
the superior articular process move anteriorly,
thus widening the gap of the fracture.
Simultaneously, the step-like arrangement of the
lumbar vertebral facets from inferior to superior
disappears. On noncontrast CT the lumbar isth-
mus should appear continuous in the transverse
plane, where the level of the isthmus of the verte-
bral arch is usually about 10–15  mm above the
level of the corresponding intervertebral disc. On
NECT displaying the isthmic fissures, the corti-
cal ring of the osseous spinal canal appears inter-
rupted, and the fissures appear low in attenuation,
343
spanning the isthmus, with irregular serrated
ends, bony sclerosis along the edges with frag-
mented bone, and narrowed caliber of the spinal
canal, neural foramina, and corresponding lateral
recesses. Such lesions can be unilateral, with uni-
lateral isthmic rupture, and bilateral defects are
characterized by bilateral isthmic rupture. If the
scan level is limited to the intervertebral disc or
facet joint level, the isthmic defect may not be
visible, possibly leading to a missed diagnosis.
9.12 Wide Canal Sign
Feature
The sagittal canal ratio (SCR) is defined as the
maximal anteroposterior diameter of the spinal
canal, divided by the diameter of the canal at the
isthmic–spondylolisthesis level of the L1 verte-
bra. The normal SCR has been determined to be
less than approximately 1.25. Thus, “wide canal
sign” refers to a SCR equal to or larger than 1.25,
mainly in isthmic spondylolisthesis patients,
caused by the increased anteroposterior
diameter.
Explanation
When the anterior vertebral body segment
becomes disconnected from the posterior seg-
ments by isthmic spondylolisthesis, this causes
the vertebral body to slip forward, whereas the
posterior segment either does not move or slips
(is displaced) posteriorly. This change increases
the anteroposterior diameter of the spinal canal,
thus leading to an increased SCR. In general, the
most common reasons for anterior slippage of a
vertebral body are osteoarthritis, remodeling of
the facet joints, disc degeneration, ligamentous
laxity, prior trauma, sequelae of an indolent
infection, etc.; however, the “degenerative dis-
ease” category is by far the most frequent cause
overall (Fig. 9.13).
Discussion
As in the foregoing discussion, a sagittal canal
ratio (SCR) of 1.25 or greater at the level of a
spondylolisthesis is considered to represent an
abnormally increased sagittal canal diameter
344
Fig. 9.13 (a–c) An 80-year old woman presented with spondylolisthesis of the L5 vertebral body
(i.e., a “wide canal sign”), indicating the pres-
ence of bilateral pars interarticularis defects
(isthmus defects). The wide canal sign on mid-
line sagittal MR images (being >1.25) is a reli-
able predictor for pars interarticularis defects at
the level of the spondylolisthesis. This sign can
be useful for distinguishing degenerative disease
from the causes of pars interarticularis defects
that mimic spondylolysis [37]. Isthmic spondylo-
listhesis is the anterior translation of one lumbar
vertebra relative to the next caudal segment as a
result of an abnormality in the pars interarticu-
laris; this causes a variable clinical syndrome of
back and lower extremity pain, and may be
accompanied by varying degrees of neurological
deficits at or below the lesion level [38], the most
common being the fourth lumbar vertebra (L4)
slipping on the fifth (L5), and L5 on S1 (sacrum).
Notably, the term spondylolysis has now been
expanded to include a spectrum of the following
pathological conditions, including (1) stress reac-
tion: no obvious cortical or trabecular disruption
but simply intraosseous edema with associated
sclerosis of the pars interarticularis, lamina, or
pedicle; (2) stress fracture: a disruption of the tra-
becular or cortical bone of the pars, but without
separation of the fracture fragments; and (3) pars
fracture: a separation of the pars interarticularis
L. Song et al.
fragments with associated displacement [39].
Degenerative spondylolisthesis is characterized
by osteoarthritis and remodeling of the facet
joints, disc degeneration, and ligamentous laxity,
resulting in anterior slippage of a vertebral body
along with an intact posterior arch. This closed-­
arch spondylolisthesis configuration is frequently
accompanied by symptoms of spinal stenosis and
nerve root compression. Surgical treatment may
be necessary in such cases, which involves
decompression of the spinal canal (and spinal
fusion if postsurgical instability is suspected). In
contrast to isthmic spondylolisthesis, which is
more common in men at the L5–S1 level, degen-
erative spondylolisthesis is more common in
women at the level of L4–L5 [37].
In adult patients with history and physical
examination findings consistent with isthmic
spondylolisthesis, standing plain film radio-
graphs, with or without oblique views or dynamic
radiographs, is considered as an appropriate,
noninvasive test to confirm the presence of isth-
mic spondylolisthesis. CT is useful in detecting
subtle but suspicious pars defects that are diffi-
cult to visualize on plain radiographs. Of note,
even on CT, the spondylolytic defects may be
missed if they are oriented in the axial plane;
sagittal and coronal reconstructions should be
­
9 Spine
routinely obtained and reviewed. Overall, the
wide canal sign is highly reliable and effective in
differentiating isthmic and degenerative spondylo-
listhesis on midline sagittal MRI images of patients
referred with lower back pain or radicular symp-
toms; other signs and modalities may initially
depict the abnormality to varying degrees [39].
9.13 The Naked Facet Sign
Feature
The naked facet sign refers to the appearance of
uncovered articular processes on CT. The affected
plane depicts the isolated facets without joint
space.
Explanation
Normally, the facet joints are symmetrical and
consistently overlap at each level, and remain in
the fixed position (i.e., do not deviate or dislocate
or change significantly on follow-up). CT can
show the facet joints and their articular spaces as
resembling hamburgers, where the upper facet
process forms a semicircular bun, and the upper
and lower articular processes form a small round
slice of bread, called the “hamburger sign.”
However, although they remain relatively fixed in
positioning, there can be slight physiological
movement in the flexion and extension positions.
Under such normal physiological conditions, the
supraspinal ligament, interspinous ligament, lig-
amentum flavum, and articular capsule maintain
their anatomical relationship; the anterior longi-
tudinal ligament and posterior longitudinal liga-
ment predominately align with the vertebral
bodies and have an indirect role in maintaining
the stability of facet joints. In severe spinal flex-
ion and separation injury, the rupture of these
ligaments with (or without) fractures can lead to
anterior subluxation of the vertebral body, thus
widening the distance between the facet joints,
and baring the upper and lower facets (i.e., mak-
ing them appear naked) (Fig. 9.14).
Discussion
Routine radiography is still the primary initial
method in examining spinal injury, so one should
345
be familiar with the routine X-ray signs of spinal
trauma. Green et al. present a list of conventional
X-ray signs of spinal injury that include local
kyphosis, anterior subluxation of the vertebral
body, posterior vertebral space widening, anterior
superior vertebral wedge fracture, and separation
of vertebral facet joint or spinous processes. These
features are critical for early diagnosis, as subse-
quent spinal instability is common (20%) [40].
CT as well as sagittal and coronal reconstructions
can provide intuitive visualization of bony and
soft-tissue injury, as well as accurately describe
the anterior and posterior structures, vertebral
alignment, and the integrity of the osseous spinal
canal. Anterior subluxation of the vertebral body
is usually the result of ligamentous complex rup-
tures. Subsequently, the upper vertebral body is
dislocated anteriorly, and the corresponding infe-
rior articular process is subluxated, resulting in
the exposed facet. The extent of facet exposure
can be partial or complete, and further flexion
forces can cause facet locking. Cross-­sectional
NECT can depict the inverted facets [41].
The naked facet sign was initially used for
thoracolumbar trauma and dislocation of lower
Fig. 9.14  A 45-year-old man who was injured in a traffic
accident. An axial NECT image through the cervical spine
shows a vertebral facet (apophyseal) joint (arrows) with
the “hamburger” appearance. The superior facet of the
lower vertebra forms the top bun of the hamburger, the
joint space is the meat patty, and the inferior facet of the
upper vertebra forms the bun beneath the hamburger. On
the patient’s left side, the facet joint is dislocated, and the
hamburger sign is no longer present
346
thoracic facets. Although normal thoracolumbar
joints differ in configuration from the cervical
spine, the mechanism is similar, and thus a simi-
larly method of evaluation can be used. In con-
clusion, the naked facet sign is a characteristic
CT finding of spinal flexion distraction injury,
suggesting severe ligamentous injury, with liga-
mentous rupture and spinal instability.
9.14 The Fat C2 Sign
Feature
The fat C2 sign represents an apparently increased
gap between the anterior and posterior margins of
the C2 vertebra when compared with that of the
C3 vertebra on a lateral plain film radiograph of
the cervical spine.
Explanation
The fat C2 sign results from an oblique fracture,
involving the C2 body, causing displacement of
either one or both anterior and posterior margins,
thus increasing the anteroposterior distance
between the two surfaces. The degree between
oblique fracture and the coronal plane determines
whether the actual fracture can be visualized on
a b
Fig. 9.15  (a–c) Both the anterior and posterior longitudinal ligament lines are interrupted. The anteroposterior dimen-
sion of C2 is much greater than that of C3
L. Song et al.
lateral plain radiograph. This injury may occur as
a result of isolated hyperflexion or hyperexten-
sion forces, or from combined hyperflexion and
hyperextension. There may also be some compo-
nent of vertical loading or distraction in these
injuries. The fracture plane is oblique when it
undergoes some degree of rotational stress. The
identification of a fat C2 sign implies a poten-
tially unstable fracture with fragment displace-
ment, which usually requires further imaging
evaluation (Fig. 9.15).
Discussion
The “fat C2 sign” was first proposed by Smoker
et al. in 1987 [42]. It was proposed that so long
as a fat C2 sign appeared on plain radiographs,
no matter whether the fracture line was clearly
identified or not, a C2 fracture could be defini-
tively diagnosed [42]. Complex fractures
involving the body of the axis may result from
a combinational injury force, such as rotation-
extension, rotation-­flexion, lateral subluxation,
or a complex of these. These forces/planes of
injury may lead to the separation of the axis
body into two or more fragments. Disruption
of the anterior longitudinal ligament line
occurs when a fracture fragment is displaced
c
9 Spine
anteriorly, whereas posterior fragment dis-
placement will result in interruption of the pos-
terior line. Also, a “burst” type of fracture, or a
combined hyperflexion-hyperextension injury,
may produce anterior shift of one fragment and
posterior shift of the other fragment, resulting
in simultaneous disruption of the longitudinal
ligament lines. This pattern of line displace-
ment is commonly encountered in the trau-
matic setting [43]. Similarly, Davis et al. found
that the combined disruption of the anterior
and posterior ligamentous lines is the most
common form of such injury in an autopsy
series [44]. In such conditions, the anteropos-
terior diameter of the axis vertebral body, as
visualized on plain radiographs, will be larger
than the anteroposterior diameter of the subja-
cent normal C3 vertebral body; hence, the fat
C2 term suggests a complex fracture involving
the axis. The horizontal fragment shift results
in the increased anteroposterior diameter of the
centrum axis on plain lateral radiographs [1].
The main implication of a fat C2, as identified
on plain radiographs, is an unstable fracture
with fragment displacement, and further imag-
ing assessment is necessary to evaluate the
effect of the fracture on the adjacent spinal
cord and meningeal structures.
Imaging is critically important in the appro-
priate management of patients presenting with
spinal trauma. Plain radiographs have essen-
tially been replaced by multi-slice CT (MSCT),
the mainstream modality utilized most in the
diagnosis of bony abnormalities in the acute set-
ting. MSCT also offers information that is use-
ful in determining spine stability. MRI is
advantageous in the delineation of spinal cord
and soft tissue/ligamentous injuries and also
offers prognostic information following spinal
cord injury. Newer studies utilizing advanced
MRI techniques have shifted the focus from
macroscopic to microscopic, with diffusion-
weighted techniques, such as diffusion tensor
imaging (DTI), offering structural information
on the integrity of white matter tracts in the spi-
nal cord [45].
347
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 Vascular Imaging
and Interventional Strategy
10
Lei Xu, Xin Chen, and Shi Zhou

