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Ultrasound
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Clinical
Ultrasound T H I R D E D I T I O N
Edited by
Section Editors
Ian Beggs MBChB FRCR David W. Pilling MBChB DCH DMRD FRCR FRCPCH
Consultant Musculoskeletal Radiologist Consultant Paediatric Radiologist
Department of Radiology Department of Radiology
The Royal Infirmary of Edinburgh Royal Liverpool Childrens Hospital Alder
Edinburgh, UK Hey
Liverpool, UK
Norman McDicken BSc PhD FIPEM
Emeritus Professor
Medical Physics
Edinburgh University
Edinburgh, UK
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PREFACE
Ultrasound remains one of the most frequently used and valuable modalities for imaging
and guiding interventional procedures. The number of ultrasound examinations carried out
world-wide continues to increase and the global sales of ultrasound equipment, both new
and refurbished, is increasing at some 3-5% each year. The flexibility, ease of use, range of appli-
cations and relatively low cost of the equipment make ultrasound an important investigative
imaging tool.
The first and second editions of this book, edited by David Cosgrove, Keith Dewbury, Hylton
Meire and Pat Farrant, were a great success, providing information and advice across the full
range of diagnostic ultrasound. They were essential reading for those training in ultrasound and
a source of information for many sonographers and sonologists across the world.
Techniques, hardware and data processing have all evolved and progressed at a rapid rate since
the second edition of this book was published in 2001. As a result of these developments, ultra-
sound equipment is now available in more sizes, specifications and complexity than ever before
and this has enabled many different types of clinician to use ultrasound in particular niche areas,
in addition to the more general imaging function that it has always provided.
The chapters in the two volumes of this book cover all aspects of general ultrasound, as well
as more specialised areas such as peripheral vascular and ophthalmic ultrasound. Some areas,
such as musculoskeletal ultrasound, have developed into major applications of ultrasound and
this is now essential to the management of patients with a wide variety of muscle and joint
disorders. There has therefore been a significant enhancement of the coverage of these areas in
this new edition.
Conversely, detailed fetal and maternal obstetric scanning in the mid and final trimesters has
followed cardiac echography into a separate sphere of expertise. There are many excellent text
books dealing with these aspects, therefore, the editors felt that a comprehensive review of obstet-
ric scanning was best left to these volumes. However, first trimester problems will still be seen
by sonographers undertaking general scanning so an account of these is included in this book.
The potential applications of echo enhancing agents, or microbubbles, have developed and
changed significantly since the publication of the second edition of this book. Originally developed
to rescue inadequate Doppler examinations, interesting properties of these agents have led to
potential uses delivering drugs and genes.
The editors of the third edition of Clinical Ultrasound are extremely grateful to the many
experts in their particular fields of ultrasound who have contributed the authoritative, compre-
hensive and informative chapters that make up this book. In particular, our thanks go to Ian
Beggs, David Pilling and Norman McDicken, who were responsible for coordinating the musculo
skeletal, paediatric and physics sections of the book. We are also very grateful to Michael Houston,
Ben Davie and all the other staff at Elsevier who have worked on the many aspects of publication
between the first outline discussions and the final published product.
Paul Allan
Grant Baxter
Michael Weston
xi
LIST OF CONTRIBUTORS
Laurence J. Abernethy MD FRCR Stefano Bianchi MD Anne Marie Coady MRCP FRCR
Consultant Paediatric Radiologist Director Consultant Radiologist
Department of Radiology CIM SA Head of Obstetric and Gynecologic
Royal Liverpool Childrens Hospital, Cabinet Imagerie Mdicale Ultrasound
Alder Hey Geneva, Switzerland Ultrasound Department
Liverpool, UK Hull and East Yorkshire Women and
Childrens Hospital
Gerd Bodner MD Hull, UK
Paul L. Allan BSc MBChB DMRD Professor of Radiology
Specialist Medical Centre
FRCR FRCPE
Gibraltar
Dennis L. Cochlin MBBCh FRCR
Consultant Radiologist Consultant Radiologist
Department of Radiology Division of Radiology
Royal Infirmary Michael J. Bradley MBChB University Hospital of Wales
Edinburgh, UK DMRD FRCR Cardiff, UK
Honorary Clinical Lecturer, Bristol
Georgina M. Allen BM MRCGP DCH University David O. Cosgrove MA MSc FRCP
Lecturer, University of the West of FRCR
MFSEM MRCP FRCR
England
Consultant Radiologist Emeritus Professor
Consultant Radiologist
Radiology Department Imaging Sciences Department
Department of Radiology
University Hospitals Birmingham Hammersmith Hospital
Southmead
Birmingham University Imperial College
Westbury-on-Trym, Bristol, UK
Birmingham, UK London, UK
David J. Breen MRCP FRCR Neil J.A. Cozens MBChB DMRD FRCR
Zahir Amin MBBS MRCP MD FRCR Consultant Abdominal Radiologist Consultant Radiologist
Consultant Radiologist Department of Radiology Derby Hospitals NHS Foundation Trust
Department of Radiology Southampton University Hospitals Derbyshire Royal Infirmary
University College London Hospitals Southampton, UK Derby, UK
London, UK
Robert S.D. Campbell MBChB Laura Crocetti MD PhD
Tom Anderson MSc DMRD FRCR Assistant Professor of Radiology
Senior Research Fellow Consultant in Musculoskeletal Division of Diagnostic Imaging and
Medical Physics Radiology Intervention
University of Edinburgh Department of Radiology Department of Liver Transplantation,
Edinburgh, UK Royal Liverpool University Hospital Hepatology, and Infectious Diseases
Liverpool, UK University of Pisa
Grant M. Baxter MBChB FRCR Pisa, Italy
Consultant Radiologist Orlando Catalano MD
Department of Radiology Assistant Colin R. Deane PhD MIPEM
Western Infirmary Department of Radiology Clinical Scientist
Glasgow, UK Pascale Institute Vascular Laboratory
Naples, Italy Department of Medical Engineering
and Physics
Ian Beggs FRCR Kings College Hospital
Consultant Musculoskeletal Radiologist Dania Cioni MD London, UK
Department of Radiology Assistant Professor of Radiology
The Royal Infirmary of Edinburgh Division of Diagnostic Imaging and
Edinburgh, UK Intervention Diane DeFriend BSc MBChB FRCR
Department of Liver Transplantation, Consultant Radiologist
Hepatology, and Infectious Diseases Imaging Directorate
University of Pisa Derriford Hospital
Pisa, Italy Plymouth, UK
xiii
LIST OF CONTRIBUTORS
Clotilde Della Pina MD PhD Simon J. Freeman MBBS MRCP FRCR Jonathan J. James FRCR
Consultant Radiologist Consultant Radiologist Consultant Radiologist
Division of Diagnostic Imaging and Department of Radiology Nottingham Breast Institute
Intervention Derriford Hospital Nottingham City Hospital
Department of Liver Transplantation, Plymouth, UK Nottingham, UK
Hepatology, and Infectious Diseases
University of Pisa Fergus V. Gleeson MBBS FRCR
Pisa, Italy Tim Jaspan MBChB BSc FRCR FRCP
Consultant Radiologist Consultant Paediatric Neuroradiologist
Department of Radiology Imaging Centre
Keith Dewbury BSc MBBS FRCR The Churchill Hospital University Hospital
Consultant Radiologist and Senior Headington, Oxford, UK Queens Medical Centre
Lecturer Nottingham, UK
Department of Clinical Radiology David E. Goss PhD MIPEM
(Ultrasound)
Southampton General Hospital Clinical Scientist Steven J. Kennish MBChB,
University of Southampton Vascular Laboratory MRCS(Ed) FRCR
Southampton, UK Department of Medical Engineering Specialist Registrar in Radiology
and Physics St James University Hospital
Kings College Hospital Leeds, UK
Rob Dineen MRCP FRCR PhD London, UK
Clinical Associate Professor
Honorary Consultant Neuroradiologist Stephen R. Killick MD FRCOG FFSRH
Andrew J. Grainger MRCP FRCR
Academic Radiology Professor of Reproductive Medicine
University of Nottingham Consultant Musculoskeletal Radiologist and Surgery
Nottingham, UK Department of Radiology University of Hull and Hull York
Leeds Teaching Hospitals Medical School (HYMS)
Leeds, UK Women and Childrens Hospital
Ferdinando Draghi
Hull, UK
Fondazione IRCCS Policlinico S. Matteo Timothy Hartshorne AVS
Universit degli Studi Istituto di
Radiologia Vascular Technologist Caren J. Landes MBChB
Pavia, Italy Department of Surgery MRCPCH FRCR
Leicester Royal Infirmary
Leicester, UK Consultant Paediatric Radiologist
Francis A. Duck PhD DSc Radiology Department
Medical Physicist Alder Hey Childrens NHS Foundation
Department of Medical Physics and
Christopher J. Harvey BSc(Hons) Trust
Bioengineering MBBS MRCP FRCR Liverpool, UK
Royal United Hospital Consultant Radiologist
Bath, UK Honorary Senior Lecturer, Imperial
College Edward Y. Lee MD MPH
Department of Imaging Assistant Professor of Radiology
Anthony J. Edey BMedSci MRCP FRCR Hammersmith Hospital Department of Radiology and
Specialist Registrar London, UK Department of Medicine
Department of Radiology Pulmonary Division
Kings College Hospital Childrens Hospital Boston and Harvard
London, UK Jeremiah C. Healy MA MB BChir Medical School
MRCP FRCR Boston, MA, USA
Simon T. Elliott MBChB FRCR Consultant Musculoskeletal Radiologist
Consultant Radiologist Honorary Senior Lecturer, Imperial
College Justin C. Lee BSc MBBS MRCS FRCR
Radiology Department
Freeman Hospital Department of Radiology Consultant Musculoskeletal Radiologist
Newcastle-upon-Tyne, UK Chelsea and Westminster Hospital Department of Radiology
London, UK Chelsea and Westminster Hospital
London, UK
Andrew J. Evans MRCP FRCR
Professor of Breast Imaging
Tracey Hughes MB, BCh, BAO, BA,
Centre for Oncology & Molecular MRCP, FRCR Edward Leen MB MD FRCR
Medicine Consultant Radiologist Professor of Radiology
Division of Medical Sciences Radiology Department MRC Clinical Sciences Centre
University of Dundee Queen Elizabeth Hospital Faculty of Medicine
Ninewells Hospital & Medical School Gateshead, UK Imperial College London
Dundee Hammersmith Hospital
Scott Inglis BSc MSc PhD MIPEM CSci London, UK
John A. Fielding MD FRCR FRCP(Edin) Senior Clinical Scientist
Consultant Radiologist Department of Medical Physics
Department of Radiology NHS Lothian / University of Edinburgh
Royal Shrewsbury Hospital NHS Trust The Royal Infirmary of Edinburgh
Shrewsbury, UK Edinburgh, UK
xiv
LIST OF CONTRIBUTORS
Riccardo Lencioni MD Eugene G. McNally MB BCh BAO Najib M. Rahman BM BCh MA(Oxon)
Associate Professor of Radiology FRCPI FRCR MRCP
Director, Division of Diagnostic and Consultant Musculoskeletal Radiologist MRC Training Fellow
Intervention Department of Radiology Specialist Registrar in Respiratory
Department of Liver Transplantation, Nuffield Orthopaedic Centre NHS Trust Medicine
Hepatology, and Infectious Diseases Headington, Oxford, UK Oxford Centre for Respiratory Medicine
University of Pisa Churchill Hospital
Pisa, Italy Headington, Oxford, UK
Carmel M. Moran PhD FIPEM
Reader in Medical Physics
Adrian Kuok Pheng Lim MD FRCR Centre for Cardiovascular Sciences Rhian Rhys MBBCh FRCS(Otol) FRCR
Consultant Radiologist University of Edinburgh Consultant Radiologist
Honorary Senior Lecturer, Imperial Queens Medical Research Institute Department of Radiology
College Edinburgh, UK Royal Glamorgan Hospital
Imaging Department Llantrisant, Cardiff, UK
Charing Cross Hospital Philip J. OConnor MRCP FRCR
London, UK Consultant Musculoskeletal Jonathan L. Richenberg MA MRCP
Radiologist FRCR
Gavin Low MBChB MRCS FRCR Department of Radiology
Leeds Teaching Hospitals Consultant Uroradiologist and
Assistant Professor Leeds, UK Honorary Senior Lecturer
Department of Radiology & Diagnostic Department of Radiology
Imaging Brighton and Sussex University
University of Alberta Hospital Simon Ostlere FRCR Hospitals NHS Trust
Edmonton, AB, Canada Consultant Musculoskeletal Brighton, East Sussex, UK
Radiologist
Department of Radiology
Gurdeep S. Mann MBChB MRCP(UK) Nuffield Orthopaedic Centre NHS Trust Philip Robinson MBChB MRCP FRCR
FRCR Headington, Oxford, UK Consultant Musculoskeletal Radiologist
Consultant Radiologist Department of Radiology
Chapel Allerton Hospital
Department of Radiology Uday Patel MBChB MRCP FRCR Leeds Teaching Hospitals
Royal Liverpool Childrens Hospital, Consultant Radiologist
Alder Hey Leeds, UK
Department of Radiology
Liverpool, UK St Georges Hospital and Medical
School Peter Rodgers MBBS FRCR
Kevin Martin BSc PhD FIPEM London, UK Consultant Radiologist
Consultant Clinical Scientist Leicester Royal Infirmary
Department of Medical Physics James M. Pilcher MSc MRCP FRCR University Hospitals of Leicester
Leicester Royal Infirmary NHS Trust
Consultant Radiologist and Clinical
Leicester, UK Leicester, UK
Lead of Adult Ultrasound
Department of Radiology
Carlo Martinoli MD St Georges Hospital Elizabeth E. Rutherford BMedSci
Associate Professor of Radiology London, UK MBBS MRCS FRCR
Radiologia DISC. Universit di Consultant Radiologist
Genova David W. Pilling MBChB DCH DMRD Department of Ultrasound
Genoa, Italy FRCR FRCPCH Southampton General Hospital
Consultant Paediatric Radiologist Southampton, UK
Catherine L. McCarthy MBChB Department of Radiology
FRCR Royal Liverpool Childrens Hospital,
Alder Hey
Suzanne M. Ryan MD MRCP(Ireland)
Consultant Musculoskeletal
Liverpool, UK FRCR
Radiologist
Department of Radiology Consultant Radiologist
Department of Radiology
Nuffield Orthopaedic Centre NHS Trust John N. Plevris MD DM PhD FRCP(E) Kings College Hospital
Headington, Oxford, UK Consultant Gastroenterologist & Reader London, UK
(hon)
Norman McDicken BSc PhD Centre for Liver & Digestive Disorders
Emeritus Professor The Royal Infirmary of Edinburgh; Maria E.K. Sellars
Medical Physics University of Edinburgh Medical School Kings College Hospital
Edinburgh University Edinburgh, UK London, UK
Edinburgh, UK
xv
LIST OF CONTRIBUTORS
Paul S. Sidhu BSc MBBS MRCP FRCR Alberto Tagliafico MD Michael J. Weston MBChB MRCP
DTMBH Staff Radiologist FRCR
Consultant Radiologist and Senior Department of Radiology Consultant Radiologist
Lecturer University of Genoa Department of Radiology
Department of Radiology Genoa, Italy St Jamess University Hospital
Kings College Hospital Leeds, UK
London, UK James Teh BSc MBBS MRCP FRCR
Consultant Musculoskeletal C. Jason Wilkins MA MRCP FRCR
Marilyn J. Siegel MD Radiologist Consultant Radiologist
Professor of Radiology and Pediatrics Department of Radiology Department of Radiology
Mallinckrodt Institute of Radiology Nuffield Orthopaedic Centre NHS Kings College Hospital
Washington University School of Trust London, UK
Medicine Headington, Oxford, UK
St Louis, MO, USA Helen Williams MRCP FRCR
Tze Min Wah MBChB FRCR Consultant Paediatric Radiologist
Rakesh Sinha MBBS MD FRCR FICR Consultant Radiologist and Lead for Radiology Department
Consultant Radiologist and Assistant Percutaneous Tumour Ablation Program Birmingham Childrens Hospital
Professor Department of Radiology Birmingham, UK
Department of Clinical Radiology Leeds Teaching Hospital NHS Trust
Warwick Hospital Foundation Trust and Leeds, UK David J. Wilson MBBS BSc FRSEM
Warwick Medical School FRCP FRCR
Warwick, UK Joanna M. Wardlaw MB ChB (Hons) Consultant Musculoskeletal Radiologist
FRCP FRCR MD FMedSci Department of Radiology
Jane A. Smith MPhil DMU DCRR Professor of Applied Neuroimaging and Nuffield Orthopaedic Centre NHS Trust
Consultant Sonographer Honorary Consultant Neuroradiologist Headington, Oxford, UK
Ultrasound Department University of Edinburgh and NHS
St Jamess University Hospital Lothian
Leeds, UK Director, Scottish Imaging Network,
A Platform for Scientific Excellence
(SINAPSE) Collaboration
Hazel C. Starritt PhD FIPEM Division of Clinical Neurosciences
Medical Physicist Western General Hospital
Medical Physics and Bioengineering Edinburgh, UK
Royal United Hospital
Bath, UK
xvi
CHAPTER
+Po
Po
A Continuous wave propagation
A Po = wave amplitude
Direction of vibration
= wavelength
+Po
Figure 1.1 The generation of continuous and pulsed wave Figure 1.3 Ultrasound wavelength and wave amplitude.
ultrasound by a vibrating source in contact with the propagating A: Continuous wave. B: Pulsed wave.
medium.
Figure 1.4 Intensity at a point rate of flow of energy through Output power in decibels ( dB) = 10log ( P Po )
unit area in an ultrasound beam. Power rate of flow of energy
The dB notation was employed in the past when it was fairly
through whole cross-section of ultrasound beam.
difficult to measure absolute values of intensity and power in units
of mW/cm2 or mW respectively and also since separate calibration
is required for each transducer. This notation is essentially an his-
INTENSITY AND POWER torical hangover and is of no value in machines designed for clinical
application. More recently the outputs of machines have been
When a transducer is excited by an electrical voltage, vibrations related to possible biological effects, in particular heating and cavi-
pass into the tissue, i.e. energy passes from the transducer to the tation. Cavitation is the violent response of bubbles when subjected
tissue. The intensity at a point in the tissue is the rate of flow of to the pressure fluctuations of an ultrasound wave (Chapter 4).
energy through unit area at that point (Fig. 1.4). For example, the Thermal (TI) and mechanical indices (MI) relate to these phenom-
intensity may be 100 milliwatts per square centimetre (100mW/ ena and are displayed onscreen (Chapter 4).
cm2). The intensity is related to the square of the pressure wave The decibel notation is also found applied to the gain of a receiver
amplitude. amplifier:
The region of tissue in front of the transducer subjected to the
Gain = Output volts Input volts
vibrations is referred to as the ultrasound field or beam. Intensity
is often measured at the focus of the field or within 1 or 2cm of the Or:
transducer face. Transducer designers will often measure the pres-
Gain in decibels = 20log ( Vout Vin )
sure amplitude or intensity over the full depth range for which the
transducer will be used. Another application relates to differences in pressure amplitude
For safety studies, intensity is often defined precisely to ensure of an ultrasound wave:
validity in the conclusions drawn; for example, Ispta is the intensity
at the spatial peak (often the focus) averaged over time. Each defini- Acoustic pressure difference in decibels = 20 log (p1 p 2 )
tion gives rise to an intensity relevant to that definition. These Absolute values of ultrasonic intensity are normally measured
intensities are not used in routine scanning but it is useful to know with a hydrophone, which takes the form of a small probe with a
their origins when the safety literature is being studied (see Appen- piezoelectric element at its tip.
dix at the end of this chapter). It will be seen in Chapter 4 that from Absolute values of ultrasonic power are measured with a radia-
a clinical application point of view, the two quantities of interest to tion power balance which is based on the following. There is a flow
optimise safety are thermal index (TI) and mechanical index (MI). of energy in an ultrasonic field from the transducer as the vibrations
The power of an ultrasonic beam is the rate of flow of energy pass into water. Associated with the flow of energy in a beam there
through the cross-sectional area of the beam (Fig. 1.4). This is a is a flow of momentum. Due to this momentum a force is experi-
quantity that is often quoted since it gives a feeling for the total enced by an object placed in the field, the force being directly related
output and is relatively easy to measure. to the power of the field. These small forces can be measured by
Power and intensity controls on ultrasonic scanners are some- placing the object under water on the pan of a sensitive chemical
times labelled using the decibel notation. This occurs less frequently balance, hence the name power balance.
on new machines. Although not essential for the operation of For a beam of power P incident perpendicularly on a totally
machines, familiarity with this labelling removes its mystique and reflecting flat surface:
can be helpful when reading the literature. The manipulation of
machine controls is covered in Chapter 3, where it is demonstrated Radiation force = 2P c
that logical operation can be readily achieved. The decibel notation The force experienced is 0.135mg per milliwatt. Power levels
basically relates the current value of intensity or power to a refer- down to 0.1mW can be measured with balances. For an object that
ence value. For example, taking the maximum intensity position of totally absorbs the beam, the force is half that of the reflection case.
the control as giving the reference output value Io, other values of
intensity I, corresponding to other control positions, are calibrated
relative to Io as:
DIFFRACTION AND INTERFERENCE
Output intensity in decibels (dB) = 10log ( I I o )
This output in dB is therefore the ratio of two intensities and is Diffraction describes the spreading out of a wave as it passes
not an absolute unit like cm or watt. Output power controls can from its source through a medium. The pattern of spread is
also be labelled in terms of dB: highly dependent on the shape and size of the source relative to the
5
CHAPTER 1 Basic physics of medical ultrasound
wavelength of the sound. To produce an approximately parallel- interference) to give an increase in amplitude. Out of step they add
sided beam, the diameter of the crystal face is typically 10 to 20 destructively (destructive interference), resulting in a lower pres-
times that of the ultrasound wavelength. The diffraction pattern of sure amplitude (Fig. 1.7B). This principle of superposition is
a disc-shaped crystal as found in basic medical ultrasound trans- widely used to predict ultrasound field shapes using mathematical
ducers is approximately cylindrical for a short distance, after which models. In such modelling the shape of the transducer field is cal-
it diverges at a small angle (Fig. 1.5). The diffraction pattern from culated by considering the crystal face to be subdivided into many
a small transducer is divergent at a larger angle from close to the small elements. The diffraction pattern for each element is calcu-
transducer (Fig. 1.6A). Within a diffraction pattern there may be lated and the effect of them overlapping and interfering gives the
fluctuations in intensity, particularly close to the transducer. Diffrac- resultant ultrasound field shape. Interference and diffraction are
tion also occurs beyond an obstacle such as a slit aperture or an rarely considered in detail since, as techniques stand at present,
array of slits which partially blocks the wavefront (Fig. 1.6B). The ultrasound beams and fields are not tightly defined.
narrowness of a beam or the sharpness of a focus is ultimately The terms ultrasound field and ultrasound beam tend to get
determined by diffraction. The submillimetre wavelengths associ- used interchangeably. It would probably be better if we restricted
ated with the high frequencies of medical ultrasound permit the field to label the transmitted ultrasound pattern in front of the
generation of well-focused beams, one of the most important facts transducer and beam to a combination of the transmitted field and
in medical ultrasound technology. The higher the frequency, the the reception sensitivity pattern in front of the transducer. For a
narrower the beam can be made and hence the finer the image single crystal transducer the two patterns are the same but for array
detail. Unfortunately, we will see later that absorption also increases transducers they are probably always different. For example, the
with frequency, which puts an upper limit on the frequency that transmission focusing and the reception focusing are usually differ-
can be employed in any particular application. ent (Chapter 2). It is the shape of the beam, i.e. the combination of
Interference of waves occurs when two or more overlap as they transmission and reception, that plays an important part in deter-
pass through the propagating medium. The resultant wave pres- mining the detail in an image. The loose usage of field and beam
sure amplitude at any point is determined by adding the pressure is not usually serious, but it is worth remembering that both trans-
amplitudes from each wave at the point (Fig. 1.7A). When the mit power and receiver gain influence the lateral resolution in an
waveforms are in step, they add constructively (constructive image. Image detail (resolution) is discussed later in this chapter.
P1
P1
P1 P1 + P2
+
P2
Resultant waveform
Resultant waveform
B Aperture diameter ~ wavelength A B
Figure 1.6 Diffraction pattern. A: For a small transducer. B: For Figure 1.7 A: Constructive interference of two waves.
a small aperture. B: Destructive interference of two waves.
6
Standing waves and resonance
f1
A
Signal amplitude
f2
B Depth (time)
B
Figure 1.8 Fluctuating echo signals resulting from constructive
and destructive interference of echoes from structures lying along
one beam direction through tissue. A: Transducer transmitting f1 and f2
ultrasound along one beam direction into complex tissue. B: Echo
signals received from one beam direction into tissue.
Voltage
Anti-nodes Nodes
A
Time
50
30 40 dB
20
10 f
B
Frequency B
C
t = o /2
one half-wavelength, a strong resonance occurs, known as the fun-
damental resonance (Fig. 1.11C).
Figure 1.11 A: The generation of a standing-wave pattern by two
At other separations equal to multiples of the half wavelength,
overlapping waves travelling in opposite directions. B: Standing
other weaker resonances are known as harmonics. Conversely har-
waves produced by waves reflected within parallel surfaces.
monics can also be seen when the separation is fixed and the wave-
C: Fundamental resonance for surfaces separated by one
length is varied. These harmonics occur when the wavelength
half-wavelength.
equals some multiple of the separation.
Piezoelectric transducer elements are made equal in thickness to
one-half of the wavelength corresponding to their desired operating
frequency to give efficient generation and detection of ultrasound.
Continuous wave Doppler transducers have little or no damping
and resonate at their operating frequency. Imaging and pulsed Interference, frequencies and resonance
wave Doppler transducers have some damping which absorbs Waves diffract and interfere.
energy and spreads their sensitivity over a frequency range; i.e. At high frequencies, and hence small wavelengths, diffraction can
they have a wider frequency response (bandwidth), which can be be controlled to produce directional beams.
desirable though the damping reduces their sensitivity. When the High frequencies produce narrow beams.
size of an object has a special numerical relationship to the wave- Image speckle is produced by interference of echoes from
length, a resonance will occur. An interesting example of resonance small-scale structures within tissue. The speckle pattern is related
is exhibited when microbubbles of a particular size resonate in an to the structure but does not represent the actual structure.
ultrasound field. This resonance is exploited to improve the detec- Complex waveforms (ultrasonic or electronic) can be broken
tion of these bubbles when they are injected into the bloodstream down into frequency components. Frequency analysis is a very
to act as imaging contrast agents (Chapter 6). By coincidence micro- powerful technique for characterising signals.
bubbles, the size of red blood cells, resonate in the same MHz The frequency spectrum of a signal is important when harmonic
ultrasound frequency range as used in tissue imaging. imaging and also Doppler blood flow detection are employed.
Standing waves and interference are of interest to the designer of Resonance can occur when ultrasound is reflected internally in a
transducers. They are two of the phenomena that contribute to the structure in which the dimensions of the structure are some
overall performance of a transducer and provide some insight into multiple of the wavelength.
its complex operation. Given this complexity and scope for varia- Resonance is commonly encountered in transducer crystals and
tion, it is always worth thoroughly assessing the performance of microbubbles.
each transducer in clinical use.
8
Scattering
Fat/muscle 1.08
Muscle/blood 0.07
Bone/fat 48.91
B Smooth reflective surface
Fat/kidney 0.64
Lens/aqueous humour 1.04
Figure 1.12 Reflection. A: Reflection at change in acoustic Soft tissue/water 0.23
impedance between two media. B: Reflection at a smooth Soft tissue/air 99.90
interface.
9
CHAPTER 1 Basic physics of medical ultrasound
Incident wave
Scattered wave
C1
Table 1.3 Scattering within organs. Scattered signal Table 1.4 Beam deviation due to refraction at typical
level compared to typical soft tissue boundary (fat/ soft/tissue boundaries (angle of incidence 30)
muscle) echo level
Bone/Soft tissue 19
Reference boundary (fat/muscle) Echo level 1.0 Muscle/Fat 2.5
Liver parenchyma Scatter level 0.032 Muscle/Blood 0.5
Placenta Scatter level 0.1 Muscle/Water 1
Kidney Scatter level 0.01 Lens/Aqueous humour 2
Blood Scatter level 0.001
Water Scatter level 0.000
Reflection, refraction and scattering
An echo is generated at a change in acoustic impedance. The
bigger the change, the bigger the echo. It does not matter if the
provides an idea of the scattering powers of some common tissues.
change is an increase or decrease.
The use of such scattering measurements has not been sufficiently
The acoustic impedance of a tissue is related to the density and
discriminatory for tissue characterisation. However, the depiction
rigidity of the tissue.
of different levels of scattered echo signals in an image provides
Bone and gas have acoustic impedances that are markedly
much of the information in the image.
different from those of soft tissue.
Reflection is said to occur at surfaces of dimensions greater than
the ultrasound wavelength and for smooth surfaces is analogous
REFRACTION to light reflecting from a mirror or glass surface.
Scattering occurs at small structures of acoustic impedance
The change in direction of a beam when it crosses a boundary different from that of the surrounding medium. Scattering
between two media in which the speeds of sound are different is redirects the incident ultrasound over a wide range of angles,
called refraction (Fig. 1.14). If the angle of incidence is 90 there is possibly through all angles in 3D.
no beam bending but at all other angles there is a change in direc- Very small tissue structures and blood cells are scattering centres
tion. Refraction of light waves in optical components such as lenses of interest.
and prisms is a common example. For an angle of incidence i, the Refraction occurs at a tissue interface where the velocity of
new angle of the beam to the boundary on passing through it (the ultrasound changes and the angle of incidence is not 90.
angle of refraction r) is easily calculated using Snells law:
sin i sin r = c1 c2 =
where is the refractive index. LENSES AND MIRRORS
Table 1.4 shows that deviations of a few degrees can occur at soft
tissue boundaries. The results in ultrasonic imaging allow us to We often think of ultrasound behaving in a manner similar to that
conclude that refraction is not a severe problem at soft tissue inter- of light. This is not surprising since both are wave phenomena. As
faces. An exception is at soft tissue/bone boundaries, where it can for light, lenses and mirrors can be constructed for ultrasound by
be a severe problem due to the big differences in speed of ultra- exploiting reflection and refraction (Fig. 1.15). Lenses are designed
sound between soft tissue and bone. by selecting material in which the velocity of ultrasound is different
10
Non-linear propagation
Table 1.5 Tissue thickness (in cm) to half intensity of ultrasound beam (3dB) for common clinical frequencies
and materials
Blood 17 8.5 3 2 1
Fat 5 2.5 1 0.5 0.25
Liver 3 1.5 0.5
Muscle 1.5 0.75 0.3 0.15
Bone 0.2 0.1 0.04
Polythene 0.6 0.3 0.12 0.6 0.03
Water 1360 340 54 14 3.4
Soft tissue (average) 4.3 2.1 0.86 0.43 0.21
from that of water or tissue. Mirror material has an acoustic imped- NON-LINEAR PROPAGATION
ance markedly different from water or tissue and hence results in
very strong reflection. Lenses are most commonly found on the Attenuation, discussed above, reduces the amplitude of ultrasound
front face of transducers. Mirrors are rarely used. as it passes through tissue. It also reduces the high-frequency com-
ponents in a pulse more than the lower ones and hence alters the
shape of the pulse. This effect is rarely considered in clinical appli-
cation. However, another phenomenon which alters the shape of a
ABSORPTION AND ATTENUATION pulse and which is routinely exploited is called non-linear propaga-
tion. It is not significant for low-amplitude waves (e.g. 50kPa) but
As an ultrasound wave passes through tissue, its orderly vibra- important for high amplitude ones (e.g. 1MPa). For waves of large
tional energy is converted into random vibrational heat energy and pressure amplitude, the speed of sound is higher in regions where
hence the wave pressure amplitude reduces with distance travelled. the pressure amplitude is positive than it is in the regions where
This process is known as absorption. The higher the ultrasound the pressure is negative. The speed is different in the regions expe-
frequency, the more rapidly is the amplitude reduced. Absorption riencing positive half-cycles than in negative half-cycles because the
rate also depends on the tissue involved. density of the medium changes with pressure. The effect is such
In addition to absorption, other effects contribute to the total that as the waveform passes through the tissue, the positive half-
attenuation of the wave amplitude. These effects are reflection, scattering cycles catch up on the negative half-cycles resulting in distortion of
11
CHAPTER 1 Basic physics of medical ultrasound
2 cm
Transducer
4 cm
the waveform (Fig. 1.16). The greater the path travelled by the
wave, the greater the distortion. The wave may become consider-
ably distorted and have sharp discontinuities in its shape. The sinu-
soidal shape seen close to the transducer has then been replaced by
a more saw-toothed shape, and the positive half-cycles can become
particularly spiked.
The amount of non-linear distortion that occurs depends on the Field focus Shear wave
nature of the propagating medium as well as the wave parameters
such as frequency and pressure amplitude. The amount of non- Figure 1.17 The generation of shear waves by the force at the
linear distortion is related to the molecular and structural proper- focus of an ultrasound beam.
ties of the medium in a complex way. However, the phenomenon
has been very successively exploited without the requirement to
consider the differences between tissues. It is employed to produce
narrower ultrasound beams rather than to provide information on
the tissues through which the ultrasound passes. of sound, attenuation coefficient and scattering coefficient. Charac-
Non-linear distortion is significant in the ultrasound methods terisation of tissue is often made difficult by the degradation of the
used in medicine and has been exploited to improve images. The ultrasound beam by fat and muscle between the transducer and the
distortion is generated where the pressure is high, i.e. along the site of interest. Invasive imaging reduces this problem, for example
central axis of the ultrasound beam. Distortion is less in the weaker by the use of catheter-based scanners to characterise blood vessel
fringes or side-lobes of the beam, i.e. away from the central axis. By walls which are examined with a short beam path through blood.
only using echoes produced by the non-linear transmitted pulse The problems are also reduced if there is a well-specified path
near the central axis, the scanning beam is effectively narrowed. It between the transducer and the tissue of interest, e.g. through the
is possible to filter out these echoes since their shock-wave shape eye to the retina or through a water-bath to skin lesions.
means that they contain a range of harmonic frequencies over and There is substantial development at the moment in the measure-
above those in the original transmitted pulse. It has been noted in ment of tissue elasticity by ultrasonic means. When a tissue is com-
the section on Fourier components that the shorter and sharper the pressed by an external force, changes in its shape and size can be
shape, the bigger is the range of frequencies. These extra frequen- measured from the changes in position of the echo speckle pattern.
cies, which are generated as non-linear propagation distorts the From the size of the force and the tissue distortion, quantities can
pulse, are called harmonics. The technique utilising harmonics to be calculated that relate to the elasticity of the tissue. This is analo-
produce narrower beams is known as harmonic imaging. The nar- gous to palpation though the aim is to develop techniques that are
rower beam improves the lateral resolution in the image. Harmonic more quantitative and can be applied to tissues deep within the
imaging is very extensively used, indeed it is often the default mode body. It is known that the hardness of a mass can often be related
which the machine is automatically programmed to activate when to its pathology. Several different methods may be employed to
first switched on. apply a force to tissue, ranging from simply pushing the scanning
transducer to using the beam radiation force to generate shear
waves which spread out around the focus of a normal ultrasound
beam. It was noted earlier that when the momentum of an ultra-
TISSUE CHARACTERISATION AND sound beam is interrupted by reflection or absorption at a target,
ELASTOGRAPHY the target experiences a radiation force. In the arrangement shown
in Figure 1.17, a target tissue at the focus of the beam will experience
When echo signals are collected there is often interest in saying a force impulse when subjected to an ultrasonic pulse. The resulting
more about the characteristics of the tissues that produced them. motion of the tissue produces a shear wave which travels sideways
The most obvious characterisation would be to distinguish benign from the direction of the ultrasound beam, not unlike the ripple on
from malignant, but other distinctions may be attempted such as a pond when a small pebble is dropped in. If several focal points
fatty from fibrotic liver or degree of calcification of arterial plaque. are targeted at successive depths by successive transmitted pulses,
Parameters related to the phenomena described in previous sec- the shear waves produced interfere with each other as they travel
tions may be measured to attempt tissue characterisation, e.g. speed sideways and produce two plane shear waves travelling in opposite
12
Doppler effect
B > f0
Attenuation, propagation and harmonics
Absorption occurs as ultrasound energy is converted into heat.
It is highly frequency and tissue dependent.
Attenuation is the reduction of beam intensity as it passes
through tissue. It is the total effect of absorption, scattering,
reflection, refraction and diffraction. It is highly frequency
dependent. To obtain adequate echo signals from deep in tissue, C < f0
the operator manipulates gain controls to compensate for
attenuation.
Non-linear propagation occurs as the wave pressure alters the
properties of the tissue as it passes through it. It distorts the
waveform which then contains additional frequency components
harmonics and subharmonics.
Non-linear propagation occurs most near the axis of the beam D > f0
where the wave amplitude is high relative to the sides of the
beam. By only detecting the harmonics the beam is effectively
made narrower, which gives better lateral resolution.
Harmonics and subharmonics frequencies are also generated
when ultrasound interacts with contrast microbubbles. Detection
of these frequencies is exploited in the location of the bubbles
in vivo.
Many operators use harmonic imaging as the method of choice.
Many attempts have been made to identify tissue types by E < f0
measuring the acoustic properties of the tissue, e.g. attenuation,
scattering and speed of sound. Some success has been
achieved where there is well-defined anatomy but difficulties often
arise where the ultrasound beam is distorted by overlying layers
of fat and muscle.
Present research into tissue characterisation seeks to develop
elastography. Figure 1.18 AE: The Doppler effect in different situations
relating to the relative motion of the source and observer.
13
CHAPTER 1 Basic physics of medical ultrasound
Transducer
Receiver Velocity component
in beam direction
Transmitter
v1 = v cos v1 = v cos
Skin surface
v1 v
v1
v (Blood velocity)
(Flow in vessel)
V A B
Doppler techniques
The Doppler effect is a very sensitive and accurate detector of
motion. It is mostly used to study blood flow but it can also be
Figure 1.19 Examination of a blood vessel with a continuous
employed to measure tissue motion.
wave Doppler transducer.
Users of Doppler techniques should be aware of the large effect
of beam/motion angle on the velocity measurement.
Most Doppler devices measure the velocity component along the
ultrasound beam axis.