Contents
10.1 Flat Cava Sign  350
10.2 String of Beads Sign  350
10.3 Hyperattenuating Crescent Sign  352
10.4 Yin-yang Sign  353
10.5 Draped Aorta Sign  354
10.6 Dog Leg Sign  355
10.7 Double Lumen Sign  356
10.8 Floating Viscera Sign  358
10.9 Double Rail Sign  359
10.10 Thread and Streak Sign  361
10.11 Angiographic String Sign  361
10.12 Snowman Sign  362
10.13 Scimitar Sign  363
10.14 Mistletoe Sign  364
10.15 The “3” Sign  365
References  367

L. Xu (*)
Department of Radiology, Beijing Anzhen Hospital,
Capital Medical University, Beijing, China
X. Chen
Department of Radiology, Affiliated Hospital of
Guizhou Medical University, Guiyang, China
S. Zhou
Department of Interventional Radiology, Affiliated
Hospital of Guizhou Medical University,
Guiyang, China

© Springer Nature Switzerland AG 2021 349

B. Gao, A. M. McKinney (eds.), Classic Imaging Signs,
https://doi.org/10.1007/978-3-030-56348-6_10
350
10.1 Flat Cava Sign
Feature
The flat cava sign refers to the inferior vena cava
(IVC) flattening on at least three consecutive
slices.
Explanation
The collapse of the IVC at multiple slices of
computed tomography (CT) in trauma patients
may be an important sign of insufficient blood
volume from massive hemorrhage. The collapse
of the IVC in patients with insufficient blood vol-
ume is most likely caused by a decrease in venous
blood flow. Some patients have a collapsed IVC
after clinical signs of shock. Because the collapse
of IVC is an important sign of insufficient blood
volume, we must pay attention to identifying it at
multiple levels (Fig. 10.1).
Discussion
In 1988 Jeffery and Federle first referred to the
phenomenon of continuous IVC flattening in
three 1-cm-thick adjacent layers as flat cava sign
[1]. The relationship between the flat inferior
vena cava (fIVC) and blood volume is compli-
cated, and current opinion is not uniform. The
wall of the IVC is weak, and its morphology
often changes significantly after traumatic blood
loss or rapid injection of contrast agent or
diuretic. The intracavitary pressure of the IVC is
closely related to its morphology. If the direct
compression and indirect traction of the distorted
blood vessels are removed, IVC morphology
Fig. 10.1  A 44-year-old man with liver rupture caused by
trauma has a flat cava sign (arrow)
L. Xu et al.
depends mainly on the comparison of intralumi-
nal pressure and abdominal pressure.
CT is widely used in the examination of
trauma patients. The morphology of the IVC is
clear. After quickly eliminating the factors that
cause flattening, such as direct compression and
indirect traction, fIVC can indirectly assess the
status of blood volume. Eisenstat et al. [2] retro-
spectively analyzed the abdominal CT of 500
nontraumatic patients and identified four planes
of observation: adjacent to the underside of the
liver, below the renal vein, above the bifurcation
of the IVC, and at the midpoint of the renal vein
and the bifurcation of IVC. If the R value (long–
short-diameter ratio) of any one of the four planes
is 3:1 or more, this is fIVC. Liao et al. [3] estab-
lished three criteria for defining fIVC: (1) R >3:1;
(2) maximum transverse diameter of IVC <9
mm; (3) these criteria appear in at least three
planes. Hypovolemia is an important factor in the
formation of fIVC, and traction of the renal vein
is one reason for the formation of fIVC and its
emergence near the entrance of the renal vein.
Moreover, fIVC is more valuable in assessing the
blood volume status of trauma patients compared
with indicators such as heart rate, blood pressure,
and respiration that reflect blood volume. fIVC
can reflect the degree of decline in blood volume
alone, and it is possible to predict the reduction of
blood volume and further deterioration into shock
[4]. In short, the flat cava sign can be seen in
blunt injury patients and may be associated with
insufficient blood volume or hypotension, but it
is also found in nontraumatic patients without
hypovolemia or hypotension, so in finding this
sign it is vital to closely combine it with clinical
observations.
10.2 String of Beads Sign
Feature
The string of beads sign is more common in renal
artery angiography, which shows that the involved
blood vessels are formed by multiple cystic
enlargements arranged in a string. This sign can
also be seen on CT angiography (CTA) and mag-
netic resonance angiography (MRA).
10  Vascular Imaging and Interventional Strategy
a b
Fig. 10.2 (a) Right renal artery angiography shows
“string of beads” appearance of right renal artery. (b)
Enhanced coronary reconstructed images of a hyperten-
Explanation
The string of beads sign is caused by a relatively
limited narrowing or dilatated area of arterial
lumen that alternates with a small fusiform or
cystic aneurysm. This sign is a more specific
indication of arterial fibromuscular dysplasia
(FMD), which is more common in the distal one
third of the renal artery trunk. The diameter of the
bead often exceeds the normal diameter of the
vessel. Other common sites of involvement are
the internal carotid, cranial, mesenteric, and
external iliac arteries (Fig. 10.2).
Discussion
FMD could be classified into the following types
based on the location of the lesion involving the
arterial wall: vascular intima fibrous hyperplasia,
vascular tunica media fibrosis hyperplasia with
microaneurysms, subadventitial fibrous hyper-
plasia, and abnormal fibromuscular dysplasia.
The typical string of beads sign is only seen in
vascular tunica media fibrosis hyperplasia. This
type is the most common FMD, more than
351
sive patient show “string of beads” changes in the middle
and distal segments of the left renal artery [5]
60–70% [5]. Renal artery vascular tunica media
fibrosis hyperplasia manifests as a single local
stenosis, but the most common manifestation is
multiple stenosis with the aneurysm protruding
outward. Two different tissue types have been
identified: peripheral and diffuse. Lesions of the
peripheral type are localized in the outer layer of
the vascular tunica media, where normal smooth
muscle tissue is replaced by fibrous tissue. The
diffuse type is more severe; it shows the whole
smooth muscle of the vascular tunica media rup-
ture and the fibrous tissue overaccumulation. In
some cases, the vascular tunica media has almost
disappeared, causing aneurysmal dilatation of the
vascular wall. The cause of the disease is not
clear, and several hypotheses are proposed: vas-
cular tunica media fibrosis hyperplasia and sub-
adventitial fibrous hyperplasia are more common
in females and hormones are among the inducing
factors. The incidence of FMD in patients with
renal ptosis is higher, suggesting that extension
of arteries may also be a disease factor. It has
been suggested that renal artery dystrophy leads
352
to wall ischemia as one of the inducing factors.
FMD accounts for 25% of renal vascular hyper-
tension, and it is the most common cause of renal
vascular hypertension in children. In addition to
vascular intima fibrous hyperplasia, all other
types of fibromuscular dysplasia are higher in
women than in men; vascular intima fibrous
hyperplasia is the most common in children, and
the incidence rates are equal for men and women.
It has been reported that 12% to 66% of patients
with renal artery disease have progression of vas-
cular tunica media fibrosis hyperplasia, and that
complete occlusion of the renal artery leads to
whole renal infarction [6]. Previously, the treat-
ment of hypertension caused by fiber dysplasia
included drug therapy and surgery; now, percuta-
neous transluminal angioplasty (PTA) has
become the preferred choice.
10.3 Hyperattenuating
Crescent Sign
Feature
The hyperattenuating crescent sign refers to a
hyperattenuation crescent region parallel to the
arterial wall or the wall thrombus of an abdomi-
nal aortic aneurysm (AAA) on CT plain scan.
The attenuation of the CT plain scan is higher
than that of blood in the aortic lumen and lower
than that of calcification of the arterial wall, and
on enhanced scan it is higher than that of the
psoas major muscle nearby.
a b
Fig. 10.3 (a) Noncontrast CT shows an abdominal aortic aneurysm (AAA) and the hyperdense crescent sign along the
anterior and left lateral wall of the abdominal aorta. (b) Schematic drawing of crescent
L. Xu et al.
Explanation
In the early stage of AAA rupture, blood in the aortic
lumen first penetrates into the wall thrombus, and as
the rupture progresses, bleeding extends to the
periphery of the thrombus and is confined to the wall
of the aneurysm. Histopathology reveals the internal
thrombus hemorrhage showing blood-filled, sepa-
rated ruptures arranged by the inner layer of the
thrombus. In the later stage, blood penetrates the
vessel wall and damages the vascular muscle fibers.
Hyperattenuating crescent sign is a CT sign of AAA
in the wall of the aneurysm or intramural thrombus
hemorrhage, which is closely related to acute rup-
ture or impending rupture of AAA (Fig. 10.3).
Discussion
The hyperattenuating crescent sign is a specific
CT sign of acute intratumoral or wall thrombus
hemorrhage in AAA. It refers to a hyperattenua-
tion crescent region parallel to the arterial wall or
the wall thrombus of the AAA on CT plain scan.
Attenuation on noncontrast CT is higher than that
of blood in the aortic lumen and lower than that
of calcification of arterial wall; on contrast-­
enhanced CT, it is higher than that of the psoas
major muscle [7]. This sign is considered as an
indication of instability and impending rupture of
the aneurysm, which represents blood perme-
ation into the wall of the thrombus or aneurysm
wall. This process weakens the protective effect
of thrombus on the prevention of aortic aneurysm
rupture, which is one of the earliest and most
characteristic imaging findings in aortic aneu-
10  Vascular Imaging and Interventional Strategy
rysm rupture, and should be used as an indicator
for emergency surgery [8]. AAA is a true aortic
aneurysm with an incidence of 1–3%. The local
aortic stenosis is abnormally dilated. The main
cause of the disease is atherosclerosis; other
causes include cystic necrosis, aortitis, and infec-
tion. CT can show the diameter of AAA and the
range of the distal and proximal ends of the aneu-
rysm, often combined with calcification of the
aneurysm wall and thrombosis of the wall.
Aneurysm rupture is a life-threatening
complication, and the likelihood of an aneurysm
rupture increases with aneurysm enlargement.
Ultrasonography (US) or CT are commonly used to
follow up signs of AAA instability. According to
US and CT studies, AAA has an acceptable rate of
expansion of 0.30–0.57 cm/year and an average rate
of expansion of 0.4 cm/year. Depending on the size
of the AAA, the risk of rupture is different. For a
4-cm aneurysm, the risk of rupture is close to 2%;
however, for aneurysms >5 cm, the risk of rupture
within 5 years increases to 25–41%; if >7 cm, the
possibility of rupture increases to 72–83%. The
imaging features suggesting that the aneurysm is
unstable or about to rupture include aneurysm
enlargement, low thrombo-luminal ratio, and
thrombus bleeding, which is the high-attenuating
crescent sign [9]. Suspected AAA rupture should be
preceded by plain CT to prevent masking of high-
attenuation crescents indicating acute or impending
a b
Fig. 10.4 (a) In this patient with aneurysm, enhanced CT
scan shows abdominal aorta enlargement; partially
enhanced and partially not enhanced areas are seen, the
353
rupture. The high-attenuating crescent sign, which
is a CT sign of unstable AAA [10], represents blood
entering the wall thrombus or the aortic wall, thus
weakening the support structure of the aneurysm,
and increasing the likelihood of complete aortic
rupture. Once this sign occurs, regardless of the
patient’s hemodynamic changes and clinical mani-
festations, surgery is required; otherwise, the mor-
tality rate of acute rupture of AAA is close to 100%.
10.4 Yin-yang Sign
Feature
Yin-yang sign is an enhanced CT finding of aneu-
rysms, mainly in the abdomen or cerebral ­vessels.
Half the round or oval shadow with clear bound-
aries is enhanced while the other half is not,
which resembles the Taiji symbol of “Yin-­Yang
and Five Elements” in China [11].
Explanation
Yin-yang sign suggests partial embolization
(eccentricity) of true aneurysms and pseudoaneu-
rysms. On postcontrast CT, increased attenuation
of the lumen is filled with contrast media whereas
the attenuation of the part embolized by mural
thrombosis is low. Yin-yang sign can also be seen
in digital subtraction angiography (DSA) and
ultrasonography [12] (Fig. 10.4).
yin-yang sign. (b) In another case, a round aneurysmal
structure is protruding from the abdominal aorta, with a
patchy nonenhanced area
354
Discussion
Aneurysms are local or diffuse dilatations of the
artery with a diameter greater than 50% of normal
size. True aneurysms are caused by acquired or
congenital lesions of the vascular wall that cause
vasodilation but remain intact; pseudoaneurysms
are caused by defects in the wall of the artery, lead-
ing to the formation of localized hematoma. True
aneurysms and pseudoaneurysms can grow rap-
idly without causing symptoms [13]. The patho-
physiological mechanism of the yin-yang sign is
an aneurysm wall thrombosis that partly blocks
the lumen. The main causes of mural thrombosis
are abnormal blood lipids, damage to the vascular
intima, and slowed blood flow. Therefore, the
mural thrombosis is often limited and is often
attached to the wall of the atherosclerotic aorta
wall or aneurysm lumen, the inner wall is irregu-
lar, and the calcified plaque is located outside the
mural thrombosis. If intramural calcification dis-
placement and intramural lesions are found, intra-
mural hematoma should be considered. The
presence of a yin-yang sign cannot be used as a
basis for the diagnosis of aneurysms [14]. In intra-
cranial cases, it is sometimes necessary to differ-
entiate it from larger suprasellar cystic
meningiomas, craniopharyngiomas, pituitary ade-
nomas, and hemorrhagic metastases.
10.5 Draped Aorta Sign
Feature
In this sign, rupture of an aortic aneurysm on CT
shows the posterior wall of aorta is close to the
spine but the demarcation is not clear.
Explanation
During the development of aortic aneurysms,
compression, displacement, or erosion of periph-
eral organs occur, which will produce the draped
aorta sign on contrast enhancement CT. This sign
strongly suggests aortic wall damage and encap-
sulated hemorrhage (Fig. 10.5).
Discussion
Aneurysm rupture is a fatal clinical emergency. If
the diagnosis or treatment is not timely, the fatal-
L. Xu et al.
Fig. 10.5  A 78-year-old woman with a ruptured abdomi-
nal aortic aneurysm. Posterior wall of the aorta is close to
the vertebral body edge, with unclear demarcation
(arrow), the draped aorta sign
ity rate can reach 90% [15]. Its clinical manifes-
tations include abdominal pain, pulsatile mass,
hypotension, and shock, but nearly one third of
the patients are misdiagnosed as urinary calculi,
diverticulitis, appendicitis, pancreatitis, or intes-
tinal obstruction because they did not have these
typical clinical manifestations. The draped aorta
sign is helpful in diagnosing aneurysm rupture. It
refers to the posterior wall of the aorta or the wall
of the aneurysm close to the vertebral body and
psoas major muscle, resulting in the disappear-
ance of the normal contour [16]. Studies have
reported that this sign may also be associated
with vertebral erosion, suggesting that rupture of
aortic aneurysm is imminent [17]. Understanding
and familiarization with the draped aorta sign are
very important to reduce mortality caused by rup-
ture of aortic aneurysms.
CT is one of the most effective examinations
for rupture of aortic aneurysm. The larger the
diameter of the aortic aneurysm, the greater the
possibility of its rupture. Aneurysms may occur
at any segment of the artery, but most of them
occur in the abdominal aorta below the renal
artery [18]. The rupture of an abdominal aortic
aneurysm often occurs in the lateral posterior
wall, and blood then flows into the retroperito-
neal space. Retroperitoneal hematoma is the
most common imaging manifestation of rupture
of abdominal aortic aneurysm. CT signs of rup-
tured aortic aneurysm include forward displace-
10  Vascular Imaging and Interventional Strategy
ment of kidney, extravasation of contrast
medium, fluid accumulation, hematoma in retro-
nephric and perinephric space, intraperitoneal
free blood, and perirenal spider web sign. Local
calcification discontinuity and unclear arterial
wall are unreliable signs if there are not previous
CT images for comparison. Chronic aortic rup-
ture and bleeding can result in stratified calcifi-
cation of the aortic wall and a mixed soft tissue
mass around the artery. An aortic hanging sign
often indicates damage of the aortic wall and
encapsulated hemorrhage. CT angiography,
which can show the extravasation of active con-
trast media, has become a routine imaging
method for ruptured abdominal aortic aneu-
rysms. However, to avoid confusion with high-
density hematoma, oral contrast agent is not
needed routinely; noncontrast CT should be per-
formed first, because intravenous contrast agent
is seldomly needed to detect definite bleeding.
Severe rupture of an aortic aneurysm can cause
massive hemorrhage and sudden death, and the
onset of the disease is more rapid. Patients with
ruptured aneurysms may experience hemody-
namic instability without any warning; early
diagnosis is the primary, and urgent, goal for
these patients.
10.6 Dog Leg Sign
Feature
This sign, seen in lower-extremity popliteal
artery angiograms, is characterized by acute cur-
vature of the popliteal artery lumen, which may
or may not be related to lumen expansion as
shown on angiography.
Explanation
The normal popliteal artery passes through the
popliteal fossa from medial to lateral, with a rela-
tively straight course. When popliteal aneurysms
are present, because of the wall-attached
­thrombus in the dilated lumen, the lumen is nar-
rowed and the contrast agent cannot fill the entire
dilated lumen. The contrast agent flow in angiog-
raphy is then called to have a dog-legged appear-
ance (Fig. 10.6).
355
Fig. 10.6  In a 50-year-old woman, lower-extremity CTA
shows acute curvature of the right popliteal artery lumen
and a right popliteal artery aneurysm
Discussion
Uppal et  al. first proposed the dog leg sign,
which is a CT sign of popliteal aneurysm [19].
When popliteal aneurysms exist, because of
the wall-­ attached thrombus in the dilated
lumen, narrowing of the lumen means the con-
trast agent cannot fill the entire dilated lumen.
Contrast agent flowing on the contrast image
has a dog-leg-like appearance. This finding
appears in lower-­extremity popliteal angiogra-
phy, is characterized by acute bending of the
popliteal artery lumen, and may or may not be
related to the luminal dilation shown on angi-
ography. The popliteal aneurysm is one of the
most common peripheral aneurysms: 50% are
bilateral, 40% have an abdominal aortic aneu-
rysm, 34% have a femoral aneurysm, and 25%
have iliac aneurysm [20]. The clinical symp-
toms are mostly related to the size of the
tumors. The main manifestations are a pulsa-
tile mass in the popliteal fossa. Some patients
complain of ischemic symptoms of the distal
limbs caused by thromboembolism in the
tumors or pseudoaneurysms caused by rupture
of the tumors, which are characterized by a
giant mass in the popliteal fossa or peripheral
compression symptoms. Arteriosclerosis,
syphilis, and trauma are the main causes of
popliteal aneurysms. Morbidity is more com-
mon in males, accounting for about 70%,
which may be related to genetic factors [21].
356
The diagnosis of popliteal aneurysms mainly
depends on the finding of dilatation of the arterial
lumen and wall calcification during angiography.
Doppler ultrasonography, CTA, and digital sub-
traction angiography can provide a definite diag-
nosis. However, when thromboembolism occurs
in the popliteal aneurysm lumen, CTA can only
show popliteal artery interruption and occlusion
but cannot show the body of the aneurysm.
Doppler ultrasound can show thromboembolism
in aneurysms and lumens at the same time, and its
cost is low. It can be followed up regularly, and it
can also dynamically observe the changes of the
aneurysms, providing guidance for surgical plan-
ning. In ultrasound, popliteal aneurysms often
present as cystic structures with blood flow, or as
cystic structures with complex echoes of blood
flow and thrombus. The differential diagnosis of
the dog leg sign includes distorted atherosclerotic
popliteal artery, popliteal artery entrapment syn-
drome, and adventitial cystic disease. These
lesions can cause an abnormal course of the pop-
liteal artery but rarely produce acute curvature of
the lumen. The popliteal artery entrapment shows
dorsal curvature stenosis during arteriography;
atherosclerosis shows irregular stenosis, and cys-
tic lesions show eccentric stenosis with external
pressure changes. For patients with the dog leg
sign, attention should be paid to looking for other
aneurysms, including contralateral popliteal
aneurysms and abdominal aortic aneurysms. This
finding may lead to changes in surgical treatment:
asymptomatic popliteal aneurysms usually have
better clinical outcomes after surgery than distal
embolization with clinical sequelae. This finding
will significantly improve the treatment of popli-
teal aneurysms.
10.7 Double Lumen Sign
Feature
On contrast enhancement CT, the aorta manifests
as both true and false lumen enhancement, or
false lumen enhancement and slightly delayed
emptying compared to the true lumen. The two
lumens are separated by dissection, so this is
called the double lumen sign.
L. Xu et al.
Explanation
Aortic dissection is an intimal rupture of the
aorta; blood enters the aortic tunica media to
form an intercalated hematoma. The original
lumen of the aorta is called the true lumen and the
newly formed lumen is called the false lumen.
The wall between the two lumens is called the
dissection. Thrombus is more likely to form in
the false lumen than in the true lumen. In a few
cases, the false lumen is filled with thrombus and
cannot be displayed, so only a single lumen (true
lumen) is displayed; the true lumen is often
increased by the compression of the false lumen
(Fig. 10.7).
Discussion
The initiating event in aortic dissection is a tear
in the aortic intima through which blood surges
into the aortic media, separating the intima from
the adventitia. Dissections usually propagate
from the intimal tear distally in the aorta,
although proximal extension can occur. The ori-
gin of any arterial trunk arising from the aorta
may be compromised, and the aortic valve may
be rendered incompetent. Blood in the false
channel can reenter the true lumen anywhere
along the course of the dissection. Rupture of the
aorta, as one of the most common causes of
death, occurs most frequently in the pericardial
space and the left pleural cavity. Aortic dissec-
tion (AD) may manifest as chest pain, back pain,
abdominal pain, neurological deficit, or syncope,
as well as with evidence of end-organ ischemic
and mechanical dysfunction. AD is rare, but car-
ries a high risk of mortality. The age distribution
is bimodal; the most common risk factor for
elderly patients is hypertension, whereas
younger patients typically have other risk fac-
tors, such as medial wall abnormality or sympa-
thomimetic toxidrome [22].
The radiologic assessment of patients with sus-
pected aortic dissection must be based on an
understanding of the treatment options and how
these are to be employed in any clinical setting.
Accurate CT differentiation between the true and
the false lumen has previously been relatively
unimportant, because surgery has been the main-
stay for therapy, and therapeutic decisions have
10  Vascular Imaging and Interventional Strategy 357