In medical ultrasound, a beam from an effectively static trans-
Processes such as absorption, attenuation, scattering, refraction
ducer is scattered back from tissues to produce echo signals (Fig.
and non-linear propagation discussed for pulse-echo imaging
1.19). The process of sending echoes back to the transducer is often
also apply to Doppler methods.
called backscatter. Weak signals from blood are detected in this
Doppler images and spectrograms are produced in real-time,
way and since the blood is moving the ultrasound has experienced
making them very useful for the study of physiological function.
a Doppler shift. In this situation if cells are moving towards the
transducer, the total Doppler effect is produced by the cells moving
through the waves plus the cells moving after the reflected ultra-
sound and hence compressing the echo signals. Motion of the cells
towards the transducer produces an increase in ultrasound fre- It is instructive to consider some numerical evaluations of this
quency due to this double Doppler effect. Likewise, a reduction in formula for values encountered in medical ultrasound. For example,
frequency is produced by cells moving away from the transducer. if v = 20cm/s, c = 154000cm/s, = 0 (cos = 1), ft = 2 106Hz,
If the direction of the beam is at an angle to the direction of then the Doppler shift equals 519Hz.
motion, it is the velocity component along the beam axis (v1) that is If the machine measures the Doppler shift and the beam angle,
the relevant velocity when the Doppler effect is considered (Fig. the velocity can be calculated and presented automatically on the
1.20A). Very often a simplified picture of blood flow is assumed in screen. The Doppler shift is seen to be small, around one part in
which the direction of flow is parallel to the walls of the blood 1000, but electronics can measure it. The Doppler shift frequencies
vessel (Fig. 1.20B). This enables the beam/flow angle to be meas- are also in the audible range, which means they can easily be
ured from an ultrasound image and hence the velocity to be calcu- studied simply by listening with earphones as well as using the
lated from the Doppler shift frequency. spectral Doppler feature of machines.
A simple but useful Doppler equation links the Doppler shift, the It will be seen in Chapter 3 that the Doppler effect is exploited in
transmitted frequency, the velocity and the angle between direc- various ways to present information on blood flow and tissue
tions of sound propagation and motion: motion. A spectrum of velocities from a sample volume at a site of
fd = 2vft cos c or v = fdc 2ft cos
interest or colour images of velocities can be produced. Doppler
methods probably provide the greatest amount of velocity informa-
where fd is the Doppler shift, ft is the transmitted frequency, v is the tion among all blood flow detection techniques.
velocity, is the angle and c is the speed of ultrasound.
So far we have discussed blood cells moving with the same veloc-
ity giving rise to one Doppler shift frequency. Obviously in blood
flow there can be many moving groups of cells with different veloc- RESOLUTION
ities in a limited region in the beam. The limited region, which
might typically be a few millimetres in diameter, is called the The detail that can be observed in ultrasound images or traces
sample volume. Each group of cells gives rise to an echo signal with depends on the smallest change that can be presented by the ultra-
a particular Doppler shift and all of these signals combine to sound systems. The detail in a particular presentation usually is
produce a complex Doppler signal from the blood. This complex said to depend on one or more resolution. These resolutions depend
signal can be analysed into a spectrum of frequencies by Fourier on the shape of the ultrasound beam, the ultrasound pulse shape
techniques. The frequency components in the spectrum can then be and the way they are transmitted. They are now listed since they
converted to velocities in the blood using the Doppler equation. apply to techniques described in later chapters.
14
References
15
CHAPTER
DOPPLER ULTRASOUND 26
Continuous wave Doppler (CW) 26
Pulsed wave Doppler (PW) 26
High pass filtering 28
Aliasing 28
Doppler frequency estimation and display 28
Colour flow imaging 28
Limitations of colour flow imaging 29
Power Doppler 30
INTRODUCTION
The clinical use of ultrasound is an interactive process, which
requires the user to manipulate the ultrasound transducer in contact
with the patients skin surface, while viewing and interpreting the
image in real-time. Before the examination, the user must select the
transducer, operating mode and system settings most relevant to
the investigation and thereafter make regular adjustments to the
system controls to optimise the diagnostic quality of the image. To
make informed choices of system components and settings, it is
essential to have an understanding of their function and how
making changes is likely to affect the resulting image. This chapter
describes the main components of the ultrasound imaging system
and explains how they operate to produce ultrasound images and
other useful diagnostic information. The aim of the chapter is to
provide a basic understanding of system function, which will help
users to produce optimum quality diagnostic information when
scanning. The intention is that these explanations should be acces-
sible to all without any detailed knowledge of physics or Figure 2.1 An ultrasound imaging system in use. (Courtesy of
technology. Siemens Healthcare.)
16
Principles of B-mode image formation
A The transmit pulse travels along the ultrasound beam into tissues.
Echoes generated at interfaces return to the transducer
Organ boundary Gas echo Transducer Transmit Returning
pulse echo
Tissue echoes
Cystic area
Depth
Received
echo signal
0 Time
B The time of arrival of echoes after transmission increases
with the depth of the reflector
Figure 2.2 A B-mode image using a curvilinear array Linear array transducer
transducer.
Backing layer
A Electrodes
ultrasound images are displayed as they are formed, resulting in a
real-time display of moving images.
Focal length F
The finite travel time of the ultrasound pulses and echoes to and
from the reflecting target results in a fundamental limitation of
ultrasound imaging systems. The time to form each image line is Focal region
the go and return time to the maximum depth. Large imaging
depths result in long line times. When coupled with a large number
B Transducer Acoustic lens
of image lines, this leads to a long frame time and low image repeat
rate or frame rate. If a high frame rate is needed to image a rapidly Figure 2.5 Transducer construction. A: A cross-section through
moving target, e.g. the heart, it may be necessary to restrict the an ultrasound transducer. B: The beam can be focused by adding
imaged depth and/or the width of the image. an acoustic lens to the transducer face, resulting in a narrower
beam in the focal region.
Figure 2.6 Common types of array transducer shape and image format.
B
A
19
CHAPTER 2 Basic equipment, components and image production
adjacent positions within the tissues, as described earlier. For most As the array elements are less than a wavelength wide, when
applications, this movement is achieved electronically using a excited by the electrical pulse waveform, they produce a wave that
transducer, which has an array of elements (typically 128 or 256). is roughly circular in shape (in the image plane). If the electrical
Array transducers are available in a variety of shapes, giving a pulse is applied to all elements simultaneously, as illustrated in
choice of image formats for different applications. Figure 2.6 shows Figure 2.9A, the circular waves merge to form a flat wavefront and
a range of common types of array transducers for transcutaneous a collimated beam in the straight ahead direction. If element 1 is
imaging. Sector transducers are used where access to the target fired first, followed after a very short delay by element 2, then
tissues is through a narrow acoustic window, e.g. approaching the element 3 and so on, by the time the last element is fired, the circular
heart through an intercostal space between the ribs. Linear and waves from the others have travelled various distances into the
curved array transducers are used where a wide anterior field of tissue and they merge to form a wavefront that propagates at an
view is needed and access is not limited by regions of bone or gas, angle to the straight ahead direction (Fig. 2.9B).
e.g. in the upper abdomen, neck or peripheral vasculature. Endo- When the echoes are received, similar delays are applied before
cavity transducers use small transducer arrays mounted on a suit- they are added together. By steadily increasing the delay between
able stem for insertion into body cavities as shown in Figure 2.7. elements on each successive pulse-echo cycle, the beam is steered
These can bring the transducer into closer proximity to the target, further away from the straight ahead position. Angles of up to 45
allowing the use of higher frequencies and avoiding intervening can be achieved by this technique.
obstructions such as gas or bone.
All array transducers make use of one or both of two methods to
scan the beam through the tissues. The beam can be electronically Other beam steering applications
stepped to different positions along the array or steered in different
directions. Beam steering is used with some linear arrays to form a trapezoidal
field of view (Fig. 2.6). Here, a half sector is added to each side of
The stepped array the normal rectangular field of view using beam steering with a
group of elements at each end of the array.
Beam steering is used by some manufacturers with linear array
Figure 2.8 illustrates the stepped array principle for a linear array
transducers to generate images of a target from a number of differ-
transducer. As explained in Chapter 1, in order to produce a rela-
ent directions. The direction of the beams from the linear array may
tively parallel-sided ultrasound beam, the active transducer width
be steered in up to nine different directions on successive image
or aperture must be at least 10 times the wavelength of the ultra-
frames, giving a so-called compound image. This technique helps
sound wave. As each element in a typical array is only about 1
to give more complete images of curved organ or lesion boundaries
wavelength wide, the electrical pulse waveform is applied simulta-
and helps to average out image speckle. However, the frame rate
neously to a group of say 10 adjacent elements, e.g. elements 110.
is reduced, as each complete compound image takes longer to form.
The echo signals received back at these elements can be added
Beam steering is used with pulsed Doppler systems (see Doppler
together also to form the first B-mode line. When this first pulse-
ultrasound section, below) to improve the angle at which the
echo cycle is complete, the beam position is stepped along the array
Doppler beam interrogates vessels that lie parallel to the skin
by applying the pulse to elements 211 and adding the returned
surface.
echoes from these. By continuing this process, the beam can be
stepped along the whole array to form a large number of closely
spaced B-mode lines.
The stepped array process is used with linear array transducers
and with curved array transducers, which are simply an array
of elements mounted onto a curved surface to give a curved field
of view. Flat wavefront
Transmit in straight ahead
The steered array pulse direction
Time delays
Matching layer Acoustic lens
Line 1
Wave travels at an
Line 2 angle to the straight
Transmit ahead direction
pulse
Line 3
Transducer element array
Active aperture
Array elements Curved wave from first element
A Cut-away of a linear array transducer, B The active aperture is stepped
showing array elements, matching along the array on each B If each element is fired in turn after a short delay, a wave is formed
layer and cylindrical lens pulseecho cycle which propagates at an angle to the straight ahead direction
Figure 2.8 The linear, stepped array transducer. Figure 2.9 The steered array principle.
20
Transducers and beam forming
Time delays
Transmit Focus
pulse
Focal depth F
A Transmit focus: if the outer elements are fired first with increasing delays a a
towards the central elements, a converging wavefront is formed which F
produces a focused transmit beam F
Time delays
Focal points on image line A The ratio of aperture a to focal depth B A higher ratio of aperture a to
F is restricted for sector transducers focal depth F can be maintained
Receive leading to weak focusing in linear arrays by increasing the
signal active aperture at larger depths
Current receive focus
Figure 2.11 Aperture control and focusing.
Array elements
of the transducer and so focusing is less effective at large depths,
B Receive focus: in reception, delays are applied to the signals received at leading to poorer resolution in these regions of the image.
each element before they are added together. The delays are calculated
for each target depth so that the receive focus tracks the current receive
depth, producing a much narrower receive beam
The beam former
Figure 2.10 Electronic focusing. In modern ultrasound systems, the beam manipulation techniques
described above are all implemented using digital techniques in a
component of the ultrasound system known as the beam former.1
The beam former is programmed to activate a chosen group of ele-
ments to transmit a focused pulse. Echo signals are then received
Electronic focusing by the elements within the active aperture. These are converted into
digital format and stored temporarily as a data series for each
Focusing of the beam in the scan plane can be achieved in both element. The beam former then uses the stored element data to
stepped and steered arrays by controlling the timing of signals to create B-mode lines by applying the techniques described above.
and from the active elements. In Figure 2.10A, the outer elements By using more than one beam former, the same stored element
of the active area are fired first, followed after small delays by signals can be used to form several adjacent B-mode lines at the
consecutive element pairs towards the centre. The circular waves same time, reducing the time needed to form each image.
from the individual elements add together to form a concave wave-
front, which converges to a focus, reducing the width of the beam. Elevation focusing
Increasing the delay time between elements reduces the distance of
the focus from the transducer.
While electronic focusing techniques can be used to produce a beam
The transmitted pulse is normally focused to a depth chosen by
that is very narrow in the direction along the scan plane, focusing
the user via the machine console and has a single value for each
at right angles to the scan plane, the slice thickness direction, often
transmission. In reception, as the depth from which echoes are
relies simply on a fixed acoustic lens as shown in Figure 2.12A. This
being received is known from the time after transmission, dynamic
fixed and relatively weak focusing results in a slice thickness that
control of the echo delays is applied so that the receive focus effec-
is much greater than the in-plane beam width. A large slice thick-
tively tracks the echo source. Focusing is applied for each point
ness can result in poor visualisation of small cysts and blood vessels.
along the line by calculating the travel time to each receive element
Slice thickness can be reduced near to the transducer by the use of
and then aligning the received signals in time before adding them
arrays containing several parallel rows of elements rather than just
together. The resulting receive beam is much narrower than the
one. These are referred to as 1.25D, 1.5D, 1.75D, 2D multi-row or
transmit beam (Fig. 2.10B).
matrix transducers according to the level of technology employed
(and manufacturer terminology). In a 1.25D array, the multiple
Aperture control rows are used simply to give aperture control, reducing the number
of rows used for superficial targets (Fig. 2.12B). The 1.5D array also
employs electronically controlled focusing in elevation but the rows
Focusing is most effective when the aperture width, i.e. the active
are paired to give symmetric delays. The 1.75D array has independ-
length of the transducer, is similar to the focal depth. If the focal
ent control of delays to each row.
depth is much greater than the aperture width, then the focusing
effect is weak. As the depth of the focus is increased by the user,
the active aperture width would normally be increased to maintain 3/4D transducers
effective focusing. For linear array transducers, the aperture can be
increased potentially to the full length of the array, maintaining an The beam manipulation techniques described so far result in a real-
effective focus to large depths (Fig. 2.11). For curved arrays and time, cross-sectional image, which allows the anatomy to be exam-
phased arrays, the maximum aperture is restricted by the geometry ined, slice by slice, as the transducer is moved by the operator. The
21
CHAPTER 2 Basic equipment, components and image production
3D transducer is used to acquire image data from a 3D volume of The alternative type of transducer that can be used for 3D acquisi-
tissue. Here, the transducer is held in a fixed position by the opera- tion is the square array transducer, which uses a square matrix of
tor as the image plane is swept sideways automatically through the transducer elements, e.g. 128128 (Fig. 2.13B). This type of trans-
target volume and a set of 2D images stored. ducer can be used in phased array mode to produce a sector image
Two types of transducer designs are available to carry out 3D in one plane as described earlier. Using beam steering in the orthog-
volume acquisitions. The most common type contains a curvilinear onal plane, the sector image can then be swept sideways on each
array mounted on a swivel within a small water bath in the trans- successive frame to interrogate a pyramid-shaped 3D volume of
ducer head (Fig. 2.13A). To acquire a 3D volume, the array is tissue.
rotated slowly by an electric motor, sweeping the image plane Both types of transducer can be used to produce continuously
sideways through the tissues. The orientation of the scan plane is updated volume data sets by repeating the volume acquisition
measured by an angle sensor coupled to the motor. The operator process. The repeat rate of the resulting 4D images may be quite
holds the transducer assembly steady as a set of 2D curvilinear low due to the time required to form a set of 2D images. By restrict-
images is acquired. ing the depth of the images and the angle of the acquired pyramid
of data, image update rates of up to 30 per second can be achieved
using a square array transducer.
Perhaps the most widely useful application of 3D transducers is
in the acquisition of a single volume data set from the target tissues
in the form of multiple adjacent planes. If the 3D volume data set
is stored, it can be interrogated and displayed in several ways. The
set of 2D views of the original scan plane being swept through the
tissues can be reviewed. Similar views can be displayed of a set of
sections orthogonal to the original 2D plane. 2D images can also be
created at a range of depths in a plane parallel to the transducer
face (C-scan). This plane is one that is not normally accessible with
a standard 2D transducer. The 3D data set can also be processed
for display in various viewing modes including see through
view and surface rendering, where a 3D surface corresponding to
the skin surface, for example, is segmented from the data and
displayed.2 Surface rendering is most effective where the surface of
interest is adjacent to a region of fluid (e.g. in obstetrics), so that the
surface echo can be detected automatically by the system
processor.
Image plane
swept sideways
through tissues
Acoustic window
Coupling fluid
Array
Gear
Motor
Position
sensing device
Cables
Housing
A A 3D volume can be imaged using a 2D curvilinear B The square array transducer has a square matrix
transducer which is rotated by an electric motor of elements, which can steer the beam to image
a pyramidal volume
B-mode system
Transmit beam former processor
Receive/
digitise
Channel
Post-processing
memory
Receive beam
Cine memory
former
Display
Echo signal
Image formation
processing
Transducer
Echo size
Echo size
Time/depth Time/depth
A Echo signals received at the transducer B TGC is used to compensate for attenuation C The user can adjust the TGC
become weaker with increasing so that echoes from similar targets are the via slide controls on the
depth/time of arrival due to attenuation same size regardless of target depth console
0 dB Tissuegas interface
-20 dB
Large tissuetissue
-40 dB interfaces
Echo size
Echo size
-60 dB
Tissue scattering
-80 dB
-100 dB Blood
Time/depth Time/depth
A Echo sizes from different target types. B Echo signals before compression C Echo signals after compression
A 60 dB range of echo strengths must
be displayed to include tissue interfaces
and scattering
Harmonic imaging
2f0 Frequency
The processing described so far has assumed that the transmitted Clutter can be suppressed by removing
pulse consists of a few cycles of the chosen transmit frequency, e.g. the fundamental frequencies and forming
5MHz, and that the returned echoes are simply miniature versions the image from the first harmonic
of the same thing. However, at the relatively high pulse amplitudes Figure 2.17 Harmonic imaging.
transmitted by modern ultrasound imaging systems, propagation
through soft tissues is non-linear and the transmitted pulse becomes When an image is formed from the original fundamental fre-
distorted as it travels into the tissue. The effect is strongest in the quency that was transmitted, it may contain clutter due to weak
centre of the ultrasound beam where the amplitude is highest. echoes from beam side lobes or multiple reflections (reverberation)
Distortion of the waveform is associated with the generation of of the pulse between strongly reflecting features (Fig. 2.17). As
harmonics or multiples of the original fundamental frequency that harmonic generation is only significant where the pulse amplitude
was transmitted. is high, the clutter can be reduced by removing the fundamental
24
Image processing
Coded pulse
Echo amplitude
waveform
RF signal
1 1 0 1
Phase
Time
A Undemodulated RF echo signal B Demodulated echo signal
Figure 2.18 Pulse coding. The phase of the elongated transmit Figure 2.19 Demodulation.
pulse is alternated according to a chosen digital code. The same
code is embedded in a digital filter applied to returned echoes to
pinpoint their time of arrival.
B-mode instrumentation and processing
Time gain compensation (TGC) is used to compensate for
frequency from the returned echoes and forming an image from the increasing attenuation of echoes with depth.
harmonic frequency. This is known as harmonic imaging.4 As The dynamic range of echoes must be compressed to display
the energy at the harmonic frequency is always less than that at the reflected and scattered echoes simultaneously.
fundamental, the system penetration may be reduced to some Harmonic imaging may be used to reduce reverberations and
extent when operating in harmonic mode. clutter in the image.
To form a harmonic image, the transducer must be able to trans- Pulse coding may be used to increase penetration for a given
mit the fundamental frequency, but also receive the second har- frequency.
monic (twice the fundamental). Hence a transducer with a wide Echoes must be demodulated to remove the transmit frequency
frequency response is required. The harmonic image can be formed before image formation.
by applying a frequency-selective filter to the returned echoes, Post-processing is applied as the image is read out from the
which rejects the fundamental frequency but allows through the image memory.
harmonic frequency.5
Harmonic images can also be produced using a method called
pulse inversion. In this method, two pulse-echo cycles are used to
form each B-mode line. In the first cycle, a short imaging pulse is
transmitted and echoes received as normal and stored. Then a its harmonics. This is referred to as the radio-frequency or RF signal.
second pulse, which is an inverted version of the first, is transmitted The brightness value that is displayed at each point in the image is
along the same path and echoes received. The second line of echoes related to the amplitude or envelope of the RF signal. The final
is subtracted from the first. In low amplitude parts of the beam, processing step in forming the B-mode image is to remove the
where there is little distortion of the transmitted pulse, the lines of radio-frequency element of the signal to leave the envelope signal.
echoes cancel out. In the high-amplitude regions, the lines of echoes This process is referred to as demodulation (Fig. 2.19).
generated from the distorted normal and inverted pulses contain
energy at the fundamental and second harmonic frequencies. The Image memory
fundamental parts cancel out leaving the second harmonic parts to
form the image.
Following the various processing steps described above, the B-mode
lines are written into the image memory to form the image as an
Pulse coding array of pixels similar to an image in a digital camera. The dimen-
sions of the image in the memory array are typically 1200 1200
The maximum depth from which echoes can be received is deter- pixels, with each pixel capable of storing up to 256 different grey
mined by the attenuation of the pulse and returning echoes by the levels (8 bits). As for a digital camera, the system is capable of
tissues they pass through. Higher frequencies give improved image storing many images (over 2000 for some models) and successive
resolution but suffer more rapid attenuation and hence reduced frames are stored in a cine memory until the memory is full. The
penetration of tissues. For a given frequency, penetration can be first image stored is then overwritten so that the last frames are
improved by using a longer transmitted pulse, making its echoes always stored. The chosen image is read out from the image
easier to detect. However, the increased pulse length degrades memory in a raster pattern which is synchronised to that of the
the axial resolution of the system. Pulse coding techniques allow display monitor.
the use of long transmit pulses while maintaining good axial The image can be written to the image memory and read out in
resolution.6 a number of different ways. If the image memory is being con-
The long transmit pulse is divided into time segments in which stantly updated with new images and the last image to be formed
the phase of the wave is alternated according to a predetermined is always read out to the display, a real-time, moving image is
code (Fig. 2.18). When the echoes are received, they are passed displayed. In freeze mode, new images are not written into the
through a digital filter which is programmed to search for the code. memory and the last image stored is read out repeatedly to the
When a match is detected, the time at which it occurs gives the display monitor. In cine loop mode, the writing process is again
effective time of arrival of the echo, restoring the axial resolution. frozen but the whole sequence of stored images is read out in a
Pulse coding allows greater penetration to be achieved at higher repeated cycle showing the last 30 seconds or so of the real-time
frequencies. image.
Receiver fT
amplifier fR
Doppler shift fD
A frequency fD B
Figure 2.22 Continuous wave Doppler. A: System block diagram. B: The demodulation process.
Transmit
Gate frequency Delay
Sample
fT
volume
Blood vessel
Low pass filter
Receiver Mixer
(fT + fR) Sample Angle cursor
amplifier fR (fT fR)
(fT fR)
Low pass
filter
Transducer
Sample volume
Doppler shift
frequency fD Figure 2.24 The pulsed Doppler sample volume and angle
cursor are adjusted by the operator to align with the vessel of
Figure 2.23 A pulsed wave Doppler system block diagram. interest.
PRF, pulse repetition frequency.
of the pulse is then received from increasing depths, following each of a cursor in the centre of the sample volume to indicate the direc-
transmission. The returned signals are processed as for CW Doppler tion of blood flow to the system.
to extract the Doppler shift frequencies. Doppler signals from a The process for extracting the Doppler shift frequency is similar
specified blood vessel are then isolated for further processing by in principle to that used for CW Doppler. However, the received
the use of a time gate, which allows through only those signals signal now consists of one brief sample of the Doppler frequency
corresponding to the depth of interest (Fig. 2.23). The position of from the depth corresponding to the target vessel, for each trans-
the time gate (the sample volume) is indicated on the B-mode image mitted pulse (Fig. 2.25). These can be thought of as a set of samples
by cursors (Fig. 2.24). The user adjusts the position of the Doppler of the equivalent CW Doppler shift frequency. The value of each
beam and the depth (or range) of the sample volume along it, so sample is determined by the phase relationship between the cor-
that the sample volume is located over the vessel of interest. As this responding fR sample and the reference transmit frequency fT. The
is a pulse-echo technique, the same transducer or active aperture continuous Doppler shift frequency signal is constructed from the
can be used to transmit and receive. The user also adjusts the angle samples by low pass filtering.7
27
CHAPTER 2 Basic equipment, components and image production
Aliasing
The sampled nature of the reconstructed pulsed Doppler signal
The pulsed Doppler gating process gives a sample leads to a major limitation of pulsed Doppler systems at high blood
of the Doppler shift frequency for each pulse echo cycle flow velocities. Each transmitted pulse leads to one sample of the
Doppler shift signal. Hence the number of samples produced per
second, the sample rate, is the same as the number of Doppler
pulses transmitted per second, the pulse repetition frequency (PRF).
To reconstruct a sine wave of a given frequency, it is necessary to
have at least two samples for each cycle of the wave, i.e. the PRF
must be at least 2fD. If the Doppler frequency for flow towards the
transducer (forward flow) increases to the point where the PRF is
The Doppler frequency is reconstructed
by further smoothing and filtering
too low, it will appear instead as an aliased, reverse flow frequency,
shifted downwards by an amount equal to the PRF.
Figure 2.25 Pulsed Doppler demodulation. Aliasing is most likely to be a problem when the Doppler shift
frequency is high (high blood flow rates and high transmit fre-
quency) and the PRF is low (due to large target depth).
A PRF
clock
Velocity
Transmit
Gate frequency
fT
Receiver Mixer
amplifier fR (fT fR)
B Mean
frequency
Image
Autocorrelator Variance Display
Power memory
Time along the line. To remove the large echoes from stationary and
slowly moving tissues, a technique called delay line cancellation is
then used rather than filtering. Each line of echoes in the ensemble
10 ms is stored digitally and compared with the next one by subtracting
intervals one from the other. This removes echoes from stationary targets,
Figure 2.27 A: A sonogram from the carotid artery. B: To which do not change, while preserving signals from those that are
construct the sonogram, the velocity distributions in consecutive moving, as they do not cancel out. Modern systems use more elabo-
10 or 20ms samples are displayed as adjacent vertical lines. rate versions of this technique to give enhanced separation of sta-
The amount of blood flowing at each velocity is represented on tionary echoes.
a greyscale. Estimation of the Doppler shift frequency is most commonly
carried out by a technique called autocorrelation.7 In essence, each
line of Doppler signals generated by each pulse-echo cycle in the
ensemble is compared with the one before it. The rate at which
the phase of the signal, at each point along the line, changes in the
interval between one line in the ensemble and the next leads to an
distribution within a stationary sample volume placed within a
estimate of the Doppler frequency at that point in the line. By
blood vessel. Colour flow imaging systems give a real-time 2D
extending this process over the ensemble of pulses, an estimate of
image of blood flow patterns in blood vessels as a colour overlay
the mean frequency is obtained for each point along the line. Mean
on a B-mode image. Here the colour of the display, at each point in
frequency is represented in the image on a colour scale, commonly
the image, represents the mean blood flow velocity at a given time.
using red for flow towards the transducer and blue for flow away
Colour flow imaging systems can be seen as an extension of the
(Fig. 2.29). Low frequencies are displayed as dark shades of red or
time gating approach from a single sample volume to multiple
blue leading, with increasing frequency, to lighter shades through
adjacent sample volumes along the Doppler beam. The beam is also
to white. The display normally includes a colour wedge showing
swept through the region of interest as in B-mode image formation,
the range of available shades of red and blue next to a correspond-
to form a 2D colour map. However, the time restrictions imposed
ing velocity scale. The velocity scale indicates the component of
by real-time 2D image formation require different techniques to be
blood flow velocity in the direction of the Doppler beam (i.e. not
used for removal of stationary tissue echoes and for Doppler fre-
corrected for Doppler angle).
quency estimation. Whereas frequency analysis in the sonogram is
The autocorrelator can also give an estimate of the variability of
performed on a 10 or 20ms sample of the Doppler signal, each line
the Doppler frequency during the ensemble for each point along
in the colour flow map must be formed in about 1ms to allow real-
the line. This is expressed in terms of the variance of the signal and
time display.
is used to display an alternative form of colour map which can
For each line in the colour flow image, the beam is held in the
indicate the degree of disturbance in the blood flow in the vessel.
same position for a number of pulse-echo cycles (typically eight).
The number of pulses transmitted in this sequence is referred to as
the ensemble length. As illustrated in Figure 2.28, the received Limitations of colour flow imaging
echoes are mixed with the transmit frequency and filtered to extract
the Doppler shift frequency as for CW and pulsed Doppler systems. As the mean frequency values displayed in each line of the colour
No gating is applied as Doppler signals are required from all depths flow image are estimated from the set of samples obtained from
29
CHAPTER 2 Basic equipment, components and image production
30
CHAPTER
3
Practical ultrasound using
scanners and optimising
ultrasound images
Colin R. Deane
1 Presets 1 Presets 1
5
Gain 2 Gain 2
TGC/DGC 3 TGC/DGC 3
1
Depth 4 Depth 4
5 6
Frequency/ 5 Frequency/ 5
4 patient type 5 patient type
3 4
2 Focus 6 3 6 Zoom 6
9 8 7
Zoom 7 7 Freeze 7
8
Freeze 8 Callipers 8
2
A Callipers 9
Figure 3.1 A and B: Control panels for two ultrasound scanners. Although there are a large number of keys and controls knobs, it is
essential to know the location and function of a few important controls before starting to scan. The main controls for B-mode imaging are
shown for these two scanners. TGC/DGC, time gain compensation/depth gain compensation.
What follows is a description of the main factors for B-mode, Colour flow imaging (CFI) and power
colour flow imaging and pulsed wave spectral Doppler. Some of
the minor controls and their effects will be discussed, but it is pos-
Doppler imaging
sible that particular controls, perhaps used by individual manufac-
turers, will not be covered.
n Power
A fairly full list of controls and a brief description of their
n Gain
n Scale
function is given in the summary boxes which follow later in the
n Colour scale invert (not applicable to all power Doppler
chapter, for B-mode, colour flow imaging and spectral Doppler.
The lists are not comprehensive but an experienced practitioner systems)
should know why they might need to be altered and how to achieve
n Focus (if the system has this)
this. For this chapter, the main controls chosen are those that it
n Frequency/patient type
n Area selected for CFI
is important to use in everyday scanning. It is also a guide for those
n For linear arrays beam steering.
using an unfamiliar scanner for the first time. The following is a list
of essential controls necessary for an operator to manipulate to Combination controls may be available that select several param-
achieve the optimum performance from the scanner. eters to optimise settings for particular applications (e.g. slow flow,
fast flow).
General controls and keys
Pulsed wave spectral Doppler (PW)
n Change/choose/switch the transducer
n Enter patient data n Power
n Application selection (for example abdominal/thyroid/leg n Gain
veins/first trimester) n Scale
n Freeze the image n Baseline
n Store images n Invert
n Review images. n For linear arrays beam steering
n Angle correction
B-mode n Sample volume/gate size
n Measurements.
n Frequency/patient or exam type
Power
TRANSDUCERS
n
n Gain
n TGC
n Dynamic range There are a wide range of transducers available for most scanners.
n Depth When choosing a transducer, the main considerations are:
n Focus (if the system has this) n transducer type, e.g. curvilinear/phased/linear array,
n Harmonics endocavity
n Zoom function n the frequency range
n Compounding/adaptive processing (if the system has this) n the size of the array: for example small linear array for
n Measurements (callipers). paediatric and perioperative work
32
Application set-ups
n additional features, for example matrix arrays for dynamic provide a uniform image of tissue that is static. Such a setting
focusing in the slice thickness/elevation plane. would be less than optimum for the carotid artery next to it, where
In recent years large frequency ranges have been quoted for some frame averaging and the slow frame rate resulting from multiple
transducers and it is tempting to believe that a single transducer transmit pulses leads to blurring of the pulsatile wall. Applications
will have good performance over a wide range of depths. Transduc- keys set a large number of parameters for B-mode, colour flow and
ers are limited by physical constraints, in particular for focusing in spectral Doppler to produce images appropriate for the particular
the elevation plane. For example, a linear array optimised for super- application. As a first step they are useful; in most systems, users
ficial work will tend to have a narrower width in the elevation plane can modify these to produce their own preferred image appearance.
for more precise beam control in the near field. A linear array suit- The difference can be marked, as shown in Figure 3.3 where the
able for investigation of deep vein thrombosis will have to have aorta is shown with an abdominal setting and abdominal vascular
good performance from 1.5 to 5cm depth; the width of the elements setting.
in the elevation plane is greater allowing better control of focusing
here through a larger aperture but with reduced precision in the Patient type/frequency
near field. Much depends on the standard of investigation required,
but for optimum performance, a range of transducers is required. In some systems, further modifications can be made by altering a
Figure 3.2 shows the range of transducers for one scanner for patient type or similar control. In one system, the type is easy,
work in our vascular laboratory. In particular, we find it useful to medium or difficult, in another the terms resolution or penetration
have low-frequency curvilinear and phased arrays for abdominal are used. For difficult patients, a lower frequency or harmonics are
vascular work. While the small aperture of the phased array leads used but other parameters are also altered. This is also a useful first
to B-mode images that have poorer spatial resolution than the cur- step to improving images but the consequences for measurements
vilinear array, the phased array has good colour sensitivity and is may be unpredictable. As an example, the use of a difficult setting
useful when overlying ribs restrict access of the curvilinear array. in the measurement of nuchal translucency may produce longer
echoes from interfaces and a slightly smaller measurement. In a
system where the frequency can be selected independently, the
reasons for this are obvious and measures can be undertaken to
APPLICATION SET-UPS standardise this. In controls and keys where manufacturers alter
several parameters to improve the appearance of the image, it may
Different applications require different scanning parameters. For not be obvious what the parameters are and how measurements or
example, imaging a thyroid setting may use a high degree of frame detectability are affected. As an example, images of a kidney with
averaging and multiple transmit focal zones to reduce speckle and resolution and penetration settings are shown in Figure 3.4.
A B
Figure 3.3 Longitudinal image of an aorta with an abdominal setting (A) and abdominal vascular setting (B). Many parameters
indicated in the yellow box are different, for example dynamic range, gain and persistence. The vascular setting has higher contrast as
a result.
A B
Figure 3.4 Longitudinal image of a kidney with a penetration setting (A) and resolution setting (B). Subtle differences in spatial
resolution, image smoothness and contrast at depths are evident. Several parameters are altered including the transmitted frequencies.
A B
Figure 3.5 Harmonic imaging of a kidney at full (A) and reduced (B) power. Thermal index (TI) and mechanical index (MI) are lower at
reduced power but in this example there is a general marked lowering of echo levels.
A B
Figure 3.6 Effect of increased gain in an image of a kidney. With the normal setting (A), a wide range of greyscales from black to
white are used. With increased gain (B), the image is brighter, more echo levels are depicted as white and contrast between adjacent
structures is reduced.
Time gain control/depth gain control as DGC (depth gain compensation) or TGC (time gain compensa-
tion) since echoes from deeper tissue take longer to return. This is
The scanner automatically compensates for attenuation as the trans- useful if there is abnormally low attenuation in the image, for
mitted and received pulses travel through the tissue. Echoes from example through fluid in ascites, the bladder, cysts or amniotic
deeper tissue are amplified on the assumption of a uniform attenu- fluid, or if there is high attenuation. In Figure 3.7 low attenuation
ation to provide uniform greyscales from similar tissue interfaces through a cyst in a thyroid causes tissue deep to the cyst to
at different depths. appear bright. By reducing gain at depth through the DGC/TGC,
The operator can usually modify this by manual control of the a more uniform image is obtained. The DGC/TGC settings
amount of amplification at different depths using a set of sliders can be displayed as a line which reflects the shape of the slider
or rotational controls (Fig. 3.1). This control is usually described controls.
35
CHAPTER 3 Practical ultrasound using scanners and optimising ultrasound images
Zoom
Depth
The zoom function is used to magnify a region of the image on the
It almost goes without saying that the depth and consequent screen. Depending on the way in which zoom is implemented,
field of view should be appropriate to the tissue under the image in this region may be improved as the scanner alters the
investigation. This is especially significant for ultrasound where scanning parameters in the selected area, for example increasing
increased image depth requires a longer time for echoes to be line density. In other implementations zoom is a simple magnifica-
received from deeper tissue. As a consequence frame rate may be tion of a portion of the scanned image in which case the resolution
reduced and image quality may deteriorate as compromises in line of the image will be similar to the original.
density, focusing and signal processing are made on the larger Zoom is useful if measurements are to be made of small distances
image. and areas since the precision may change to suit the change in scale
Using an inappropriately large depth is a common error for those of the image shown. Accurate location of the callipers may be
new to ultrasound imaging. Large depths have the advantage that enhanced (Fig. 3.12).
surrounding anatomy can be viewed and the effects of some arte- The zoom or res key/control is one for which manufacturers have
facts, notably speckle, may be less apparent, but the image of the used considerable imagination and originality. Both the area and
target is suboptimal (Fig. 3.10). size of the enlarged area can usually be adjusted prior to the zoom
A B
Figure 3.8 Image of a kidney transplant with low dynamic range (A) and high dynamic range (B). With a low dynamic range there
is increased contrast between the medulla/cortex and surrounding tissue but speckle is more obvious and detail in the cortex/medulla may
be lost.
36
B-mode parameters
A B
artefact from the near field, a theoretical tighter beam in the trans-
verse and elevation plane and an inherently reduced dynamic
range all combine to produce images that often demonstrate
improvements in resolution over fundamental images (Fig. 3.13).
The development of harmonics has continued since their intro-
duction in the mid 1990s. Originally thought to be mainly applica-
ble to low-frequency imaging for abdominal and cardiac
applications, harmonic imaging now finds itself the default appli
cation for many manufacturer presets including high-frequency
scanning for musculoskeletal applications. Since harmonics are
generated by passage of the ultrasound pulse through tissue, the
images that result appear to combine harmonics and non-harmonic
components. Harmonics are also used in conjunction with spatial
and frequency compounding (see below) and adaptive processing
(see below) so that there may be several combinations from these
three parameters alone.
Figure 3.10 Inappropriate depth setting. The deep image is Spatial and frequency compounding
redundant, no information is displayed and the kidney is not
displayed to best advantage. The frame rate also suffers because Several versions and implementations of compounding are mar-
of the need for long pulse-echo times. keted. One method of spatial compounding uses transmit beam
steering to produce echoes from several different transmit beam
angles. This has the effect of providing strong echoes from inter-
faces over a wider range of angles than in conventional imaging.
key being activated but there are a variety of means to do this and
The images from different transmit beam directions have variations
the user might like to try out the various permutations before they
in speckle distribution; compounding images averages this and
begin scanning clinically.
reduces its effect on the final image (Fig. 3.14). Spatial compounding
requires more time to complete a compounded image.
Harmonics Frequency compounding is offered in some scanners. The speckle
pattern in images is frequency dependent; by combining images
Native tissue harmonics are now commonplace in scanners from obtained from several transmitted frequencies, the effect of speckle
small portable devices to flagship models. The benefits of reduced is reduced.
37
CHAPTER 3 Practical ultrasound using scanners and optimising ultrasound images
A B
Figure 3.11 Influence of transmit focus. With the focus set for superficial tissue (A, arrow) the upper pole of the kidney is not displayed
as clearly as it is when the focal depth is set to the appropriate depth (B).
A B
Figure 3.12 Zoom function. In a measurement of intimamedia thickness, an area of the image is selected for investigation (A).
Scanning parameters are optimised for this area and the image allows more precise measurements (B).
A B
Figure 3.13 Longitudinal image of an aorta with fundamental (A) and harmonic (B) imaging. Reduced echo levels in the aorta
increases contrast in the harmonic image.