a b

Fig. 10.7 (a) A patient with aortic dissection shows an obvious “double lumen sign” on enhanced CT scan. (b, c) In
another patient, the double lumen sign is seen on axial and sagittal views of CTA

relied predominantly on the presence or absence
of involvement of the ascending aorta [23].
However, at the present time, percutaneous treat-
ment methods are maturing and have become
more prevalent, partly fueled by advances in CT
angiography. Reliable CT findings that differenti-
ate the true and false lumen may become particu-
larly important in planning endovascular treatment
of dissection. Beak sign and large cross-sectional
area on contrast-enhanced CT are the most useful
indicators of the false lumen in classical acute and
chronic aortic dissection. The pattern of mural
calcification, presence of intraluminal thrombus
or cobwebs, and wraparound feature in the trans-
verse arch are less common and less reliable iden-
tifiers of the true and false lumens [24]. The
358
diagnosis and differential diagnosis of dissection
must be quickly confirmed, and the type and
extent of dissection must be established to aid in
formulating an appropriate therapy plan.
10.8 Floating Viscera Sign
Feature
The floating viscera sign is the image of the visceral
branches of the aorta when the catheter is located in
the compressed aortic true lumen for angiographic
examination. These vessels (including the celiac
trunk, superior mesenteric artery, and renal artery)
seem to have no origin, so the anterograde blood
flow in the true aorta is slightly or not visualized.
Explanation
When aortic dissection occurs, there are two patho-
physiological mechanisms of branch vessel com-
pression. One is called stationary stenosis, which
refers to the origin of the branching ­vessels involved
by the intimal patches raised by the interlayer, so
that the subintimal hematoma extends to the wall of
the branching vessels, resulting in true lumen steno-
sis of the branching vessels. Another is called active
a b
Fig. 10.8  A 53-year-old man. (a) Cather angiography
shows catheter located downstream of the obstructive
branch of the aortic true lumen. Visceral vessels (celiac
L. Xu et al.
stenosis, which means that the intima of the inter-
layer does not involve the opening of the branch
vessels, but the raised intima sheet crosses the
branch level like a curtain. Because of the impact of
blood flow, the active intima sheet blocks the branch
vessels like a towel at the drain of a bathtub. The
two mechanisms may occur simultaneously in the
same patient. Moreover, if the intimal dissection
does not involve a branch, the diameter of the sup-
ply vessel (aortic true lumen) on the plane of the
branch is larger than that of the branch. At this time,
the true lumen of the aorta upstream of the branch is
compressed by the enlarged pseudo-­lumen of the
aorta, and blood flow in the true lumen of the aorta
downstream and its branches is reduced or disap-
pears accordingly. If contrast agent is injected into
the downstream aortic true lumen during angiogra-
phy, the visceral branch vessels will be visible, that
is, will show the floating viscera sign. At this time,
the visceral vascular branches originating from the
aortic pseudo-lumen will not be visualized unless
there is a re-entry at the corresponding branch level.
When resting stenosis occurs, angiography does not
show the floating viscera sign, but a fan-­shaped
margin (no re-entry) or a linear filling defect can be
seen in the branching vessel lumen (Fig. 10.8).
trunk, superior mesenteric artery, and left renal artery) are
visible. (b) The catheter is located in the pseudo-lumen,
and the main visceral branches are not visible
10  Vascular Imaging and Interventional Strategy
Discussion
Aortic dissection is caused by an intimal tear of
aorta for various reasons. Blood in the aortic cav-
ity enters the middle layer of the aortic wall
through the intimal tear, forming two lumens,
true and false [25]. Aortic dissection is a serious
aortic disease with dangerous conditions, rapid
development, and high mortality. In about 30%
of patients the aortic dissection is accompanied
by compression and ischemia of branches, which
can lead to disappearance of pulse, poor renal or
other visceral perfusion, stroke, and paraplegia.
Branch vessel involvement often predicts a higher
mortality rate, so the floating viscera sign is very
important in judging prognosis. The floating vis-
cera sign was first proposed by Switzer in 2004
[26]. Both dynamic stenosis and static stenosis
can lead to damage of the branches of aortic dis-
section. In the dynamic stenosis of aortic dissec-
tion, the true lumen of the aorta upstream of the
visceral branch is narrowed by the pressure of the
dilated pseudo-lumen of the aorta, which reduces
the anterograde blood flow in the true lumen of
the aorta downstream and in the branches.
Injecting contrast agent into the downstream aor-
tic true lumen can develop the branching vessels
and produce visceral vascular floating sign.
Branches of the aortic pseudo-lumen will not be
visible unless there is a reentrant tear. The float-
ing viscera sign not only indicates the existence
of aortic dissection but also demonstrates the
dynamic damage of the aortic true lumen and
related visceral branches.
Conventional angiography is invasive and
may not be effective in judging the extent of the
pseudo-lumen. If a thrombus is formed in the
pseudo-lumen and does not appear, the diagnosis
may be missed. Noninvasive imaging including
CT, magnetic resonance imaging (MRI), and
transesophageal ultrasound has been widely used
in the diagnosis of aortic dissection. Especially,
multi-slice CT has become the preferred imaging
examination for aortic dissection with nearly
100% sensitivity and specificity. However, no
matter what kind of examination is used, the most
important need is to identify the true and false
lumen of aortic dissection. When aortic dissec-
tion occurs at the root of the aorta and involves
359
the whole aorta, iliac artery, or even femoral
artery and aortic root annular dissection, if the
clinical symptoms are atypical and only abdomi-
nal or thoracic scans are performed, judgment of
true lumen continuity is limited.
10.9 Double Rail Sign
Feature
Double rail sign refers to an embolus in the lumen
of the pulmonary artery causing a central filling
defect with contrast agent surrounding it; it forms
a strip of low density in the center of the lumen,
surrounding a high-density orbital image. Other
name: railway track sign.
Explanation
The double rail sign is a feature of pulmonary
artery thrombosis on postcontrast CT resulting
from contrast between the embolus located in the
center of the lumen and contrast agent surround-
ing it (Fig. 10.9).
Discussion
Pulmonary thromboembolism (PTE) is a disease
caused by thrombosis from the venous system or
right heart that blocks the pulmonary artery or its
branches. Pulmonary circulation and respiratory
dysfunction are the main clinical and
­pathophysiological characteristics. The thrombus
that causes PTE comes mainly comes from deep
vein thrombosis. It can be classified into four
types according to the location and attachment
site of the thrombus in the endovascular cavity
[27]. (1) The partial filling defect shows filling
defect in different degrees in the vascular cavity;
it is irregular in shape and can be filled with con-
trast media. (2) The thrombus with a wall-filled
defect is attached to the vessel wall, and the con-
trast agent is concave or convex, filling on the
side of the vessel. (3) The thrombus of the central
filling defect is filled in the center of the vascular
lumen. If the scanning plane is perpendicular to
the blood vessel, a central point-like filling defect
is seen in a cross section of the blood vessel. The
contrast agent is surrounded by a ring and is
called a target. If the scanning plane is parallel to
360 L. Xu et al.

a b

c d

Fig. 10.9 (a–c) Double rail sign in bilateral pulmonary arteries and branches. (d) In a 23-year-old man, axial recon-
struction of lung CTA shows filling defects in the right middle lobe pulmonary artery

the blood vessel, the strip filling defect appears
located in the middle of the longitudinal plane of
the blood vessel, and the contrast agent on both
sides is symmetrically distributed; this is called
the railway track sign. (4) Completely obstructed
blood vessels have a truncated obstruction with
no contrast agent filling, and no contrast agent
passes through the distal end of the blood vessel.
The direct signs of PTE include filling defects of
contrast agent in the pulmonary blood vessels,
with or without blood flow blockage of orbital
signs, and delayed venous return. However,
because of the high technical requirements, about
6% of complications and a mortality rate of 0.5%
occur.
Multi-slice CT (MSCT) is a reliable, safe, and
simple method for diagnosing a pulmonary embo-
lism. Not only can the direct signs of pulmonary
embolism be seen above the pulmonary segment,
but the pathological changes of pulmonary paren-
chyma can also be simultaneously evaluated. An
embolus found in the pulmonary artery above the
segment is one of the diagnostic methods of
PTE. The direct sign of PTE is a low-­density filling
defect in the pulmonary artery, partially or com-
pletely surrounded by opaque blood flow (railway
track sign), or a complete filling defect, and the dis-
tal vessel is not developed (sensitivity, 53–89%;
specificity, 78–100%). Indirect signs include high-
density wedges in the lobe, banded high-density
areas or discoid atelectasis, central pulmonary
artery dilatation, and reduced or absent branching
of distal vessels. CT has limited diagnostic value
for PTE in the ­subsegment, but it can simultane-
ously show other chest diseases of lung and extra-
pulmonary diseases. MRI has potential ability to
identify new and old thrombi, which may provide a
basis for future thrombolysis. On T1WI and T2WI,
10  Vascular Imaging and Interventional Strategy
it can better show double rail sign according to the
formation time of the thrombus. The double rail
sign is a direct sign of diagnosis of pulmonary
infarction; this sign is very helpful for radiologists
and also nonradiologists to increase learning and
assimilation of concepts [28]. Pulmonary embo-
lism is treated by timely thrombolysis, and the
embolus may be dissolved. Therefore, the double
rail sign is of great significance for the diagnosis of
emergency pulmonary infarction.
10.10 Thread and Streak Sign
Feature
“Thread and streak sign” is usually described as
the thread and chain-like contrast agent filling in
the portal vein, hepatic vein, renal vein, or infe-
rior vena tumor thrombus at the early and middle
stages of angiography, contrast CT, or MRI,
forming continuous or discontinuous parallel
arrangement lines with contrast agent filling or
abnormal enhancement.
Explanation
The tumor invades venous blood vessels into an
embolus, vessels of the tumor grow into a cancer
suppository or the long narrow blood sinus formed
in the emboli, in which the sign is formed by con-
trast agent filling. The sign reflects the growth of
tumor, such as hepatocellular ­carcinoma growing
into the portal or hepatic vein, kidney tumor into
renal vein, and retroperitoneal osteosarcoma into
inferior vena cava, often accompanied by arterio-
venous malformations.
Discussion
The sign was initially described as indicating
tumor vessels in portal thrombi seen on angiogra-
phy. The sign represents blood spaces and vessels
(both veins and arteries) located in and around a
tumor cast that is growing in a large branch and
trunk of the portal vein. The tumor cast contains
many small, narrow blood spaces inside, as well
as between, the tumor and vessel wall. The spaces
are lined with a layer of endothelium and extend
along the long axis of the vein. Arterial blood
enters the tumor thrombus, flows through and
361
around the thrombus longitudinally, and mixes
with the portal vein blood near the portal hilum.
The thread and streak sign therefore reflects the
growth of tumor, such as hepatocellular carci-
noma, into the portal vein. The thread and streak
signs may be seen in other hypervascular tumors
that grow into a large vein and demonstrate arte-
riovenous shunting. The sign has also been noted
in patients with renal neoplasms, as well as in a
case of retroperitoneal osteosarcoma growing
into the inferior vena cava that had an appearance
similar to malignant liver tumors [29].
In the hepatic artery, the clearest retrograde
development of the portal vein can been seen
after the contrast agent is injected within 3–4s,
which can be mistaken for small arterial plexus.
This sign is not associated with the injection
pressure. The sign can be distinguished from the
portal vein thrombosis. The thrombus appears as
a filling defect in the portal vein or there is no
contrast agent filling in the portal vein, and there
is a lack of early linear enhancement of the artery.
Portal vein thrombosis indicates the presence of a
clot in the portal vein lumen or a permanent oblit-
eration of the portal vein as a result of prior
thrombosis with replacement by numerous tortu-
ous venous channels (termed cavernomas) [30].
In patients with hepatocellular carcinoma,
whether the sign is seen on angiography or post-
contrast CT and MRI, it should be considered
that the portal vein, hepatic vein, or inferior vena
cava is invaded. Contrast-enhanced ultrasonogra-
phy also demonstrates intratumoral blood flow in
tumor thrombi. It converts adjacent spotty signals
into a linear signal and enables vessel recogni-
tion. Tumor vessels are clearly demonstrated by
the presence of the thread and streak sign [31].
10.11 Angiographic String Sign
Feature
Atherosclerosis leads to stenosis or occlusion of
the initial lumen of the internal carotid artery. In
the arterial angiography image, the former shows
a long-distance narrower lumen behind the initial
segment, which appears as a thin line or curved
shape. The latter manifests as one or several
362
c­ ollateral circulations around the occluded blood
vessels, and the two ends of which coincide with
the distal and proximal ends of the occluded
blood vessels, respectively. These two signs are
called angiographic string sign.
Explanation
Atherosclerotic plaque leads to stenosis or occlu-
sion of initial segment of internal carotid artery.
The former is caused by a decrease in vascular
pressure in the distal part of the plaque, causing
collapse of the lumen and stratification of con-
trast agent and blood. The lumen is narrowing
with a thin line or curved. The latter is caused by
atheromatous plaque that stimulates neovascular-
ization and forms a collateral circulation.
Discussion
The “angiographic string sign” is common in
the internal carotid artery, being caused by the
stenosis from atherosclerosis. The initial athero-
matous plaque can be recanalized after endarter-
ectomy or arterial stenting; the collapsed vessels
in the distal segment can return to normal. In the
distal part of the plaque, intravascular contrast
agent and blood can be stratified, and the thicker
the tube diameter, the slower the blood flow, and
the greater the difference in the specific gravity
of contrast agent and blood flow, thus the more
obvious the stratification phenomenon. Because
the velocity of the contrast agent is less than that
of blood flow, if a blood vessel moves in the
direction of countergravity, the direction of con-
trast agent and blood flow may be opposite,
forming a phenomenon in which contrast agent
is poorly filled. Therefore, angiographic string
sign is caused by the combination of vessel wall
collapse caused by reduced intravascular pres-
sure and contrast agent and blood flow stratifi-
cation [32].
In selective carotid angiography, the blood
vessels in the proximal segment of internal
carotid artery are narrowed; the distal lumen is
narrowed for a long distance, appearing linear or
curved, and even becomes thinner or indistin-
guishable, forming the angiographic string sign
[33]. The proliferation of neovascularization,
increase in density of the vascular network
L. Xu et al.
around the plaques, and communication between
neovascularization and vascular wall-nourishing
blood vessels and the formation of collateral cir-
culation can also form the angiographic string
sign. The angiographic string sign formed by this
collateral circulation is phlegm and multiple, and
some patients have larger collateral vessels,
which is different from the sign formed by the
collapse of the vessel wall [34]. Arteriography
can show the degree of stenosis, partial or multi-
ple, and the oblique image can also distinguish
the illusion caused by the overlap of the external
carotid artery. The branch of the latter does not
enter the internal carotid artery of the pyramid,
and the angiographic string sign is formed by the
occlusion of the blood vessel; the contrast agent
is in a thin bead shape along the internal carotid
artery and finally enters the basilar artery ring.
10.12 Snowman Sign
Feature
Snowman sign is seen on radiography of the
supracardiac total anomalous pulmonary venous
connection (TAPVC), showing the quasi-circular
contour of superior vena cava and vertical vein
laid on the upper side of the cardiac border, which
looks like a snowman.
Explanation
TAPVC refers to a cyanotic congenital defect in
which all four pulmonary veins fail to make their
normal connection to the left atrium. This defect
results in drainage of all pulmonary venous return
into the right-heart-systemic-venous circulation.
The classic snowman sign is present in young
children with supracardiac TAPVC (Fig. 10.10).
Discussion
Among all the four anatomical variants of
TAPVC, supracardiac TAPVC is the most fre-
quent type seen, according to the multicenter
study. Supracardiac TAPVC is caused by retained
pulmonary vein connections to the cardinal
venous systems. In affected patients, the pulmo-
nary veins from both lungs gather and form a
common chamber from which blood can ascend
10  Vascular Imaging and Interventional Strategy
Fig. 10.10  Chest radiograph of an infant with supracar-
diac total anomalous pulmonary venous connection
(TAPVC) shows dilation of the superior vena cava,
innominate vein, and the silhouette produced by the verti-
cal vein. Pulmonary vasculature is engorged; the cardiac
silhouette is mildly enlarged
through a “vertical vein.” The vertical vein often
connects to the innominate vein and then affluxes
into the superior vena cava.
The diagnosis of TAPVC can be made by vari-
ous modalities, but the typical “snowman sign” is
not always seen on chest radiography. Findings
on X-ray are not specific and cannot be simply
used to diagnose TAPVC. The clinical manifesta-
tion and imaging findings mainly depend on the
presence and severity of the obstruction. Patients
with unobstructed TAPVC may have a mildly
enlarged heart size and the parenchyma of the
lung may be normal. The classic snowman sign is
present in young children with supracardiac
TAPVC as there is no significant stenosis or com-
pression affecting the pulmonary veins and the
venous confluence. In patients with obstructed
TAPVC, however, the size of heart may be nor-
mal and pulmonary congestion and parenchyma
edema may exist, along with the dilation of the
pulmonary artery. The typical snowman sign may
not be found in these patients. Although the X-ray
is not specific enough for the diagnosis of
TAPVC, echocardiography serves as the most
frequently modality to diagnose the underlying
causes of such cyanotic congenital heart disease
[35]. The gold standard for the diagnosis of
TAPVC has been interventions such as cardiac
catheterization. Both CTA and MRA can evalu-
363
ate pulmonary pathways and connections in great
detail. As CTA better shows lung parenchyma,
the bronchia, and pulmonary vasculature, expo-
sure to radiation during the examination remains
a problem to be solved [36, 37]. MRA requires a
long scanning time, which may not be available
to infants as they are not sedated enough to finish
the examination. Snowman sign on radiography
may hint to the existence of supracardiac TAPVC
but cannot establish the diagnosis.
10.13 Scimitar Sign
Feature
Scimitar sign refers to the abnormal connection
from right lower pulmonary venous to hepatic
vein, portal vein, or inferior vena cava (IVC).
Chest radiography shows the tubular high-­density
shadow extending from the right margin of heart
to the diaphragm, which parallels the right heart
border. The curved course of the right pulmonary
vein shows the characteristic appearance of a
Turkish sword, a scimitar, on radiography.
Explanation
The term “scimitar” was suggested to character-
ize the radiographic finding of a curvilinear,
scimitar- or Middle Eastern sword-shaped den-
sity along the right cardiac border. The typical
scimitar sign is usually seen in the partial anoma-
lous pulmonary venous connection (PAPVC)
with only a single pulmonary vein abnormally
affluxing into the inferior vena cava, whereas the
total anomalous pulmonary venous connection
may not have this kind of sign (Fig. 10.11).
Discussion
A variety of congenital defects are commonly
associated with this specific type of anomalous
pulmonary venous connection. It is a rare autoso-
mal dominant disorder with an incidence of 2 in
100,000, affecting more women than men [38].
The syndrome is characterized by the combina-
tion of hypoplasia of the right lung and right pul-
monary artery, cardiac dextroposition, and
extracardiac left-to-right shunting through the
scimitar vein. Adults or elder children with
364
Fig. 10.11  Scimitar vein on CTA. Curved density from
scimitar-like right lower lobe vein is draining into inferior
vena cava (IVC)
s­ cimitar syndrome may present with manifesta-
tions of fatigue, dyspnea, recurrent pneumonia,
and some signs of right heart failure; symptoms
of infantile scimitar syndrome include failure to
thrive, cyanosis, and pulmonary artery hyperten-
sion. However, patients with a single anomalous
pulmonary vein without associated defects are
usually asymptomatic and have a good prognosis
[39]. The scimitar sign on chest radiography may
offer the first clue to find the defect, but other
conditions may also produce the sign without the
features of scimitar syndrome, which should
draw our attention to differentiation. The term
“meandering right pulmonary vein” was coined
to describe the presence of the scimitar sign and
an anomalous right pulmonary vein that drains
normally and tortuously into the left atrium [40].
The initial diagnosis of scimitar syndrome is
often made by echocardiography and confirmed
by other imaging modalities such as CTA or
MRA. CT can better demonstrate the anomalous
pulmonary veins and other associated abnormali-
ties; CTA especially is an invasive angiography
intuitively showing the scimitar sign that the right
pulmonary vein abnormally drains into IVC, por-
tal vein hepatic vein, or the right atrium; also, it
may show some cases with right lung hypoplasia
and other malformations. Cardiac MRI can accu-
rately assess the pulmonary venous anatomy,
quantification of the ratio of pulmonary to sys-
tematic blood flow, the dilation of the right heart
and pulmonary artery, and the left-to-right shunt.
Thus, cardiac MRI also serves as a modality well
suited to aid in the decision making of the syn-
L. Xu et al.
drome [40]. The diagnosis could also be made by
interventional modalities such as cardiac cathe-
terization or pulmonary artery angiography.
Interventional cardiology can also occlude small
anomalous connections to refrain left-to-right
shunting.
10.14 Mistletoe Sign
Feature
The perivascular masses around the coronary
arteries on coronary CT angiography (CCTA)
and cardiac magnetic resonance (CMR) resemble
the shape of mistletoe.
Explanation
Mistletoe is a plant that attaches to the branches
of other plants, which is like the perivascular soft
tissue masses attached to the coronary tree. Also,
the mass around the coronary artery may have
some relationship with retroperitoneal fibrosis
(RPF), according to some case reports, as a mani-
festation of the RPF cardiac involvement
(Fig. 10.12).
Discussion
RPF is a perplexing disorder characterized by
excessive tissue proliferation, consisting of
chronic inflammation and marked fibrosis in
periaortic or peri-iliac retroperitoneum that
entraps the ureters or other abdominal organs
[41]. RPF includes two kinds of forms, the
idiopathic forms or Ormond disease, and sec-
ondary forms caused by malignancy or chronic
inflammations and other conditions [42]. The
clinical symptoms may conclude atypical chest
or abdominal pain, weight loss, and fatigue.
Maurovich-Horvat et al. reported a 69-year-old
woman in whom was first found a confluent,
irregularly shaped retroperitoneal tissue mass
on CT growing around the aorta and trunk of
the iliac artery, with the obstruction of both
sides of the ureters. Follow-up biopsy and his-
tological analysis confirmed the diagnosis of
RPF. After 4 years of immunosuppressant ther-
apy, there was no significant change of the ret-
roperitoneal mass, and the same was seen on
10  Vascular Imaging and Interventional Strategy
a b
Fig. 10.12 (a, b) Curved multiplanar reconstruction of
coronary CT angiography (CCTA) shows the size of peri-
vascular soft tissue (white arrow) around the middle seg-
the consequent ­biological therapy. Then, trans-
thoracic echocardiography was performed, and
no abnormality was found, although the cine
CMR on transverse view demonstrated a soft-
tissue mass around the proximal part of right
coronary artery (RCA) and the left anterior
descending (LAD), showing delayed material
enhancement. Subsequently, CCTA was per-
formed to assess whether there was obstruction
or narrowing of the coronary lumen caused by
the mass, and the finding showed mild to mod-
erate stenosis to the proximal segment of RCA,
LAD, and ramus intermedius (RI). From this
case, a relationship between the peri-coronary
mass and retroperitoneal fibrosis is likely [43].
In another, different, case reported by Xiao
et al., RPF had an excess level of IgG4, but the
imaging examination also showed soft-tissue
masses growing around the left circumflex
artery (LCX) and RCA with histological con-
firmation [44]. So, RPF can also be regarded as
a kind of immunological disease, occurring
independently but associated with other auto-
immune disease. RPF can also demonstrate
multifocal fibroinflammatory lesions, which
belong to the range of immunoglobulin
G4-related disease (IgG4-RD) [45]. The differ-
ential diagnosis for the described coronary
pathological abnormality includes coronary
arteritis, which is also a rare finding in
365
ment of the left anterior descending artery (LAD). The
lumen is moderately narrowed
CCTA.  The imaging manifestations of sys-
temic vasculitides, such as Takayasu disease,
Kawasaki disease, and Behcet disease, include
aneurysms, stenoses, mural thickening, and
dissections. The presence of mistletoe sign on
CMR and CCTA is probably rare, but it might
be a characteristic manifestation of RPF. With
the increasing number of noninvasive cardiac
imaging tests performed worldwide, the recog-
nition of the mistletoe sign could be helpful in
diagnosing RPF [43].
10.15 The “3” Sign
Feature
The “3” sign (also called incisura of the aortic
arch) is a characteristic imaging finding for diag-
nosing coarctation of the aorta (especially tubular
hypoplasia) on X-ray radiography.
Explanation
On posteroanterior or left anterior oblique radio-
graphs, the conjunction of the aortic arch (or
dilated left subclavian artery, LSCA) and the
descending aorta shows a double arch-like notch
or defect that looks like the number “3.”
Indentation of the aortic wall at the site of coarc-
tation with pre- and postcoarctation dilatation
can produce this sign (Fig. 10.13).
366
a b
Fig. 10.13 Chest radiography and CT angiography
(CTA) show typical “3” sign consisting of the enlarged
and distorted aortic knob and LSCA forming the upper
Discussion
Coarctation of the aorta (CoA) is a narrowing of
the aorta, usually located at the insertion of duc-
tus arteriosus and distal to the left subclavian
artery. This defect accounts for 4% to 6% of all
congenital heart disease [46]. The precise patho-
genesis is still unknown, and there may be a
genetic predisposition and association with
Turner syndrome (loss of an X chromosome)
[47]. As mentioned previously, although most
patients have a discrete narrowing of the descend-
ing aorta at the insertion of the ductus arteriosus,
there is a spectrum of aortic narrowing that
encompasses the usual discrete thoracic lesions,
long segmental defects, and tubular hypoplasia.
In a considerable proportion of patients, this
defect is accompanied by complex cardiovascu-
lar abnormalities such as bicuspid aortic valve,
ventricular septal defect (VSD), and transposi-
tion of the great artery and patent ductus arterio-
sus (PDA) [48].
The findings on chest radiograph vary with
age and the severity of the coarctation. In infants
with heart failure, the chest radiograph shows
generalized heart size with increased pulmonary
vascular markings caused by pulmonary conges-
tion. A barium swallow radiograph, although not
routinely performed nowadays, may demonstrate
L. Xu et al.
portion of the arch, the waist at the site of the coarctation,
and the lower portion formed by the poststenotic proximal
descending aorta
a “reverse 3” or “E” sign. The diagnosis may be
accurately confirmed by noninvasive imaging
methods, particularly echocardiology. In most
patients, high-quality transthoracic two-­
dimensional and Doppler echocardiography can
make the diagnosis and detect an accompanying
congenital heart defect, including infants with
PDA [49]. Color and pulsed Doppler echocar-
diography can localize the area of coarctation by
demonstrating increased velocities and turbu-
lence, as well as forward diastolic flow. The
severity of CoA can also be estimated by continu-
ous wave Doppler and calculating the ratio of the
maximal velocity across the narrow area [49].
Cardiovascular MRI (CMRI) or CTA clearly
defines the location and severity of CoA, as well
as collateral vessels [49]. Echocardiography
often provides adequate anatomical and hemody-
namic information, and CMRI or CTA serves as
a complementary diagnostic tool providing
important anatomical data before intervention or
surgery. For adults or adolescent patients with
CoA, CMRI or CTA is recommended for initial
and follow-up diagnosis, and cranial MRA or
CTA is also appropriate to search for underlying
intracranial aneurysms [50]. CMRI is generally
preferred over CTA to decrease the radiation and
contrast burden. Given the accuracy of noninva-
10  Vascular Imaging and Interventional Strategy
sive modalities for diagnosis and determination
of severity, cardiac catheterization for CoA is
generally performed in conjunction with a thera-
peutic intervention and evaluation of patients
with complex congenital heart disease [51]. In
adults, interventional methods are indicated
when coronary artery disease is suspected. The
clinical diagnosis of CoA can be made based
upon the characteristic findings of systolic hyper-
tension in the upper extremities, diminished or
delayed femoral pulses, and low or unobtainable
arterial pressure in the lower extremities. The 3
sign serves as a typical imaging finding on radi-
ography, but further accurate diagnosis is
expected to be made by echocardiology, with
CMRI or CTA to provide complementary
information.
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 Index