A B
C D
Figure 3.14 Longitudinal image of a kidney. The four images show a standard image (A), use of spatial compounding (B), use of
adaptive processing (C) and a combination of spatial compounding, adaptive processing and harmonics (D).
B-mode parameters
Power: Alters the output power. This is usually set to a maximum especially speckle are random and the effect of speckle is
but is reduced for specific applications, for example imaging reduced.
through the eye. Some scanners do not have a separate output Depth: Alters the depth of the image. Greater depths require more
control. time, resulting in a decreased frame rate.
Gain: Alters the amplification of the overall received signal. Zoom/Res: Magnifies an area of the image. The zoom can
Increasing gain boosts the signals and makes the overall image magnify an area of the scanned image or can be used to image a
brighter. reduced area.
Time gain control/depth gain control/swept gain: Alters the Adaptive processing: Many variations of these are marketed and
gain at a specific depth range. Compensates for variation in aim to reduce the effect of speckle and accentuate true differences
attenuation. in the acoustic properties within tissue.
Frequency/Patient type: Trades resolution for penetration. Temporal/spatial controls: The image may be optimised for high
Focus: Transmit focus improves lateral resolution and image temporal resolution, for example by using a lower line density and
quality at a specific depth. Multiple transmit focal zones may be reducing lateral resolution. High spatial resolution may be chosen
used which may reduce frame rate. at the expense of frame rate.
Dynamic range: Selects the range of echoes to display on Persistence/frame averaging: Successive frames may be
the greyscale. A low dynamic range produces high contrast in the combined to produce a smoother image with less speckle.
image. Moving structures may appear blurred. For fast moving structures,
Harmonics: Harmonic images have a lower dynamic range, are low persistence may be used.
less prone to artefacts, especially near-field artefacts. They tend to Edge enhancement: Large changes in amplitude may be
produce a higher contrast image. Axial and lateral resolution may accentuated to display shaper edges. This may aid calliper
be altered. placement but makes speckle appear more prominent.
Compounding: Many scanners now offer spatial or frequency Post-processing: Allocates a greyscale to the range of echoes.
compounding where images are reconstructed from several images Colour maps are possible but are not commonly used.
obtained with different beam steering or transmit frequencies. Measurements: Linear and area measurements may be made
Tissue structures are common to each individual image, artefacts from the frozen image.
39
CHAPTER 3 Practical ultrasound using scanners and optimising ultrasound images
designed to enhance the ultrasound signals from tissue features from moving tissue with colour bleeding into surrounding tissue
while reducing artefactual signals in the image, particularly those (Fig. 3.15). Inadequate gain leads to poor sensitivity to blood flow.
from speckle. Adaptive processing algorithms permit changes in The gain is usually set by the application key at a new patient
response to local changes in time and space and may be based on investigation but in some systems the gain last set is retained. The
the statistical analysis of signals. Manufacturers of commercial gain value can be expressed in decibels (dB) or as a percentage.
scanners use proprietary descriptive terms, for example Dynamic There is inconsistency between manufacturers as to the default set-
Tissue Contrast Enhancement TCE (Siemens), Delta function tings; in our own department one scanner has a default setting of
(Acuson), XRES (Philips), SRI Speckle Reduction Imaging (GE) 50%, another is optimised at between 60% and 75% and yet another
for their own implementation of processing. Different levels of has a value of 25 with no units listed.
processing may be offered. Images may appear smoother and detail
of tissue structure or texture may appear freer of speckle (Fig.
3.14C). The difference in algorithms between systems may lead to Scale/pulse repetition frequency (PRF)
differences in image appearance which may in turn be disconcert-
ing to those comparing clinical images. Perhaps the most important control for CFI is the scale setting.
Spatial compounding may be used in combination adaptive Changing the scale alters the rate at which pulses are transmitted,
processing and harmonic imaging (Fig. 3.14D). The utility of each the pulse repetition frequency (PRF). For slow flows, scale/PRF is
or in combination is the subject of objective study and subjective set low to detect the small movement between pulses. This can lead
preference. to problems of aliasing for high velocities since PRF may not be
sufficient for unambiguous measurement of the Doppler frequency.
For high velocities, a high scale uses high PRFs to depict the result-
ing Doppler shifts unambiguously although very high velocities
COLOUR FLOW IMAGING may lead to aliasing. The effect is shown in an image of arterial and
venous flow (Fig. 3.16). Scale settings are shown on the colour bar
All the following factors, with the exception of colour scale invert, in the image; the number at the extremity of the scale represents
also apply to power Doppler (also called energy Doppler/ampli-
tude Doppler).
Power
Colour flow imaging uses several pulses along each scan line to
obtain the information necessary to give a colour map of velocity
vectors. Blood is a weak scatterer and higher amplitude pulses with
a longer pulse length may be employed to provide adequate signals
for processing. As a consequence, outputs from colour flow imaging
are often higher than for B-mode. Where there are issues of safety,
particularly in first and second trimester scanning and imaging
through the eye, particular consideration should be given to output
limits and, in those scanners where output power is adjustable,
operators should be aware of its effect on image quality and indi-
cated output through the output display standards of MI and TI
(Chapter 4).
Gain
Figure 3.15 The colour flow gain is too high; there is
By increasing gain, the colour flow image is more sensitive to overwriting (bleeding) of colour flow signals extending beyond the
moving echoes. However, increasing gain may lead to artefacts vessel under examination.
A B
Figure 3.16 Images of a femoral artery and the confluence of the deep and superficial veins. With a high scale setting (A)
indicated by a scale of 24.1cm/s, flow in the artery is displayed but venous velocities are too low for the high pulse repetition frequency.
By lowering the scale to 9.6cm/s (B), flow in the veins is now displayed. There is aliasing in the artery because the PRF is too low for the
high arterial Doppler shifts.
40
Colour flow imaging
the velocity vector corresponding to that colour. More importantly, the beam direction, which in turn is dependent on the transducer
since colour is seldom used to quantify velocities, the number rep- type and, in linear arrays, beam steering. There is no established
resents a range of velocities shown so that a scale value of 0.03m/s standard for allocating colour to direction. For curvilinear
or 3cm/s is appropriate for low velocities, a scale value of, for and phased arrays, users tend to choose red as flow towards the
example 0.4m/s or 40cm/s is appropriate for arterial flow. Both transducer (e.g. Fig. 3.20). For linear arrays, where the beam
m/s and cm/s values are used by manufacturers, who seem unable direction is changed to improve insonation of vessels lying
to agree a standard. parallel to the skin, users may choose to invert the colour
The maximum scale is dependent on the maximum PRF possible scale to suit their preference for a particular application or
due to the depth of the image, and is also dependent on the trans- anatomy (Fig. 3.18), for example showing flow in carotid arteries
mitted frequency used. Users may find that the maximum scale as red.
changes automatically as depth is changed in an investigation.
The appropriate scale is selected when an application is chosen.
For arterial flow, the colour image will vary throughout the cardiac Frequency/patient type
cycle since systolic velocities are higher than diastolic. In investiga-
tions of arterial disease, aliasing is invaluable to identify areas of
As in B-mode, low frequencies give better penetration into tissue
high velocities at sites of narrowing (Fig. 3.17).
and can improve sensitivity to flow in deep tissue. Low frequencies
also give higher aliasing limits at depth since the resulting Doppler
Invert frequencies are lower, allowing a lower maximum PRF. In some
systems the frequency can be altered as a separate control. In others
The colour scale shows the direction of flow relative to the ultra- the frequency is one of several parameters altered to improve pen-
sound beam. This varies depending on the course of the vessels and etration (Fig. 3.19).
A B
Figure 3.17 Using aliasing in arterial investigation. The colour flow image of a femoral artery shows a small length of aliasing (arrow)
indicating raised velocities at this point (A). Spectral Doppler images (B) show a change of velocity as the cursor is moved into the area of
colour aliasing indicating severe arterial narrowing.
A B
Figure 3.18 Colour flow invert. Flow in an internal carotid artery is from right to left in image A. The colour scale shows blue as Doppler
shifts away from the beam direction. By inverting the scale the image can display this flow as red (B). In some systems this can be done
after the image is frozen.
41
CHAPTER 3 Practical ultrasound using scanners and optimising ultrasound images
A B
Figure 3.19 In image A there is an area within the artery where colour flow signals are poor. By changing the setting to improve
penetration (B), colour filling is improved. In other scanners this can be achieved by lowering transmit frequency.
A B
Figure 3.20 Colour box size. By setting the colour box area across the entire image (A) there are large demands on time to obtain flow
information. Indicated frame rate is 6fps and the quality of the colour image is limited, possibly because line density and ensemble length
is restricted. By reducing the area of colour investigation (B), the CF image of aorta and renal artery origins shows improved colour quality.
Frame rate is doubled.
Colour flow imaging box/area size beam/flow angles close to 90 lead to confusing images. In trans-
verse imaging, adequate Doppler angles are obtained by tilting the
In most colour flow scans, a particular area of the B-mode image is transducer. In longitudinal section there is limited scope to do this.
selected for CFI investigation. CFI requires several pulses for each Beam steering produces an offset colour, and spectral Doppler,
line of the image to detect the movement between pulses. This is beam direction so that unambiguous colour flow images may be
comparatively time-intensive and many compromises are made to obtained by reducing the beam/flow angle (Fig. 3.22). The amount
ensure an acceptable frame rate in the combined CFI/B-mode of steering available depends on the transducer and the frequencies
image. Engineers adjust line density, the number of pulses used for used; lower frequencies tend to have a larger range of steering
each line of colour and the use of advanced B-mode techniques to angles. It is not always advantageous to steer the colour box;
ensure a satisfactory image appearance. Improvements in frame unsteered colour areas sometimes have better sensitivity (Fig. 3.23),
rate, colour sensitivity and spatial resolution can often be seen if a especially in images of vertebral arteries where the vertebral proc-
small area of colour flow is selected. Examples of improvements in esses can shield the arteries from the steered beam.
spatial resolution and frame rate are shown in Figure 3.20.
A B
Figure 3.21 Transmit focus. A: With a focus set for superficial tissue (arrow), the colour flow image of the aorta and renal artery flow at
depth is suboptimal. With the focus set for deeper tissue (B), the image is improved.
A B
Figure 3.22 Beam steering in linear arrays I. In this image of the carotid bulb (A), flow is predominantly from right to left.
The flow vectors are close to 90 from the beam direction and variations in the artery lead to flow away from (red) and towards (blue)
the beam. By angling the colour box, the transmit beam is steered so that flow is consistently away from the beam with a uniformly red
image of flow (B).
A B
Figure 3.23 Beam steering in linear arrays II. Beam steering doesnt always give the best colour image in linear arrays. In this image
of an internal carotid artery (A), there is a void in the colour image (arrowed), possibly due to the long path length and refraction lowering
the intensity of the transmitted and scattered signal. In this case, slightly contrary to expectations, the colour flow image is improved with
no steering (B), despite poorer beam/flow angles.
43
CHAPTER 3 Practical ultrasound using scanners and optimising ultrasound images
A B
Figure 3.24 Mixing B-mode and colour images priority. A colour flow image is a superimposition of colour flow information on a
B-mode image. Colour may overwrite B-mode levels and vice versa. The extent to which one mode has priority over the other is variable
as shown in these two images where colour overwriting of B-mode images is suppressed (A) and is maximum (B). The level of priority is
shown on the colour scale (arrow).
appearance, and an experienced operator may wish to change indi- Flow settings combination controls
vidual parameters to optimise a particular scan. An example of
changes in the priority setting is shown in Figure 3.24 where the Many scanners offer settings for different flow states, for example
emphasis of the colour and B-mode images relative to each other is slow flow or fast/high flows which optimise several parameters to
altered. suit the flow conditions. For fast flows, high PRFs, low persistence,
One control and concept that does require further explanation is low ensemble lengths and high filters may be employed. For slow
the space/time balance of a colour image. Because a colour flow flows, parameters will be selected to best show colour flow images
image requires several pulses for each line to obtain measurement in these vessels. The controls and the way in which they are imple-
of movement, it imposes limits on the frame rate. Several compro- mented are specific to manufacturers and individual scanners; an
mises are made to ensure acceptable images, such as removing example of the effect of these controls is shown in Figure 3.26.
multi-beam B-mode options, reducing frame rate or reducing the
spatial resolution of the colour image, for example by using a lower
line density.
Many scanners offer user-modification of the colour image in PULSED WAVE SPECTRAL DOPPLER (PW)
terms of improved temporal resolution with a reduction in spatial
resolution or improved spatial detail with a lower frame rate There are several controls that affect the appearance of the spectral
(Fig. 3.25). The controls to do this are variously described and Doppler sonogram. Just as importantly, many of these controls
implementations include pre-processing, space/time controls or also affect the accuracy of measurements made from the
colour line density. sonogram. Doppler measurements of velocity and, for appropriate
44
Pulsed wave spectral Doppler (PW)
A B
Figure 3.25 Space/time priority. With temporal priority (A), frame rate (11Hz) is improved but the spatial resolution of the image is
degraded. With a higher spatial setting (B), frame rate is reduced but the colour image appears to have improved spatial resolution.
A B
C D
Figure 3.26 Low flow/fast flow settings. In this scanner, several parameters are altered to suit a particular flow state. A low flow setting
is good to display flow within a kidney (A) but leads to aliasing at the renal artery bifurcation (C). A fast flow settings barely displays any
flow in the kidney (B) but is appropriate for the renal artery bifurcation (D). Factors changed include transmit frequency and scale/PRF.
investigations, volume flow are highly susceptible to errors in scan- Basic rules beam/flow angle and angle
ning technique and manipulation of controls. Velocity measure-
ment errors of over 10% are commonplace in clinical practice.
correction
Volume flow errors can exceed 20% even in ideal circumstances.
The fact that these values are frequently displayed to four signifi- There are two basic rules for spectral Doppler investigation.
cant figures is a testament to the optimism and sense of humour of 1. Obtain a good sonogram by aligning the Doppler beam so
the engineers. However, the seemingly high degree of precision can that there is a good (typically <6070 depending on the
lead the unwary to assume that this reflects the accuracy of the investigation) beam/flow angle to obtain adequate Doppler
measurements made. shifts. This is done by moving the transducer so that there is
45
CHAPTER 3 Practical ultrasound using scanners and optimising ultrasound images
A B
an adequate beam/flow angle. For linear arrays, beam stronger backscattered signals than do arteries and this can lead to
steering may be used. Alter the scale so that the sonogram is suboptimal sonogram images if the gain is set incorrectly for the
clearly displayed. vessel under investigation. If gain is too high then cross-talk can
2. If measurements of velocity are required, alter the Doppler appear in the Doppler sonogram with apparent flow in the opposite
cursor angle correction so that it is aligned with the direction direction (Fig. 3.28). In general, low gains reduce the brightness of
of flow. Without this correction, the velocity scale and the sonogram display and some frequencies may not be displayed.
measurements made from it are incorrect (unless the beam Conversely, high gains amplify weaker Doppler frequencies in the
and flow direction are very closely aligned). sonogram and can lead to apparently higher velocities being dis-
These principles are shown in Figure 3.27 for measurements of played and measured (Fig. 3.29). High gains may also increase the
velocity in a carotid artery. noise, confusing automatic measurements.
If velocities are not required then rule 2 is not appropriate and it
may be sufficient to obtain a good sonogram and make qualitative Invert baseline
assessment of flow or measurements of non-dimensional indices
such as resistance/resistive index and pulsatility index for which The direction of flow is indicated by whether the sonogram appears
angle correction is not required. above or below the baseline. The sonogram scale can be inverted
when necessary so that the flow display appears above the baseline.
This tends to make flow waveforms easier to understand. There is
Power an indication on the sonogram as to whether this is inverted or not
(Fig. 3.30). If flow is predominantly in one direction then the posi-
Intensities for spectral Doppler are generally higher than for tion of the baseline in the sonogram can be set so that the sonogram
B-mode. For applications where there is risk from higher output can be shown to best advantage (Fig. 3.30B, C).
levels (see section above on application set-ups), the operator
should ensure that recommendations are followed and that the
output display guidelines are observed, monitored and used to Scale and HPRF
ensure good practice.
The scale alters the pulse repetition frequency for spectral
Doppler and has a similar function to the scale control for colour
Gain flow imaging (see section above on scale/pulse repetition fre-
quency). Typically, low scales are used for venous flow and for
Increasing the gain increases sensitivity to weak scatterers by flow in small vessels. Flow in large arteries is faster and requires a
amplifying the received signal. In general, venous flow provides high scale. If too low a scale is used, aliasing may occur (Fig. 3.31);
46
Pulsed wave spectral Doppler (PW)
Figure 3.28 Gain in the spectral Doppler. The sonogram shows Figure 3.29 Effect of gain on measurements made from a
flow in a vein. If gain is too high as in the left of the sonogram sonogram. The spectral Doppler trace from flow in a dialysis fistula
image, cross-talk may be displayed (arrow). By reducing gain a shows the effect of change in peak velocity as gain is reduced in
better quality sonogram is seen (right of image). the right of the sonogram. Peak velocity falls from 205 to 184cm/s.
A B
if too high a scale is used, the sonogram shape may not be clear to be measured unambiguously. In some systems the limits can be
(Fig. 3.32). extended by choosing a low transmit frequency (typically 2MHz)
A major limitation of pulsed wave Doppler ultrasound is that the which in turn leads to lower Doppler frequencies, thereby allowing
scale is limited by the depth of investigation. Conventionally, the lower PRFs for the same velocity.
scale is limited by the need for pulses from the sample volume to In order to circumvent this, many ultrasound systems offer an
return before the next pulse is transmitted. This leads to difficulties option whereby the PRF limit can be overridden and a second pulse
for high velocities in deep tissue, for example in renal artery steno- sent out before the first has returned. This setting, usually referred
sis where the high Doppler frequencies that result are often too high to as HPRF high pulse repetition frequency, leads to an additional
47
CHAPTER 3 Practical ultrasound using scanners and optimising ultrasound images
Figure 3.32 With too high a scale, the shape of the flow Figure 3.33 Investigation of high velocities in deep arteries
waveform is unclear and measurements are difficult. may require high pulse repetition frequencies (HPRF) whereby
a second pulse is transmitted before the first returns. An additional
superficial sample volume appears in the image (arrow) and the
sonogram has more background noise.
A B
Figure 3.34 Sample volume/gate size. With a larger sample volume (A), the sonogram shows low velocities from flow near the vessel
wall. With a sample volume limited to the centre of vessel (B), the sonogram does not show the low velocities near the wall.
48
Pulsed wave spectral Doppler (PW)
A B
Figure 3.35 Wall filter. In the sonogram the wall filter is increased to remove the low velocities from wall movement in the left of the
sonogram (arrow). This has a profound effect on the measurement of time-averaged velocity. With the filter allowing strong echoes from
wall movement (A), the mean velocity (short arrow) measured is 8cm/s. When the filter removes low-velocity echoes, the measurement of
mean velocity is now 61cm/s (B).
49
CHAPTER 3 Practical ultrasound using scanners and optimising ultrasound images
A B
C D
Figure 3.37 Errors in velocity arising from a 10 change in beam/flow correction angle. In images A and B, the peak velocities in the
aorta change from 45 to 56cm/s when the angle correction is changed from 46 to 56 (the image and sonogram are identical, only the
angle correction is changed). In images C and D the peak velocity in the renal artery changes only slightly from 37 to 38cm/s with a
change from 1 to 11. The images demonstrate that velocity measurements are increasingly prone to error as the beam/flow angle
increases.
50
CHAPTER
4 Safety
Hazel C. Starritt and Francis A. Duck
Greater temperature increases have been reported where bone increase excessively if operated in air under maximum output con-
is located in the path of the acoustic beam. For example, at the ditions.17 An upper limit for the permitted temperature of the trans-
bone/brain interface in the skull of guinea-pig fetuses a ducer face has now been set by the IEC;18 when coupled to tissue
maximum temperature rise of 5.2C was measured adjacent to the the temperature is limited to 43C after 30 minutes, i.e. an increase
parietal bone (260mW, 3.2MHz).7 In a separate study the degree of 6C, and if operated in air prior to scanning the temperature must
of heating was found to increase with fetal gestational age as the not exceed 50C. In general transducer heating is now well managed
bone became denser.8 A similar effect was observed with human and transducers are designed to operate with the constraint imposed
fetal femurs.9 Doody etal.10 reported temperature measurements by the IEC limits.
on the surface of unperfused human fetal vertebrae. The
maximum temperature reached in this bone, exposed in vitro to a
simulated, medium-power, Doppler ultrasound beam (50mW), Implications of heating
increased from 0.6C to 1.8C with increasing gestational age
from 13 weeks to 39 weeks. Current ultrasound equipment has the potential to cause heating in
Heat generated at the bone/brain interface is of particular concern tissue and to raise the temperature locally due to absorption when
for obstetric scanning because of the risk of damage to the develop- operated towards the upper end of available powers and intensities.
ing brain and central nervous system. In anaesthetised mice, a The greatest temperature increase due to ultrasound absorption
maximum temperature elevation in the mouse skull of 5C was occurs at the surface of ossified bone; in soft tissues it is very
recorded after 90s exposure (I(spta) 1.5Wcm2).11 Temperature unlikely that the temperature would be increased above 2C due to
elevations were 10% higher when repeated after the animals had absorption. Uncalcified bone does not absorb ultrasound strongly.
been killed, showing that the effect of blood perfusion on tempera- The potential for heating resulting from obstetric applications is
ture elevation in the mouse skull was small. Other studies have of concern because hyperthermia is known to be a teratogen in
reported differences in the ultrasound-induced temperature eleva- animals. In obstetric examinations the developing brain is within
tion in guinea-pig fetuses depending on gestational age. Horder the ultrasound beam and in close proximity to the skull.
etal.12 reported a 12% reduction in the temperature increase in Animal studies have shown that abortion or reabsorption may
guinea-pig fetuses near to full term due to a better developed vas- occur in early embryos and that developmental effects are most
cular system. Investigations have also been carried out on fetal likely when hyperthermia occurs during organogenesis, with the
sheep brain in utero.13 A temperature increase of 1.7C in 120s was central nervous system being most at risk. In the following studies
measured in soft tissue adjacent to the parietal skull bone which the core temperature of pregnant animals was elevated by immer-
was approximately 40% lower than the unperfused value measured sion in water in order to investigate the effect of heat on fetal
postmortem (spatial-average temporal-average intensity, I(sata) development. In studies investigating brain development following
0.3Wcm2). Different responses to changes in perfusion have been whole body heating of pregnant rats19,20 it was found that the
associated with different beam areas, with heating in the smaller threshold temperature for abnormalities was 4C increase in mater-
focal regions of diagnostic beams being less affected by altered nal core temperature maintained for 5 minutes. The majority of
perfusion.14 abnormalities involved encephaloceles and microphthalmia. A 5C
increase in maternal temperature resulted in developmental abnor-
malities in the fetal rat brain when maintained for less than 1
Heating in tissue minute. In mice a threshold for exencephaly has been reported at a
More heating occurs in bone than in soft tissue. temperature increase of 4.5C above normal body temperature,
The fetal brain may be at greater risk of heating as the skull maintained for 5 minutes21 and in mice and rats at 3.5C maintained
ossifies during gestation. for 10 minutes22 following whole body hyperthermia. Abnormali-
Temperature rises measured in vitro from diagnostic ultrasound ties in proliferating bone marrow cells were found in guinea-pigs
exposure are small. heated in a hot air incubator23 and similar effects were observed
when an equivalent temperature elevation was produced by
ultrasound.
In summary, there is a large body of evidence demonstrating that
Transducer heating heat induces developmental abnormalities in a range of animal
Until now we have been considering heating effects in tissue result- species. The sensitivity varies with stage of gestation and peaks
ing from direct transfer of energy from the ultrasound beam to the during neurogenesis. At this stage, a sustained temperature eleva-
tissue. A separate mechanism for heating tissue has been identified tion of about 2.0C above maternal body temperature results in
and occurs when the temperature of the ultrasonic transducer developmental defects such as micrencephaly, microphthalmia and
increases due to inefficient energy conversion. Pulsed transducers retarded brain development in a wide range of animals. The same
in particular are often inefficient in converting electrical energy into types of developmental defects were observed following heating
acoustic energy. Heat generated within the transducer is conducted for shorter periods where the temperatures were higher. Thus, the
from the front face of the transducer into adjacent soft tissues. This risk depends on both the temperature elevation and the time for
is the dominant source of heat for tissue in contact with the surface which that temperature elevation is maintained. The time to cause
of the transducer and exceeds that arising from the absorption of any particular biological effect becomes shorter as the temperature
ultrasound by tissue.15 elevation increases. At high temperatures (above about 43C), the
If uncontrolled, transducer heating could result in thermal time is halved for each additional 1C.
damage to surrounding tissues. Transvaginal scanning has been a For these reasons it is important to consider how the changes in
situation of particular concern due to the proximity of the trans- the absorption coefficient of human embryonic and fetal tissues will
ducer to fetal tissue. Calvert etal.16 investigated the heating depth- affect local heating. Ossification only commences towards the end
profile in a tissue-mimicking material (TMM) for two transvaginal of the first trimester, starting with the cranial and jaw bones. Until
transducers operated at output conditions close to maximum. The this stage in gestation, the absorption coefficient of embryonic
greatest temperature increase was found to always occur at the tissue is thought to be at the lower end of soft tissue absorption and
interface between the transducer and TMM and to reduce to 10% significant heating is unlikely to occur. Later in pregnancy, as the
of the surface value at about 1cm depth. Temperature increases fetal skeleton develops, absorption is greater and heating is more
were higher when the transducers were operated in colour flow and likely. During the third trimester, it is possible for a stationary
pulsed Doppler modes than for pulse-echo mode. Doppler beam to heat fetal bones lying approximately at the focus
In the past there has been experimental evidence demonstrating of the beam, especially when a large proportion of the acoustic path
that the surface temperature of ultrasound transducers could is though amniotic fluid.
53
CHAPTER 4 Safety
For adult scanning, transcranial pulsed Doppler studies have temperature rise in situ and that inferred from the displayed TI
been judged to carry the greatest risk of localised heating.3 This is have been reported. These are most probably due to differences
due to the relatively high acoustic output used and because the between the assumed tissue models and the actual tissue structure,
transducer is held in a fixed position and orientation for extended but may also reflect real differences in individual transducer per-
periods. Bone is exposed, with no overlying tissue attenuation and formance. In addition it must be stressed that displayed TI is not
conducted heat from any transducer self-heating will add to the the actual temperature increase in degrees Celsius generated in
heat generated by absorption of ultrasound in bone. tissue while scanning. TI is, however, the best indication of thermal
hazard available to the user and allows risk to be quickly assessed
during an ultrasound examination.
Risks associated with tissue heating There are a number of ways in which the operator can adjust scan
conditions in order to reduce TI and to minimise risk when neces-
Sustained heating of the embryo is known to cause sary. In all operating modes and all clinical applications, reducing
developmental abnormalities in animals. the acoustic output power will reduce TI. Using a lower acoustic
In the adult, the greatest risk of localised heating arises during frequency may result in lower TI due to less local absorption.
transcranial Doppler studies. Reducing the frame rate or increasing the sector width may again
reduce TI. If the transducer dwell time is short, the risk of heating
will be reduced. This will not, however, be reflected in the dis-
played value of TI because the model assumes that the transducer
Hazard indication thermal index (TI) is stationary for a sufficient time for a steady state to be reached.
The user could be forgiven for thinking that the evidence for heating In 2008 a survey of TI displayed during a range of scans in clinical
by ultrasound in vivo is unclear, suggesting that heating may or practice was carried out in the United Kingdom by the Safety Com-
may not occur and if it does occur it may be to a greater or lesser mittee of the British Medical Ultrasound Society.25 The results
extent. Primarily this is because of the wide range of variables that showed that the greatest range of TI values (0.1 to 2.5) and the
need to be considered in each situation. One of the most important average of the highest TI values (0.98) were displayed during
aspects is the ultrasound mode, for example the potential for obstetric examinations. The average examination time (15.4
heating may increase in moving from pulse-echo to colour flow 0.7minutes) was also longest for obstetric examinations. The highest
imaging. The acoustic output power and the beam properties deter- TI values were associated with pulsed Doppler examinations.
mine the acoustic energy available, whilst the tissue absorption and Deane and Lees26 also found TI to be highest during pulsed Doppler
perfusion determine the temperature rise generated by absorption examination. A similar study in the USA27 concentrated on obstetric
of acoustic energy. Ideally, a user would need to give due consid- scanning. The conclusion was that while acoustic power levels, as
eration to each of these factors for each ultrasound examination in expressed by TI and MI, were generally low, TI >1.5 could be
order to assess the risk and act accordingly. However, this is not reached during colour Doppler examination and accounted for a
practical and a simplified approach has been adopted by displaying small proportion of the total examination time.
the thermal safety index (TI) on the ultrasound scanner.1,2 The success of TI as a safety indicator depends on the extent to
The display of TI on many modern scanners allows the operator which it is understood and used by the user. There is some evi-
to identify scanner operating conditions most likely to cause tissue dence24,28 that obstetric ultrasound users do not, in general, use the
heating in a range of situations and, if necessary, to make adjust- indices and are not confident of their meaning, in spite of extensive
ments to minimise the heating caused by ultrasound absorption. At training opportunities.
present, the display does not include information about surface
temperature caused by transducer self-heating.
The thermal index (TI) is defined as the ratio W/Wdeg, where W is The thermal index (TI)
the acoustic power emitted by the transducer at any time, and Wdeg TI is the thermal safety index.
is the power required to cause a maximum temperature rise of 1C It is displayed to guide users in assessing the likelihood of
anywhere in the beam, contributed by ultrasound absorption heating.
alone.24 It is assumed that a steady state is reached and hence would It should be kept to a value minimum consistent with diagnostic
require that the beam remains stationary with respect to the tissue quality.
for several minutes. Three simple physical models are assumed for
the computational programs that generate the TI values displayed
on ultrasound scanners. These are:
1. Soft tissue thermal index (TIS). The soft tissue model assumes a CAVITATION AND GAS BODY EFFECTS
uniform homogeneous tissue-mimicking material with an
absorption coefficient somewhat lower than soft tissue to In addition to the thermal safety index (TI), a mechanical safety
allow for fluid pathways, and makes some allowance for heat index (MI) is displayed on many ultrasound scanners. This index
loss from blood perfusion. is intended to warn the user about the hazard arising from inertial
2. Bone-at-focus thermal index (TIB). This model includes a layer cavitation due to the behaviour of bubbles or gas bodies in the
of strongly absorbing material (bone mimic) within the soft acoustic beam. Although MI relates to inertial cavitation, gas body
tissue model at the depth that maximises temperature rise. activity can produce a range of effects which need to be considered
3. Cranial bone thermal index (TIC). The third tissue model omits in the context of patient safety.
soft tissue, and considers the absorption of ultrasound in a
bone-equivalent layer coupled directly to the transducer.
What do we mean by acoustic cavitation?
These three models can be used to estimate TI in scanned beams
(pulse-echo B-mode, and Doppler imaging/colour flow) and Acoustic cavitation is a term used to refer to the behaviour of a gas
unscanned beams (M-mode and pulsed Doppler). bubble contained in a liquid, in an acoustic beam. The bubble expe-
riences variations in pressure due to the acoustic wave. It expands
in size during the period of decreased pressure and contracts
Use of TI during ultrasound examination during compression to an extent dependent on the acoustic pres-
Most scanners now display TI values calculated from these models sure. At low acoustic pressure, these oscillations in bubble size
and this provides a clear and simple indication of thermal hazard occur broadly in step with variations in acoustic pressure in a stable
to the user. Occasionally differences between the actual worst-case fashion. This is known as non-inertial, or stable, cavitation.
54
Cavitation and gas body effects
However, if the peak acoustic pressure increases, different motions mouse lung have been determined experimentally37,38 to be 1.4MPa
may be induced until finally the bubble becomes unstable and col- for pulsed ultrasound in the frequency range 14MHz, with a
lapses under the inertia of the surrounding liquid. This is known dependence on pulse length. Typically damage included extravasa-
as inertial cavitation or collapse cavitation. The term acoustic cavi- tion of blood cells into the alveolar spaces suggesting ruptured
tation also refers to the generation of bubbles in a liquid by a sound capillaries. The exact mechanism remains unclear, since it is
wave. For this to occur pre-existing nucleation sites such as micro- difficult to explain all the experimental results on the basis of
scopic impurities are required. ultrasound-induced cavitation occurring in the alveolar spaces.39
Thresholds for lung damage have been determined for monkey,40
rat41 and rabbit lung,42 for neonatal pig43 and mouse.44 Gas in the
Hazards from gas bubble activity intestine has been associated with damage to the intestinal wall in
and cavitation mice45,46 on exposure to ultrasound.
The injection of microbubbles into the circulation as contrast
Inertial cavitation, in which very rapid bubble collapse occurs, agents causes effects that do not occur under normal conditions.
results in the generation of extremely high instantaneous tempera- There is evidence that ultrasound and microbubbles can lead to
tures and pressures within the bubble cavity. The temperature increased permeability of the bloodbrain barrier.47 It may be pos-
can increase by thousands of degrees. This is sufficient for highly sible to use this effect to assist the delivery of macromolecular
chemically reactive free radicals to be formed which are known to agents to the brain. It has been shown that the bloodbrain-barrier
be potentially damaging to molecules in the body. can be transiently opened using focused ultrasound and introduced
A different hazard is posed by the complex mechanical forces microbubbles without acute neuronal damage.48 However, there is
associated with bubble activity. For example, the shear forces insufficient evidence to conclude that there is no damage to the
exerted at the bubble surface by a pulsating bubble can generate a barrier as a result of the effects of ultrasound and microbubbles.
small steady flow of fluid via a process known as microstreaming.29 To date there has been one experimental study reporting an
The variation of this flow with distance from the bubble creates observed bioeffect associated with ultrasound which is not easily
extremely high shear stresses near the bubble surface, which have explained by any of the accepted mechanisms. Ang etal.49 reported
been associated with cell destruction (haemolysis), and temporary increased migration of neurons in fetal mice with exposure to diag-
alteration in permeability (sonophoresis).30 These mechanical forces nostic ultrasound. The mechanism is unclear and the need for
occur with both non-inertial and inertial cavitation, but are signifi- further research is indicated.
cantly higher in the latter case. Furthermore, additional heating of
the surrounding medium may result.31
Factors affecting incidence of cavitation
Review of experimental work associated and gas body activity
with cavitation and gas body activity
Physical factors
Modelling Before cavitation can occur, gas bubbles or nucleation sites within
the fluid or tissue are required. Once this condition is met, the likeli-
Cavitation has been investigated theoretically using mathematical
hood and amount of cavitational activity will depend on two physi-
modelling.32,33 Maximum collapse pressures and temperatures
cal properties of the acoustic beam. Firstly it depends on the acoustic
within bubble cavities and collapse speeds of the cavities were
frequency and is more likely at lower frequencies. Secondly there
calculated for a range of nucleus sizes.33 Further work gave evi-
is a threshold level of the peak acoustic pressure in the decompres-
dence that cavitation could, in theory, occur in the type of pulsed
sion phase of the acoustic wave, below which inertial cavitation will
acoustic beams employed in diagnostic ultrasound. Holland and
not occur. Bubble activity is influenced by surface tension and
Apfel34 predicted the threshold acoustic pressure required for cavi-
viscosity.
tation to occur at different frequencies, and this analysis was used
as the basis for MI. In practice pre-existing gas bubbles are required
for cavitation and these are unlikely to occur naturally in the body. Biological factors
Church35 has published perhaps the most relevant theoretical paper
for diagnostic ultrasound. He examined the likelihood that cavita- The use of contrast materials, which introduce gas bubbles into an
tion nuclei could give rise to acoustic cavitation within soft tissue, acoustic field, significantly increases the potential for cavitation
under diagnostic conditions. He determined that the threshold during clinical ultrasound examinations. Contrast agents consist of
acoustic pressure for such events lay above those used in current stabilised bubbles, 110m in diameter, typically surrounded by a
practice, and that even at slightly higher acoustic pressures, viscous lipid or polymeric shell. When activated by high acoustic pressures,
and other forces within the tissue made the likelihood of cavitation these shells may become damaged, allowing the release of free gas
events vanishingly small. bubbles. Demonstrable harm can result when tissues containing
gas-filled contrast agents are exposed to ultrasound under so-called
high MI conditions. Capillary rupture can occur, with leakage of
In-vivo animal and human effects blood contents into the surrounding extravascular space.50,51 In
addition, ventricular extra-systolic contractions can be induced
Biological effects attributed to cavitation and other gas body effects during cardiac scanning.52 Without the addition of contrast materi-
have been observed in association with the use of ultrasound in als other gas body activity of the type outlined above may occur at
extra-corporeal shock-wave lithotripsy (ESWL) where bruising may any gas/tissue interfaces within the body for example in the lung
sometimes be observed on the skin on the exit beam side of the or intestinal tract.
patient. There is evidence that the destruction of gallstones and
renal calculi is due to cavitation effects.36 In ESWL the peak acoustic
Cavitation and tissue
pressure is typically 20MPa compared to approximately 2MPa for
diagnostic ultrasound and the acoustic frequency of ESWL pulses Inertial cavitation is potentially damaging to tissue.
is much lower than diagnostic pulses. These factors make cavitation The use of contrast agents enhances the likelihood of ultrasound-
more likely to occur. induced cavitation.
Lung tissue is vulnerable to damage from diagnostic ultrasound In the absence of contrast agents there is no evidence of
because of the presence of air. Damage has been demonstrated in cavitation occurring in vivo at current diagnostic exposures.
mammals, and acoustic pressure thresholds for haemorrhage in
55
CHAPTER 4 Safety
Definition of MI EPIDEMIOLOGY
A safety index displayed on a scanner allows a user to manage
acoustic exposure in such a way that the risk of cavitation effects is Epidemiology studies allow the effects of prenatal diagnostic ultra-
minimised. The mechanical index, (MI) is formally a predictor of sound on the exposed population to be studied directly. Necessarily
inertial cavitation and was derived from a theoretical analysis such studies lag behind changes in practice and technology; much
which predicts the onset of inertial cavitation in water or blood, of the current evidence from epidemiology is based on examina-
given the existence of available bubbles. The index is related to tions carried out 10 or more years in the past. During that time
acoustic pressure and frequency according to the equation: many changes have occurred. Equipment operating at higher
maximum acoustic pressures and intensities is much more widely
MI = pr f used; also transvaginal transducers, harmonic imaging, pulsed
Doppler and contrast materials have all become available and are
where pr is the in-situ rarefaction pressure and f is the acoustic commonly employed. Hence epidemiological evidence can never
frequency. be used to prove that current ultrasound practice is risk free.