A Black hole sign (BHS), 19

Absent bow tie sign, 293–294 Black pleural line sign, 141–142
Accordion sign, 261–263 Black target sign, 42
Ace-of-spade sign, 160–161 Blood–brain barrier (BBB), 329
Acetabulum, 287 Blurred cortex sign, 30, 32
Acoustic neuromas (AN), 69 Bowel wall fat halo sign, 254–255
Acute angle sign, 68 Brain
Acute disseminated encephalomyelitis (ADEM), 71 acute angle sign, 68
Acute ischemic cerebral infarction, 33 aura sign, 52
Acute laryngotracheobronchitis, see Viral howling basilar artery encasement sign, 53
Acute subdural hematoma, 16 black target sign, 42
Adrenoleukodystrophy (ALD), 48, 49 butterfly-like lesions, 47
Aggressive angiomyxoma (AAM), 320 caput medusa sign, 75
Air bronchiologram sign, 115–116 coarse flecks of calcification, 35
Air bronchogram, 114, 116–117 cord sign, 27
Air crescent sign, 132–133 CSF cleft sign, 12
Air–fluid level sign, 156–157 dense artery sign, 21
Angiographic string sign, 361–362 disappearing basal ganglia sign, 30
Anterior cerebral artery (ACA), 21, 297 dural tail sign, 67
Anterior tibial translocation sign, 297–298 empty delta sign, 60
Appendices epiploicae, 256 ependymal dot-dash sign, 69
Appendicitis, 256, 261 eye of the tiger sign, 51, 52
Apple core sign, 263–264 false falx sign, 57
Arcuate sign, 303–304 fogging effect, 33
Arrowhead sign, 260–261 gyri gathering sign, 14
Arterial epidural hematoma, 18 hoop sign, 45
Artificial intelligence (AI), 6 hot cross bun sign, 72
Astrocytoma, 53 hummingbird sign, 71
Atypical hepatic hemangiomas, 180 infundibulum sign, 39
Atypical sign, 3 insular ribbon sign, 29
Aunt Minnie approach, 5 interhemispheric fissure sign, 13
Aura sign, 52 interpeduncular fossa sign, 59
Avulsion injury, 304 ivy sign, 47
lateral ventricular depressing sign, 16
little ventriculus sign, 17
B middle cerebral artery dot sign, 23
Bare area sign, 144 molar tooth sign, 74
Basal ganglia, 31 mount Fuji sign, 50
Basilar artery encasement sign, 53 multilocular ring-like enhancement, 43
Beaded septum sign, 112–113 obscured lentiform nucleus sign, 32
Beaded sign, 208–209 parasagittal sinus sign, 61
Benign lobulation, 106 primary damage, 17
Bird's beak sign, 242–243 pulvinar sign, 62
Bitten cookie sign, head-and-neck abnormalities, 97 radial bands sign, 64