There are a number of issues surrounding the design of epidemi-
ology studies. First of these is the need to find a matched unexposed
Mechanical index in clinical practice control group. Since its introduction into clinical practice 40 years
ago the use of ultrasound in fetal scanning has increased dramati-
cally. It is now very unusual in the developed world for a fetus not
Situations of potentially higher risk to be scanned routinely with ultrasound. This makes it impossible
to design new, large randomised studies which have unexposed
In the following situations tissue is particularly vulnerable to gas control groups.
bubble activity and/or acoustic cavitation in an acoustic beam and Very commonly, ultrasound exposures are poorly documented,
exposures should be well managed: often including no record of acoustic power settings or duration of
1. Echocardiography in premature infants, particularly in exposure, so making it impossible to demonstrate any relationship
combination with lung surfactant therapy. between effect and acoustic exposure. In any epidemiological study
2. Any clinical application of ultrasound involving contrast the selected outcomes are likely to be influenced by additional
materials (further discussed in Chapter 6) or saline for factors other than ultrasound exposure. Any clinical reason for
endometrial evaluation. additional or extensive ultrasound examination in utero may be
3. The incidental exposure of any tissue/air interfaces such as associated with outcomes that are unrelated to the acoustic expo-
lung and intestine. sure. In order to produce statistically valid results, studies require
4. Mechanical effects are equally likely to occur in pulsed very large groups of participants because, if there are ultrasound-
Doppler beams and in B-mode imaging beams, since a very induced effects, they would appear to be subtle and to occur with
similar range of acoustic pressures is used in each mode. very low probability.
None of this negates the importance of epidemiology studies;
developments in ultrasound technology and increased acoustic
Reduction of MI during scanning power levels53,54 make it essential that further epidemiological
research into possible adverse effects of ultrasound on the develop-
To reduce the MI, the acoustic pressure may be decreased by reduc- ing brain continues.55
ing the acoustic output power using the transmit control. It is not
possible to predict the outcome of altering the acoustic frequency,
because any frequency change will also change the acoustic Review of epidemiological studies
pressure.
An excellent review56 of epidemiological studies which focuses on
several key biological endpoints is summarised here.
Conclusion
Epidemiology studies to date show no association between ultra-
sound exposure during pregnancy and childhood malignancies, 3. TIC must be displayed for adult or neonatal transcranial
reduced birth weight, dyslexia, or abnormal neurological develop- applications.
ment. It is impossible, however, to rule out an association between When TIs are sufficiently low for display not to be required, some
ultrasound and left-handedness among males. Further research is manufacturers display the value, some do not. This may be advan-
essential to ensure the continuing safety of ultrasound for obstetric tageous for reasons not associated with safety, for example in the
examination. use of MI to control the behaviour of contrast agents.
BMUS guidelines
Evidence from epidemiology
In the UK guidance on the safe use of ultrasound equipment is
Epidemiology provides direct information on human population provided by the British Medical Ultrasound Society (BMUS). The
exposed to ultrasound. information in this section is taken from the current guidelines
To date studies show no effect from prenatal ultrasound on birth available on the BMUS website.63
weight, dyslexia, childhood cancer or neurological development.
General guidelines
1. Medical ultrasound imaging should only be used for medical
REGULATIONS AND GUIDELINES diagnosis.
2. Ultrasound equipment should only be used by people who
are fully trained in its safe and proper operation. This
A number of statements have been issued by national and interna-
requires:
tional organisations concerning the safe use of medical ultrasound.
n an appreciation of the potential thermal and mechanical
What follows is a summary of the main points of these guidelines
bio effects of ultrasound
and is not complete. Ultrasound practitioners are advised of the
n a full awareness of equipment settings
need to be familiar with the full guideline recommendations.
n an understanding of the effect of machine settings on
power levels.
Food and Drug Administration (FDA) 3. Examination times should be kept as short as is necessary to
produce a useful diagnostic result.
Two alternative routes exist by which manufacturers can obtain 4. Output levels should be kept as low as is reasonably
Food and Drug Administration (FDA) approval in the USA for the achievable whilst producing a useful diagnostic result.
manufacture and sale of ultrasound scanners,1,2 The original 5. The operator should aim to stay within the BMUS
requirement was for application-specific limited acoustic output recommended scan times (especially for obstetric
and is rarely applied now. Currently the more commonly adopted examinations).
route permits all equipment, except ophthalmology scanners, to 6. Scans in pregnancy should not be carried out for the sole
operate to the maximum limit previously applied only for vascular purpose of producing souvenir videos or photographs.
scanning (so-called Track 3). This route also requires on-screen
displays indicating to the user the likelihood of thermal and
mechanical effects. Current limits for this option are shown in Specific guidance for use of thermal and
Table 4.2. mechanical Indices
The following requirements apply to the display of safety
indices:18
Obstetric examination
1. Not all ultrasound equipment is required to display on-screen
safety indices. Only those systems capable of reaching an MI n TIS should be monitored for scans during the first 10 weeks
or TI of 1.0 are required to display that index, beginning at a after LMP.
value of 0.4 and increasing to the maximum in increments of n TIB should be monitored for scans following 10 weeks after
no less than 0.2. LMP.
2. Only one thermal index will be displayed (TIS, TIB or TIC) n TI up to 0.7: no time restriction, but observe ALARA.
but the equipment must allow the user to retrieve the n TI up to 1.0: maximum exposure time of an embryo or fetus
other two. should be restricted to no more than 60 minutes.
57
CHAPTER 4 Safety
The mechanical index (MI) is a useful but imperfect guide for 20. Sasaki J, Yamaguchi A, Nabeshima Y, et al. Exercise at high
safety and no absolute threshold can be defined. Bioeffects have temperature causes maternal hyperthermia and fetal anomalies in rat.
been observed in small animals in ultrasound contrast agent studies Teratology 1995;51:233236.
21. Shiota K. Induction of neural tube defects and skeletal malformations
with MI as low as 0.4; the clinical implications are yet to be
in mice following brief hyperthermia in utero. Biol Neonate
determined. 1988;53:8697.
Strategies that reduce the likelihood of bioeffects include: 22. Edwards MJ, Shiota K, Smith MSR, Walsh DA. Hyperthermia and
1. scanning at lower MI birth defects. Reprod Toxicol 1995;9:411442.
2. scanning at higher frequencies 23. Edwards MJ, Penny RHC. Effects of hyperthermia on the myelograms
3. reducing total acoustic exposure time of adult and fetal guinea-pigs. Br J Radiol 1985;59:93101.
4. reducing contrast agent dose 24. Abbott JG. Rationale and derivation of MI and TI a review.
Ultrasound Med Biol 1999;25:431441.
5. adjusting the timing of cardiac triggering (end-systole being,
25. ter Haar G. Results of a survey of exposure conditions used in
in general, the most vulnerable phase for triggering ultrasound scans in the UK, February 2007. BMUS Bulletin
ventricular arrhythmias). 2008;16:110113.
The use of contrast agents in a diagnostic ultrasound study 26. Deane C, Lees C. Doppler obstetric ultrasound: a graphical display of
should be avoided 24 hours before lithotripsy procedures. temporal changes in safety indices. Ultrasound Obstet Gynecol
2000;15:418423.
27. Sheiner E, Freeman J, Abramowicz J. Acoustic output as measured by
REFERENCES mechanical and thermal indices during routine obstetric ultrasound
examinations. J Ultrasound Med 2005;24:16651670.
1. FDA. Information for manufacturers seeking marketing clearance of 28. Marl K. The output display standard: has it missed its target?
diagnostic ultrasound systems and transducers. US Department of Ultrasound Obstet Gynecol 2005;25:211214.
Health and Human Services: Food and Drug Administration; 2008. 29. Nyborg WL. Acoustic streaming. In: Hamilton MF, Blackstock DT,
www.fda.gov/cdrh/ode/guidance/560.pdf. editors. Nonlinear acoustics. New York: Academic Press; 1998.
2. IUM/NEMA 1992: revision 2 2004. Standard for real-time display of p. 207231.
thermal and mechanical acoustic output indices on diagnostic 30. Wu J, Ross JP, Chiu J-F. Reparable sonoporation generated by
ultrasound equipment. UD 3-2004. American Institute for microstreaming. J Acoust Soc Am 2002;111:14601464.
Ultrasound in Medicine/National Electrical Manufacturers 31. Holt RG, Roy RA. Measurements of bubble-enhanced heating from
Association, USA. focused, MHz-frequency ultrasound in a tissue-mimicking material.
3. Duck F. Hazards, risks and safety of diagnostic ultrasound. Med Eng Ultrasound Med Biol 2001;27:13991412.
Phys 2008;30:13381348. 32. Flynn HG. Cavitation dynamics. II. Free pulsation and models for
4. ICRU. Tissue substitutes, phantoms and computational modelling in cavitation bubbles. J Acoust Soc Am 1975;58:11601170.
medical ultrasound. ICRU Report 61. Bethesda, MD: International 33. Apfel RE. Acoustic cavitation: a possible consequence of biomedical
Commission on Radiation Units and Measurements; 1998. uses of ultrasound. Br J Cancer 1982;45:140146.
5. Barnett SB. Can ultrasound heat tissue and cause biological effects? 34. Holland CK, Apfel RE. An improved theory for the prediction
In: Barnett SB, Kossoff G, editors. Safety of diagnostic ultrasound. of microcavitation thresholds. IEEE Trans UFFC 1989;36:
New York: Parthenon Publishing Group; 1998. p. 2738. 204208.
6. ter Haar G, Duck FA, Starritt HC, Daniels S. Biophysical 35. Church CC. Spontaneous, homogeneous nucleation, inertial cavitation
characterisation of diagnostic ultrasound equipment preliminary and the safety of diagnostic ultrasound. Ultrasound Med Biol
results. Phys Med Biol 1989;34:15331542. 2002;28:13491364.
7. Bosward KL, Barnett SB, Wood AKW, et al. Heating of the guinea-pig 36. Coleman AJ, Saunders JE, Crum LA, Dyso M. Acoustic cavitation
fetal brain during exposure to pulsed ultrasound. Ultrasound Med generated by an extracorporeal shockwave lithotripter. Ultrasound
Biol 1993;19:415424. Med Biol 1987;15:213227.
8. Horder MM, Barnett SB, Edwards, MJ, Kossoff G. In utero 37. Penney DP, Schenk EA, Maltby K, et al. Morphological effects of
measurements of ultrasound-induced heating in guinea-pig fetal brain pulsed ultrasound in the lung. Ultrasound Med Biol 1993;19:
(Abstr. 2300). In: Proceedings of the 41st Annual Convention of AIUM. 127135.
San Diego, USA; 1997:22. 38. Child SZ, Hartman CL, Schery LA, Carstensen EL. Lung damage
9. Drewniak JL, Carnes KI, Dunn F. In-vitro ultrasound heating of fetal from exposure to pulsed ultrasound. Ultrasound Med Biol
bone. J Acoust Soc Am 1989;88:2634. 1990;16:817825.
10. Doody C, Porter H, Duck FA, Humphrey VF. In-vitro heating of 39. OBrien WD Jr. Ultrasound biophysics mechanisms. Prog Biophys
human fetal vertebra by pulsed diagnostic ultrasound. Ultrasound Molec Biol 2007;93:212255.
Med Biol 1999;8:12891294. 40. Tarantal AF, Cranfield DR. Ultrasound-induced lung hemorrhage in
11. Carstensen EL, Child, SZ, Norton S, Nyborg W. Ultrasonic heating of the monkey. Ultrasound Med Biol 1994;20:6572.
the skull. J Acoust Soc Am 1990;87:13101317. 41. Holland CK, Zheng X, Apfel RE, et al. Direct evidence of cavitation
12. Horder MM, Barnett SB, Edwards MJ, Kossoff G. In-vivo temperature in-vivo from diagnostic ultrasound. Ultrasound Med Biol
rise in the fetus from duplex Doppler ultrasound (Abstr). In: 1996;22:917925.
Proceedings of the 23rd Annual Conference of the Australasian 42. Delecki D, Child SZ, Raeman CH, et al. Ultrasonically induced
Society of Ultrasound in Medicine. September 1993;Australia. lung haemorrhage in young swine. Ultrasound Med Biol 1997;23:
13. Duggan PM, Liggins GC, Barnett SB. Ultrasound heating of the brain 777781.
of fetal sheep in utero. Ultrasound Med Biol 1995;21:553560. 43. Baggs R, Penney DP, Cox C, et al. Thresholds for ultrasonically
14. Vella GJ, Humphrey VF, Duck FA, Barnett SB. Ultrasound-induced induced lung haemorrhage in neonatal swine. Ultrasound Med Biol
heating in a foetal skull bone phantom and its dependence on beam 1996;22:119128.
width and perfusion. Ultrasound Med Biol 2003;29:779788. 44. Frizzell LA, Chen E, Chong L. Effects of pulsed ultrasound on the
15. Thomenius KE. Estimation of the potential for bioeffects. In: Ziskin mouse neonate: hind limb paralysis and lung hemorrhage. Ultrasound
MC, Lewin PA, editors. Ultrasonic exposimetry. Boca Raton, FL: CRC Med Biol 1994;20:5363.
Press; 1992. p. 371407. 45. Miller DL, Thomas RM. Thresholds for haemorrhages in mouse skin
16. Calvert J, Duck F, Clift S, Azaime H. Surface heating by transvaginal and intestine induced by lithotripter shock waves. Ultrasound Med
transducers. Ultrasound Obstet Gynecol 2007;29:427432. Biol 1995;21:249257.
17. Duck FA Starritt HC, ter Haar GR, Lunt MJ. Surface heating of 46. Delecki D, Raeman CH, Child SZ, Carstensen EL. Intestinal
diagnostic ultrasound transducers. Br J Radiol 1989;67:10051013. haemorrhage from exposure to pulsed ultrasound. Ultrasound Med
18. IEC, 2005. IEC 60601 part 237: Medical Electrical Equipment: Biol 1995;21:10671072.
Particular requirements for the safety of ultrasound diagnostic and 47. Taniyama Y, Tachibana K, Hiraoka K, et al. Local delivery of plasmid
monitoring equipment 2001 & Amendment 1 2005. International DNA into rat carotid artery using ultrasound. Circulation
Electrotechnical Commission, Geneva. 2002;105:12331239.
19. Germain MA, Webster WS, Edwards MJ. Hyperthermia as a teratogen: 48. Hynynen K, McDannold N, Vykhodtseva N, Jolesz FA. Non-invasive
parameters determining hyperthermia-induced head defects in the rat. MR imaging-guided focal opening of the blood-brain-barrier in rabbit.
Teratology 1985;31:265272. Radiology 2001;220:640646.
59
CHAPTER 4 Safety
49. Ang E, Gluncic V, Duque A, et al. Prenatal exposure to ultrasound 58. Stark C, Orleans M, Haverkamp A, Murphey J. Short and long term
waves impacts neuronal migration in mice. Proc Natl Acad Sci USA risks after exposure to diagnostic ultrasound in utero. Obstet Gynecol
2006;103:1290312910. 1984;63:194200.
50. Skyba DM, Price RJ, Link AZ, et al. Direct in vivo visualization of 59. Salvesen KA, Bakketeig LS, Eik-Nes SH, et al. Routine
intravascular destruction of microbubbles by ultrasound and its local ultrasonography in utero and school performance at age 89 years.
effects on tissue. Circulation 1998;98:290293. Lancet 1992;339:8589.
51. Miller DL, Quddus J. Diagnostic ultrasound activation of contrast 60. Salvesen KA, Vatten LJ, Eik-Nes SH, et al. Routine ultrasonography in
agent gas bodies induces capillary rupture in mice. Proc Natl Acad Sci utero and subsequent handedess and neurological development. BMJ
USA 2000;97:1017910184. 1993;307:159164.
52. Van der Wouw PA, Brauns AC, et al. Premature ventricular 61. Keiler H. Epidemiological studies on adverse effects of prenatal
contractions during triggered imaging with ultrasound contrast. J Am ultrasound what are the challenges? Prog Biophys Mol Biol
Soc Echocardiogr 2000;13:288294. 2007;93:301308.
53. Duck FA, Martin K. Trends in diagnostic ultrasound exposure. Phys 62. Neilson JP. Ultrasound for fetal assessment in early pregnancy.
Med Biol 1991;38:14231432. Cochrane Database Syst Rev 1998;4: Art. No. CD000182/
54. Henderson J, Whittingham TA, Dunn T. A review of the acoustic 63. BMUS. Guidelines for the safe use of diagnostic ultrasound
output of modern diagnostic equipment. BMUS Bull equipment. 2009. www.bmus.org
1997;November:1014. 64. EFSUMB. European Committee of Medical Ultrasound Safety. Clinical
55. Keiler H. Epidemiological studies on adverse effects of prenatal Safety Statement for Diagnostic Ultrasound 2008 (www.efsumb.org).
ultrasound what are the challenges? Prog Biophys Mol Biol 2007;93: 65. Barnett SB, ed. Conclusions and recommendations on thermal and
301308. non-thermal mechanisms for biological effects of ultrasound. In:
56. Salvesen KA. Epidemiological prenatal ultrasound studies. Prog World Federation for Ultrasound in Medicine and Biology Symposium
Biophys Mol Biol 2007;93:295300. on Safety of Ultrasound in Medicine. Ultrasound Med Biol 1998;SI
57. Newnham J, Evans S, Machael C, et al. Effects of frequent ultrasound 24:155.
during pregnancy: a randomized controlled trial. Lancet 66. Barnett SB, Duck F, Ziskin M. Recommendations on the safe use of
1993;342:887891. ultrasound contrast agents. Ultrasound Med Biol 2007;33:173174.
60
CHAPTER
A B
Figure 5.1 Gain-related noise. A: The combination of high overall gain and the high TGC amplification at depth may produce random
noise in the image. Though this is present throughout the deeper parts of the image, because it is masked by the echoes from tissue
structure, the noise is most obtrusive in echo-free regions such as within the urinary bladder. B: In this case, correction of the excessive
gains removed the noise but this cannot always be achieved without also darkening the structure whose display is required.
s l
Figure 5.2 Structured noise. Persistent oblique bars (arrowheads) Figure 5.3 Specular and scattered echoes. Scattered signals
on these images were found to be due to electrical interference account for the low-intensity parenchymal echoes from the liver
to the scanner by a nearby diathermy apparatus. Similar effects (l) and kidney (k). Their appearance is independent of the direction
can be produced by radio transmitters and by stray fields from of the ultrasound beam. Specular echoes arise from the flatter
poorly shielded television monitors and video recorders. CB radio structures of the peritoneal and fascial layers separating the liver
transmitters are particularly troublesome offenders. Note also the from the kidney. These echoes are strongly dependent on the angle
comet-tail artefact (arrow) (see also Fig. 5.15). between the beam and the surface, being intense when the surface
is aligned at 90 (arrow) but weak or even completely absent when
the beam runs along the interface (arrowhead). Note also the rib
shadow (s).
under laser light, for example in a hologram. The ultrasound
pattern, though isotropic (i.e. uniform regardless of scanning direc-
tion), is only indirectly related to the real tissue structure: the dis- reflection equals the angle of incidence. Since the focused beam of
played texture is actually a convolution of the real structure by the ultrasound is not dispersed, all of the reflected energy can be picked
ultrasound pulse shape. Thus a pixel on the ultrasound image of up by the transducer so that the signals are much stronger than for
the parenchyma of, say, the liver cannot be expected to correspond scatterers. However, they are intensely directional and thus are only
to a histological interface in the organ. Because the speckle pattern detected when the transducer is correctly directed, i.e. when the
is as much produced by the transducer as by the tissue, the same surface is at right angles to the beam in standard pulse-echo
organ will produce a different texture with different transducers imaging. As the surface is tilted away from the right angle, the
and tissues with different histological structures may have indistin- signal intensity falls off rapidly; in fact, were it not for the tolerance
guishable appearances on ultrasound an example is the near- afforded by the beam width and the fact that real biological surfaces
identical texture of liver and spleen. are rarely mirror-smooth, any tilting of the surface from 90 would
When the reflecting surface is flat (relative to the ultrasound cause the echo to be lost and this constraint would apply in both
wavelength), it behaves like a mirror so that the direction of the scanned and orthogonal planes. In practice most interfaces are
62
Scattering and specular interfaces
A B
C D
Figure 5.4 Missing echoes. When flat surfaces that lie along
the beam are not depicted, very confusing images are produced.
A: An example is the wall between a dilated lower common bile
duct and the adjacent portal vein in the head of the pancreas. The
duct seems to form part of the vein and may be missed altogether.
B: The interface is readily detected when the transducer is
appropriately angled (arrow). (The obstruction was caused by
enlarged lymph nodes (n) in the head of the pancreas.) C: A similar
situation can be seen in this hyperstimulated ovary: when the
ultrasound beam runs along the interface between the largest cysts
(c) it is hard to make out, but D: moving the transducer a little to
one side reveals it clearly (arrowheads). E: In this scan of a normal
rotator cuff in the shoulder, the tendon (arrowheads) appears more
reflective where the beam strikes it at right angles anteriorly. As the
E ligament curves laterally, it seems to be less reflective. This artefact
can erroneously suggest tendon damage. h, head of humerus.
detectable up to angles of more than 60, albeit with diminished apparent communication sometimes seen between the inferior
intensity, depending on the particular structures involved (Fig. 5.3). vena cava and the aorta when these lie close together, for the
A situation where this may cause confusion is in scanning tendons, failure to image the sides of the globe of the eye, and for the
whose fibrillar structure gives strong echoes when they lie at right invisibility of the superior surface of the urinary bladder in
angles to the beam but at oblique angles appear as relatively echo- ascites scanned from certain angles. Such missing surfaces can
poor, simulating a tear or tendinosis.7,8 be demonstrated by scanning from other angles: the sonographer
However, beyond some limiting angle, flat surfaces are not needs to be aware of the problem to avoid serious diagnostic
imaged and this can be confusing (Fig. 5.4). It accounts for the errors.
63
CHAPTER 5 Artefacts in B-mode scanning
A B
Figure 5.5 Acoustic shadowing. When a structure absorbs more sound energy than its surroundings, the TGC correction is inadequate
for that region and the deeper structures appear darker: this is known as acoustic or distal shadowing. A: Produced by fibrosis in a breast
surgery scar and B: by gallstones in the gallbladder (arrowhead). p, portal vein; s, shadowing.
Type Source
Attenuation Attenuation higher than
TGC compensation
Reflective Near-total reflection
Edge From curved surfaces
Interfaces
Speckle is often misinterpreted as information.
Loss of signal from specular interfaces beyond a critical angle
leads to confusing gaps in the image.
Mirror artefacts can be very confusing, especially from pelvic
bowel gas.
Figure 5.6 Increased through transmission. The fluid in a cyst
absorbs very little of the sound energy passing through it so that
the TGC, which has been adjusted to correct for attenuation in
the surrounding tissues (here, the liver) is locally excessive. The
deeper tissues are depicted as being more reflective giving a lighter
SHADOWING AND INCREASED SOUND band (arrows) known as distal or acoustic enhancement. c, cyst;
p, portal vein.
TRANSMISSION
The commonest form of shadowing (and its counterpart, increased
through transmission of sound) are perhaps not true artefacts and
their presence provides important diagnostic information about the
attenuation of the tissues responsible for them (Table 5.1).9,10 Shad- difference in attenuation from the surrounding structures as well as
owing occurs when a region of the tissue has a higher attenuation the path length through the anomalous region. Thus these effects
coefficient than the majority of the tissue in the scan; since the TGC provide clues to the attenuation of the tissue regions responsible
(which corrects for the attenuation with depth) can only be set for they can be thought of as friendly artefacts. Ways to reduce shad-
an average value, an inadequate correction will be applied to this owing and increased through transmission have been developed
region so that both it and the tissues deep to it are depicted as less and promise to facilitate correct setting of the TGC.3
reflective than they actually are (Fig. 5.5). The dark band is referred Since shadowing is simply loss of acoustic signal for a tissue
to as an acoustic or distal shadow. Conversely, if a region of tissue region, it can also be produced by an extremely efficient reflector
attenuates less than its surroundings, echoes from it and the deeper (Fig. 5.7).11 Gas bubbles or regions of calcification, for example,
tissue are overcorrected and appear as a bright band known as where 99% and 80% of the incident sound beam is reflected back
enhancement but, in view of the enhancing effects of microbubble respectively, cast acoustic shadows because very little of the sound
contrast agents (see Chapter 6), it is perhaps better termed increased energy penetrates to insonate the deeper tissues (in addition, any
through transmission or distal bright-up (Fig. 5.6). The degree of echoes from them would probably not cross the reflective layer on
shadowing and increased sound transmission is determined by the the return journey since they would be re-reflected distally).
64
Multiple echoes
Sound transmission
May be friendly, as increases behind cysts.
Intense shadowing deletes information.
Enhancement suggests an effect of microbubble contrast
However, it should be noted that, for most soft tissues, only a small agents, so increased sound transmission is preferred.
proportion of the loss of energy from the beam (i.e. the attenuation)
is due to reflection (in fact only between 1% and 20%) so that echo-
genicity does not correlate closely with attenuation. Echogenic
fluids (e.g. crystalline bile or a pyonephrosis) are examples where Edge or refractive shadows do not have the same diagnostic
strong echoes are associated with increased through transmission significance as bulk shadowing. Unfortunately, edge shadows com-
(Fig. 5.8). monly occur in situations where shadowing suggests calcification
An interesting and sometimes confusing form of shadowing (e.g. in the kidney, arising from vessel walls in the renal sinus) or
occurs deep to the edges of strongly curved surfaces such as vessels, malignancy (e.g. in the breast, where they arise from Coopers liga-
cyst walls and fetal skull (Fig. 5.9). Fine, dark lines are seen extend- ments); they must be recognised for what they are and dismissed.
ing distal to such edges; in the case of a cyst, they are striking by
contrast with the increased through transmission behind the cyst
itself. Two explanations have been offered (Fig. 5.10). In the refrac-
tive model, the ultrasound beam is dispersed as it is reflected from MULTIPLE ECHOES
the curved edge because the leading edge of the ultrasound beam
strikes it at a different angle than the trailing edge. Thus the ultra- A basic and critical assumption in pulse-echo ultrasound is that the
sound energy is spread through a larger tissue region and so the ultrasound beam returns directly to the transducer after a single
returning echoes are weaker, resulting in a shadow; at the same reflection.13 Where the geometry allows multiple reflections to
time, the velocity differences may focus the beam in the region occur, multiple images are formed, and sometimes these are confus-
immediately deep to the structure, increasing the signals here.12 ing. Repeat echoes are more likely to occur where the reflections
Simple geometric reflection, as from a flat surface, would not have are strong and this implies flat surfaces giving specular echoes.
the same effect, for a mirror image of the tissues it strikes will be Since the path lengths for multiples are longer, the corresponding
superimposed on the band immediately behind the edge; this is the images are depicted as lying deeper in the body and they are weak-
mirror image artefact (see below). The other explanation presumes ened as the ultrasound is attenuated. Therefore, multiple echoes are
that the tissue of the wall of the curved structure has a higher more likely to be observed when the surfaces are close together and
attenuation than the surrounding tissue; the ultrasound beam when the intervening tissue is of low attenuation, for example when
passing along the edge must pass through three to four times as it is a fluid.
much of this tissue than that crossing at the diameter and therefore An example of a single echo is the mirror image artefact where a
will be attenuated more. The effect is familiar to those who have repeat of a structure is depicted on the other side of a specular
used a hacksaw in plumbing: cutting a pipe is difficult at first, reflector and equidistant from it.14,15 This effect is readily demon-
becoming easier towards the centre of the pipe before becoming strated for the diaphragm: imaged from below through the liver,
more difficult again as the full thickness of the other side is cut. In echoes commonly appear above the diaphragm and sometimes dis-
this model the edge shadows are a form of attenuation, but only of crete structures in the normal liver or focal lesions can be recognised
the wall material, not of the contents. The two mechanisms could there (Fig. 5.11). This is not the appearance of lung (which is seen
coexist in different situations. as an intensely reflective band when imaged intercostally) and is
65
CHAPTER 5 Artefacts in B-mode scanning
Attenuation model Figure 5.10 Mechanisms of edge shadows. Edge shadows are fine echo-poor
A B Refraction model lines extending deep to the edges of strongly curved structures. Two possible
mechanisms are illustrated. On the left is the attenuation model, which proposes
that the wall is more attenuating than the surrounding tissue; since the beam
traversing the edge of the wall A must traverse three times the thickness of the
wall as the beam B passing through the diameter of the curved structure, it is
more heavily attenuated. On the right is the refractive model, which proposes that
the beam is dispersed as it reflects from the curved edge which is struck at more
than the critical angle; the returning echoes from the spreading beam have less
energy than echoes from a confined beam, so that, even though they are reflected
from the interfaces they encounter, their intensity is reduced. In either case the
Total path A
shadows should not be construed as signifying high attenuation, as would
= 6 x wall thickness
ordinarily be the case.
Total path B
= 2 x wall thickness
66
Multiple echoes
A B
C D
Figure 5.11 Mirror image artefacts. The apparent tissue normally visualised above the diaphragm in the right lower zone of the chest is
actually artefactual, being produced by the airpleura interface acting as an acoustic mirror. Sometimes recognisable structures feature
in the artefact, forming ghost images. An example (A) is a branch of the right hepatic vein (arrow), while in B a blood vessel (arrow)
is cut in cross-section. In this image the diaphragm appears as a triple-layered structure: probably this is a mirror image of thickening of
the diaphragmatic peritoneum. C: Since the artefact depends on reflection from the air surface, where this is replaced, such as by
consolidation or a pleural effusion (pe), the artefact no longer occurs. D: Pathological changes may appear as ghost lesions; an example
is the haemangioma in the upper part of the right lobe of the liver. It has its mirrored counterpart (arrow), seemingly within the chest. d,
diaphragm; hv, hepatic vein.
attributable to the beam reflecting back into the liver from the dia- sense. A further clue is the weak superior and inferior walls com-
phragm.16 Actually the reflecting surface is probably the airpleura pared to the strong anterior and posterior walls.
interface since the muscle of the diaphragm itself would be expected Multiple repeat echoes are known as reverberations. They are
to act as a scatterer rather than a specular reflector. produced when two strong reflectors lie parallel to each other. By
Generally this artefact is not a diagnostic problem and on rare far the commonest example of this is when a flat surface such as a
occasions it may actually be useful, for example when it reveals gas pocket or a stone is parallel to the skin surface where the skin
increased sound transmission beyond a peripheral liver cyst where transducer interface forms the second reflector (Fig. 5.14). Ultra-
it would otherwise be invisible as it falls onto the diaphragm; since sound reflected from the gas travels back to the transducer in the
this is already shown as a full white on the screen no further usual way to generate a correctly placed image, but a proportion of
increase in intensity can be depicted. In other situations the mirror the echo is re-reflected back into the tissue, retracing its path. On
artefact is confusing; in the pelvis, for example, a repeat echo of the its second reflection from the gas surface it produces a second
bladder or of structures immediately posterior to it (the rectum or image at twice the depth of the real image. Sequential repeat echoes
sigmoid) may appear as a deeper line marking the back of an echo- are depicted deeper behind the first (real) echo. A striped pattern
poor mass (Figs 5.12 and 5.13). In fact the echo-poor region is the results, with the deeper multiple echoes becoming weaker because
mirror image of the bladder. The typical position should arouse of loss of sound energy due to incomplete reflection at the surfaces
suspicion that it is artefactual and the back wall of the mass often and to attenuation by the intervening tissues. Since weaker echoes
lies beyond the position of the sacrum and so is anatomical non- appear to be narrower than stronger ones, the reverberating bands
67
CHAPTER 5 Artefacts in B-mode scanning
Reverberation
Multipath signals can be very confusing.
Vigilance is required to avoid misinterpretation.
Reverberations in cysts are especially troublesome.
Sometimes helpful as comet tails behind gas and metallic
bodies.
Skin
A B
C D
Figure 5.14 Reverberation artefacts. A: A second-time-around signal occurs when a strong reflector, in this example the anterior
surface of the bladder, lies parallel to the skin-transducer surface so that some of the received signal is re-reflected into the tissue to be
received as a false surface (arrowhead) at twice the depth of the real surface. The mechanism is the same as for the false pelvic mass (see
Fig. 5.13) There are also complex reverberations (r) giving an impression of noise in the anterior part of the bladder. B: The same effect
occurs in solid tissue, here across a kidney (arrowheads), though here it is often masked by the tissue echoes themselves.
A B
Figure 5.15 Comet-tail artefact (A and B): When a pocket of gas forms a foam, there is the possibility for multiple, almost random
reflection paths between the bubbles to produce trains of echoes. They are seen as intensely reflective lines (arrows) extending deep to
the gas. This is most commonly seen from the duodenum (arrowheads).
69
CHAPTER 5 Artefacts in B-mode scanning
A B
Figure 5.16 Velocity errors. When traversing a region where it is conducted slowly, the sound beam takes longer to complete the
go-and-return pathway, so that echoes from beyond it are depicted deeper in the image than their real positions. A: In this example,
a fatty metastasis (m) in the liver has slowed the sound beam so that the diaphragm (d) appears to have a shelf (arrow). B: The reverse
situation, where a high-velocity region is traversed, as is the case for the lens (l) of the eye, moves the portion imaged through it closer.
The resulting distortion, known as Baums bumps (arrows), can cause serious errors in eye diameter measurements.
A B
Rectus
Velocity errors
Linear array muscle Refraction
Refraction errors produce stretched or even double images.
Fat prism behind the linea alba is a common cause.
Possible cause of lost twins in early pregnancy.
Fat
Bladder
The mechanism by which the ultrasound beam is focused
depends on the compression and rarefaction waves of which it is
Uterus Expanded composed coinciding in their proper phase at the focal zone and,
uterus in the same way, at the transducer surface during receive focusing.
If the velocity in the intervening tissue is different from the cali-
brated value, the focal zone is shifted and, when the intervening
A Transverse sectional B Ultrasound ray C Artefactual distortion tissue has heterogeneous velocities, defocusing will occur because
anatomy paths the waves no longer coincide precisely, some arriving early when
the propagation path includes tissues of a high velocity, others
Figure 5.19 Double images in the pelvis. (A) When the arriving late when the path includes fat, for example. The beam is
ultrasound beam strikes the slower-conducting layer of fat, it is bent thus defocused, degrading the lateral resolution. This effect partly
towards the midline so that medial structures are displayed lateral accounts for the marked variation in ultrasound image quality from
to their true position (B). They therefore appear laterally stretched patient to patient, despite which the quality of images from obese
(C) or even duplicated, leading to confusing or even serious subjects is sometimes surprisingly good. The larger the transducer
diagnostic errors. aperture used, the worse the effect; this is probably why
71
CHAPTER 5 Artefacts in B-mode scanning
sophisticated systems such as high-resolution linear arrays in which disturbed region immediately in front of the transducer surface,
500 or more elements are used to form each ultrasound line give then a near field that progressively narrows to the focus, after which
such exquisite images in easy subjects, but perform badly with it spreads rapidly in the far field. In addition to this main beam
difficult subjects, in whom images from smaller, simple transduc- there are side lobes, low-energy beams directed at angles away from
ers may be less degraded. the centre line.
Axial resolution depends on the pulse length, which is mainly
determined by the wavelength; typically this might be 0.3mm for
a 5MHz transducer and it does not change greatly with depth. In
BEAM WIDTH contrast, the width of the main beam defines the lateral resolution
of the ultrasound image because adjacent objects can only be
Unfortunately the real ultrasound beam shape falls far short of the resolved separately if the beam is narrower than the distance
desired uniformly narrow laser-like configuration that would be between them.29 If the beam is wider, they are depicted as one
optimal.28 A typical actual focused beam (Fig. 5.20) consists of a larger object on the screen. Because of the complex shape of
the typical practical ultrasound beam, lateral resolution varies
with depth, being best at the focal zone and deteriorating rapidly
beyond it.
The edges of the beam are not sharply defined; the ultrasound
energy is concentrated on the centre line of the beam and falls off
progressively from the centre line with a Gaussian distribution.
This means that a strong reflector will continue to give detectable
echoes further from the central axis than a weak reflector. In clinical
terms this means that the resolution of ultrasound is better for weak
reflectors. Strong reflectors tend to blur laterally and are therefore
seen as cigar-shaped smears or streaks so that their width is exag-
gerated. This is the beam width artefact (Fig. 5.21), and is most
obvious when the smearing overlaps an echo-free structure, often
encountered when a gassy or bony structure lies adjacent to a fluid
space.30 However, it also leads to the general tendency to fill in small
Figure 5.20 Ultrasound beam shape. In this Schlieren tank echo-free regions, such as ducts, and in part for the discrepancy
photograph of the ultrasound field from an unfocused disc between the ultrasound and X-ray measurements of the calibre of
transducer, the main beam is accompanied by several side lobes the bile and pancreatic ducts (the remaining discrepancy being
emitted at angles from the central axis. The width of the main beam attributable to the magnification on X-ray and to duct dilatation
limits resolution in the transverse direction. The side lobes cause caused by contrast agents).
falsely positioned images. (Taken by Hiedemann E and Beam width artefacts also occur in the orthogonal plane, i.e. in
Osterhammel K; discussed in Hiedemann E and Osterhammel K, the slice thickness. With circular transducers (either the simple disc
Optische Untersuchung der Richtcharakteristik von type or annular arrays) the beam is symmetrical in all planes but,
Ultraschallquellen. Z Phys 1937;107:272-282, Hiedemann E and for linear and phased arrays, the beam is wider in the orthogonal
Osterhammel K: Untersuchung von Schallamplitudenfeldern mittels plane. These artefacts are exactly the same as the slice thickness
einer Methode der Isochromaten. Proc Ind Acad 1938;8:275-80 artefact in CT except that the ultrasound beam is not uniform with
and 1938;8:23, and Osterhammel K, Optische Untersuchung der depth; low-level information derived from signals in adjacent
Schallfelder kobenfrmig schwingender Quarze. Akust Z planes is spuriously depicted in the image plane.31,32 Typically,
1941;6:78-86). bands or lines are noted within echo-free spaces (Fig. 5.22). They
A B
Figure 5.21 Beam width artefact. Echoes arising from structures at the edge of the ultrasound beam, which has a finite width, are
depicted as lying in the centre line of the beam. The more intense the reflection, the further off-axis its echoes will be received. A: In this
example the strong echoes from a pocket of gas in pelvic gut loops (g) smear across the bladder (arrowheads). B: A beam spread artefact
misplaces echoes from the reflective gas in gut loops (g) spread across the ascitic fluid (arrowheads). As is often the case with artefacts,
they are more obvious when the false signal overlies an echo-free region but, in fact, are present everywhere to a greater or lesser extent,
depending on the beam shape (mainly determined by focusing) and the reflectivity of the off-axis interfaces. a, ascites.
72
Beam width
A B
Figure 5.22 Orthogonal beam width artefact. A: The low-level echoes (arrowheads) within this longitudinal section of the bladder are
not due to debris or echogenic urine but are a beam width artefact arising from gas in adjacent bowel loops seen in B, the transverse
section (arrow); because the artefact arises out of the plane of the tomogram, this variant of the beam width artefact is more difficult to
recognise. b, bladder.
may mislead the operator into thinking that the fluid contains
debris. Because the offending reflector is not visualised within the
image, the orthogonal beam width artefact is more difficult to rec-
ognise than the same artefact occurring within the scanned plane.