© Springer Nature Switzerland AG 2021 369

B. Gao, A. M. McKinney (eds.), Classic Imaging Signs,
https://doi.org/10.1007/978-3-030-56348-6
370
Brain (cont.)
reversal sign, 55
secondary damage, 17
spot sign, 19
swirl sign, 18
target sign, 41
tau sign, 55
tram-track sign, 37
triangular pattern, 65
tuft sign, 38
white target sign, 42
Breast calcifications, 169
Bridging vascular sign, 284–285
Bright dot sign, 180–181
Bronchiectasis, 149
Bronchioloalveolar carcinoma (BAC), 113–115
Bronchogenic pulmonary carcinoma, 117
Bucket-handle tear (BHT), 294, 295, 299
Bulging fissure sign, 155–156
Bull’s eye sign, 184–185
Butterfly-like lesions, 47
Button sequestrum sign, 322–323
C vascular convergence sign, 108–109
Calyceal crescent sign, 218–220
Caput medusa sign, 75
Cavernous angioma, 46
Cavernous hemangioma, 86
Celery stalk sign, 298–299
Central arrowhead sign, 215–216
Central dots sign, 214–215
Cerebral infarction, 34
Cerebral tuberculosis, 41
Cerebral venous sinus thrombosis (CVST), 61
Cerebral venous thrombosis (CVT), 27
Chest
ace-of-spade sign, 160–161
air bronchiologram sign, 115–116
air bronchogram, 116–117
air crescent sign, 132–133
air–fluid level sign, 156–157
beaded septum sign, 112–113
black pleural line sign, 141–142
bulging fissure sign, 155–156
coarse spicules sign, 109
comet tail sign, 129–130
crazy paving appearance, 140–141
CT angiogram sign, 114–115
deep sulcus sign, 152–154
double-wall sign, 139–140
fallen lung sign, 150–151
feeding vessel sign, 120–121
gloved finger sign, 119–120
Golden S sign, 124–125
grey snow sign, 158–160
ground-glass opacity, 136–138
halo sign, 131–132
hampton’s hump sign, 125–126
honeycomb sign, 113
incomplete border sign, 157–158
Index
linguine sign, 163–164
lobulation sign, 106–107
luftsichel sign, 123–124
mosaic pattern, 135–136
mucous bronchogram, 118–119
multinodule accumulation sign, 105
peach-tip sign, 128–129
peripheral washout sign, 164–166
pleural indentation sign, 110–112
positive bronchus sign, 117–118
reversed halo sign, 130–131
ring around the artery sign, 151–152
SAM sign, 161–163
sarcoid galaxy sign, 142–144
scimitar sign, 154–155
silhouette sign, 122–123
spicular sign, 166–167
spinous protuberant sign, 107–108
split pleura sign, 147–148
square sign, 126–128
tattoo sign, 169–170
tiny calcium sign, 167–168
tree-in-bud sign, 138–139
vacuole sign, 108–109
water-lily sign, 133–134
withered tree sign, 114
Chest X-ray scan, 149
Chronic subdural hematomas (CSDH), 14, 16
CJD, see Creutzfeldt-Jakob disease
Cluster sign, 188–189
Coarctation of the aorta (CoA), 366
Coarse flecks of calcification, 35
Coarse spicules sign, 109
Cobra head sign, 231–232
Cochlear otosclerosis, 92
Coffee bean sign, 245–246
Comb sign, 252–253
Comet tail sign, 129–130, 228–229
Concentric ring sign, 275–276
Congenital pulmonary vein syndrome (CPVS), 154
Contrast-enhanced CT (CECT), 60
Contrast-enhanced MR angiography
(CE-MRA), 95
Cord sign, 27
Corkscrew sign, 248–249
Cortical rim sign, 220–221
COVID-19, 159
Crazy paving appearance, chest, 140–141
Crescent sign, 197–198, 301–302
Creutzfeldt-Jakob disease (vCJD), 63
Crohn’s disease, 252
CSF cleft sign, 12
C sign, 317–318
CT angiogram sign, 114–115
CT angiography (CTA), 33, 62
CT perfusion (CTP), 33
Curved knife sign, 154
CVT, see Cerebral venous thrombosis
Cyclops lesion, 295–296
Cyst-in-cyst sign, 206–207
Index 371

D False falx sign, 57

Deep sulcus sign, 152–154 Fat–blood interface sign, 314–315
Dense artery sign, 21 Fat C2 sign, 346–347
Dense triangle sign, 61 Fat halo sign, 255
Dependent viscera sign, 267–269 Fat ring sign, 258–259
Developmental venous anomaly (DVA), 75 Feeding vessel sign, 120–121
Diaphragm sign, 144 Finger-in-glove sign, chest, 119
Diffuse cerebral swelling, 18 Flat cava sign, 350
Diffusion-tensor imaging (DTI), 14 Flipped meniscus sign, 292–293
Diffusion-weighted imaging (DWI), 95 Floating aorta sign, 278–279
Direct sign, 3 Floating ball sign, 281–282
Disappearance of the sulcus, 30 Floating membrane sign, 207–208
Disappearing basal ganglia sign, 30, 32 Floating viscera sign, 358–359
Displaced crus sign, 144 Flow void sign, 321–322
Disproportionate fat stranding sign, 255–257 Focal cortical dysplasia, 65
Diverticulitis, 256 Focal hepatic hot spot sign, 205–206
DNET, see Dys-embryoplastic neuroepithelial tumor Fogging effect, 33
Dog leg sign, 355–356 Football sign, 266–267
Double bubble sign, 240–241 Fragment-in-notch sign, 294–295
Double duct sign, 211
Double halo sign, 251–252
Double lumen sign, 356–358 G
Double oreo cookie sign, 304–305 Gallbladder (GA), 200
Double peak sign, 286–287 Garland sign, 200–201
Double posterior cruciate ligament sign, 299–300 Gas bubble sign, head-and-neck abnormalities, 98
Double rail sign, 359–361 Gastrointestinal tracts
Double-line sign, 300–301 accordion sign, 261–263
Double-ring sign, head-and-neck abnormalities, 92 apple core sign, 263–264
Double-wall sign, 139–140 arrowhead sign, 260–261
Draped aorta sign, 354–355 bird's beak sign, 242–243
Drooping lily sign, 233–234 bowel wall fat halo sign, 254–255
DTS, see Dural tail sign coffee bean sign, 245–246
Duct-penetrating sign, 213 comb sign, 252–253
Duodenal wind sock sign, 264–265 corkscrew sign, 248–249
Duplex kidneys, 234 dependent viscera sign, 267–269
Dural tail sign (DTS), 67 disproportionate fat stranding sign, 255–257
Dynamic contrast-enhanced (DCE), 95 double bubble sign, 240–241
Dys-embryoplastic neuroepithelial tumor (DNET), 65 double halo sign, 251–252
Dysgenesis of corpus callosum (DCC), 13 duodenal wind sock sign, 264–265
fat ring sign, 258–259
football sign, 266–267
E hyperattenuating ring sign, 259–260
Echinococcosis granulosus, 206 misty mesentery sign, 257–258
Elbow fat pad sign, 315–317 northern exposure sign, 269–270
Elephant trunk sign, 313–314 rigler sign, 265–266
Empty delta sign, 60 small-bowel feces sign, 241–242
Empty sella, 39 spoke wheel sign, 246–247
Endometriosis, 283 string of pearls sign, 243–245
Endometriotic cysts, 282 string sign, 253–254
Endoscopic retrograde cholangiopancreatography target sign, 249–251
(ERCP), 208 whirl sign, 247–248
Ependymal dot-dash sign, 69 GBE, see Giant bullous emphysema
Epidural hematoma, 18 Gestalt theory, 5
Eponymous signs, 2 GGO, see Ground-glass opacity (GGO)
Eye of the tiger sign, 51 Giant bullous emphysema (GBE), 140
Gloved finger sign, 119–120
Gluteal muscle contracture (GMC), 310
F Golden S sign, 124–125
Faceless kidney, 229–230 Golf ball-on-tee sign, 216–218
Fallen fragment sign, 308–309 Granulation tissue, 43
Fallen lung sign, 150–151 Gray-white matter interface (G-WMI) displacement, 20
372 Index