Unfortunately, even this rather complex description of the shape
of the ultrasound beam is incomplete because the profile is even
further complicated by the inevitable presence of side lobes and, for
array transducers, of grating lobes also.3335 Both these are misdi-
rected, aberrant lines of ultrasound energy transmitted alongside
the main beam. They have their exact counterpart in off-axis regions
of sensitivity when the transducer is in the receive mode. Side lobes
are generated as part of the beam focusing mechanism, whether by
applied lenses or by curving of the transducer face, and consist of
ill-defined beams, the first some 20 away from the main beam and
much weaker than it (by about 40dB). For a disc transducer they
form a series of rings, while in the case of linear arrays they are
asymmetrical, being differently positioned in the two planes.
Grating lobes are similar but are produced by array transducers
of all types; however, they tend to be more discrete and powerful.
Grating lobes are less marked when the elements are small and
numerous because the array then approximates more closely to a
continuous transducer. Because they are weaker than the main Figure 5.23 Grating lobe artefact. Grating lobe artefacts have
beam, only strong reflectors cause serious side and grating lobe essentially the same effects as simple beam spread artefacts but
artefacts in clinical practice but if a gas bubble or bone surface are more severe and only occur with array transducers. They often
happens to lie at the position of a side lobe then its grating lobe have a convex shape (arrows). This example arose from a gas-
echo will be depicted in the line of the main beam (Fig. 5.23). The containing pelvic gut loop (arrowhead). b, bladder.
result is a convex-shaped streak that has been dubbed the Chinese
hat artefact (Fig. 5.24). Because these artefacts may appear consist-
ently on rescanning the same region, they may be rather confusing. Beam width
Often the cause can be visualised within the image, but side lobes May produce lateral smearing of strong signals in the
can extend beyond the imaged area and do also occur in the orthog- scan plane.
onal plane. Because the same focusing mechanisms are used in Can exaggerate fetal measurements.
Doppler, the same misregistration of signals may occur and be quite Produce slice thickness effects in the z plane.
difficult to recognise. Also occur with Doppler.
The introduction of tissue harmonic modes has reduced some of
these artefacts and produces cleaner images, especially in difficult
subjects.36 They operate by exploiting the fact that harmonics are sound pressures. There are two ways to exploit the phenomenon.
only generated at relatively high acoustic powers and so the lower In one, the receiver circuitry is tuned to accept echoes at twice the
powers that occur in side and grating lobes and in reverberations frequency of the transmitted sound. In another approach, the phase
do not excite harmonics and therefore echoes are not detected (Fig. inversion mode, each image line is formed from the sum of the
5.25). Such harmonic signals are generated because tissue resists echoes from a pair of pulses sent in the same direction, the second
compression more than it resists expansion so that an ultrasound of which is inverted with respect to the first. Where the sound is
pulse that begins as a symmetrical sine wave becomes asymmetrical conducted in a linear fashion, the echoes are out of phase and cancel
as it propagates through the tissue. The harmonics are represented out, but asymmetries caused by non-linear conduction result in
by the asymmetry, and are much more strongly formed with higher differences that do not cancel and these are used to form the image.
73
CHAPTER 5 Artefacts in B-mode scanning
Linear array
1 2 3 4 c 20dB
Signal intensity
Side lobe
Fundamental
1 2 3 4
Both modes give cleaner images with less clutter; the phase inver-
sion mode images have half the frame rate, while dual frequency
harmonics have some compromise in spatial resolution because
they use longer narrower band pulses. Both have limited depth
penetration because the high powers that are critical to the genera-
tion of the harmonics are attenuated at depths greater about
1015cm.
A B
Figure 5.26 Ranging artefact. If the manufacturer exceeds the limit in the pulse repetition frequency in an attempt to increase
the frame rate late echoes from pulse 1 overlap early echoes from pulse 2, etc. and signals are falsely depicted in the near field.
A: The phenomenon is most obvious when a fluid path is traversed and so is well seen in transabdominal pelvic scanning, as in this
example (arrows). B: Reducing the PRF eliminates this range overlap or wraparound artefact.
This phenomenon, known as aliasing, is rare in real-time imaging 4. Hope-Simpson D, Burns PN. Pulse inversion Doppler: a new method
but is important in Doppler. for detecting nonlinear echoes from microbubble contrast agents. IEEE
Ultrasound Symposium 1999.
5. Wells PNT, Halliwell M. Speckle in ultrasonographic imaging.
Ultrasonics 1981;19:225232.
6. Burchard CB. Speckle in ultrasound B-scan. IEEE Trans Son Ultrason
ARTEFACTS IN THREE-DIMENSIONAL 1978;SU-25:16.
7. Grechenig W, Clement HG, Fellinger M, et al. Value of ultrasound
SCANNING imaging of the Achilles tendon in traumatology. Radiologe
1997;37:322329.
Some artefacts are only encountered in three-dimensional (3D) 8. Bachmann GF, Melzer C, Heinrichs CM, et al. Diagnosis of rotator cuff
ultrasound.38 They may stem from errors in the data collection lesions: comparison of US and MRI on 38 joint specimens. Eur Radiol
process, for example movements of the probe that are too rapid 1997;7:192197.
9. Suramo I, Paivanslo M, Vuoria P. Shadowing and reverberation
result in gaps in the final image that may be depicted as such in
artifacts in abdominal ultrasonography. Eur J Radiol 1985;5:147151.
registered 3D but when the data are collected freehand (where no 10. Robinson DE, Wilson LS, Kossoff G. Shadowing and enhancement in
correction is made for the z-plane movement), they produce errors ultrasonic echograms by reflection and refraction. J Clin Ultrasound
in the geometry of this axis that are not necessarily apparent in the 1981;9:181188.
image: this is why measurements from this type of unregistered 3D 11. Sommer FG, Taylor KJ. Differentiation of acoustic shadowing due to
scan are unreliable.39 Obviously errors in the system that generated calculi and gas collections. Radiology 1980;135:399403.
the spatial coordinates of the raw images distort the final rendered 12. Ziskin MC, LaFollette PS, Blathras K, et al. Effect of scan format on
image. refraction artefacts. Ultrasound Med Biol 1990;16:183191.
Speckle in the ultrasound data also produces defects in the final 13. Bly SH, Foster FS, Patterson US, et al. Artefactual echoes in B-mode
images due to multiple scattering. Ultrasound Med Biol
image and they are particularly obvious in surface-rendered dis-
1985;11:99111.
plays where they show as serpiginous holes.40 Though unaesthetic, 14. Cosgrove DO, Garbutt P, Hill CR. Echoes across the diaphragm.
they do not affect the validity of the image; speckle reduction tech- Ultrasound Med Biol 1978;3:388392.
niques can be used to mitigate the problem. 15. Gardner FJ, Clark RN, Kozlowski R. A model of a hepatic mirror
If the rendering algorithm does not interpolate adequately for image artifact. Med Ultrasound 1980;4:1821.
missing slices, a gappy rendered image results giving a toothcomb 16. Fried AM, Cosgrove DO, Nassiri DK, et al. The diaphragmatic echo
appearance when the three-dimensional set is rotated to align the complex: an in vitro study. Invest Radiol 1985;20:6267.
z-axis. 17. Thickman DI, Ziskin MC, Goldenburg NJ, et al. Clinical manifestations
If the structure being imaged moves during the data of the comet tail artifact. J Ultrasound Med 1983;2:225230.
18. Lichtenstein D, Meziere G, Biderman P, et al. The comet-tail artifact:
collection, the final rendered set will be distorted. This is particu-
an ultrasound sign ruling out pneumothorax. Intensive Care Med
larly a problem with an active fetus and produces bizarrely dis- 1999;25:383388.
torted three-dimensional images. It is also a problem with vascular 19. Ahuja A, Chick W, King W, et al. Clinical significance of the comet-tail
three-dimensional imaging because of vessel pulsations. artifact in thyroid ultrasound. J Clin Ultrasound 1996;24:129133.
20. Wells P. Physical principles of ultrasonic diagnosis. London: Academic
Press; 1969.
REFERENCES 21. Goss SA, Johnstone RL, Dunn F. Comprehensive compilation of
empirical ultrasound properties of mammalian tissues. J Acoust Soc
1. Robinson DE, Kossoff G, Garrett WJ. Artefacts in ultrasonic echoscopic Am 1978;64(2):423457.
visualisation. Ultrasonics 1966;14:186194. 22. Bamber JC. Attenuation and absorption. In: Hill CR, editor.
2. Laing FC. Commonly encountered artifacts in clinical ultrasound. Physical principles of medical ultrasonics. Chichester: Ellis Horwood;
Semin Ultrasound 1983;4:125. 1986.
3. Sanders RC. Atlas of ultrasonographic artifacts and variants. In: Year 23. Pierce G, Golding RH, Cooperberg PL. The effects of tissue velocity
book of ultrasound. Chicago: Mosby; 1986. changes on acoustical interfaces. J Ultrasound Med 1982;1:185187.
75
CHAPTER 5 Artefacts in B-mode scanning
24. Richman TS, Taylor KJW, Kremkau FW. Propagation speed artefact in 33. Laing FC, Kurtz AB. The importance of ultrasonic side-lobe artifacts.
a fatty tumour (myelolipoma). J Ultrasound Med 1983;2:4547. Radiology 1982;145:763768.
25. Baum G. Ultrasonography in clinical ophthalmology. Trans Am Acad 34. McKeighen RE. The influence of grating lobes on image quality using
Ophthalmol Otolaryngol 1964;68:265276. real-time linear arrays. J Ultrasound Med 1982;1(S):83.
26. Mller N, Cooperberg PL, Rowley VA, et al. Ultrasonic refraction by 35. Balthez PY, Leveille R, Scrivani PV. Side lobes and grating lobes
the rectus abdominis muscles: the double image artefact. J Ultrasound artifacts in ultrasound imaging. Vet Radiol Ultrasound
Med 1984;3:515520. 1997;38:387393.
27. Sauerbrei EE. The split image artefact in pelvic ultrasonography: 36. Tranquart F, Grenier N, Eder V, Pourcelot L. Clinical use of ultrasound
anatomy and physics. J Ultrasound Med 1985;4:2934. tissue harmonic imaging. Ultrasound Med Biol 1999;25:889894.
28. Goldstein A, Parks JA, Osborne B. Visualization of B-scan transducer 37. Goldstein R, Downey DB, Pretorius DH. Three dimensional
transverse cross-sectional beam patterns. J Ultrasound Med ultrasound. Philadelphia: Lippincott; 1999.
1982;1:2335. 38. Eckersley RJ, Goldberg BB, Cosgrove DO, et al. Vessel beading in
29. Jaffe CC, Taylor KJ. The clinical impact of ultrasonic beam focusing normal vessels using three dimensional ultrasound imaging.
patterns. Radiology 1979;131:469472. Radiology 1999;213:396.
30. Finet G, Cachard C, Delachartre P, et al. Artifacts in intravascular 39. Tong S, Cardinal HN, Downey DB, et al. Analysis of linear, area and
ultrasound imaging during coronary artery stent implantation. volume distortion in 3D ultrasound imaging. Ultrasound Med Biol
Ultrasound Med Biol 1998;24:793802. 1998;24:355373.
31. Fiske OE, Filly RA. Pseudo-sludge. Radiology 1982;144:631632. 40. Rohling R, Gee A, Berman L. Three-dimensional spatial compounding
32. Goldstein A, Madrazo BL. Slice-thickness artifacts in gray-scale of ultrasound images. Med Image Anal 1997;1:177193.
ultrasound. J Clin Ultrasound 1981;9:365375.
76
CHAPTER
Microbubble dynamics
Microbubbles oscillate in response to the ultrasound beam.
It is the compressibility of the gas within the microbubbles that
makes them such efficient scatterers.
The resonant frequency of commercial microbubbles lies in the
diagnostic frequency range of ultrasound scanners.
The ultrasound beam may force the microbubbles to oscillate in a
non-linear manner, resulting in the generation of harmonics.
At high acoustic pressures, the microbubbles can be forced to
collapse or fragment, releasing free gas bubbles which diffuse
rapidly in the blood.
Table 6.1 Examples of commercially developed ultrasonic contrast agents. Early-generation agents that encapsulated air
have been omitted
HEPS, hydrogenated egg phosphatidyl serine; DMPC, dimyristoylphosphatidylcholine; DPPC, dipalmitoyl glycerophosphocholine; DPPA, dipalmitoyl
glycerophosphate; DPPE, dipalmitoyl glycerophosphoethanolamine; DSPC, distearoyl glycerophosphocholine; DPPG, dipalmitoyl glycerophosphoglycerol.
No US
Low intensity US
High intensity US
Figure 6.2 Preparation kit for SonoVue. Figure 6.4 Schematic representation of lipid (left column) and
polymer (right column) microbubble interaction with
ultrasound of increasing intensity (top to bottom). (Reprinted
from Advanced Drug Delivery Reviews, Vol 60, Hernot S, Klibanov
AL. Microbubbles in ultrasound-triggered drug and gene delivery.
11531166.Copyright (2008) with permission of Elsevier.)
Albumin-coated microbubbles
Optison
Optison (GE Healthcare) microbubbles are a development from the
first-generation contrast agent Albunex, which was one of the first
commercially available agents to demonstrate EBD. In Optison,
octafluoropropane has replaced the air that was encapsulated in
Figure 6.3 Vialmix with inset of Definity/Luminity vial. Albunex. The shell of Optison microbubbles is of denatured human
serum albumin and the size distribution is such that 93% are less
than 10m in diameter. A typical concentration is 5 108mL1. The
It is a lipid bi-layer microbubble encapsulating octafluoropropane. agent is supplied in vials that must be refrigerated prior to use. The
The size distribution of the microbubbles is such that 98% are less agent is hand agitated to produce a milky solution prior to with-
than 10m in diameter. A typical concentration is 109mL1. The drawal of the agent from the vial. Optison is licensed for EBD and
agent is supplied in vials as a clear liquid with a head-space of LVO in the USA and EU.
octafluoropropane. To form the bubbles, the vial must be agitated
in a mechanical shaker (Vialmix) for 45 seconds prior to withdrawal PESDA
of the milky solution (Fig. 6.3). The vial is vented using a needle
prior to withdrawal of the solution. The agent must be refrigerated PESDA (perfluorocarbon exposed dextrose albumin) comprises
prior to use. Luminity is licensed in the EU but is not currently sonicated dextrose albumin microbubbles containing decafluorobu-
marketed there. In the USA and Canada the agent is licensed for tane gas. It has been developed by Porter etal. exclusively for
LVO and EBD. research use.17 The mean size of the microbubbles is 5.1m and the
concentration is 3.1 109mL1.
Imavist CARDIOsphere
Imavist (IMCOR Pharmaceuticals Inc) is a lipid-encapsulated, per- CARDIOsphere microbubbles (POINT Biomedical Corp) are manu-
fluorohexane and nitrogen encapsulated microbubble. The size factured using a technique described as BiSphere technology in
80
Imaging of contrast microbubbles
Contrast agents
Ultrasonic contrast agents are micron-sized encapsulated
bubbles.
The shells of the microbubbles are generally either lipid or
polymer.
The gases within current contrast microbubbles are
perfluorocarbons.
There are approximately 109 microbubbles/mL of contrast agent
solution. A B
Contrast agents are generally injected into the femoral vein as
either a bolus or infusion. Figure 6.5 A: Suspected middle cerebral artery (MCA) stenosis on
unenhanced transcranial colour-coded duplex sonography. In the
Doppler frequency spectrum only suspicious low-frequency
bidirectional signals can be obtained. In colour mode the MCA is
barely visible. B: Improvement of the Doppler frequency spectrum
which microbubbles are produced comprising an outer layer of a and the colour mode depiction of the MCA after application of an
biocompatible material (albumin) and an inner polymer layer. The ultrasound contrast agent. Flow velocities >300cm/s ascertain the
microbubbles are filled with air and have been developed for myo- presence of a high-grade MCA stenosis. (Reprinted from Seminars
cardial perfusion studies. Their mean diameter is 4.0m. Using in Cerebrovascular Diseases and Stroke, Vol 5, Stolz EP and Kaps
BiSphere technology, smaller sub-micron microbubbles have also M, Ultrasound contrast agents and imaging of cerebrovascular
been manufactured for lymphatic imaging. disease 111131.Copyright (2005) with permission from Elsevier.)
Imagify (AI-700)
Imagify (Acusphere Inc) consists of a synthetic polymer poly(L-
lactide co-glycolide) shell and a phospholipid layer encapsulating scattered wave to provide sensitive contrast imaging techniques.
a perfluorobutane gas. The agent is made using a spray drying Current contrast imaging techniques can be divided into either low
technique to produce microbubbles. The mean size of the microbub- MI imaging techniques which minimise destruction of the micro-
bles is 2.0m. FDA approval is currently being sought for this agent bubbles or high MI techniques which maximise microbubble
for myocardial contrast perfusion imaging. destruction.
Pulse 1
Amplitude
Transmit Receive
bandwidth bandwidth Pulse 2
Pulse 1 + Pulse 2
f0 2f0
Frequency
Figure 6.7 Schematic diagram illustrating the principle of the
Figure 6.6 Schematic diagram illustrating the overlap in the pulse inversion imaging technique. Two pulses are transmitted
transmit and receive bandwidths with second harmonic down each line, the second pulse the inverse of the first. The sum
imaging, where f0 is the central transmit frequency. of the scattered pulses from linear scatterers will sum to zero, while
the sum from non-linear scatterers will not equal zero.
Figure 6.9 A flash frame acquired during a perfusion study. Figure 6.10 Contrast perfusion study using infusion of
A high mechanical index frame disrupts SonoVue microbubbles SonoVue with graphical display illustrating variation in
within the myocardium and ventricle. backscatter signal in selected ROI within the myocardium. A pulse
inversion imaging technique is used to image reperfusion of the
myocardium following application of a high MI pulse. (Image
courtesy of Dr Stephen Glen, Stirling Royal Infirmary, Scotland.)
CLINICAL APPLICATIONS OF
CONTRAST IMAGING
Figure 6.12 Image of a benign splenic lesion showing the pulse One of the most significant advantages of the use of contrast agents
inversion harmonic image on the right side (about 15 seconds after is the real-time nature of contrast enhancement and the resultant
injection of SonoVue), and the microbubble trace image on the left real-time diagnostic potential. In addition, the ability provided by
side. (Courtesy of Christoph Dietrich.) some commercial ultrasound manufacturers to view the B-mode
image and the contrast image simultaneously using a split-screen
function (Fig. 6.12) enables visualisation of the organ of interest on
one half of the screen, while simultaneously visualising the uptake
microbubbles are summated over time, thus showing the path of of contrast on the other half. The conventional B-mode image is
the microbubbles through the vascular bed. In addition, the echoes acquired at low MI to avoid disruption of the microbubbles.
are weighted such that the intensity decreases with elapsed time so The number of applications for which contrast agents are now
that the direction of movement of the microbubbles can be studied used has increased significantly over the past 5 years and has been
(Fig. 6.12). Early studies have indicated that these techniques can reviewed by the European Federation of Societies for Ultrasound
illustrate arterial structure but the diagnostic benefit is as yet in Medicine and Biology (EFSUMB).28 In this review the guidelines
undetermined. for each contrast procedure and recommendations for good clinical
practice are presented. Some of these applications are not currently
Newer imaging techniques licensed (e.g. myocardial perfusion, renal applications) but the
diagnostic benefits that clinicians have observed using contrast
agents for applications other than those for which the agent is
Subharmonic imaging licensed (off-label applications) merit a mention in this chapter and
elsewhere in this book.
Subharmonic imaging is based upon the principle that contrast
microbubbles when scattering non-linearly not only generate har-
monics higher than the fundamental but also generate subharmon-
Radiology applications
ics. In addition, tissue does not generate subharmonics and therefore
at subharmonic frequencies the contrast-to-tissue ratio is generally The initial use of ultrasonic contrast agents was primarily focused
higher than that achieved at second harmonic frequencies. Much of on rescuing colour Doppler studies where the signal from blood
the work associated with subharmonic imaging has been performed was too small to be detected. Injection of contrast microbubbles
at frequencies normally associated with intravascular ultrasound increased these low signals so that they could be detected and
imaging (30MHz). An improvement of contrast-to-tissue ratio of displayed (Fig. 6.5).35
30dB at the subharmonic (15MHz) in comparison to the funda-
mental (30MHz) has previously been achieved, highlighting the Liver
potential of using subharmonic imaging for vasa vasorum imaging.25
The organ in which contrast agents have provided substantial diag-
nostic impact is in the liver for the characterisation of focal liver
Coded excitation lesions. There is now substantial evidence to suggest that ultrasonic
Coded excitation involves the transmission of a high energy long contrast agent imaging using low MI techniques (during the arte-
transmit pulse with limited peak amplitude and is well known as rial, portal venous and late phases) is an effective diagnostic tool
a means of improving signal-to-noise ratio in ultrasound B-mode for the characterisation of focal liver lesions29 (Fig. 6.13). Maximum
imaging. Recovery of axial resolution is achieved by the receive diagnostic potential from these studies is achieved when the pre-
electronics examining the signals and picking out the echoes of contrast image is such that there is little tissue structure visible and
similar shape to the transmitted pulse. Use of coded excitation in only major anatomical markers such as the diaphragm are presented.
combination with phase and amplitude modulation techniques has This relies upon interplay of both the gain and MI controls.
been shown to improve sensitivity to non-linear signals from micro-
bubbles at relatively low signal to noise but with limited benefit at Renal
high signal-to-noise levels. A review of coded excitation techniques
is given elsewhere.26 No contrast agents have currently been licensed for the assessment
of renal lesions. However, there has been substantial documenta-
Radial modulation imaging tion of the benefits of using contrast microbubbles in the assessment
of complex cystic lesions (Fig. 6.14), vascular diseases and trans-
Radial modulation imaging is based upon the premise that contrast planted kidneys.30 For the assessment of renal lesions, contrast is
microbubbles respond differently to an incident acoustic imaging injected as a bolus and low MI imaging techniques are used.
84
Clinical applications of contrast imaging
A B
Figure 6.13 A: Image of an echogenic liver metastasis (between callipers) acquired in fundamental imaging. B: Image acquired 1 minute
and 24 seconds after bolus injection of SonoVue (portal-venous stage). Low reflective area in the contrast-enhanced image is indicative of
malignancy. (Images courtesy of Dr Paul Sidhu, Kings College Hospital, London, UK.)
A B
Figure 6.14 A: Image acquired in fundamental mode and suggestive of a complex renal cyst. B: Image acquired after a bolus injection of
SonoVue using a low MI imaging technique. No septation enhancement evident, therefore lesion unlikely to be malignant. (Images courtesy
of Dr Paul Sidhu, Kings College Hospital, London, UK.)
A B
Figure 6.15 A: Image acquired in fundamental mode and suggestive of a possible splenic cyst. B: Image acquired after a bolus injection
of SonoVue and using a low MI technique to image the spleen. Honeycomb pattern suggestive of a spleen abscess. (Images courtesy of
Dr Paul Sidhu, Kings College Hospital, London, UK.)
A B
C D
Figure 6.16 Cardiac parasternal short-axis view of the heart Figure 6.17 Contrast-enhanced images of a cardiac
during a pharmacologically stressed cardiac stress-echo study. A thrombus obtained in three imaging planes. (Images courtesy of
low MI imaging technique is used. Images acquired at baseline (A), Dr Stephen Glen, Stirling Royal Infirmary, Scotland.)
low dose stress (B), high dose stress (C) and recovery (D). (Images
courtesy of Dr Stephen Glen, Stirling Royal Infirmary, Scotland.)
diagnostic stress test, where regions of the myocardium are indi- Ultrasonic contrast agents can also be used to assess other abnor-
vidually assessed for movement under rest, stress and recovery malities such as LV apical thrombus many of which are difficult to
conditions. Such studies are normally undertaken at low MI, ensur- image without the use of contrast microbubbles (Fig. 6.17). A com-
ing that the complete ventricular endocardial border can be visual- prehensive review of clinical applications of ultrasonic contrast
ised without microbubble disruption and associated shadowing agents in echocardiography is given in a recent American Society
effects (Fig. 6.16).33 of Echocardiography Statement.34
There are currently no ultrasonic contrast agents that are licensed
to aid in the assessment of myocardial flow and hence perfusion.
As described previously, when microbubbles are administered as OTHER POTENTIAL USES OF CONTRAST
an infusion and a consistent level of enhancement is achieved, it is MICROBUBBLES
possible to destroy the microbubbles in the scan-plane using a
single or several high MI pulses. By then returning to low MI
imaging, the time required for segments within the myocardium to Targeted contrast microbubbles
become enhanced can be measured. Since this value is related to
myocardial blood flow, areas of the myocardium that have a One of the most exciting areas of progress in contrast agent devel-
reduced blood flow take longer to enhance. opment has been that of selective targeting of the microbubbles to
86
Safety of contrast microbubbles
HN
C=O HN
COO C
=O
=O
C
Gas inside Gas inside HN Gas inside
COO
the bubble the bubble the bubble
C OO
O
C=
HN
C HN
=O COO
A B C
Figure 6.18 Methods to attach targeting ligands to microbubble shell. A: Non-covalent method, where avidin is embedded in the
shell during bubble formation. B: Biotinylated bubble is coated with streptavidin and then biotinylated ligand. C: Ligand is covalently
attached to the bubble shell by a peptide bond. (Reprinted from Klibanov AL. Ultrasound molecular imaging with targeted microbubble
contrast agents. J Nucl Cardiol 2007;14:876884.)
particular sites within the body, enabling acoustic visualisation of microbubble to fuse with the cell membrane. However, from the
localised biological markers expressed in disease processes. literature it appears that many factors affect the size and perma-
However, the proportion of microbubbles that bind to the surface nency of the opening in the cell wall not least the relative closeness
is dependent on many factors including the number of receptor of the microbubble to the cell wall.42
sites available for binding and the shear stress exerted on the micro- Once sonoporation has occurred, extracellular molecules, such as
bubbles at the receptor sites.35 Initial in-vitro studies demonstrated drugs or genes, either incorporated within the microbubbles or
encouraging results under well-controlled flow dynamics36 and a injected near the site of sonoporation, may then enter the cells
review of this field is given elsewhere.37 Figure 6.18 illustrates sche- during this period of permeability thus enhancing the payload of
matically the potential methods of attaching ligands onto the the drugs or genes to the cell.43 Comprehensive reviews of this topic
surface of lipid- or albumin-coated microbubbles. Most commonly are available.44
the binding for liposomal agents is achieved by formulating the
liposome using a biotinylated lipid and using streptavidin as the
linking mechanism between the biotinylated liposome and a bioti-
nylated ligand. The antibody-loaded microbubble when injected SAFETY OF CONTRAST MICROBUBBLES
into the body is then targeted to biological markers in which the
receptor antigens are expressed. Increases in attachment can also be
The main area of concern over the safety of ultrasonic contrast
achieved using the radiation force of an ultrasound beam to push
agents is based around the likelihood of acoustic cavitation taking
the targeted microbubbles towards the cell receptors by applying
place under routine clinical scanning conditions. The potential
the ultrasound beam perpendicularly to blood flow.38 Although this
hazards and risks of diagnostic ultrasound with and without con-
has been shown to be useful for in-vitro applications, it is difficult
trast agents have recently been addressed.45 In summary, since
to assess how controllable this would be in clinical situations.
acoustic cavitation is extremely unlikely to occur in a conventional
Early results in this area have shown promise with applications
scan due to the lack of pre-existing gas bubbles within the body,
that include targeting of microbubbles to atherosclerosis,
the probability of harm is extremely low. If contrast is introduced
intravascular thrombi39 and sites of angiogenesis and tissue
the risk of acoustic cavitation and the severity of harm induced by
inflammation.40
it are considered higher.
The safety of two contrast agents (Definity and Optison) has
Drug and gene delivery recently been assessed retrospectively in a large multicentre clinical
study. The conclusions of the study indicated that the agents had a
Although targeting mechanisms enable the microbubbles to become good safety profile in both cardiac and abdominal ultrasound appli-
attached to particular biological markers, it is the ability of ultra- cations and the incidence of severe adverse reactions is less than
sound in the presence of the microbubbles to cause transient pora- that associated with other contrast agents used with other imaging
tion of the cell wall that enables the microbubbles, their contents or modalities.46
other localised extracellular materials to pass into the cell. This The World Federation for Ultrasound in Medicine and Biology
transient permeability of the cell wall is known as sonoporation. To (WFUMB) published a series of articles as a result of a safety sym-
date, it is unclear from the literature the exact range of phenomena posium dedicated to the use of ultrasonic contrast agents in diag-
that are responsible for sonoporation. Although early research sug- nostic applications. This series of articles comprehensively addresses
gested that inertial cavitation was the source, more recent work clinical applications and safety concerns for contrast agents,47
using high speed cameras suggests that micro-streaming associated in-vitro bioeffects,48 in-vivo bioeffects,49 exposures from diagnostic
with non-inertial cavitation may also be associated with sonopora- ultrasound equipment50 and mechanisms for the interaction of
tion.41 Alternatively, the generation of extremely high temperatures ultrasound.51 As a result of this symposium, recommendations for
associated with inertial cavitation may result in an increase in reducing the likelihood of bioeffects when using ultrasound con-
the fluidity of the phospholipid membranes thus allowing the trast agents included: (i) scanning at low MI, (ii) scanning at higher
87
CHAPTER 6 Ultrasonic contrast agents
A B C
Figure 6.19 Example of acoustic shadowing during a cardiac study after a bolus injection of contrast. A: complete shadowing
of left ventricle by contrast in right ventricle. B: contrast begins to clear from right ventricle, shadowing reduces. C: complete left ventricular
opacification is now visualised.
Doppler artefact
frequencies, (iii) reducing total acoustic exposure time, (iv) reduc-
ing contrast agent dose and (v) adjusting the timing of cardiac
After the injection of a bolus of contrast agent, an artefact known
triggering to avoid systole where most ventricular arrhythmias
as colour blooming may be observed during colour Doppler studies.
have been shown to occur.52 The safety of ultrasound is discussed
When contrast agent enters a vessel the magnitude of the signal
more fully in Chapter 4.
scattered from within the vessel increases, giving a corresponding
increase in the Doppler signal. This effectively broadens the width
of the scanning beam, allowing flow to be detected in the weaker
IMAGING ARTEFACTS regions of the beam. The resulting degradation of the lateral resolu-
tion causes the colour-coded flow region in the image to expand,
There are several artefacts that must be taken into consideration i.e. bloom. The effect is similar to having the Doppler gain too high
when making clinical ultrasound measurements after the injection and may be compensated by reducing the gain.
of a bolus of contrast. These may be subdivided into propagation
artefacts and Doppler artefacts.
REFERENCES
Propagation artefacts 1. Gramiak R, Shah P, Kramer D. Ultrasound cardiography: contrast
study in anatomy and function. Radiology 1969;92:939948.
2. Feinstein SB, ten Cate FJ, Zwehl W, et al. Two-dimensional contrast
When contrast is injected into the body, although it scatters ultra- echocardiography. I. In vitro development and quantitative analysis of
sound strongly it also strongly attenuates and consequently as the echo contrast agents. J Am Coll Cardiol 1984;3(1):1420.
bolus of contrast passes through a vessel or through the heart, 3. Ophir J, Parker KJ. Contrast agents in diagnostic ultrasound.
organs distal to the vessels will temporarily disappear from the Ultrasound Med Biol 1989;15(4):319333.
screen until the bolus clears through the system. This is readily 4. Keller M, Feinstein SB, Watson DD. Successful left ventricular
observed in cardiac scanning where a large amount of the contrast opacification following peripheral venous injection of sonicated
contrast agent: an experimental evaluation. Am Heart J 1987;114:
agent can build up within the ventricles and obscure the posterior
570575.
walls (Fig. 6.19). Shadow artefacts are commonly helpful in making 5. Schlief R, Schurmann R, Balzer T, et al. Saccharide based contrast
a diagnosis in ultrasonic imaging; however, those created by con- agents. In: Nanda C, Schlief R, eds. Advances in echo imaging using
trast agents have not been used in that way. contrast enhancement. Dordrecht: Kluwer Academic Publishers; 1993.
Although a single bubble can be detected as a single spot in an 6. Rayleigh L. On the pressure developed in a liquid during the collapse
image, when there are a large number of bubbles the spots in the of a spherical cavity. Philosophy Magazine 1917;6:9498.
88
References
7. Plesset MS. The dynamics of cavitation bubbles. J Appl Mech 30. Jiang J, Chen Y, Zhou Y, Zhang H. Clear cell renal carcinoma:
1949;16:272282. contrast-enhanced ultrasound features relation to tumor size.
8. de Jong N. Acoustic properties of ultrasound contrast agents. PhD Eur J Radiol 2010;73:162167.
thesis, Erasmus University, Rotterdam, 1993. 31. Droste DW, Jurgens R, Weber S, et al. Benefit of echocontrast-enhanced
9. Doinikov AA, Haac JF, Dayton PA. Resonance frequencies of transcranial color-coded duplex ultrasound in the assessment of
lipid-shelled microbubbles in the regime of non-linear oscillations. intracranial collateral pathways. Stroke 2000;31:
Ultrasonics 2009;49:263268. 920933.
10. Sboros V. Response of contrast agents to ultrasound. Adv Drug Deliv 32. Darge K. Contrast-enhanced voiding urosonography for diagnosis of
Rev 2008;60:11171136. vesicoureteral reflux in children. Pediatr Radiol 2007;38:4063.
11. Chomas JE, Dayton PA, May D, et al. Optical observation of contrast 33. Mathias W Jr, Arruda AL, Andrade JL, et al. Endocardial border
agent destruction. Appl Phys Lett 2000;77:10561058. delineation during dobutamine infusion using contrast
12. Boukaz A, Versluis M, de Jong N. High speed optical observations of echocardiography. Echocardiography 2002;19:109114.
contrast agent destruction. Ultrasound Med Biol 2005;31:391399. 34. Mulvagh SL, Rakowski H, Vannan MA, et al. American Society of
13. Stride E, Saffari N. Microbubble ultrasound contrast agents: a review. Echocardiography consensus statement on the clinical applications of
Proc Inst Mech J Eng Med H 2003;217:429447. ultrasonic contrast agents in echocardiography. J Am Soc Echocardiogr
14. Boukaz A, de Jong N. WFUMB safety symposium on echo-contrast 2008;21:11791201.
agents: nature and types of ultrasound contrast agents. Ultrasound 35. Butler MB, Moran CM, Anderson T, et al. Laser Doppler anemometry
Med Biol 2007;33(2):187196. measurements of the shear stresses on ultrasonic contrast agent
15. Huang S-L, Hamilton AJ, Pozharski E, et al. Physical correlates of the microbubbles attached to agar. Ultrasound Med Biol 2005;31:545552.
ultrasonic reflectivity of lipid dispersions suitable as diagnostic 36. Takalkar AM, Klibanov AL, Rychak JJ, et al. Binding and detachment
contrast agents. Ultrasound Med Biol 2002;28:339348. dynamics of microbubbles targeted to P-selectin under controlled
16. Sontum PC. Physiochemical characteristics of Sonazoid, a new shear flow. J Control Release 2004;96:473482.
contrast agent for ultrasound imaging. Ultrasound Med Biol 37. Klibanov AL. Ultrasound molecular imaging with targeted
2008;34:824833. microbubble contrast agents. J Nucl Cardiol 2007;14:876884.
17. Porter TR, Xie F, Kilzer K. Intravenous perfluoropropane-exposed 38. Rychak JJ, Klibanov AL, Ley KF, Hossack JA. Enhanced targeting of
sonicated dextrose albumin produces myocardial contrast which ultrasound contrast agents using acoustic radiation force. Ultrasound
correlates with coronary blood flow. J Am Soc Echocardiogr Med Biol 2007;33:11321139.
1995;8:710718. 39. Lanza GM, Wallace KD, Scott MJ, et al. A novel site-targeted ultrasonic
18. Bloch SH, Dayton PA, Wan M, Ferrara KW. Optical observation of contrast agent with broad biomedical application. Circulation
lipid- and polymer-shelled ultrasound microbubble contrast agents. 1996;94:33343340.
Appl Phys Lett 2004;84:631633. 40. Linder JR, Song J, Xu F, et al. Noninvasive ultrasound imaging of
19. Hope Simpson D, Chin CT, Burns P. Pulse inversion Doppler: a new inflammation using microbubbles targeted to activated leukocytes.
method for detecting nonlinear echoes from microbubble contrast Circulation 2000;102(22):27452750.
agents. IEEE Trans Ultrason Ferroelectr Freq Control 1999;46:372382. 41. Wu J, Ross JP, Chiu JF. Reparable sonoporation generated by
20. Eckersley RJ, Chin CT, Burns PN. Optimising phase and amplitude microstreaming. J Acoust Soc Am 2002;111:14601464.
modulation schemes for imaging microbubble contrast agents at low 42. Prentice P, Cuschieri A, Dholakia K, Prausnitz M, Campbell P.
acoustic power. Ultrasound Med Biol 2005;31:213219. Membrane disruption by optically controlled microbubble cavitation.
21. Wei K, Jayaweera AR, Froozan S, et al. Quantification of myocardial Nature Phys 2005;1:107110.
blood flow with ultrasound-induced destruction of microbubbles 43. Van Wamel A, Kooiman K, Harteveld M, et al. Vibrating microbubbles
administered as a constant venous infusion. Circulation 1998;97: poking individual cells: drug transfer into cells via sonoporation.
473483. J Control Rel 2006;112:149155.
22. Tiemann K, Lohmeier S, Kuntz S, et al. Real-time contrast echo 44. Hernot S, Klibanov AL. Microbubbles in ultrasound-triggered drug
assessment of myocardial perfusion at low emission power: first and gene delivery. Adv Drug Deliv Rev 2008;60:11171136.
experimental and clinical results using power pulse inversion imaging. 45. Duck FA. Hazards, risks and safety of diagnostic ultrasound. Med Eng
Echocardiography 1999;16:799809. Phys 2008;30:13381348.
23. Blomley MJK, Albrecht T, Cosgrove DO, et al. Stimulated acoustic 46. Wei K, Mulvagh SL, Carson L, et al. The safety of Definity and
emission in the liver parenchyma with the ultrasound contrast agent Optison for ultrasound image enhancement: a retrospective analysis of
Levovist. Lancet 1998b;351:568. 78,383 administered contrast doses. J Am Soc Echocardiogr 2008;21:
24. Wilson SR, Jang H-J, Kim TK, et al. Real-time temporal maximum- 12021206.
intensity-projection imaging of hepatic lesions with contrast-enhanced 47. Blomley M, Claudon M, Cosgrove D. WFUMB safety symposium on
sonography. Am J Roentgenol 2008;190:691695. echo-contrast agents: clinical applications and safety concerns.
25. Goertz DE, Frijlink ME, Tempel D, et al. Subharmonic contrast Ultrasound Med Biol 2007;33(2):180186.
intravascular ultrasound for vasa vasorum imaging. Ultrasound Med 48. Miller DL. WFUMB safety symposium on echo-contrast agents: in
Biol 2007;33:18591872. vitro bioeffects. Ultrasound Med Biol 2007;33(2):197204.
26. Eckersley RJ, Tang M-X, Chetty K, Hajnal JV. Microbubble contrast 49. Dalecki D. WFUMB safety symposium on echo-contrast agents:
agent detection using binary coded pulses. Ultrasound Med Biol bioeffects of ultrasound contrast agents in vivo. Ultrasound Med Biol
2007;33:17871795. 2007;33(2):205213.
27. Cherin E, Brown J, Masoy S-E, et al. Radial modulation imaging of 50. Whittingham TA. WFUMB safety symposium on echo-contrast agents:
microbubble contrast agents at high frequency. Ultrasound Med Biol exposure from diagnostic ultrasound equipment relating to cavitation
2008;34:949962. risk. Ultrasound Med Biol 2007;33(2):214223.
28. EFUSMB study group. Guidelines and good clinical practice 51. Nyborg W. WFUMB safety symposium on echo-contrast agents:
recommendations for contrast enhanced ultrasound (CEUS) Update mechanisms for the interaction of ultrasound. Ultrasound Med Biol
2008. Ultraschall Med 2008;29:2844. 2007;33(2):224232.
29. Tranquart F, Le Gouge A, Correas JM, et al. Role of contrast enhanced 52. Barnett SB, Duck F, Ziskin M. WFUMB symposium on safety of
ultrasound in the blinded assessment of focal liver lesions in ultrasound in medicine: Recommendations on the safe use of
comparison with MDCT and CEMRI: results from a multicentre study. ultrasound contrast agents. Ultrasound Med Biol 2007;33(2):
EJC Suppl 2008;6:915. 173174.
89
CHAPTER
ment is a long triangular fold that lies between the liver and the
INTRODUCTION 93 anterior parietal peritoneum, attached anteriorly from the dia-
ANATOMY 93 phragm down to the umbilicus, and posteriorly to the liver
from the upper end of the ligamentum teres and along its
VASCULAR AND BILIARY ARCHITECTURE 94 anterior surface. It shows a third, free edge extending from the
SEGMENTAL ANATOMY OF THE LIVER 95 inferior argin of the liver to the umbilicus, enclosing the ligamen-
tum teres.
VARIATIONS IN ANATOMY AND DEVELOPMENT 96 The lesser omentum is an important anatomical landmark in the
SCANNING TECHNIQUES 98 abdomen, but also is usually only seen when surrounded by fluid.
Segmental approach 98 It is a double layer of peritoneum that extends as a sheet from the
Liver parenchyma 100 lesser curve of the stomach to the liver and is also known as the
Liver surface 101 hepatogastric ligament. It attaches in the fissure for the ligamen-
Liver size 101 tum venosum and from there folds back on itself to continue as the
Vascular and ductal morphology 102 peritoneal layer covering the liver itself. At the oesophagogastric
region the anterior layer continues over the diaphragm as the pari-
etal peritoneum while the posterior layer is reflected over the pos-
terior abdominal wall (mainly covering the body and tail regions
INTRODUCTION of the pancreas) as the posterior wall of the lesser sac. On the right
the two layers separate to enfold the hepatic pedicle (comprising
The liver is the largest organ in the human abdomen. Due to its size, the portal vein, the hepatic artery and the bile duct), fusing lateral
position and architecture, it has a special place in abdominal ultra- to them to form a free border that stretches up from the first part of
sound, often influencing both the selection and set-up of ultrasound the duodenum to the lateral part of the porta hepatis where the
scanners. Knowledge of the normal anatomy and appearances is layers again continue into the peritoneum covering the liver. Thus
essential, in view of developments in hepatic surgical and interven- a foramen is formed immediately posterior to the porta hepatis
tional techniques, and the worldwide increase in chronic liver where the general peritoneum communicates with the recess (the
diseases. lesser sac); it is known as the foramen of Winslow and its poste-
rior margin overlies the inferior vena cava. The other walls of the
lesser sac are formed by the posterior wall of the stomach and the
peritoneum over the upper retroperitoneal structures so that part
of the pancreas lies immediately posterior to it. On the left it
ANATOMY extends up to the splenic hilum. Most of the caudate lobe lies
within it.
The normal liver lies mostly in the right upper abdomen, protected The coronary ligaments over the diaphragmatic surface of the
by the lower right rib cage; only its thin left part lies to the left of liver divide the subphrenic peritoneal space into anterior and pos-
midline. It is a solid organ, weighing approximately 1.5kg.1 It terior portions which are more completely separated on the right
shows a basic wedge shape, rounded on the right and tapering to where the ligament is more extensive. The posterior subphrenic
the left. The domed superior surface fits smoothly under the cupola space continues into the hepatorenal space (Morisons pouch).
of the right diaphragm and adjacent right ribs; the flatter inferior These spaces delimit regions in which ascitic fluid and infective
surface is tilted such that it faces posteriorly and to the left, and is collections are confined.
described as the visceral surface due to its contact with a number The ligamentum teres and ligamentum venosum are remnants
of other abdominal structures (Fig. 7.1). of the fetal circulation (Fig. 7.2) which appear as fibrous, reflective
Whereas the superior surface is smooth, the visceral surface is bands on ultrasound. Ligamentum venosum (fetal ductus
more complex, and most significantly contains the hilum, or porta venosus) extends from the left portal vein branch, upwards and
hepatis. Organs in contact with the visceral surface include, from to the right of the caudate lobe to join the vena cava at the orifice
right to left: right kidney, gallbladder, duodenum and stomach. The of the left hepatic vein. Ligamentum teres (fetal umbilical vein)
generally smooth surface of the liver is indented anteroinferiorly by runs in the liver from the anteroinferior fissure of the left lobe to
the gallbladder and ligamentum teres. join the left portal vein branch. Small, normally invisible vessels
The liver is clothed in adherent peritoneum, apart from the run along it: the hepatic branch of the superior epigastric artery,
fossae for the inferior vena cava and the gallbladder, and the so- and small veins connecting portal vein to the umbilicus (the latter
called bare area posteriorly. At certain points, however, the may dilate markedly in portal hypertension to form the para-
peritoneum is reflected off the surface of the liver to form complex umbilical vein and subcutaneous periumbilical collaterals caput
folds which connect with neighbouring structures; the coronary Medusae).
ligament, and right and left triangular ligaments are situated The liver is traditionally divided into left and right lobes, and
posteriorly, related to the bare area, and are not seen in currently the most widely accepted segmental classification is that
abdominal scans. However, the two other peritoneal folds described by Couinaud (see below), which is based on the vascular
may be seen clearly in the presence of ascites. The falciform liga- architecture of the liver.2
93
CHAPTER 7 Liver: anatomy and scanning techniques
Left coronary
ligament
VIII VII
II
III II I
Porta hepatis
V VI
Ligamentum Ligamentum
teres venosum
Ductus venosus Right hepatic vein Inferior vena cava Middle hepatic vein Left hepatic vein
Ligamentum venosum
Hepatic veins
VIII II
III
VII
IV
Umbilical vein
V
Inferior vena cava Portal vein Main portal vein
VI
Figure 7.2 Fetal circulation through the liver. The venous
bypass in the fetus takes blood returning from the placenta via the
umbilical vein to the left portal vein and thence directly to the left
hepatic vein and on into the inferior vena cava. The temporary
vessels that carry this blood (the umbilical vein and the ductus Right portal vein Gallbladder Left portal vein
venosus) undergo vasospasm at birth and they subsequently
thrombose to form the ligamentum teres and ligamentum venosum, Figure 7.3 Blood vessels of the liver. The main branches of the
respectively. If the spasm extends into the left portal vein itself, portal vein and the way they interdigitate with the three main
lateral parts of the left lobe of the liver become ischaemic. This may hepatic veins are illustrated. Couinauds segmental divisions are
account for the marked variability in size of this segment. indicated in Roman numerals.
origin occur,3 including separate left and right supplies from the
VASCULAR AND BILIARY ARCHITECTURE coeliac axis and superior mesenteric artery (SMA), or common
supply from the SMA alone. Identification of these vessels is impor-
The generally smooth liver parenchyma is traversed by several tant in preoperative assessment of liver transplant recipients. The
vascular structures: the portal veins, hepatic veins, hepatic arteries diameter of the normal common hepatic artery is 5mm or less. On
and the bile ducts. The liver is unique in receiving two blood sup- ultrasound images, the artery is roughly parallel with the portal
plies: the hepatic artery provides approximately 25% of the inflow vein at the porta, but is more tortuous, and is seen coming in and
at rest, in the form of oxygenated blood direct from the systemic out of the scan plane.
arterial system; the portal vein provides partially deoxygenated The portal vein originates as the confluence of the splenic and
blood (75%) via the bowel, spleen and other viscera. Both pass superior mesenteric veins, and enters the liver at the porta hepatis.
through the porta hepatis, along with the bile duct. Venous drain- It runs roughly transversely in the right upper abdomen, angled
age occurs via the hepatic veins, directly into the upper inferior superiorly and to the right, and always lies posterior to the hepatic
vena cava to the right atrium of the heart (Fig. 7.3). artery and bile duct. The main portal vein is a short trunk, a few
The common hepatic artery is normally a branch of the coeliac centimetres in length and around 1cm in diameter, which divides
axis, and divides into left and right branches at or somewhere as it enters the liver into left and right branches. The left branch
before the porta hepatis. In around 50% of people variations in its curves anteriorly before dividing further into segmental branches.
94
Segmental anatomy of the liver
The right portal vein passes transversely for a few centimetres to simply as the common duct. From the liver, the common duct
before dividing into anterior and posterior branches, then further passes down anterolateral to the portal vein, then posterior to the
subdividing into segmental veins. Within the liver parenchyma the first part of duodenum, through the posterior border of the head of
hepatic arteries follow the same course. pancreas, and turns sharply and transversely to the right to empty
The hepatic veins comprise three main veins left, middle and into the second part of duodenum at the ampulla of Vater. The
right. The left vein is relatively short, and lies approximately in the common duct does not lie perfectly parallel with the main portal
midline sagittal plane; the middle vein courses from the line of the vein, but sits in a very slightly more sagittal plane, so that it appears
gallbladder fossa towards the inferior vena cava, usually joining to cross the portal vein as it passes inferomedially to the duodenum.
with the left vein to form a short trunk before draining into the This difference in duct/vein plane may become more pronounced
inferior vena cava (Fig. 7.4). The right vein lies in the coronal plane in older patients.
and empties directly into the vena cava. In addition to this normal The liver also possesses a lymphatic system. The network of
arrangement of the three major veins, some liver segments which lymph vessels lies predominantly within the portal tracts, and like
lie in direct contact with the vena cava are drained directly by the elsewhere in the body is not seen with ultrasound. However, their
short inferior hepatic veins; these segments include the caudate lobe distribution can be revealed in the presence of lymphoedema (for
and the superomedial part of the right lobe (Fig. 7.5). instance in some forms of cirrhosis or after liver transplantation),
The bile ducts drain bile from the liver into the duodenum. The when low reflectivity cuffing may be seen surrounding the portal
intrahepatic arrangement of the ducts is similar to that of the portal tracts.4
venous system, with the small segmental ducts joining to form left Microscopically, the anatomy of the liver is still a matter of inter-
and right ducts, which normally lie anterior to their companion esting debate.5 Functional units within the liver structure have been
portal vein branches. Close to the porta hepatis, the right hepatic described since 1833, in the form of Kiernans classic lobule a
duct passes over the right portal vein, usually with the hepatic hexagonal lobule made up of the sinusoids, with portal tracts
artery in between. The confluence of the left and right ducts lies just (including portal vein, hepatic artery and bile ducts) at the six
outside the liver parenchyma, forming the common hepatic duct. corners and a draining hepatic vein at the centre. Later models
At a variable point along its length, the common hepatic duct is include the portal lobule portal tract at the centre and hepatic
joined by the cystic duct (which drains the gallbladder) to form the venules at the periphery and the liver acinus. Current concepts
common bile duct. Since this point cannot always be identified with favour primary and secondary lobules, with vascular septa as the
transabdominal ultrasound, the extrahepatic duct is often referred basis for the lobular architecture. It should be noted that the micro-
anatomy of the liver differs across species, both between animal
species and between animals and humans. Also, that these relation-
ships apply only to the adult liver; the arterial and biliary systems
are immature at birth, and in humans the hepatic arterial system
may only proliferate to reach the adult state at 15 years of age, sug-
gesting that the portal blood supply may be more important than
the arterial in establishing the lobular architecture.5
Overview of liver
The liver is the largest organ in the abdomen.
Knowledge of its complex three-dimensional structure is essential
for localisation and surgical planning.
Peritoneal folds, other ligaments and vascular structures are
important landmarks.
The liver receives a dual blood supply: 25% from hepatic artery,
75% from portal vein.
A B
95
CHAPTER 7 Liver: anatomy and scanning techniques
Segmental approach
The examination is ideally based upon mentally following the seg-
mental anatomy, e.g. from I to VIII, so that no part of the organ is
overlooked. The Couinaud segments can be followed by a sequence
of simple and easily identifiable landmarks: the central portal veins,
the caudate lobe itself, ligamentum teres, the gallbladder, right
kidney, middle and right hepatic veins.
Each segment or group of segments should be examined
by sweeps in two orthogonal planes, e.g. sagittal and transverse,
wherever possible. Sweeps should extend beyond the liver
capsule, to identify exophytic liver lesions or adjacent extrahepatic
pathology.
Starting in the midline sagittal plane with the transducer posi-
tioned just below the xiphisternum, the normal left lobe shows a
Figure 7.13 Adult polycystic liver and kidney. The polycystic triangular shape with a sharp anteroinferior border (Fig. 7.14). The
liver in the near field is difficult to differentiate from the polycystic caudate lobe can be seen deep to the left lobe, separated by the
right kidney in the far field. In real time, visceral slide can be used to reflective fissure line. This view also allows identification of other
identify the planes of tissue separation. epigastric structures, notably the pancreas, stomach, aorta,
mesenteric artery origins and adjacent lymph nodes.
Note that in thin subjects, in deep inspiration, the crura of the
has an advantage, in that by observing visceral slide between the diaphragm may also appear as a pre-aortic wedge-shaped structure
two during respiration, it is usually possible to identify their plane of varying reflectivity (Fig. 7.15).
of separation. Rotate the transducer anticlockwise into the transverse plane; in
this plane, the segments I to IV are arranged anticlockwise, so
identify the caudate lobe (I) again, then the segmental portal vein
branches supplying segments II (posterior) and III (anterior), and
SCANNING TECHNIQUES sweep through the segments accordingly (Fig. 7.16). The ligamen-
tum teres appears as a highly reflective fibrous band passing down
The liver is a large, complex three-dimensional structure, so it is from the anterior surface of the liver towards the left portal vein
important that the ultrasound practitioner develops a steady, sys- (Fig. 7.17). It is often dense enough to cast a significant acoustic
tematic approach to the assessment of each component of the exam- shadow. The inferior margin of the ligament and the left portal vein
ination. These components should include: are important landmarks for identifying, using colour Doppler, the
n segmental approach presence of a patent para-umbilical vein in portal hypertension. In
n parenchyma the presence of ascites, the falciform ligament can be seen extending
n reflectivity from the ligamentum teres to the anterior parietal peritoneum.
98
Scanning techniques
Figure 7.19 Right lobe the blind area. The intercostal section
Figure 7.17 Ligamentum teres. Transverse (left image) and (left image) shows lack of information in the upper segments close
sagittal (right) sections. The ligamentum teres appears as a highly to dome of diaphragm, usually due to overlying rib or aerated lung.
reflective band which is usually linear in transverse section and may These segments may be seen by taking a right subcostal approach
be triangular or sheet-like in sagittal. It often cast a dense acoustic in deep inspiration, with cephalad angulation of the transducer
shadow. (right image).
99
CHAPTER 7 Liver: anatomy and scanning techniques
Liver parenchyma
The ideal ultrasound image of the normal liver is very much a
matter of personal preference, and can be a major influence on
purchasing decisions. The assessment of liver parenchymal texture
is notoriously subjective, and can give rise to a confusing range of
reporting terminology in both normal and abnormal situations.
Some users prefer to see a smooth texture with minimum speckle
pattern, others prefer a sharper, more speckly image. Modern
ultrasound scanners possess a vast range of beam-forming and
image processing techniques, each of which can significantly alter Figure 7.22 Liver reflectivity. The normal liver texture is uniform
the perceived echotexture of the liver; just changing transducers and shows slightly increased reflectivity compared with adjacent
on the same scanner can markedly affect interpretation, and it may normal renal cortex.
take several scanning sessions to get a feel for normal liver texture
for each individual transducer/scanner combination. The aim in
every department should be to develop agreed standards, both for
imaging technique and reporting terminology.
Liver assessment
The key to ultrasound examination of liver parenchyma is image
optimisation. Firstly, depth should be adjusted to include only the Scanning technique should be systematic and segmental.
section of liver down to its deepest surface, followed by optimisa- Perception of liver texture is highly subjective.
tion of 2D gain. Time gain compensation should be adjusted to Parenchymal appearances can be markedly changed using
produce an image that is as uniform as possible from near to far different systems and imaging parameters.
field. Focus depth is generally positioned at the area of interest, but Accurate assessment of liver size is difficult.
may be placed in the far field to improve penetration. An increasing Assessment of the liver surface is an important component of the
number of systems provide semi-automated optimisation controls, examination.
which alter several parameters simultaneously; these are remark-
ably effective and can be used for rapid image optimisation. Tissue
harmonic imaging may be used for baseline scanning or activated
when increased tissue contrast is required this again is a matter
of personal preference depending on the system used (Fig. 7.21). cortex (Fig. 7.22). The parenchymal texture should be homogene-
High-resolution or read zoom should be used to interrogate areas ous. Since the time gain compensation curves of most scanners are
of interest. set up using the right lobe of liver as a reference, there should be
Normal liver has a uniform reflectivity that is the same or is little or no appreciable attenuation of echoes when progressing
slightly increased compared to the adjacent normal right renal from near to far field in normal circumstances.
100
Scanning techniques
Portal
vein
Transverse section
Figure 7.23 Liver surface. Sagittal section of left lobe using a Figure 7.24 Measurement of the caudate lobe. The position for
linear 517MHz transducer with spatial compound imaging. Normal measurement of the caudate lobe in the transverse plane is shown.
linear appearance (arrows) with no irregularity. The normal caudate is less than two-thirds the transverse diameter
of the right lobe.
Table 7.1 Dimensions of the normal liver3
Liver surface
The surface of the normal liver presents as a very smooth reflective
interface. Identification of a change to an irregular or nodular
surface is extremely important in the assessment of diffuse chronic
liver disease, e.g. cirrhosis, so an ultrasound examination of the
liver should include a high-resolution image of its surface. This is
best obtained from a free edge (usually the anterior border of the
left lobe, as the right lobe intercostal surface may be compressed by
the adjacent chest wall) using a high-frequency linear transducer
(Fig. 7.23). Spatial compound imaging assists in improving the edge Figure 7.25 Volume ultrasound. Volume acquisition of the left
definition of the liver surface, allowing detection of subtle varia- lobe of liver (segments II and III) using a 26MHz mechanically
tions. Systems are also increasingly able to provide improved edge swept curvilinear transducer, 3 second scan time. Multiplanar
definition at depth, e.g. of the free inferior (visceral) surfaces of both images (right) have been measured using a stacked contour
left and right hepatic lobes. technique, to produce a surface-rendered representation of this
part of the left lobe. Volume calculation 250mL.
Liver size
Clinical hepatomegaly is defined by palpation of the liver edge However, the size of the caudate lobe is relatively easily assessed
below the costal margin, but this evaluation is notoriously unreli- using linear ultrasound measurements, and this may be helpful in
able.10,11 For example, a normal size liver may be displaced inferi- confirming enlargement in conditions such as cirrhosis or hepatic
orly by overinflated lungs or by an enlarged heart, or a Riedels lobe vein occlusion (BuddChiari syndrome). The transverse diameter
may be present. One advantage of ultrasound is that the inferior can be obtained as shown in Figure 7.24, where this diameter at the
border of the liver can rapidly be located in relation to the clinical level of the porta can be compared with that of the right lobe. The
marker of the costal margin, so that a clinical diagnosis of hepatome- normal caudate lobe should be less than two-thirds the diameter of
galy can be correlated directly with normal or abnormal ultrasound the right lobe.13 The anteroposterior diameter of the caudate lobe
findings. can also be measured and compared with that of the adjacent left
Wide variations in the configuration of the liver make any assess- lobe; the normal caudate diameter should be less than half that of
ment of its overall size difficult, and like so many aspects of liver the left lobe.
ultrasound, this evaluation is subjective. Ultrasound assessment of Recent and ongoing developments in volume acquisition ultra-
liver size is possible, using linear measurements in standard posi- sound, using mechanical and true matrix transducers, provide for
tions, and these may be useful in specific circumstances.12 For refer- more accurate volumetric analysis, but the size of the normal liver
ence, longitudinal (maximum supero-inferior span) measurements is too great for their current acquisition range. However, these tech-
of the left lobe in the midline and right lobe in midclavicular line niques can be used for measuring the volume of specific parts of
from 1000 healthy subjects are listed in Table 7.1. the liver, e.g. left lobe (Fig. 7.25), and are increasingly being used to
101
CHAPTER 7 Liver: anatomy and scanning techniques
assess more accurately the size and progress of neoplastic masses techniques can markedly alter the appearances of both liver texture
in the liver. Since assessment of overall liver size is now achievable and linear structures within the liver another case for learning the
using rapid MR or CT sequences, these may be the method of capabilities of, and variations produced by, individual systems. It
choice. should be noted that a number of diffuse liver diseases are more
likely to show changes around the portal tracts than around the
Vascular and ductal morphology hepatic veins.
As well as developments in image processing, progressive
These structures can be imaged at the porta hepatis, and in their improvements in spatial resolution are making it possible routinely
intrahepatic and extrahepatic portions. to identify the components within the portal tracts (vein, artery and
The porta hepatis is usually assessed from the right intercostal duct) as discrete vessels, down to at least segmental level (Fig. 7.28).
approach. This approach also provides an optimal incident angle For quantification and surveillance purposes, a transverse view of
(around 30) for Doppler studies. The portal vein should be identi- the left lobe should be recorded with the portal tracts of segments
fied as the largest vessel at the porta, and the scan plane oriented 2 and/or 3 seen lengthways, i.e. perpendicular to the beam.
such that it is seen lengthways (Fig. 7.20). With slight variations Although clearly there may be asymmetry of these structures
from this plane, the common duct will be seen as a smaller vascular between left and right lobes, in diffuse disease these tracts are more
structure lying above the portal vein. Closer to the hilum of the easily assessed than those in the right lobe.
liver, the right and left ducts, and the right and left portal veins,
may be traced as separate structures. At the hilum, the hepatic
artery, more likely the right branch of the hepatic artery, may be
identified in cross-section lying between the duct and portal vein.
The relationship of the hepatic artery and common duct shows
variations along their lengths, but the pair almost without exception
lie above the portal vein on this projection.
In transverse section, the portal vein appears as the largest vas-
cular ring, with the hepatic artery and common duct lying imme-
diately anteriorly.
The portal vein can be traced from the porta into left and right
branches. Each of these generally divides in H form, with the H
appearing to lie on its side, to supply the lobar segments6 (Fig. 7.16).
The intrahepatic portal and hepatic veins can be differentiated by
their anatomical orientation, rather like the interlocking fingers of
two hands, and to some extent by their structural appearances.
Portal veins tend to have thicker, more reflective walls, whereas
hepatic veins may appear to have no walls at all (Fig. 7.26). The
portal vein wall borders are enhanced by the accompanying bundle
of hepatic artery, bile duct and associated connective tissue. Figure 7.27 Hepatic vein walls. The effect of incident beam
However, this is a very variable difference, and depends markedly angle on wall reflectivity (right hepatic vein). With an acute angle of
on the incident angle of the ultrasound beam. Thus normal hepatic approach (left) the hepatic vein shows little or no wall reflectivity.
veins lying perpendicular to the beam may show a reflective wall, The same vein imaged with a perpendicular approach (right) shows
which disappears when approached from a different, more acute highly reflective walls, similar to a normal intrahepatic portal vein.
angle (Fig. 7.27). In addition, modern adaptive image processing
Figure 7.29 Right hepatic vein. Intercostal coronal oblique Figure 7.31 Cystic duct insertion. Subcostal oblique section.
showing right hepatic vein entering inferior vena cava. The cystic duct (arrow) is seen entering the deep wall of the
common hepatic duct, combining to form the common bile duct.
Note the slight dilatation of the common duct at this point.
REFERENCES
1. Gelfand DW. Anatomy of the liver. Radiol Clin North Am
1980;18:187194.
2. Couinaud C. Le foie; tudes anatomiques et chirurgicales. Paris:
Masson; 1957.
3. Sidhu PS, Chong WK. Measurement in ultrasound: a practical
handbook. London: Arnold; 2004.
4. Worthy SA, Elliott ST, Bennett MK. Low-reflectivity periportal collar
on hepatic ultrasound. Br J Radiol 1994;67:10501051.
Figure 7.30 Common hepatic duct measurement. Intercostal 5. Saxena R, Theise ND, Crawford J. Microanatomy of the human liver
view of porta hepatis. The common duct is measured (callipers) at exploring the hidden interfaces. Hepatology 1999;30:13391346.
the point where it crosses the hepatic artery (arrow) in cross- 6. LaFortune M, Madore F, Patriquin H, Breton G. Segmental anatomy of
section. PV, portal vein. the liver: a sonographic approach to the Couinaud nomenclature.
Radiology 1991;181:443448.
7. Massaro M, Valencia MP, Guzman M, Mejia J. Accessory hepatic lobe
mimicking an intra-abdominal tumor. J Comput Assist Tomogr
2007;31:572573.
8. Aktan ZA, Savas R, Pinar Y, Arslan O. Lobe and segment anomalies of
the liver. J Anat Soc India 2001;50:1516.
The three main hepatic veins can sometimes be seen at once in 9. Torra R. Polycystic kidney disease. http://emedicine.medscape.com/
subxiphoid high transverse sections of the liver as they converge article/244907-overview. 2008.
towards the inferior vena cava. More often, several different planes 10. Naftalis J, Leevy CM. Clinical estimation of liver size. Am J Dig Dis
are required to image them individually. The right hepatic vein can 1963;8:236243.
be seen in a coronal oblique plane from the intercostal window, and 11. Sullivan S, Krasner N, Williams R. The clinical estimation of liver size.
BMJ 1976;2:10421043.
traced directly into the vena cava (Fig. 7.29). Left and middle
12. Niederau C, Sonnenberg A, Mller JE, et al. Sonographic
hepatic veins can be seen converging into their common trunk from measurements of the normal liver, spleen, pancreas and portal vein.
a transverse plane with some cephalad angulation (Fig. 7.4). Radiology 1983;149:537540.
The common duct is conventionally measured at the porta 13. Harbin WP, Robert NJ, Ferrucci JT. Diagnosis of cirrhosis based on
hepatis, around the point where the triad of vein, duct and artery regional changes in hepatic morphology: a radiological and
are seen, and the artery is in cross-section (Fig. 7.30). Taking an pathological analysis. Radiology 1980;135:273283.
103
CHAPTER
A
B
Sonographic features of normal liver triglycerides within the cytoplasm of hepatocytes as a result of
disruption to normal lipid metabolic pathways, predominantly
Liver reflectivity right kidney those of free fatty acids.11 Initially hepatocyte accumulation of lipid
Liver reflectivity < spleen is centrilobular (around the hepatic vein) in distribution, but with
Defined reflective periportal tracts increasing severity this extends out towards the portal tracts
Visible diaphragmatic interface (Fig. 8.3A and B).
Uniform parenchymal speckle pattern Worldwide the commonest two causes of a fatty liver are alcohol
and non-alcoholic fatty liver disease (NAFLD).11,12 Other important
secondary causes include obesity, diabetes mellitus, hyperlipidae-
true anatomical structure, with a significant contribution towards mia, pregnancy, starvation, drugs (especially steroids), severe hepa-
the altering echo amplitude arising from scatter. Echotexture is also titis, gastrointestinal bypass surgery, cystic fibrosis and glycogen
dependent upon technical factors within the ultrasound scanner storage disease (Table 8.1). As the process behind fatty liver is
and therefore speckle reduction techniques such as spatial or fre- dynamic any correction of the primary cause will frequently result
quency compounding can dramatically alter the apparent liver in its rapid reversal (Fig. 8.4A and B).13
texture (Fig. 8.2A and B). On ultrasound the presence of multiple fat interfaces throughout
the liver causes a diffuse increase in parenchymal reflectivity,
making it greater than that of the adjacent normal right kidney, or
more reliably the spleen. Unlike other causes of a bright liver
FATTY LIVER (Table 8.2), the echo pattern is fine and uniform, and with increasing
fat deposition there is attenuation of the ultrasound beam, through
Fatty liver is one of the commonest abnormal findings on an both absorption and scatter.11,14,15
abdominal ultrasound and its incidence across Western countries Diffuse fatty liver can be described as: mild when there is
is increasing. It represents the reversible accumulation of minimal increase in parenchymal reflectivity, moderate when
105
CHAPTER 8 Diffuse parenchymal liver disease
A B
Figure 8.2 Alteration of liver echotexture with machine settings. A: Identical view to Figure 8.1 with spatial compounding showing a
fine interleaving echo pattern from the liver parenchyma. B: Same view with frequency compounding switched on resulting in a much more
uniform echotexture.
A B
Figure 8.3 Fatty liver histology. A: Normal liver biopsy (H&E stain, 100 magnification), demonstrating uniformity of hepatocyte
distribution, interrupted by sinusoidal spaces. B: Liver biopsy (H&E stain, 100 magnification) showing moderate diffuse fatty change;
at ultrasound the fat globules act as multiple acoustic interfaces hence increasing the parenchymal reflectivity.
there is loss of intrahepatic vessel wall definition with impaired in a number of the conditions associated with fatty liver. Despite
visualisation of the diaphragm, and severe when there is poor its apparent sensitivity, the detection of fatty liver at ultrasound can
penetration of the posterior aspect of the right lobe of the liver with be highly subjective, with only moderate inter-observer agreement
very poor or non-visualisation of the hepatic vessels and dia- reported.19 In acute fatty liver of pregnancy the liver most often
phragm.16 With increasing severity there is often a degree of appears normal on ultrasound.20
hepatomegaly (Fig. 8.5AC). As well as the greyscale changes, increasing hepatic steatosis can
The reported sensitivity and specificity for ultrasound in assess- cause dampening of the normal hepatic vein spectral Doppler
ing the presence of fatty liver depends upon the degree of severity triphasic waveform, resulting in a biphasic or monophasic pattern.
and is therefore variable at 60100% and 7795%, respectively.17,18 A reduction in the hepatic artery resistive index has also been
The lower specificity may well be due to the coexistence of fibrosis reported.21
106
Fatty liver
Table 8.1 Conditions associated with fatty liver Table 8.2 Causes of increased liver reflectivity
Other:
Cystic fibrosis
A B
Figure 8.4 Temporal changes in fatty infiltration. A: Moderate fatty liver with a focal heterogeneous mass in a patient with high
alcohol consumption. B: Repeat scan 16 days later shows complete resolution of fatty infiltration revealing a typical haemangioma.
Focal fatty change metastases.24 Careful ultrasound examination will show that these
areas lack any mass effect and do not alter the course of regional
Although fatty infiltration is usually a diffuse process, it may vessels.21 An interval scan may also reveal a rapid change in size or
sometimes affect only one lobe, segment or subsegment of the shape of these areas. If there is still concern, contrast-enhanced
liver. In these cases it usually has a fairly characteristic geographic ultrasound should demonstrate iso-enhancement of the focal area
pattern, with relatively well-defined, straight or angulated margins in comparison to the adjacent normal liver. Liver MRI with in and
between areas of differing reflectivity: less frequently an interdigi- out of phase gradient echo sequencing can also confirm the pres-
tating pattern has been described.14,22,23 When subsegmental, pref ence of focal fat.11
erred locations for this distribution include the porta hepatis, Subcapsular fatty infiltration in diabetic patients receiving
gallbladder fossa and areas adjacent to the falciform ligament2123 intraperitoneal insulin, and perivascular infiltration (predomi-
(Fig. 8.6AC). nantly affecting the hepatic veins) in high alcohol consumers
Focal fatty infiltration can sometimes be more rounded in appear- are more unusual patterns that have been described on CT and
ance and may also be multifocal in distribution, so that on ultra- MRI.11,25 The latter has a rather non-specific distribution on
sound it can potentially be mistaken for haemangiomas or echogenic ultrasound.
107
CHAPTER 8 Diffuse parenchymal liver disease
A B
Figure 8.5 Differing degrees of diffuse fatty infiltration. A: Mild, with diffuse increased reflectivity, but good vessel visualisation and
penetration. B: Moderate, with indistinct vessel walls and reduced penetration. C: Severe, with poor vessel visualisation and very limited
penetration.
Focal fatty sparing directly into the liver.11 A number of studies have now described
this phenomenon using colour Doppler, contrast ultrasound and
CT angiography to demonstrate the aberrant vessels.2730
Within a diffusely fatty liver there may be focal areas of relatively On the whole the location and contour of fatty sparing is usually
normal liver parenchyma. At ultrasound these appear as low reflec- characteristic enough on ultrasound, to recognise it for what it is.
tive focal lesions, which can be misinterpreted as discrete hepatic However, as with focal fatty infiltration, it can have a more nodular
masses. The common locations for this appearance are similar to appearance so that, on occasion, further assessment is required.
those of focal fatty change, namely the gallbladder fossa, periportal Contrast ultrasound will show a uniform enhancement pattern
region and around the falciform ligament, where they typically identical to background liver (Fig. 8.8B) throughout all phases.31 As
demonstrate a geographic pattern (Fig. 8.7A and B).11,14,26 Focal with focal fatty infiltration, liver MRI with in and out of phase
nodular like areas in segment II of the liver have also been gradient echo will confirm the altered fat content.32
described (Fig. 8.8A). Areas of focal fatty sparing may also be seen around benign and
These focal areas of fatty sparing are thought to be due to regional malignant focal liver lesions, including: haemangiomas, focal
reduction in portal vein perfusion, most often as a result of aberrant nodular hyperplasia, hepatocellular carcinoma and metastases. In
splanchnic veins or divisions of normal (non-portal) veins draining these cases compression of adjacent hepatocytes by the focal tumour
108
Fatty liver
B
A
A B
Figure 8.7 Patterns of focal fatty sparing. A: Fatty liver, with a typical wedge-shaped area of focal sparing adjacent to the gallbladder.
B: More extensive area of fatty sparing in segments II and III of the liver, again showing a geographical pattern. 109
CHAPTER 8 Diffuse parenchymal liver disease
A B
Figure 8.8 Patterns of focal fatty sparing. A: Oval shaped area of focal sparing in segment II with moderate background fatty change.
B: CEUS confirms iso-enhancement of the area with respect to the background liver consistent with focal fatty sparing.
A B
Figure 8.9 Perilesional focal fatty sparing. A: Mild-moderate fatty liver with focal lesion in left lobe (arrow) showing a peripheral
low reflective halo (perilesional fatty sparing) suggestive of a metastasis. B: Post contrast the lesion shows early arterial enhancement of
the central component (arrow), becoming isoechoic with background liver and apparent halo during the parenchymal phase: biopsy
confirmed focal nodular hyperplasia.
A B
Figure 8.12 Cirrhotic liver morphology. A: Transverse measurements of caudate (6cm) and right lobe (9cm) in a patient with
established cirrhosis. B: Enlarged caudate lobe in a cirrhotic liver giving a pseudo-mass appearance.
A B
Figure 8.15 Surface nodularity. A: In the absence of ascites high-resolution ultrasound of a hepatic vein contour can help demonstrate
surface nodularity. B: Irregular liver surface demonstrated against the gallbladder wall.
Dysplastic nodules tend to be larger than regenerative nodules Other greyscale findings in cirrhosis reflect the altered haemody-
and are considered premalignant, the hepatocytes showing histo- namics associated with portal hypertension, including splenomeg-
logical features of atypical growth. With increasing dysplasia ang- aly, enlarged venous collaterals and intrahepatic arterial branches,
iogenic pathways are activated leading to the development of a gallbladder and stomach wall thickening and the presence of ascites
predominantly arterial supply.45,63 On contrast-enhanced ultra- (Fig. 8.19A and B). All of these are covered in more detail in Chapter
sound (CEUS) low-grade dysplastic nodules tend to have an identi- 12. The altered haemodynamics seen in cirrhosis can also be
cal enhancement pattern to that of regenerating nodules; however, demonstrated using functional imaging methods with ultrasound
increasingly high-grade dysplastic nodules will begin to show arte- contrast agents. There is a significant reduction in the transit
rial phase enhancement64 (Fig. 8.18). time of these intravascular agents through the liver in cirrhosis,
which can be detected using either spectral Doppler or contrast
harmonic imaging.1,2,65 The details of this technique are described
in Chapter 10.
Sonographic features of cirrhosis
Biliary cirrhosis
Relative enlargement of left lobe and caudate
Coarse echotexture Primary biliary cirrhosis (PBC) is a slowly progressive autoimmune
Surface irregularity disease of the liver that primarily affects women in the fifth decade
Focal nodules (hypo/hyperechoic) of life. Histopathologically there is periportal inflammation with
Splenomegaly, ascites and visceral congestion immune-mediated destruction of the intrahepatic bile ducts, leading
Damped hepatic vein spectral traces. to accumulation of toxic substances and further hepatic damage
Reduced liver transit times with CEUS with fibrosis and finally cirrhosis.66 Serologically anti-mitochondrial
Increased tissue stiffness on sonoelastography antibodies are present in the majority of patients.66
In early stages the liver is usually normal or slightly enlarged,
with no textural changes: a pattern of periportal low reflectivity has
been described; however, this is a non-specific finding.67 With pro-
gressive disease the liver tends to appears nodular, and shows
coarse thickening of the periportal tracts (Fig. 8.20A). The coexist-
ence of gallstones is a common finding and a significant number of
patients will have enlarged periportal, gastro-hepatic ligament or
upper retroperitoneal lymph nodes (Fig. 8.20B). Enlarged perihe-
patic lymph nodes are also a common described finding in hepatitis
C and autoimmune hepatitis.68,69
Secondary biliary cirrhosis is a result of longstanding biliary
obstruction, often with only minor visible bile duct dilatation.
Underlying conditions include sclerosing cholangitis, choledochal
cyst, bile duct strictures or atresias. The subsequent cirrhotic
changes have no particular features.