Grey snow sign, 158–160 Interhemispheric fissure sign, 13

Ground glass opacity (GGO), 136–138 Internal carotid artery (ICA), 30
Gyriform calcifications, 37 Interpeduncular fossa sign, 59
Gyri gathering sign, 14 Intracranial tuberculosis, 41
Intraparenchymal hemorrhage (IPH), 19
Intravenous urography, 231
H Intravertebral vacuum cleft sign, 337–339
Half delta sign, 62 Intussusception, 249
Halo sign, 131–132, 191–192 Inverted Napoleon’s hat sign, 339–340
Hampton’s hump sign, 125–126 Iso-attenuation hematoma, 16
Head-and-neck abnormalities Ivory vertebra sign, 333–334
bitten cookie sign, 97 Ivy sign, 47
double-ring sign, 92
gas bubble sign, 98
progressive enhancement sign, 85 J
prominent ear sign, 98 Joubert’s syndrome (JS), 74
salt-and-pepper sign, 93 J sign, 305–306
steeple sign, 95
teardrop sign, 90
tendon sign, 86 L
tram-track sign, 91 Late gadolinium enhancement (LGE), 161
V-shape sign, 88 Lateral capsular sign, 307–308
Hemangiomas, 180 Lateral femoral notch sign, 312–313
Hepatic echinococcosis, 206, 208 Lateral ventricular depressing sign, 16
Hepatic hemangioma, 179 Lenticular nucleus, 31
Hepatic hydatidosis, 206 Light bulb sign, 179–180
Hepatic metastases, 184 Linguine sign, 163–164
Heterogeneous signal intensity, 184 Little ventriculus sign, 17
High-resolution CT (HRCT), 112 Liver capsule depressed sign, 195–196
Hodgkin's lymphomas, 279 Lobulation sign, 106–107
Honeycomb sign, 113 Lollipop sign, 186–187
Hoop sign, 45 Loss of the insular ribbon sign, 30, 33
Horizontal tear, 293 Luftsichel sign, 123–124
Hot cross bun sign, 72 Lung abscess, 156
Hummingbird sign, 71
Hydatidosis, 207
Hyperattenuating crescent sign, 352–353 M
Hyperattenuating ring sign, 259–260 Malignant mass, 164
Hyperdense artery sign, 33 Malignant tumor cells, 107
Hyperdense hematoma, 21 Marginal tear, 293
Hyperdense MCA sign (HMCA sign), 21, 30, 32 Mature cystic teratoma, 281
Hyperintense rim sign, 277–278 Medical imaging, 1
Hypoxic-ischemic injury (HII), 55 Meningiomas, 11
Meniscus of knee, 292
Metaphoric sign, 2
I Microcalcification, 167, 168
Iliac hyperdense line, 309–311 Middle cerebral artery (MCA), 21, 30
Imaging signs, 1 Middle cerebral artery dot sign, 23
classification, 3 Middle cerebral artery susceptibility sign, 24
decision-making, 4 Minute gas, 99
features, 2 Mistletoe sign, 364–365
formation, 2 Misty mesentery sign, 257–258
role, 4 Molar tooth sign (MTS), 74
Incomplete border sign, 157–158 Mosaic pattern, 135–136, 184
Incomplete vertebral ring sign, 342–343 Mother-in-law sign, 181–182
Indirect sign, 3 Mount Fuji sign, 50
Inflammatory pseudotumor of the lung (IPL), 128 Moya-moya disease (MDD), 47
Infundibulum sign, 39 MR cholangiopancreatography (MRCP), 211
Insular ribbon sign, 29, 32 MRI fluid sign, 336–337
Interface sign, 144 MTS, see Molar tooth sign
Index
Mucoid impaction, 119
Mucous bronchogram, 118–119
Multidetector computed tomography (MDCT), 284
Multilocular ring-like enhancement, 43
Multinodule accumulation sign, 105
Multi-planar reformat (MPR) image, 90
Multiple low-density nodules, 186
Multiple sclerosis (MS), 69
Multiple-vessel-oriented nodules, 122
Multi-slice CT (MSCT), 90, 161
Musculoskeletal
absent bow tie sign, 293–294
anterior tibial translocation sign, 297–298
arcuate sign, 303–304
button sequestrum sign, 322–323
celery stalk sign, 298–299
crescent sign, 301–302
C sign, 317–318
cyclops lesion, 295–296
double-line sign, 300–301
double oreo cookie sign, 304–305
double posterior cruciate ligament sign, 299–300
elbow fat pad sign, 315–317
elephant trunk sign, 313–314
fallen fragment sign, 308–309
fat–blood interface sign, 314–315
flipped meniscus sign, 292–293
flow void sign, 321–322
fragment-in-notch sign, 294–295
iliac hyperdense line, 309–311
J sign, 305–306
lateral capsular sign, 307–308
lateral femoral notch sign, 312–313
secondary cleft sign, 306–307
swirl sign, 320–321
target sign, 318–320
Terry Thomas sign, 311–312
yo-yo on string sign, 302–303
Mycobacterium tuberculosis, 41
N Possible sign, 4
Naked facet sign, 345–346
Nasopharyngeal swab test, 159
Necessary sign, 3
Negative sign, 4
Neurocysticercosis (NCC), 42
Northern exposure sign, 269–270
O Pseudo-capsule sign, 225–226
Obscured lentiform nucleus sign, 30, 32
Oligodendroglioma, 35
Omentum, 256
Onion skin sign, 276–277
Optic nerve sheath meningiomas (ONSMs), 92
Orbital myositis, 86
Otosclerosis, 92
Oto-spongiosis, see Cochlear otosclerosis
Ovarian suspensory ligament, 284
373
Ovarian teratoma, 281
Ovarian vascular pedicle sign, 283–284
P
Pagoda-like multinodule accumulation sign, 105
Pancreatic cancer, 212
Pantothenate kinase-associated neurodegeneration
(PKAN), 51
Parasagittal sinus sign, 61
Peach-tip sign, 128–129
Pearl necklace sign, 198–200
Peripheral spinal cord hypointensity sign, 327–329
Peripheral washout sign, 164–166, 189–191
Periportal halo sign, 203–205
Periportayl tracking sign, 202–203
Perirenal cobwebs sign, 224–225
Perirenal halo sign, 223–224
Peritoneum and pelvis
bridging vascular sign, 284–285
concentric ring sign, 275–276
double peak sign, 286–287
floating aorta sign, 278–279
floating ball sign, 281–282
hyperintense rim sign, 277–278
onion skin sign, 276–277
ovarian vascular pedicle sign, 283–284
sandwich sign, 279–280
sentinel clot sign, 273–274
shading sign, 282–283
spongiform gas bubbles, 280–281
Persistent trigeminal artery (PTA), 55
Phleboliths, 228
Pleural indentation (PI) sign, 110–112
Pneumomediastinum, 151, 152
Pneumonia pseudotumor, 127
Pneumoperitoneum, 266
Polka-dot sign, 330–332
Popcorn sign, 45
Portal vein, 212
Positive bronchus sign, 117–118
Posterior cerebral artery (PCA), 21
Posterior vertebral scalloping sign, 334–336
Primary capillary network, 38
Primary sclerosing cholangitis, 208
Primary sign, 3
Progressive enhancement sign, head and neck, 85
Progressive supranuclear palsy (PSP), 71
Prominent ear sign, head-and-neck abnormalities, 98
Pseudo-delta sign, 61
PSP, see Progressive supranuclear palsy
PTA, see Persistent trigeminal artery
Pulmonary alveolar microlithiasis (PAM), 142
Pulmonary echinococcosis, 133, 134
Pulmonary hydatid disease, 133
Pulmonary thromboembolism (PTE), 359
Pulvinar sign, 62
Pupil-like sign, 185–186
374 Index

Purulent cholangitis, 215 MRI fluid sign, 336–337

Pyogenic micro-abscesses, 189 naked facet sign, 345–346
peripheral spinal cord hypointensity sign, 327–329
polka-dot sign, 330–332
R posterior vertebral scalloping sign, 334–336
Radial bands sign, 64 rugger jersey spine sign, 332–333
Radiology, 1 scotty dog collar sign, 340–342
Radiomics, 6 sugarcoating sign, 329–330
Rapid wash-in followed by washout, 182–184 wide canal sign, 343–344
Recurrent artery of Huebner, 31 Spinous protuberant sign, 107–108
Relapsing polychondritis (RP), 98 Split pleura sign, 147–148
Renal halo sign, 221–222 Spoke wheel sign, 226–227, 246–247
Renal oncocytoma (RO), 226 Spongiform gas bubbles, 280–281
Retinal detachment, 89 Spot sign, 19
Retroperitoneal lymphoma, 279 Square sign, 126–128
Retroperitoneal space, 221 Steeple sign, head-and-neck abnormalities, 95
Reversal sign, 55 Stenotic cholangitis, 209
Reversed halo sign, 130–131 Straight border sign, 196–197
Rigler sign, 265–266 Straight line sign, 194–195
Ring around the artery sign, 151–152 String of beads sign, 350–352
Rokitansky-Aschoff sinus (RAS), 201 String of pearls sign, 243–245
Rounded atelectasis, 129 String sign, 253–254
Rugger jersey spine sign, 332–333 Sturge-Weber syndrome (SWS), 37
Subacute subdural hematoma, 16
Subarachnoid hemorrhage (SAH), 59, 61
S Subdural hematomas (SDH), 20
Sagittal canal ratio (SCR), 343 Subdural hemorrhage, 16
SAH, see Subarachnoid hemorrhage Subdural hyperintense band, 15
Salt-and-pepper sign, head-and-neck abnormalities, 93 Subpleural curvilinear shadow (SCLS), 148
SAM sign, 161–163 Subpleural line, 148–149
Sandwich sign, 279–280 Sufficient sign, 3
Sarcoid galaxy sign, 142–144 Sugarcoating sign, 329–330
Schistosomiasis, 201 Superior labrum anterior and posterior (SLAP) tear, 305
Scimitar sign, 154–155, 363–364 Superior sagittal sinus thromboses, 61
Scimitar syndrome, 155 Suppurative cholangitis, 215
Sclerosing mesenteritis (SM), 259 Susceptibility effect, 26
Scotty dog collar sign, 340–342 Susceptibility-weighted imaging (SWI), 15
Secondary capillary bed, 38 Swirl sign (SS), 18, 320–321
Secondary capillary network, 38
Secondary cleft sign, 306–307
Secondary sign, 3 T
Sentinel clot sign, 273–274 Target sign, 41, 187–188, 197–198, 249–251, 318–320
Septic pulmonary embolus, 120 Tattoo sign, 169–170
Shading sign, 282–283 Tau sign, 55
Signet ring sign, 149–150 Teardrop sign, head-and-neck abnormalities, 90
Silhouette sign, 122–123 Teardrop superior mesenteric vein sign, 212–213
Small cell lung cancer (SCLC), 121 Tendon sign, in head and neck, 86
Small-bowel feces sign, 241–242 Tension pneumocephalus, 50
Snowman sign, 362–363 Terry Thomas sign, 311–312
Soft rattan sign, 209–210 Thoracic empyema, 147
Soft-tissue rim sign, 227–228 Thread and streak sign, 361
“Spherical” retinal detachment, 89 “3” sign, 365–367
Spicular sign, 166–167 Thyroid dysfunction myopathy, 88
Spicule, 107 Tiny calcium sign, 167–168
Spine Tortoise shell sign, 201–202
fat C2 sign, 346–347 Total anomalous pulmonary venous connection
incomplete vertebral ring sign, 342–343 (TAPVC), 362
intravertebral vacuum cleft sign, 337–339 Tram-track sign, 37, 91
inverted Napoleon’s hat sign, 339–340 Transparent ring sign, 192–193
ivory vertebra sign, 333–334 Transverse tear, 293
Index
Traumatic brain injury (TBI), 18
Tree-in-bud sign, 138–139
Triangular pattern, 65
Tuft sign, 38
Typical sign, 3
U V
Upper abdomen
beaded sign, 208–209
bright dot sign, 180–181
bull’s eye sign, 184–185
calyceal crescent sign, 218–220
central arrowhead sign, 215–216
central dots sign, 214–215
cluster sign, 188–189
cobra head sign, 231–232
comet-tail sign, 228–229
cortical rim sign, 220–221
crescent sign, 197–198
cyst-in-cyst sign, 206–207
double duct sign, 211
drooping lily sign, 233–234
duct-penetrating sign, 213
faceless kidney, 229–230
floating membrane sign, 207–208
focal hepatic hot spot sign, 205–206
garland sign, 200–201
goblet sign, 230–231
golf ball-on-tee sign, 216–218
halo sign, 191–192
light bulb sign, 179–180
liver capsule depressed sign, 195–196
lollipop sign, 186–187
mosaic pattern, 184
mother-in-law sign, 181–182
pearl necklace sign, 198–200
peripheral washout sign, 189–191
periportal halo sign, 203–205
periportal tracking sign, 202–203
perirenal cobwebs sign, 224–225
perirenal halo sign, 223–224
pseudo-capsule sign, 225–226
pupil-like sign, 185–186
rapid wash-in followed by washout, 182–184
renal halo sign, 221–222
soft rattan sign, 209–210
spoke wheel sign, 226–228
straight border sign, 196–197
straight line sign, 194–195
target sign, 187–188, 197–198
375
teardrop superior mesenteric vein sign, 212–213
tortoise shell sign, 201–202
transparent ring sign, 192–193
wedge-shaped sign, 193–194
Ureteral cyst, 231, 232
Vacuole sign, 108–109
Vacuum phenomena, 99
Vanishing lung syndrome, 140
Variant Creutzfeldt-Jakob disease (vCJD), 63
Vascular and interventional
angiographic string sign, 361–362
dog leg sign, 355–356
double lumen sign, 356–358
double rail sign, 359–361
draped aorta sign, 354–355
flat cava sign, 350
floating viscera sign, 358–359
hyperattenuating crescent sign, 352–353
mistletoe sign, 364–365
scimitar sign, 363–364
snowman sign, 362–363
string of beads sign, 350–352
thread and streak sign, 361
“3” sign, 365–367
yin-yang sign, 353–354
Vascular convergence sign, 108–109
Vasogenic edema, 42
vCJD, see Variant Creutzfeldt-Jakob disease
Venous epidural hematoma, 19
Venous hypertensive myelopathy (VHM), 327
Viral howling, 95
V-shape sign, head and neck, 88
W
Wall ischemia, 251
Water-lily sign, 133–134
Wedge-shaped sign, 193–194
Whirl sign, 247–248
White target sign, 42
Wide canal sign, 343–344
Withered tree sign, 114
Y
Yin-yang sign, 353–354
Yo-yo on string sign, 302–303