A B
Figure 8.19 Associated findings in cirrhosis. A: Enlarged segmental hepatic artery due to portal hypertension, which may be mistaken
for intrahepatic bile duct dilatation. B: Congestive cholecystopathy in cirrhotic portal hypertension causing moderate gallbladder wall
oedema.
115
CHAPTER 8 Diffuse parenchymal liver disease
A B
Figure 8.20 Primary biliary cirrhosis. A: High-resolution scan through the left lobe showing marked periportal echogenic thickening.
B: Longitudinal scan showing enlarged lymph nodes in the hepatoduodenal ligament in a patient with PBC.
periportal tract reflectivity and thickening, with a generalised coars- findings and diagnosis using MR imaging. Eur Radiol
ening of the parenchymal texture.8689 Surface irregularity, with 2000;10:10951100.
regenerating nodules 23cm in size, is seen in diffuse cirrhosis 25. Hamer OW, Aguirre DA, Casola G, Sirlin CB. Imaging features of
perivascular fatty infiltration of the liver: initial observations.
along with atrophy of the right lobe and possibly signs of portal
Radiology 2005;237:159169.
hypertension. The coexistence of a micro-gallbladder in CF patients 26. Sauerbrei EE, Lopez M. Pseudotumor of the quadrate lobe in hepatic
is a well-described feature.89 sonography: a sign of generalized fatty infiltration. AJR Am J
Roentgenol 1986;147:923927.
27. Tochio H, Kudo M, Okabe Y, et al. Association between a focal spared
area in the fatty liver and intrahepatic efferent blood flow from the
REFERENCES gallbladder wall: evaluation with colour Doppler sonography. AJR
1. Albrecht T, Blomley MJ, Cosgrove DO, et al. Non-invasive diagnosis of Am J Roentgenol 1999;172:12491253.
hepatic cirrhosis by transit-time analysis of an ultrasound contrast 28. Liu LP, Dong BW, Yu XL, et al. Analysis of focal spared areas in fatty
agent. Lancet 1999;353:15791583. liver using color Doppler imaging and contrast-enhanced microvessel
2. Lim AK, Taylor-Robinson SD, Patel N, et al. Hepatic vein transit times display sonography. J Ultrasound Med 2008;27:387394.
using a microbubble agent can predict disease severity non-invasively 29. Gabata T, Matsui O, Kadoya M, et al. Aberrant gastric venous
in patients with hepatitis C. Gut 2005;54:128133. drainage in a focal spared area of segment IV in fatty liver:
3. Forner A, Vilana R, Ayuso C, et al. Diagnosis of hepatic nodules demonstration with colour Doppler sonography. Radiology
20mm or smaller in cirrhosis: prospective validation of the 1997;203:461463.
noninvasive diagnostic criteria for hepatocellular carcinoma. 30. Matsui O, Takahashi S, Kadoya M, et al. Pseudolesion in segment IV
Hepatology 2008;47:97104. of the liver at CT during arterial portography: correlation with
4. Jang H-J, Kim TK, Wilson SR. Small nodules (12cm) in liver cirrhosis: aberrant gastric venous drainage. Radiology 1994;193:3135.
characterization with contrast-enhanced ultrasound. Eur J Radiol 2008 31. Bleuzen A, Tranquart F. Incidental liver lesions: diagnostic value of
Sep 30; Epub 2008 Sep 30. cadence contrast pulse sequencing (CPS) and SonoVue. Eur Radiol
5. Friedrich-Rust M, Ong MF, Herrmann E, et al. Real-time elastography 2004;14(Suppl 8):P5362.
for noninvasive assessment of liver fibrosis in chronic viral hepatitis. 32. Tom WW, Yeh BM, Cheng JC, et al. Hepatic pseudotumor due to
AJR Am J Roentgenol 2007;188:758764. nodular fatty sparing: the diagnostic role of opposed-phase MRI. AJR
6. Dahl JJ, Pinton GF, Mark L, et al. A parallel tracking method for Am J Roentgenol 2004;183:721724.
acoustic radiation force impulse imaging. IEEE Trans Ultrason 33. Duvnjak M, Leroti I, Bari N, et al. Pathogenesis and management
Ferroelectr Freq Control 2007;54:301312. issues for non-alcoholic fatty liver disease. World J Gastroenterol
7. Kurtz AB, Dubbins PA, Rubin CS, et al. Echogenicity: analysis, 2007;13:45394550.
significance, and masking. AJR Am J Roentgenol 1981;137: 34. Angulo P. Non-alcoholic fatty liver disease. N Engl J Med
471476. 2002;346:12211231.
8. Chiou S-Y, Forsberg F, Fox TB, Needleman L. Comparing 35. Farrell GC, Larter CZ. Nonalcoholic fatty liver disease: from steatosis
differential tissue harmonic imaging with tissue harmonic and to cirrhosis. Hepatology 2006;43:S99S112.
fundamental gray scale imaging of the liver. J Ultrasound Med 2007; 36. Powell EE, Cooksley WGE, Hanson R, et al. The natural history of
26:15571563. nonalcoholic steatohepatitis: a follow-up study of forty-two patients
9. Garra BS, Insana MF, Shawker TH, Russell MA. Quantitative for up to 21 years. Hepatology 1990;11:7480.
estimation of liver attenuation and echogenicity: normal state versus 37. Hui JM, Kench JG, Chitturi S, et al. Longterm outcomes of cirrhosis in
diffuse liver disease. Radiology 1987;162:6167. nonalcoholic steatohepatitis compared with hepatitis C. Hepatology
10. Oosterveld BJ, Thijssen JM, Hartman PC, et al. Ultrasound attenuation 2003;38:420427.
and texture analysis of diffuse liver disease: methods and preliminary 38. Charlton M, Kasparova P, Weston S, et al. Frequency of nonalcoholic
results. Phys Med Biol 1991;36:10391064. steatohepatitis as a cause of advanced liver disease. Liver Transpl
11. Hamer OW, Aguirre DA, Casola G, et al. Fatty liver: imaging patterns 2001;7:608614.
and pitfalls. Radiographics 2006;26:16371653. 39. Moriyasu F, Iijima H, Tsuchiya K, et al. Diagnosis of NASH using
12. Farrell GC, Larter CZ. Nonalcoholic fatty liver disease: from steatosis delayed parenchymal imaging of contrast ultrasound. Hepatol Res
to cirrhosis. Hepatology 2006;43:S99S112. 2005;33:9799.
13. Clain JE, Stephens DH, Charboneau JW. Ultrasonography and 40. Friedrich-Rust M, Ong M-F, Martens S, et al. Performance of transient
computed tomography in focal fatty liver. Report of two cases with elastography for the staging of liver fibrosis: a meta-analysis.
special emphasis on changing appearances over time. Gastroenterology 2008;134:960974.
Gastroenterology 1984;87:948952. 41. Saverymuttu SH, Joseph AEA, Maxwell JD. Ultrasound scanning in
14. Tchelepi H, Ralls PW, Radin R, Grant E. Sonography of diffuse liver the detection of fibrosis and steatosis. BMJ 1986;292:1315.
disease. J Ultrasound Med 2002;21:10231032. 42. Zheng R-Q, Wang Q-H, Lu M-D, et al. Liver fibrosis in chronic viral
15. Joseph AE, Saverymuttu SH, al-Sam S, et al. Comparison of liver hepatitis: an ultrasonographic study. World J Gastroenterol
histology with ultrasonography in assessing diffuse parenchymal liver 2003;9:24842489.
disease. Clin Radiol 1991;43:2631. 43. Nishiura T, Watanabe H, Ito M, et al. Ultrasound evaluation of the
16. Scatarige JC, Scott WE, Donovan PJ, et al. Fatty infiltration of the liver: fibrosis stage in chronic liver disease by the simultaneous use of low
ultrasonographic and computed tomographic correlation. J Ultrasound and high frequency probes. Br J Radiol 2005;78:189197.
Med 1984;3:914. 44. Wolf DC. Cirrhosis. emedicine [ONLINE] 2008 Aug [update 22 Dec
17. Joy D, Thava VR, Scott BB. Diagnosis of fatty liver disease: is biopsy 2009]. Available from: http://emedicine.medscape.com/
necessary? Eur J Gastroenterol Hepatol 2003;15:539543. article/185856-overview.
18. Saadeh S, Younossi ZM, Remer EM, et al. The utility of radiological 45. Anthony PP, Ishak KG, Nayak NC, et al. The morphology of cirrhosis.
imaging in nonalcoholic fatty liver disease. Gastroenterology J Clin Pathol 1978;31:395414.
2002;123:745750. 46. MacSween RNM, Anthony PP, Scheuer PJ. Pathology of the liver.
19. Strauss S, Gavish E, Gottlieb P, Katsnelson L. Interobserver and 2nd edn. New York: Churchill Livingstone; 1987:342363.
intraobserver variability in the sonographic assessment of fatty liver. 47. Rumack CM, Wilson S, Charboneau JW. Diagnostic Ultrasound.
AJR Am J Roentgenol 2007;189:W320W323. 3rd edn. Missouri: Mosby; 2004.
20. Van Le L, Podrasky A. Computed tomographic and ultrasonographic 48. Zaman SN, Melia WM, Johnson RD, et al. Risk factors in development
findings in women with acute fatty liver of pregnancy. J Reprod Med of hepatocellular carcinoma in cirrhosis: prospective study of 613
1990;35:815817. patients. Lancet 1985;1:13571360.
21. Karcaaltincaba M, Akhan O. Imaging of hepatic steatosis and fatty 49. Harbin WP, Robert NJ, Ferrucci JT. Diagnosis of cirrhosis based on
sparing. Eur J Radiol 2007;61:3343. regional changes in hepatic morphology. Radiology 1980;135:273.
22. Quinn SF, Gosink BB. Characteristic sonographic signs of hepatic fatty 50. Giorgio A, Amoroso P, Lettiri G, et al. Cirrhosis: value of caudate
infiltration. AJR Am J Roentgenol 1985;145:753755. to right lobe ratio in diagnosis with ultrasound. Radiology
23. Jain KA, McGahan JP. Spectrum of CT and sonographic appearance of 1986;161:443.
fatty infiltration of the liver. Clin Imaging 1993;17:162168. 51. Goyal AK, Pokharna DS, Sharma SK. Ultrasonic diagnosis of cirrhosis:
24. Kroncke TJ, Taupitz M, Kivelitz D, et al. Multifocal nodular fatty reference of quantitative measurements of hepatic dimensions.
infiltration of the liver mimicking metastatic disease on CT: imaging Gastrointest Radiol 1990;15:32.
118
References
52. Paruleker SG, Bree RL. Liver. In: McGahan JP, Goldberg BB, editors. 71. Larcos G, Sorokopud H, Berry G, Farrell GC. Sonographic screening
Diagnostic ultrasound. 2nd edn. New York: CRC Press; 2008. for hepatocellular carcinoma in patients with chronic hepatitis or
p. 339426. cirrhosis: an evaluation. AJR Am J Roentgenol 1998;171:433435.
53. Martnez-Noguera A, Calonge E, Coscojuela P, et al. Chronic liver 72. Wun YT, Dickinson JA. Alpha-fetoprotein and/or liver
disease: comparison of ultrasound patterns with laparoscopy and ultrasonography for liver cancer screening in patients with chronic
biopsy. J Clin Ultrasound 1993;21:325330. hepatitis B (Review). Cochrane Database of Systematic Reviews 2003,
54. Taylor KJW, Gorelick FS, Rosenfield AT, Riely CA. Ultrasonography of Issue 2. Art. No.: CD002799. DOI: 10.1002/14651858.CD002799.
alcoholic liver disease with histological correlation. Radiology 73. Ozen H. Glycogen storage diseases: new perspectives. World J
1981;141:157161. Gastroenterol 2007;13:25412553.
55. Caturelli E, Castellano L, Fusilli S, et al. Coarse nodular US pattern 74. Lee P, Mather S, Owens C, et al. Hepatic ultrasound findings in
in hepatic cirrhosis: risk for hepatocellular carcinoma. Radiology glycogen storage diseases. Br J Radiol 1994;67:10621066.
2003;226:691697. 75. Grossman H, Ram P, Coleman R, et al. Hepatic ultrasonography in
56. Freeman MP, Whitley Vick C, Taylor KJW, et al. Regenerating nodules type I glycogen storage disease (von Gierke disease): detection of
in cirrhosis: sonographic appearance with anatomic correlation. hepatic adenoma and carcinoma. Radiology 1981;141:753756.
AJR Am J Roentgenol 1986;146:533536. 76. Dachman A, Ros P, Goodman Z, et al. Nodular regenerative
57. Simonovsky V. The diagnosis of cirrhosis by high resolution hyperplasia of the liver: clinical and radiologic observations. AJR Am J
ultrasound of the liver surface. Br J Radiol 1999;72:2934. Roentgenol 1987;148:717722.
58. Colli A, Fraquelli M, Andreoletti M, et al. Severe liver fibrosis or 77. Leung V, Ng W-L, Luk I, et al. Unique hepatic imaging features in a
cirrhosis: accuracy of US for detection-analysis of 300 cases. Radiology patient with nodular regenerative hyperplasia of the liver associating
2003;227:8994. with systemic lupus erythematosus. Lupus 2007;16:205208.
59. Laing FC, Jeffrey RB, Federle MP, et al. Noninvasive imaging of 78. Clouet M, Boulay I, Boudiaf M, et al. Imaging features of nodular
unusual regenerating nodules in the cirrhotic liver. Gastrointest Radiol regenerative hyperplasia of the liver mimicking hepatic metastases.
1992;7:245. Abdom Imaging 1999;24:258261.
60. Kraus GJ, Schedlbauer P, Lax S, et al. The reverse target sign in liver 79. Smevik B, Swensen T, Kolbenstvedt A, Trygstad O. Computed
disease: a potential ultrasound feature in cirrhotic liver nodules tomography and ultrasonography of the abdomen in congenital
characterization. Br J Radiol 2005;78:355357. generalized lipodystrophy. Radiology 1982;142:687689.
61. Solbiati L, Martegani A, Leen E, et al. Contrast-enhanced ultrasound 80. Monzawa S, Tsukamoto T, Omata K, et al. A case with primary
of liver diseases. Milan: Springer-Verlag; 2003. amyloidosis of the liver and spleen: radiologic findings. Eur J Radiol
62. Lencioni R, Crocetti L, Della Pina MC, Cioni D. Guidelines for 2002;41:237241.
imaging focal lesions in liver cirrhosis. Expert Rev Gastroenterol 81. Kim S, Han J, Lee K, et al. Abdominal amyloidosis: spectrum of
Hepatol 2008;2:697703. radiological findings. Clin Radiol 2003;58:610620.
63. Ueda K, Terada T, Nakanuma Y, Matsui O. Vascular supply in 82. Mergo P, Ros P, Buetow P, Buck J. Diffuse disease of the liver:
adenomatous hyperplasia of the liver and hepatocellular carcinoma: radiologic-pathologic correlation. Radiographics 1994;14:12911307.
a morphometric study. Hum Pathol 1992;23:619626. 83. Vogel W, Kathrein H, Dietze O, Judmaier G. Sonography of the liver in
64. Nicolau C, Vilana R, Catal V, et al. Importance of evaluating all Wilsons disease. Sonographic studies of the liver in Wilsons disease
vascular phases on contrast-enhanced sonography in the significance for assessing prognosis? Ultraschall Med 1988;9:270273.
differentiation of benign from malignant focal liver lesions. AJR Am J 84. Akpinar E, Akhan O. Liver imaging findings of Wilsons disease.
Roentgenol 2006;186:158167. Eur J Radiol 2007;61:2532.
65. Bang N, Nielsen MB, Rasmussen AN, et al. Hepatic vein transit time 85. Akhan O, Akpinar E, Oto A, et al. Unusual imaging findings in
of an ultrasound contrast agent: simplified procedure using pulse Wilsons disease. Eur Radiol 2002;12:S66S69.
inversion imaging. Br J Radiol 2001;74:752755. 86. Stewart L. The role of abdominal ultrasound in the diagnosis, staging
66. Kaplan MM, Gershwin ME. Primary biliary cirrhosis. N Engl J Med and management of cystic fibrosis liver disease. J R Soc Med
2005;353:12611273. 2005;98(Suppl. 45):1727.
67. Worthy SA, Elliott ST, Bennett MK. Low-reflectivity periportal collar 87. Ling S, Wilkinson J, Hollman A, et al. The evolution of liver disease in
on hepatic ultrasound. Br J Radiol 1994;67:10501051. cystic fibrosis. Arch Dis Child 1999;81:129132.
68. Soresi M, Bonfissuto G, Magliarisi C, et al. Ultrasound detection of 88. Graham N, Manhire A, Stead R, et al. Cystic fibrosis: ultrasonographic
abdominal lymph nodes in chronic liver diseases. A retrospective findings in the pancreas and hepatobiliary system correlated with
analysis. Clin Radiol 2003;58:372377. clinical data and pathology. Clin Radiol 1985;36:199203.
69. Del Olmo J-A, Esteban J-M, Maldonado L, et al. Clinical significance of 89. Fields T, Michel S, Butler C, et al. Abdominal manifestations of cystic
abdominal lymphadenopathy in chronic liver disease. Ultrasound fibrosis in older children and adults. AJR Am J Roentgenol
Med Biol 2002;28:297301. 2006;187:11991203.
70. Thompson Coon J, Rogers G, Hewson P, et al. Surveillance of cirrhosis
for hepatocellular carcinoma: systematic review and economic
analysis. Health Technol Assess 2007;11(34):1206.
119
CHAPTER
FUNGAL INFECTION 127 Hepatitis is any inflammatory process affecting the liver leading to
Candidiasis 127 hepatocyte injury. This may be an acute, self-limiting event or
chronically progressive leading to scarring and ultimately cirrhosis,
SCHISTOSOMIASIS 128
with the associated risk of hepatocellular carcinoma.
TOXOCARIASIS 129
Diagnostic
Virus Transmission Chronicity serology Specific features
HAV FaecalOral No HAV-IgM Younger patients affected. Mortality rate 0.1%, usually
fulminant hepatitis
HBV Percutaneous/ Yes HBsAg HBsAg may be seen in acute of chronic infection. HBeAg
Venereal Majority vertical detected with active viral replication, i.e. highly infective
infection
HCV Percutaneous Yes (75%) Anti-HCV Majority of acute cases clinically mild. Histology unable to
distinguish progressive disease
HDV Percutaneous Yes Anti-HDV Requires the presence of HBsAg for its expression. Either
Majority simultaneous co-infection of subsequent superinfection
superinfection
HEV Faecal Oral No Anti-HEV Leading cause of infective hepatitis in a number of
developing countries. High mortality in pregnancy
HGV Percutaneous Yes (mild) Research tool Association with hepatocellular carcinoma remains unclear
Table 9.2 Causes of acute hepatitis Differential diagnosis for starrysky appearance
Alcoholic
Acute alcoholic hepatitis is a defined clinicopathological condition
of varying severity, which can present both in long-term alcohol
abusers and in moderate drinkers following a short-term alcohol
Figure 9.1 Hepatitic liver. Adult male with recent history of binge.7 At histology there is neutrophilic infiltration with centri-
influenza-like illness and right upper quadrant pain now presenting lobular ballooning and necrosis of hepatocytes with Mallory hyaline
with jaundice. The liver shows apparent reduction in parenchymal inclusions: fatty infiltration and cirrhosis may also be seen in more
reflectivity and increased periportal reflectivity. chronic cases.
The clinical features are fever, right upper quadrant pain and
jaundice, with a neutrophilia, hyperbilirubinaemia, elevated aspar-
thickening relating to the level of enzyme elevation.6 However, the tate aminotransferase and prothrombin time. In its most severe
pathogenesis for this thickening remains uncertain. Portal lym- form the mortality rate can approach 50%.8 At ultrasound the liver
phadenopathy is another finding typically seen with hepatitis C is often enlarged, with diffuse increased reflectivity as a result of
infection, but also hepatitis A and non-viral causes of hepatitis fatty infiltration or fibrosis8 (Fig. 9.5). A described ultrasound
(Fig. 9.4). feature in acute alcoholic hepatitis is the pseudo-parallel channel
121
CHAPTER 9 Liver: infections and inflammations
sign representing a dilated hepatic artery adjacent to a portal (hepatitis B, C, D and G), but also metabolic (Wilsons disease,
venous branch.9 Peak systolic velocity measurements in the right alpha-1-antitrypsin deficiency, and haemochromatosis), autoim-
hepatic artery are also elevated compared to normal subjects.10 Both mune and drugs. Histologically there is infiltration of the portal
findings are thought to reflect increased arterial flow to the liver to tracts by predominantly mononuclear cells, which when confined
compensate reduced portal venous flow as a result of rising sinu- to the portal triads is defined as mild. In moderate CH there is
soidal resistance. increasing extension of inflammatory infiltrate into the adjacent
parenchyma and it becomes severe when there is confluent necrosis
between portal triads and/or the central veins, the latter being
Chronic hepatitis much more likely to progress to cirrhosis.11
The main role of ultrasound in patients with CH is in monitoring
Chronic hepatitis (CH) is defined as continued disease activity for evidence of developing cirrhosis, portal hypertension and hepa-
beyond 6 months, detectable by persistent elevation of liver tocellular carcinoma. There are no diagnostic ultrasound features
enzymes, and has a number of aetiologies: most commonly viral for CH and the liver often appears normal, with adenopathy in the
122
Hepatitis
A
B
LIVER ABSCESS
Necrotic infection within the liver can be caused by a number of
bacterial, fungal and parasitic organisms. Ultrasound plays an
important role in the diagnosis, management and follow-up of
these infections, although frequently the appearances can be non-
specific or frankly misleading. Access to epidemiological and clini-
cal information, including the patients immune status, is therefore
vital in order to enable a more accurate presumptive diagnosis.
Bacterial
The aetiology of pyogenic liver abscess formation from bacterial
spread to the liver has changed significantly in the past twenty
years. Currently the most common source of infection is direct
extension from the biliary tract in patients with suppurative cholan-
gitis or cholecystitis.14 Direct extension may also sometimes come
from the lung, kidney or colon. Other sources include: portal
venous spread from appendicitis, diverticulitis or other inflamma-
tory bowel disease; hepatic artery spread from distant infection
such as subacute bacterial endocarditis or osteomyelitis; and pen-
etrating injury from trauma, surgical intervention and more recently
minimally invasive ablative techniques.15
Escherichia coli has traditionally been the most common organism
isolated from pyogenic liver abscesses, with Staphylococcus aureus,
Streptococcus milleri and the anaerobes Clostridia and Bacteroides also
Figure 9.8 Liver abscess containing gas. Focal liver abscess
being found: the latter two are likely to have been significantly
with cystic and solid components. There are several strongly
under-reported in the past due to inadequate culture techniques.16
echogenic linear areas, some with acoustic shadowing,
Recent case reviews, however, have identified Klebsiella pneumoniae
representing air within the abscess.
as an increasingly important pathogen, particularly amongst Asians
and people with diabetes.1719 The clinical presentation for all these
infections is variable, and can be non-specific, such as fever, malaise
and anorexia. More specific features include right upper quadrant
pain, pleuritic pain, vomiting and jaundice. At laboratory analysis,
most patients will have a leukocytosis and marked elevation of the
alkaline phophatase.17 In patients with a K. pneumoniae liver abscess, enhancement, followed by arterial rim enhancement and septations
bacteraemia is extremely common with end-organ seeding and (if present) (Fig. 9.9AC). There tends to be lesion washout in the
distant abscess formation well reported.19,20 portal venous phase or late phase of imaging.12
The main treatment approach for a pyogenic liver abscess is The traditional management approach of surgical drainage for
systemic antibiotics and percutaneous drainage/aspiration (see pyogenic liver abscess has long been superseded by percutaneous
below); however, despite this approach mortality rates can still aspiration or drainage under image guidance combined with
reach 614%.21 parenteral broad-spectrum antibiotics.21,2731 Ultrasound is fre-
On ultrasound pyogenic liver abscesses are highly variable in quently employed to guide needle placement within the abscess
appearance and can range from resembling a simple cyst to a solid and the majority of reported series have used a freehand approach
echogenic mass, or multiple low reflective nodules suggestive of in order to allow adjustment to its trajectory. For percutaneous
metastatic disease (Fig. 9.7AC). Appearances are closely related to aspiration a 22-18-gauge trocar needle is used depending upon the
the pathological process, with early suppuration prior to hepato- size of the liver abscess (Fig. 9.10).28 If there are multiple abscesses,
cyte necrosis appearing as a solid mass with altered, usually the deepest one is targeted first to avoid overlying artefact from gas
reduced, reflectivity and frequently demonstrating distal acoustic bubbles. Repeated aspirations may be required if the patient has
accentuation.22 With necrosis and liquefaction abscesses become persistent fever, leukocytosis or the abscess cavity remains signifi-
increasingly heterogeneous in reflectivity and eventually demon- cant on ultrasound follow-up: this appears to be unrelated to the
strate central cystic change, which may contain septations or echo- initial size of the abscess.28,29 Percutaneous drainage is performed
genic debris. With gas-forming organisms, the abscess may contain either as a single-stick procedure,30 or using the Seldinger tech-
highly reflective foci demonstrating reverberation artefact, and if nique,31 with an 810F pigtail catheter being introduced into the
more extensive, strong linear echoes with acoustic shadowing (Fig. abscess (Fig. 9.11). This is fixed to the skin and left on free drainage
9.8). The fibrous walls of the abscess can vary in appearance from until the patient shows clinical improvement or there is a fall in
irregular and indistinct to well defined and, less frequently, irregu- catheter output to <10mL/24h.31 Both procedures appear to be
lar and thick.23 In patients with Klebsiella pneumoniae infection tolerated well by the patient, although there is a recognised risk of
abscesses tend to have a predominantly solid appearance, with lack post-procedure sepsis following catheter drainage.32 There is a con-
of through-transmission of sound,24 while with Staphylococcus tinuing debate amongst centres as to whether aspiration or drain-
aureus infection a pattern of multiple micro-abscesses (<2cm) mim- age should be the first-line approach to liver abscess management.
icking fungal infection has been described.25 It has been suggested that for abscesses less than 5cm in size,
The sensitivity of ultrasound for liver abscess detection is up to aspiration is a reasonable first-line approach, with drainage
97%.26 However, there is a differential for the varied appearance reserved for larger abscesses or complex loculated abscesses. With
including a haemorrhagic simple cyst, focal haematoma or malig- regard to aspiration, abscesses secondary to Klebsiella pneumoniae
nant tumour. Contrast-enhanced ultrasound (CEUS), may help infection appear to aspirate poorly compared to other pyogenic
make the distinction, with the most common enhancement pattern abscesses, with only a couple of millilitres of pus being obtained in
for a confirmed abscess showing early peripheral parenchymal many cases.24
124
Liver abscess
A B
B
A
Ultrasound follow-up of treated pyogenic abscesses shows a necrosis, with little leukocytic response or fibrotic reaction.38
resolution time that lags significantly behind the clinical findings. Abscess formation is most commonly seen in the posterior right
The majority will resolve to sonographically normal parenchyma hepatic lobe, typically measuring 410cm in size although in 20
(Fig. 9.12AC), but a few will continue to show a persisting cystic 25% of cases they can be small and multiple.38 For some unknown
cavity, even at 2 years, or focal areas of calcification.33 reason males are affected four times more frequently than females.39
Patients present with fever and right upper quadrant pain, but
Brucellar abscess frequently lack any associated gastrointestinal symptoms (65
90%).37 There is often a leukocytosis and serology for anti-amoebic
antibodies will be positive in 7080% in the acute phase, increasing
Brucellosis is a worldwide zoonosis, which is endemic in parts of
to over 90% after a week and remaining positive long term in about
the Mediterranean, India, Mexico and Central America. Infection
10%.37 More recently introduced highly specific diagnostic tests
can involve any organ of the body and in the liver this usually
involve the detection of protein antigens in serum or faeces using
manifests as a granulomatous hepatitis.34 A brucellar abscess is far
monoclonal antibodies.40
less common (0.21.6%). On ultrasound these appear as low reflec-
At ultrasound the typical described features of an amoebic
tive hepatic masses, with central areas of liquefaction and one or
abscess are36,38,39,41:
more areas of focal calcification (65% of reported cases).35 A recent
report describes its appearance on CEUS as a thick enhancing rim n an absence of significant wall echoes
of inflammatory tissue surrounding a non-enhancing central area n oval or round shape
with subsequent washout.35 These findings, however, are not totally n reduced reflectivity to background liver with fine internal
specific and need to be combined with positive serology or blood echoes
cultures. n mild distal acoustic enhancement that increases with
treatment
Amoebic abscess n subcapsular location.
All of these features may also be seen in pyogenic abscesses,
Liver abscess is the commonest extraintestinal manifestation (1 however, and there is significant overlap. A blinded comparison
25%) of infection by the protozoan parasite Entamoeba histolytica36 between these two types of liver abscess found that a rounded
and outside the Western world is far more common than bacterial shape and low reflectivity with fine internal echoes were features
sources of focal liver infection. Transmission is by the faecaloral more prevalent in an amoebic abscess, yet this was not sufficient to
route, with ingestion of the cysts through contaminated food or make a distinction between the two (Fig. 9.13).39 Ultrasound find-
water. These excystate in the small bowel to release the trophozoites ings need to be combined with relevant clinical history and sero-
that adhere to and sometimes invade the colonic mucosa.37 logical testing to reach the correct diagnosis. In about 5% of cases
Amoebic colitis may then develop, although infection can often be amoebic abscesses will be echogenic in appearance and can be
asymptomatic.37 Invasion of the colonic mucosa into the mesenteric mistaken for solid masses.38 Other less typical findings are: thick
venules allows the amoebae to reach the liver via the portal vein, echogenic walls which tend to resolve with treatment, mural
where they lodge in the peripheral capillaries leading to hepatocyte nodules and septations.3639,41,42
126
Fungal infection
A B
Following diagnosis and the commencement of appropriate anti- lymphoproliferative disorders and recipients of organ transplants.
biotic therapy, namely metronidazole, patient symptoms usually Systemic candidiasis is the commonest underlying organism and
resolve rapidly over 48 hours, with the liver abscess tending to should be suspected in any patients with a resolving neutropenia
become more sonolucent and reducing in size.38 For uncomplicated and a fever unresponsive to antibiotic treatment. Other recognised
amoebic liver abscess there is no convincing evidence to support hepatic fungal infections include cryptococcosis, histoplasmosis,
percutaneous aspiration or drainage over standard medical treat- murcomycosis and occasionally aspergillosis.
ment.43 There are, however, a limited number of indications for
percutaneous drainage, namely: continuing diagnostic uncertainty, Candidiasis
lack of response to drug therapy, a left lobe abscess close to the
pericardium, or pregnancy.42 Potential complications include
Diagnosis of systemic candidiasis can be challenging. Targeted
rupture of the abscess into the pleural cavity, pericardium or peri-
aspiration of the focal liver lesions may be falsely negative44 or
toneal cavity or compression of the inferior vena cava.
aspiration is contraindicated due to impaired coagulation. Imaging
With successful treatment the majority of abscesses disappear
therefore plays a key diagnostic role, with MRI seen as the most
sonographically within 523 weeks. In a number of cases resolution
sensitive modality for detection of focal fungal disease.44 However,
of the abscess cavity may take over a year and in a minority of
ultrasound is often used as the first-line investigation.
patients a residual focus resembling a hepatic cyst may persist
On ultrasound hepatic candidiasis has four described appear-
(Fig. 9.14).40
ances, which are believed to relate both to the timing of the infection
and to the extent of the patients neutropenia.45 In the absence of an
inflammatory response there may be nothing focal to see. Type I is
FUNGAL INFECTION seen early in the disease and is described as a wheel within a wheel
appearance, with a low reflective or anechoic central nidus centred
Disseminated fungal infection involving the liver primarily affects in an echogenic ring, surrounded by a low reflective halo. Histologi-
patients with prolonged or recurrent neutropenia: in particular cally this has been shown to represent a central area of necrosis with
patients with leukaemia, patients undergoing chemotherapy for fungal elements, surrounded by inflammatory cells and a ring of
127
CHAPTER 9 Liver: infections and inflammations
fibrosis. Type II is the bulls eye lesion, appearing later when the
neutrophil count has recovered and measuring 14cm in size. The SCHISTOSOMIASIS
echogenic centre with a low reflective halo can potentially mimic
metastatic disease, but here the centre contains inflammatory cells Schistosomiasis is one of the most common parasitic infections in
(Fig. 9.15A, B). Type III is the most common appearance reported: humans, affecting around 200 million people worldwide. Hepatic/
seen with healing of the lesions, these uniformly hypoechoic intestinal schistosomiasis is caused by the trematodes Schistosoma
nodules represent fibrosis. Type IV is echogenic foci, sometimes mansoni, S. japonicum and less commonly S. mekongi and S. interca-
with acoustic shadowing representing focal calcification as a result latum.47 Infection occurs through contact with contaminated water,
of scarring.44,46 with the cercaria penetrating the skin/mucosa and migrating first
to the lungs and then to the venules of the mesentery.48 Here the
mature flukes release eggs into the venules which enter the portal
venous system, lodging in the periportal spaces and along the liver
capsule. The resulting chronic granulomatous inflammation leads
to periportal fibrosis described by Symmers as clay-pipestem in
the healing stage, with the development of portal hypertension
without frank cirrhosis.48,49
In the acute stage of infection patients may complain of fever,
itching and diarrhoea, with an eosinophilia found on full blood
count and positive serology to schistosome antigen. There are no
reliable imaging features at this stage, although low reflective
nodules scattered throughout the liver of uncertain aetiology have
been described.50 The more chronic changes are somewhat depend-
ent upon the trematode present:
n Schistosoma mansoni causes a more central periportal fibrosis,
with marked echogenic thickening of the portal tracts (up to
2cm) seen on ultrasound, predominantly around the porta
hepatis. Left lobe hypertrophy, portal vein enlargement with
venous collaterals, echogenic thickening of the gallbladder
wall and splenomegaly are other typical findings
(Fig. 9.16).48,49
n Schistosoma japonicum has a more peripheral pattern of portal
tract fibrosis giving a reticular pattern/fish-scale network to
the appearance of the liver on ultrasound, with relatively
normal appearing parenchyma between these echogenic septa
that extend out to a thickened liver capsule.48,51 Doppler
studies of the portal vein in these patients tend to be within
normal limits.51
Figure 9.14 Resolving amoebic abscess. Four-month follow-up
on patient seen in Figure 9.13A showing significant reduction in size
of abscess cavity with more uniform, reduced reflectivity and
through-transmission.
A B
Figure 9.15 Hepatic candidiasis. A and B: Hepatic candidiasis in two immunocompromised patients, both showing a type II pattern,
i.e. discrete low reflective focal lesions with an echogenic central nidus.
128
Echinococcal infection
inner germinal layer; this gives rise to brood capsules which in turn
form infectious scolices, both of which may precipitate within the
cyst to form hydatid sand. Between these is a thin laminated acel-
lular membranous layer known as the ectocyst that allows the
passage of nutrients to the cyst. The cyst fluid is clear or pale yellow
in colour, may contain scolices and is antigenic, with a risk of ana-
phylaxis if the cyst ruptures.56 In certain circumstances, not clearly
understood, daughter cysts develop within the mother cyst which
are an exact replica of the mother cyst, but lack a pericyst.
At ultrasound hydatid cysts may be single or multiple and have
a number of described appearances, largely dependent upon the
stage of the disease56,57:
n Initially they can appear as simple cysts. Distinguishing
features include a double linear echo to the cyst wall, fine
echogenic debris (hydatid sand) within the cyst, which can be
accentuated by moving the patient and there may be evidence
of cyst wall calcification.
n A cyst showing detachment of the endocyst from the pericyst,
which may be due to falling cyst pressure, host response,
Figure 9.16 Periportal fibrosis seen with schistosomiasis trauma or treatment. This results in the ultrasound water lily
mansoni. Marked echogenic periportal thickening in a patient with sign seen as an undulating series of echogenic linear
schistosomiasis mansoni. (Courtesy of Dr N. Arafa.) interfaces that appear to float in relatively anechoic fluid.
Ultrasound is the most sensitive modality for the detection of
membranes, septa and hydatid sand.
n Multivesicular cysts represent the presence of multiple
TOXOCARIASIS daughter cysts, sometimes separated by echogenic matrix
material (cyst fluid containing scolices, broken brood
capsules). The appearance is a characteristic cartwheel or
Toxocariasis is caused by the human ingestion of eggs from the honeycomb cyst. Large amounts of matrix material can result
faeces of dogs and cats infected with the nematodes Toxocara canis in a pseudo-solid echogenic mass.
and T. catis. The larvae are liberated in the intestine and burrow n Calcification of the cyst wall can be partial or complete and
through the wall to reach the liver, but may migrate on to involve dense, with the latter producing a strong acoustic shadow.
a number of organs. The migrating larvae stimulate a localised Partial calcification does not always indicate death of the cyst
eosinophilic infiltration leading to granuloma or eosinophilic (Fig. 9.17).
abscess formation.52,53 On ultrasound the liver is seen to contain
multiple oval shaped or elongated, low reflective lesions with Ultrasound has a >90% sensitivity for the diagnosis of
poorly defined margins usually measuring <2cm in size. Follow-up hydatid cyst, based on its sonographic features, which can be
ultrasound may see resolution of these focal areas, or a change in confirmed on antibody titres to hydatid antigen using counter
location thought to indicate migration of the larvae.54 immunoelecrophoresis.55
The main complication of hepatic hydatid is cyst rupture (50
90%), which can be contained, communicating or direct. In con-
tained rupture the endocyst ruptures, but the pericyst remains
ECHINOCOCCAL INFECTION intact. The collapsed floating membranes are seen on ultrasound as
serpiginous linear echoes: this may occur as a result of cyst degen-
eration, medical treatment or following trauma. Communicating
Echinococcal cyst (hydatid disease) rupture into the biliary system, via biliary radicles within the peri-
cyst, can lead to cholangitis and death of the parasite due to an
There are two types of Echinococcus infection causing hydatid influx of bile into the cyst. Biliary obstruction is more often seen
disease in humans. By far the most common is that by the larval with a wide neck rupture into a main biliary branch due to the
stage of the cestode (tapeworm) Echinococcus granulosus, resulting extrusion of daughter cysts, membrane debris and hydatid sand
in the formation of hydatid cysts in the liver or other organs. into the central bile ducts. The cyst becomes increasingly echogenic
Traditionally E. granulosus is prevalent in sheep- and cattle- and layering of echogenic hydatid sand or linear membranous
raising countries, being endemic throughout the Middle East, material has been described in the dilated biliary system, in up to
South America, Australia and parts of the Mediterranean. Increas- 77% of cases. Biliary dilatation can sometimes be seen proximal to
ing travel and tourism, however, means it can now potentially be the cyst simply due to pressure effect rather than obstruction sec-
seen anywhere in the world.55 The adult tapeworn usually resides ondary to rupture. Direct rupture into the peritoneal cavity or
in the intestine of dogs or another carnivore (the definitive host) transdiaphragmatic rupture into the pleural space can carry serious
and its eggs are excreted in their faeces. These are then ingested by consequences, with seeding throughout the abdomen and a high
the intermediate host, namely sheep, cattle, goats and sometimes risk of anaphylaxis.58 Biliarybronchial fistulas can sometimes arise
humans. The eggs hatch in the intestine and the freed larvae perme- when a transdiaphragmatic rupture involves the lung. In direct
ate the intestinal mucosa to enter the portal venous system. The ruptures ultrasound can demonstrate the wall defect as well as
majority become trapped in the hepatic capillary system, where track the passage of cyst content.
they either die or encyst and grow slowly (approximately 23cm Cyst infection only occurs following rupture and can result in
per year depending upon host immunity).56 Some will, however, abscess formation, which on ultrasound is indistinct from other
pass through the liver to reach the lungs and other organs.55 types of liver abscess, and may have a pseudo-solid appearance on
The right lobe of the liver is most commonly affected and the wall ultrasound, with or without airfluid levels.56 Traditionally
of the developing hydatid cyst is made of three layers: The outer contrast-enhanced CT has been decreed as the investigation of
pericyst represents the inflammatory response by the host and is choice to assess infection, yet there may now be a role for CEUS.
predominantly dense connective tissue, sometimes containing Medical treatment for hydatid with mebendazole or albendazole
biliary radicals: this will often partially calcify. The endocyst is the has a variable success rate and should be monitored with
129
CHAPTER 9 Liver: infections and inflammations
B
A
ultrasound. A good response is confirmed by a reduction in cyst (Fig. 9.19). Persistence of a round anechoic cyst is seen as an indi-
dimensions, detachment of the endocyst from the pericyst, some- cation of treatment failure.
times with the development of calcification, and an alteration in
cyst content echotexture towards a more uniform echogenic Hepatic alveolar echinococcosis
pseudo-solid lesion.59 Doubts over its clinical efficacy, however,
mean that medical treatment tends to be reserved for disseminated Hepatic alveolar echinococcosis (HAE) is a rare disease caused by
disease or cases where intervention/surgery is contraindicated.55 larvae of Echinococcus multilocularis, which behaves in a very differ-
Although surgery is still seen by some groups as the definitive ent way from the more common hydatid disease. The primary host
treatment for intrahepatic hydatid disease,55 there is increasing evi- is the fox, with humans becoming infected either through direct
dence that percutaneous aspiration/drainage procedures are not contact or indirectly from contaminated water of plant life in the
only safe but offer a highly effective treatment alternative. The wild. It is endemic in parts of the USA, Canada, Japan and Central
technique known as PAIR (percutaneous aspiration injection and Europe.63
re-aspiration) involves the insertion of a fine needle (e.g.19G) into The liver is involved in 90% of infections, with E. multilocularis
the hydatid cyst under ultrasound guidance followed by the aspi- producing multiple alveolar cysts, each containing a germinal layer,
ration of half the cyst volume. Hypertonic saline is then injected that grow by exogenous proliferation, aggressively invading host
into the cyst, left for a period and then the entire cyst content is tissue. As the multicystic masses expand they are highly prone
aspirated.60 A variation of this technique describes repeated injec- to central necrosis, leaving a surround of viable metacestoidal
tion and aspiration until the endocyst is seen to separate from the vesicles.
pericyst on ultrasound.61 For larger cysts (>6cm) a drainage cath- At ultrasound the typical described finding is a hailstorm
eter is inserted at the end of the procedure and left in situ for 24 pattern made up of multiple poorly defined echogenic nodules due
hours. Other groups have tried injecting alcohol as a scolicidal to numerous cyst wall interfaces and microcalcification, interspaced
agent with good results (Fig. 9.18A, B),62 although care must be by areas of necrosis.64 Large areas of central necrosis appear similar
taken to ensure there is no fistulous communication with the to pyogenic abscesses although they tend to have thick, irregular,
biliary tree. The reported complication rate for this procedure is echogenic margins. With progressive disease, coarse peripheral cal-
around 8%, with liver abscess formation being the most significant. cification can be seen to surround areas of necrosis. The latter can
The concern over severe anaphylaxis from leakage of cyst content mimic a calcified liver cyst, and if suspected, serology for HAE
would appear to be unjustified, but prophylactic mebendazole is antibodies can help make the distinction.
often administered to reduce the risk of dissemination. Following Complications from HAE arise from hilar infiltration of the
successful treatment ultrasound shows a gradual reduction in biliary tree, leading to intrahepatic duct dilatation, and invasion of
cyst size, eventually concluding with a small residual cyst, an the portal and hepatic veins resulting in ischaemic atrophy of liver
echogenic focus in the liver parenchyma or complete resolution62 segments, both of which can be identified at ultrasound.
130
HIV/AIDS
A B
Figure 9.18 Ethanol injection of hydatid. A: Ultrasound-guided needle puncture of a hydatid cyst. B: Following aspiration of cyst
content, 95% alcohol is injected into the cyst cavity causing a strongly echogenic focus (arrow). (From Giorgio A et al. Clinical and
sonographic management of viable hydatid liver cysts. Journal of Ultrasound 2008;11:107112.)
INFLAMMATORY PSEUDO-TUMOUR
Inflammatory pseudo-tumour (IPT) of the liver is a rare condition
of uncertain aetiology producing a chronic inflammatory mass in
the liver consisting of collagenous tissue infiltrated with plasma
cells and other inflammatory cells. More common in young men, it
tends to present with fever, weight loss, abdominal pain and
general malaise.67 Although the imaging findings can be concern-
ing, the prognosis for IPT is good and therefore needs to be consid-
ered, to avoid unnecessary surgical intervention.
At ultrasound the findings can be concerning, with a well or
poorly defined mass of either increased or decreased reflectivity,
sometimes showing through-transmission of sound. CEUS gives a
variable pattern, with either increased or reduced enhancement in
Figure 9.19 Old hydatid. Calcified rounded focus in the right lobe
the arterial phase, but all lesions showing reduced enhancement
of the liver, in a patient previously treated for hydatid.
during the portal venous phase, suspicious for a malignant focal
liver lesion.27 CT or MRI may demonstrate a delayed enhancement
pattern suggestive of IPT.68
ACUTE FASCIOLIASIS
Fasciola hepatica is a trematode that commonly infests sheep or HIV/AIDS
cattle. Human infestation occurs through the consumption of con-
taminated aquatic vegetables and has an acute, latent and chronic Throughout the clinical course of the human immunodeficiency
phase. In the acute phase the larvae penetrate the small intestine virus, from the initial infection through to early symptomatic
entering the peritoneal cavity and then pass through Glissons disease and finally late stage AIDS, the liver is affected by a wide
capsule to migrate through the liver towards the bile ducts. Patients range of pathologies and frequently appears abnormal on ultra-
typically experience fever, upper abdominal pain and have sound examination. At the time of primary infection the liver may
a marked eosinophilia. Anti-fluke antibody serology becomes show features of associated infections, namely acute or chronic
131
CHAPTER 9 Liver: infections and inflammations
Table 9.3 Focal liver lesions in HIV/AIDS patients Table 9.4 Causes of granulomatous hepatitis
Infective: Tuberculoma Malignant: Lymphoma Bacterial: Mycobacterium Viral: Infectious mononucleosis
Mycobacterium avium Kaposis sarcoma Brucellosis Cytomegalovirus
complex (rare) Spindle cell tumour Actinomycosis Drugs: Allopurinol
CMV Hepatocellular carcinoma Q fever Phenytoin
Toxoplasmosis Drug reaction: Trimethoprim/ Fungal: Histoplasmosis Idiopathic: Sarcoid
Metabolic: Focal fatty sulfamethoxazole Blastomycosis
infiltration Cryptococcosis
Vascular: Peliosis hepatis Parasitic: Schistosomiasis
Toxoplasmosis
A B
Figure 9.23 Large tuberculoma pre- and post-contrast scan. A: Left lobe 3cm heterogeneous mass in a patient with confirmed
hepatic tuberculosis. B: Post contrast there was no convincing enhancement even in the arterial phase.
Figure 9.24 Examples of incidental hepatic calcification, with varying degrees of acoustic shadowing. The linear calcification in A was
thought to be a result of previous trauma, while in B and C the most likely cause is granulomatous.
17. Lederman ER, Crum NF. Pyogenic liver abscess with a focus on 45. Pastakia B, Shawker TH, Thaler M, et al. Hepatosplenic candidiasis:
Klebsiella pneumoniae as a primary pathogen: an emerging disease with wheels within wheels. Radiology 1988;166:417421
unique clinical characteristics. Am J Gastroenterol 2005;100:330332. 46. Miller JH, Greenfield LD, Wald BR. Candidiasis of the liver and spleen
18. Rahimian J, Wilson T, Oram V, Holzman RS. Pyogenic liver abscess: in childhood. Radiology 1982;142:375380.
recent trends in etiology and mortality. Clin Infect Dis 47. Chiavaroli R, Grima P, Grima P. Detection of early liver fibrosis in
2004;39:16541659. patients with intestinal schistosomiasis: sonographic and histologic
19. Wang JH, Liu YC, Lee SS, et al. Primary liver abscess due to Klebsiella findings in Schistosoma mansoni infection. Infection 2008;36:585589.
pneumoniae in Taiwan. Clin Infect Dis 1998;26:14341438. 48. Manzella A, Ohtomo K, Monzawa S, Lim JH. Schistosomiasis of the
20. Cheng DL, Liu YC, Yen MY, et al. Pyogenic liver abscess: clinical liver. Abdom Imaging 2008;33:144150.
manifestations and value of percutaneous catheter drainage treatment. 49. Cerri GG, Alves VAF, Magalhaes A. Hepatosplenic schistosomiasis
J Formos Med Assoc 1990;89:571576. mansoni: ultrasound manifestations. Radiology 1984;153:777780.
21. Yu SC, Ho SS, Lau WY, et al. Treatment of pyogenic liver abscess: 50. Cesmeli E, Vogelaers D, Voet D, et al. Br J Radiol 1997;70:758760.
prospective randomized comparison of catheter drainage and needle 51. Chou Y-H, Chiou H-J, Tiu C-M, et al. Duplex Doppler ultrasound of
aspiration. Hepatology 2004;39:932938 hepatic schistosomiasis japonica: a study of 47 patients. Am J Trop
22. Terrier F, Backer CD, Triller JK. Morphologic aspects of hepatic Med Hyg 2003;68:1823.
abscesses at computed tomography and ultrasound. Acta Radiol 52. Clarke HM, Hinde FRJ, Manns RA. Case report: hepatic ultrasound
1983;24:129137. findings in a case of toxacariasis. Clin Radiol 1992;45:135136.
23. Kuligowska E, Connors SK, Shapiro JH. Liver abscess: sonography in 53. Chan S, Lim JH, Choi D, et al. Hepatic visceral larva migrans of
diagnosis and treatment. AJR Am J Roentgenol 1982;138:253257. Toxocara canis: CT and sonographic findings. AJR Am J Roentgenol
24. Hui JY, Yang MK, Cho DH, et al. Pyogenic liver abscesses caused by 2006;187:W622W629.
Klebsiella pneumoniae: US appearance and aspiration findings. 54. Lim JH. Toxocariasis of the liver: visceral larvae migrans. Abdom
Radiology 2007;242:769776. Imaging 2007;33:151156.
25. Verbanck J, Ponette J, Verbanck M, et al. Sonographic detection of 55. Safioleas MC, Misiakos EP, Kouvaraki M, et al. Hydatid disease of
multiple Staphylococcus aureus hepatic microabscesses mimicking the liver. A continuing surgical problem. Arch Surg 2006;141:
Candida abscesses. J Clin Ultrasound 1999;27:478481. 11011108.
26. Vassiliades VG, Bree RL, Korobkin M. Focal and diffuse benign 56. Pedrosa I, Saiz A, Arrazola J, et al. Hydatid disease: radiologic and
hepatic disease: correlative imaging. Semin Ultrasound CT MR pathologic features and complications. Radiographics 2000;20:
1992;13:313335. 795817.
27. Liu GJ, Lu MD, Xie XY, et al. Real-time contrast-enhanced ultrasound 57. Lewall DB, McCorkell SJ. Hepatic echinococcal cysts: sonographic
imaging of infected focal liver lesions. J Ultrasound Med appearances and classification. Radiology 1985;155:773775.
2008;27:657666. 58. Lewall DB. Hydatid disease: biology, pathology, imaging and
28. Giorgio A, Stefano G, Di Sarno A, et al. Percutaneous needle aspiration classification. Clin Radiol 1998;53:863874.
of multiple pyogenic abscesses of the liver: 13-year single-centre 59. Bezzi M, Teggi A, De Rosa F, et al. Abdominal hydatid disease: US
experience. AJR Am J Roentgenol 2006;187: findings during medical treatment. Radiology 1987;162:9195.
15851590. 60. Ustnsz B, Akhan O, Kamiloglu MA, et al. Percutaneous treatment of
29. Ch Yu S, Hg Lo R, Kan PS, Metreweli C. Pyogenic liver abscess: hydatid cysts of the liver: long-term results. AJR Am J Roentgenol
treatment with needle aspiration. Clin Radiol 1997;52:912916. 1999;172:9196.
30. Zerem E, Hadzic A. Sonographically guided percutaneous catheter 61. Akhan O, Ozmen MN, Diner A, et al. Liver hydatid disease:
drainage versus needle aspiration in the management of pyogenic long-term results of percutaneous treatment. Radiology
liver abscess. AJR Am J Roentgenol 2007;189:W138W142. 1996;198:259264.
31. Rajak CL, Gupta S, Jain S, et al. Percutaneous treatment of liver 62. Giorgio A, Di Sarno A, de Stefano G, et al. Sonography and clinical
abscess: needle aspiration versus catheter drainage. AJR Am J outcome of viable hydatid liver cysts treated with double
Roentgenol 1998;170:10351039. percutaneous aspiration and ethanol injection as first-line therapy:
32. Thomas J, Turner SR, Nelson RC, Paulson EK. Postprocedure sepsis in efficacy and long-term follow-up. AJR Am J Roentgenol
image guided percutaneous hepatic abscess drainage: how often does 2009;193:W186W192.
it occur? AJR Am J Roentgenol 2006;186:14191422. 63. Didier D, Weiler S, Rohmer P, et al. Hepatic alveolar echinococcosis:
33. Sudhamshu KC, Sharma D. Long-term follow-up of pyogenic liver correlative US and CT study. Radiology 1985;154:179186.
abscess by ultrasound. Eur J Radiol 2009; doi:10.1016/j. 64. Czermack BV, Unsinn KM, Gotwald T, et al. Echinococcus
ejrad.2009.01.017. multilocularis revisited. AJR Am J Roentgenol 2001;176:12071212.
34. Pappas G, Akritidis N, Bosilkovski M, Tsianos E. Brucellosis. N Engl J 65. Andresen B, Blum J, Weymarn AV, et al. Hepatic fascioliasis: report of
Med 2005;352:23252336. two cases. Eur Radiol 2000;10:17131715.
35. Meloni MF, Andreano A, Laeseke PF, et al. Contrast-enhanced 66. Cosme A, Ojeda E, Poch M, et al. Sonographic findings of hepatic
ultrasonographic findings in a Brucellar hepatic abscess. J Ultrasound lesions in human fascioliasis. J Clin Ultrasound 2003;31:358363.
Med 2008;27:15111515. 67. Soudack M, Shechter A, Malkin L, et al. Inflammatory pseudotumor of
36. Ralls PW, Colletti PM, Quinn MF, Halls J. Sonographic findings in the liver: sonographic and computed tomographic features with
hepatic amebic abscess. Radiology 1982;145:123126. complete regression. J Ultrasound Med 2000;19:501504.
37. Haque R, Huston CD, Hughes M, et al. Amebiasis. N Engl J Med 68. Yan FH, Zhou KR, Jiang YP, Shi WB. Inflammatory pseudotumor of
2003;348:15651573. the liver: 13 cases of MRI findings. World J Gastroenterol
38. Stoopen ME, Kimura-Fujikami K, Quiroz y Ferrari FA, Barios-Boullard 2001;7:422424.
V. Ultrasound imaging of hepatic amebic abscess. Ultrasound Q 69. Ng VL, Yajko DM, Hadley WK. Extrapulmonary pneumocystis. Clin
1999;15:189200. Microbiol Rev 1997;10:401418.
39. Shamsi K, De Schepper A, Deckers F, et al. Role of ultrasound in the 70. Keane MA, Finlayson C, Joseph AE. A histological basis for the
diagnosis and treatment follow-up of amoebic abscess. Eur Radiol sonographic snowstorm in opportunistic infection of the liver and
1993;3:434438. spleen. Clin Radiol 1995;50:220222.
40. Sharma MP, Ahuja V. Amoebic liver abscess. JIACM 2003;4:107111. 71. Spouge AR, Wilson SR, Gopinath N, et al. Extrapulmonary
41. Ralls PW, Barnes PF, Radin DR, et al. Sonographic features of amebic Pneumocystis carinii in a patient with AIDS: sonographic findings. AJR
and pyogenic liver abscesses: a blinded comparison. AJR Am J Am J Roentgenol 1990;155:7678.
Roentgenol 1987;149:499501. 72. Reeders JWAJ, Yee J, Gore RM, et al. Gastrointestinal infection in the
42. Berry M, Bazaz R, Bhargava S. Amebic liver abscess: sonographic immunocompromised (AIDS) patient. Eur Radiol 2004;14:E84E102.
diagnosis and management. J Clin Ultrasound 1986;14:239. 73. Wetton CW, McCarty M, Tomlinson D, et al. Ultrasound findings in
43. Chavez-Tapia NC, Hernandez-Calleros J, Tellez-Avila FI, et al. hepatic mycobacterial infections in patients with acquired immune
Image-guided percutaneous procedure plus metronidazole versus deficiency syndrome (AIDS). Clin Radiol 1993;47:3638.
metronidazole alone for uncomplicated amoebic liver abscess. 74. Bray HJ, Lail VJ, Cooperberg PL. Tiny echogenic foci in the liver and
Cochrane Database of Systematic Reviews 2009, Issue 1. Art. No.: kidney in patients with AIDS: not always due to disseminated
CD004886. DOI: 10.1002/14651858.CD004886.pub2. Pneumocystis carinii. AJR Am J Roentgenol 1992;158:8182.
44. Semelka RC, Kelekis NL, Sallah S, et al. Hepatosplenic fungal disease: 75. Glasgow BJ, Anders K, Layfield K, et al. Clinical and pathologic
diagnostic accuracy and spectrum of appearances on MR imaging. findings of the liver in the acquired immunodeficiency syndrome
AJR Am J Roentgenol 1997;169:13111316. (AIDS). Am J Clin Pathol 1985;83:582588.
136
References
76. Vieco PT, Rochon L, Lisbona A. Multifocal cytomegalovirus-associated 84. Akhan O, Pringot J. Imaging of abdominal tuberculosis. Eur Radiol
hepatic lesions simulating metastases in AIDS. Radiology 2002;12:312323.
1990;176:123124. 85. Garel LA, Pariente DM, Nezelof C, et al. Liver involvement in chronic
77. Gaya DR, Thorburn D, Oien KA, et al. Hepatic granulomas: a 10 year granulomatous disease: the role of ultrasound in diagnosis and
single centre experience. J Clin Pathol 2003;56:850853. treatment. Radiology 1984;153:117121.
78. Mills P, Saverymuttu S, Fallowfield M, et al. Ultrasound in the 86. Larsen CE, Patrick LE. Abdominal (liver, spleen) and bone
diagnosis of granulomatous liver disease. Clin Radiol 1990;41:113115. manifestations of cat-scratch disease. Pediatr Radiol 1992;22:353355.
79. Monill-Serra JM, Martinez-Noguera A, Montserrat E, et al. Abdominal 87. Kim GB, Kwon JH, Kang DS. Hypereosinophilic syndrome: imaging
ultrasound findings of disseminated tuberculosis in AIDS. J Clin findings in patients with hepatic involvement. AJR Am J Roentgenol
Ultrasound 1998;25:16. 1993;161:577580.
80. Kessler A, Mitchell DG, Israel HL, Goldberg BB. Hepatic and splenic 88. Nam K-J, Jung W-J, Choi J-C, et al. Hepatic involvement in
sarcoidosis: ultrasound and MR imaging. Abdom Imaging hypereosinophilia: sonographic findings. J Ultrasound Med
1993;18:159163. 1999;18:475479.
81. Xu HX, Xie XY, Lu MD, et al. Unusual benign focal liver lesions: 89. Lee WJ, Lim HK, Lim JH, et al. Foci of eosinophil related necrosis in
findings on real-time contrast-enhanced sonography. J Ultrasound the liver: imaging findings and correlation with eosinophilia. AJR Am
Med 2008;27:243254. J Roentgenol 1999;172:12551261.
82. Huang W-T, Wang C-C, Chen W-J, et al. The nodular form of hepatic 90. Reeder MM. Gamut: liver calcification. Semin Roentgenol 1975;10:171.
tuberculosis: a review with five additional new cases. J Clin Pathol 91. Stoupis C, Taylor HM, Paley MR, et al. The rocky liver: radiologic-
2003;56; 835839. pathologic correlation of calcified hepatic masses. Radiographics
83. Blangy S, Cornud F, Sibert A, et al. Hepatitis tuberculosis presenting 1998;18:675685.
as tumoral disease on ultrasonography. Gastrointest Radiol
1988;13:5254.
137
CHAPTER
solid liver pathologies that may be encountered in clinical practice respect there are some similarities to the haemodynamic profiles
and the sonographic findings on both conventional and contrast- observed during CT or MR examinations, except for the volumes
enhanced US that enable lesion characterisation are discussed. of the agents required and their transit times. A very small volume
(0.2 to 2.4mL) of USCA is sufficient in enhancing the liver paren-
chyma as a result of the higher sensitivity of the US non-linear
CONTRAST AGENTS FOR LIVER IMAGING modes compared with CT or MR imaging; the intensitytime curves
of USCA are shifted by 1015 seconds earlier. In the late phase the
Based on evidence from clinical trials, expert committee reports and tumour to liver contrast ratio is increased sevenfold.15 This may
consensus, the European Federation of Societies of Ultrasound in enable the detection of very small liver metastases. In addition,
Medicine and Biology (EFSUMB) has already issued guidelines on imaging with USCA is in real-time with the added advantage that
use of ultrasound contrast agents (USCAs) in clinical practice.13 USCA is truly intravascular, which may be particularly useful for
For liver imaging, it is more appropriate to classify USCAs more accurate perfusion quantification.16
according to their specificity for normal hepatic parenchymal Primary and secondary neoplasms of the liver demonstrate wide
uptake (Tables 10.1 and 10.2). Earlier agents were primarily variability in their vascularity, which is dependent on their size and
designed to be blood pool agents to salvage conventional Doppler growth rate. When the tumour is small (about 1mm) its main blood
examinations and have been shown to be highly effective in enhanc- supply is via the portal vein and as it grows, a new arterial system
ing the macrovasculature on spectral/colour/power Doppler develops and becomes the predominant or exclusive blood supply.17
modes lasting for up to 7 minutes following a bolus intravenous However only 2025% of the blood supply to the normal liver origi-
administration. Agents such as NC100100 (GE Healthcare, Oslo), nates from the hepatic artery and the remainder is from the portal
SHU 508A and SHU 563A (Bayer AG, Berlin) have additional vein. After a bolus intravenous injection of USCA, hypervascular
tissue-specific properties; they are selectively taken up by the tumours show hyper-enhancement compared with the adjacent liver
Kupffer cells of the reticuloendothelial system after the vascular in the arterial phase, which ranges between 15 and 25 seconds from
phase and enhance the normal hepatic parenchyma for up to an the time of the injection. As blood with the higher volume of USCA
hour with non-linear imaging modes depending on the dosage is then delivered to the liver via the portal vein, the echogenicity of
used. The advantage of such agents is that lesions, which are defi- the liver rises rapidly; in contrast within malignant tumours, USCA
cient of Kupffer cells or associated with Kupffer cell dysfunction, washout is observed during that period. The reversal in the enhance-
do not retain the agents, thereby improving the lesion to tissue ment between the liver and the tumour is accentuated during this
contrast ratio resulting in higher sensitivity for detection as well as phase and peaks from 35 to 90 seconds. All contrast agents will
specificity in tissue characterisation. Other agents such as SonoVue display such arterial and portal phases. Therefore optimal scanning
(Bracco SPA, Milan) or Definity (BMS, Billerica, USA), which for detection of hyper- and hypovascular malignant tumours is
were also primarily designed to be blood pool agents, are during the hepatic arterial and portal venous phases respectively.
known to be trapped or slowed in the hepatic sinusoids, thereby However, beyond the vascular phases, some agents such as Optison
demonstrating late phase uptake, which may last for up to clear out of the circulation fairly rapidly whilst other agents such
6 minutes.14 This characteristic confers similar advantage clinically SonoVue or Definity are held in the sinusoids for up to 56 minutes
to those Kupffer cell targeted agents. from the time of the bolus injection and this phase can be called the
late phase.10,18 On the other hand, with USCAs, which are taken up
by the Kupffer cells, liver parenchymal enhancement continues
beyond the 5 minutes and may last for up to an hour depending on
CONTRAST AGENT KINETIC the dose use.19 Optimal imaging for malignant tumours for detection
DISTRIBUTION and characterisation is during this late phase.
systematically throughout the hepatic arterial, portal venous and frequently detected in the 30- to 40-year-old age group and has a
late phases. The whole examination should be recorded digitally 25 times higher incidence in females than males.23 Haemangioma
and archived for further review. The hepatic arterial phase may be is often solitary but can be multiple in 1050% of cases.24,25 It
too short to complete a full liver coverage to specifically detect all may occur anywhere in the liver but has a predilection for periph-
the hypervascular malignant tumours; however, the contrast eral and subcapsular locations and is most frequently found in
washout is usually rapid for these lesions and the portal and late the posterior segment of the right lobe.26 Due to their benign
phases are long enough for them to be depicted. Irrespective of the nature, haemangiomas are predominantly asymptomatic although
tumour vascularity, the vast majority of malignant lesions are complications can occur, particularly in large haemangiomas. The
detectable using the standardised protocol described. For the incidence of complications occurring in haemangiomas >5cm in
purpose of characterisation it is important to understand the tem- size is 520%.27 Potential complications include inflammation, Kasa-
poral changes in the lesional enhancement during the three phases. bachMerritt syndrome, intra-tumoral haemorrhage, volvulus and
Agents with late phase uptake have the advantage that there is compression of adjacent structures.21 An inflammatory process of
sufficient scanning time and are ideally suited for both detection uncertain aetiology has been reported in large haemangiomas,
and characterisation. which may lead to rapid tumour growth, and non-specific clinical
In the characterisation of focal liver tumours, a standardised findings such as fever, weight loss and abdominal pain. Kasabach
scanning protocol is also useful to evaluate the tumoral vascular Merritt syndrome is a coagulopathy consisting of intravascular
morphology during the hepatic arterial, portal venous and the late coagulation, clotting and fibrinolysis within the haemangioma that
phase by observing the relative contrast entrapment/uptake within can lead to systemic thrombocytopenia. Intra-tumoral haemorrhage
the tumour compared to the surrounding normal liver parenchyma is a rare complication in large haemangiomas and can occur spon-
in. Following the administration of the contrast agent, gentle sweeps taneously or following anticoagulation therapy. Rarely, large hae-
to cover the whole lesion are recommended instead of maintaining mangiomas may present as pedunculated masses and there are two
the same scanning plane continuously; although there is minimal case reports of these masses having undergone volvulus.28,29 A large
destruction when scanning at low MI, microbubble destruction still haemangioma can exert local compressive effects on adjacent biliary
occurs if the probe is kept constantly at the same scan plane. In (particularly for those situated at liver hilum) and hepatic vascular
addition, when sweeping through the lesion, a three-dimensional structures or on neighbouring organs such as the kidney or a loop
perspective of the lesional vascular morphology and geometry is of bowel.
obtained. These sweeps can be repeated over the whole vascular Haemangiomas are composed of blood-filled cavernous spaces
phase and into the late phase. However, for suspected benign hae- lined with a single layer of flat endothelial cells and separated by
mangiomas the protocol needs to be tailored to demonstrate the fibrous septa. At microscopy, they have a honeycomb appearance.
centripetal progression of the peripheral nodular enhancement by On US, haemangiomas are typically well-defined, round or lobu-
progressively increasing the delays between sweeps thereby mini- lated lesions, measuring 3cm in size, and have a uniformly hyper-
mising microbubble destruction, to allow for the accumulation of echoic appearance with or without posterior acoustic enhancement.
agent throughout the lesion. The increased echogenicity on US is due to the multiple interfaces
However, the equipment settings and scanning protocols are dif- between the walls of the cavernous spaces and the blood within
ferent for agents such as Levovist and Sonavist as they are best them.30 The posterior acoustic enhancement reflects the low acous-
displayed using non-linear imaging modes set at high MI (over 1.0). tic impedance of blood-filled spaces and tends to occur in lesions
The scanning protocol for detection is as follows: the left lobe and 2.5cm in size.31 Colour Doppler US is limited in assessment of
then the right lobe is scanned axially or sagittally at 45 minutes haemangiomas as it is not sensitive enough to detect the slow flow
post Levovist or Sonavist injection. Oblique scans at the intercostal in the cavernous spaces of these focal lesions, particularly in small
spaces can also be performed to complete the right lobe examina- lesions and lesions located deep within the liver.32,33 Power Doppler
tion. As this is a destructive mode, the contrast display with Levo- has a higher sensitivity in detecting slow flow compared with
vist is transient; the first sweep through each lobe will provide the colour Doppler but suffers from being more sensitive to motion
best and possibly the only chance to visualise tissue enhancement. artefact thus limiting its value.34
Pre-contrast scan planning is therefore essential to ensure complete In patients where a confident diagnosis of cavernous haemangi-
coverage of the whole liver. If the examination is incomplete after oma can be made based on typical US findings, no further confirma-
the first injection, repeated contrast administration is possible. With tory imaging test is required except perhaps for a routine follow-up
the transience of the contrast display, biopsy of newly identified ultrasound to determine interval stability consistent with a benign
lesions is difficult with this agent. For characterisation, single aetiology. However, haemangiomas can present with atypical US
sweeps through the lesion can be performed at the hepatic arterial findings in 2040% of cases with potential for misdiagnosis.35 In a
(1520 seconds) and portal venous (6090 seconds) phases at high retrospective study of 29 proven atypical haemangiomas in 29
MI to demonstrate the lesion vascular morphology and then in the patients, Moody and Wilson observed a number of sonographic
late phase to demonstrate the amount of contrast uptake within the features that suggest a haemangioma.35 The most useful feature is
lesion. During the vascular phase following Levovist administra- an echogenic border around a solid tumour while other suggestive
tion, the number of sweeps over the lesion should be minimised, as features include a partially hypoechoic internal echo pattern and a
it may spoil the late phase imaging. However, with Sonavist, curvilinear outline, which may be scalloped. The hypoechoic inter-
despite the destructive high MI mode being used, repeated sweeps nal echo pattern is postulated to be secondary to degenerative
are possible to complete the liver examination in the vascular and changes in a haemangioma such as haemorrhage, necrosis, fibrosis
late phases; this is most likely because of the much higher dose of or myxomatous change. Less frequently, atypical haemangiomas
Sonavist used.20 may rapidly enlarge in size, calcify, present as a cystic/ multilocular
lesion, contain fluidfluid levels or become hyalinised.21 Growth in
haemangiomas is thought to be due to vascular ectasia. Some hae-
mangiomas have oestrogen receptors and rapid growth has been
BENIGN FOCAL LIVER LESIONS observed during oestrogen influence during puberty, pregnancy,
oral contraceptive use and hormonal treatment.36 Fluidfluid
levels in a haemangioma are thought to represent stagnant or slow-
Cavernous haemangioma flowing blood with red blood cell sedimentation on the dependent
portion of the tumour. Hyalinisation is believed to represent the
Cavernous haemangioma is a common benign liver tumour with a end-stage involution of a haemangioma with replacement of the
prevalence of 0.520% in the general population21 and it is often vascular spaces by hyalinised fibrotic tissue leading to loss of
detected as an incidental finding on abdominal imaging.22 It is most the typical morphological appearance and enhancement pattern of
140
Benign focal liver lesions
A
B
C D
Figure 10.1 Haemangioma. A: Baseline scan showing central lesion with mixed echoes almost isoechoic to adjacent liver. B: Arterial
phase scan showing peripheral rim enhancement with nodular outline. C: Portal phase scan shows centripetal filling-in with more
prominent peripheral globular enhancement. D: Late phase scan shows further centripetal filling-in of the peripheral globular enhancement.
a haemangioma. In addition, haemangiomas occurring in a back- portal or late phase filling it was 78% (6588%); and for the combi-
ground of diffuse hepatic steatosis may have variable echogenicity, nation of both, it was 98% (91100%) (Fig. 10.2). In 22% of cases,
making pattern recognition difficult. Haemangiomas may appear haemangiomas demonstrated incomplete centripetal filling in the
slightly hypoechoic, isoechoic or hyperechoic compared to the stea- portal or late vascular phases. Quaia et al.40 also noted this similar
totic liver but usually maintain their posterior acoustic enhance- finding in a study of atypical haemangiomas on CEUS and showed
ment (which may be the only clue to their aetiology).37 High flow that in these cases of incomplete centripetal filling (Fig. 10.3), a
haemangiomas are reported to have a tendency for a hypoechoic thrombotic or fibrosclerotic pattern was proven at histology. In
appearance compared to the typically seen hyperechoic appearance general, this pattern is seen in larger haemangiomas >4cm.41 In
in most slow flow haemangiomas, and may be associated with an small haemangiomas (usually <1cm in size) an immediate homo-
arterio-portal shunt.38 geneous enhancement pattern may be seen in the arterial phase,
Cavernous haemangiomas, even those with atypical appearances due to rapid filling within these haemangiomas. These flash filling
on conventional US, can be confidently diagnosed based on their haemangiomas account for about 16% of all cases.36 Rarely, a cen-
enhancement pattern on CEUS36,39,40 (Fig. 10.1). Peripheral nodular trifugal (inside out) enhancement pattern has been described on
enhancement in the arterial phase with centripetal filling on the CEUS whereby there is a central enhancing focus in the arterial
portal venous and late vascular phases is a typical feature seen on phase followed by centrifugal enhancement in the portal and late
CEUS, and resembles the pattern seen on contrast-enhanced CT and vascular phases.41 Assessment of lesion enhancement in the portal
MRI. A study of the CEUS enhancement pattern of histologically and late vascular phases is also important to determine whether a
proven haemangiomas in 58 patients36 found that the sensitivity for liver tumour is benign or malignant. Consistent with other benign
detecting haemangiomas based on peripheral nodular enhance- tumours, haemangiomas are hyperechoic or isoechoic compared
ment was 74% (95% confidence interval, 6185%); for complete with the background liver during these phases, whilst malignant
141
CHAPTER 10 Focal liver lesions/echo enhancing agents and the liver
A B
tumours show contrast washout and are therefore typically contains normal hepatocytes and Kupffer cells and proliferating
hypoechoic. malformed bile ducts with absence of portal triads and central
veins.46 FNH is divided into two types: classic (80%) and non-classic
(20%). Classic FNH contains all components, including an abnor-
Fibronodular hyperplasia mal nodular architecture, malformed vessels, and bile duct prolif-
eration. The non-classic type contains two of the three components
Fibronodular hyperplasia (FNH) is another common benign liver but always shows bile duct proliferation.
tumour representing 8% of all liver tumours.42 It has a prevalence FNH is typically not well visualised on conventional US as the
of 35% in the general population, a female to male ratio of 8:1 and lesion is usually of similar echogenicity to the surrounding liver.
occurs most frequently in the 2050-year-old age group.42 When Detection is challenging for this stealth lesion with displacement
occurring in men, atypical presentation is more common with of adjacent intrahepatic vessels by mass effect occasionally being
lesions usually detected at a smaller size and at an older age.43 FNH the only clue to its presence.47 FNH is usually a well-defined and
is usually a solitary lesion <5cm in size but can be multiple in up homogeneous lesion with sharp margins and may be slightly hypo
to 20% of cases. An FNH syndrome of simultaneous occurrence of echoic (85% of cases), isoechoic or hyperechoic relative to normal
multiple FNHs and haemangiomas has been recognised.44 FNH is liver. A peri-lesional hypoechoic halo simulating a pseudo-capsule
usually diagnosed incidentally on imaging but may be sympto- has been observed which is thought to represent compressed liver
matic in up to 20% of cases, mainly in patients with larger lesions tissue or vessels around the liver. The central scar and the septa are
where the mass effect causes abdominal pain and distension.45 often difficult to appreciate on US but occasionally when apparent,
The aetiology of FNH is uncertain but dominant theories include they are usually hyperechoic in appearance. The addition of colour
a hyperplastic response to a pre-existing vascular malformation or and power Doppler48,49 to conventional US interrogation has been
a response to ischaemia due to an occult vascular occlusion. On shown to be useful for FNH characterisation showing a spoke
pathological examination, FNH is composed of circumscribed wheel arterial pattern of vessels, radiating from the central feeding
nodules of hyperplastic parenchyma surrounded by radiating artery to the periphery of the lesion. However, colour and power
fibrotic septa originating from a central scar, which contains fibrous Doppler US have limitations, particularly in detection of slow flow
connective tissue and malformed vascular structures. The arterial in intra-tumoral vessels and particularly in small lesions deep
vessels in FNH are most prominent in the central scar but are also within the liver parenchyma.
present along the septa, which extend from the centre to the periph- USCAs can improve the demonstration of tumoral microvascu-
ery of the lesion with a recognised centrifugal flow pattern. FNH larity in FNH thereby facilitating its diagnosis. USCAs enable the
142
Benign focal liver lesions
A B
detection of low-velocity blood flow because they increase the in the right lobe of liver (75% of cases) but may be intraparenchymal
signal to noise ratio so improve display of vascular pattern50 (Figs or pedunculated (10% of cases).59
10.4 and 10.5). The central feeding vessel with the FNH scar and Long-term oral contraceptive usage is linked with development
the communicating network of surrounding arteries is displayed as of adenomas with only a few cases of this disease being recorded
a centrifugal spoke wheel pattern of enhancement51 (Fig. 10.5). prior to introduction of the contraceptive pill in the 1960s.60 An
Central scar is present in 35% of lesions <3cm and in 65% of lesions extensive epidemiological study61 showed a 25 times higher inci-
>3cm.52 On CEUS, it has been reported in 3156% of cases.1,11,53,54 dence of hepatic adenoma in women on long-term oral contracep-
CEUS compares favourably with other modalities for detecting the tives compared to those who had either never used oral contraception
characteristic vascular pattern and central scar in FNH55,56 (Fig. or had used it for less than 24 months. Adenomas rarely occur in
10.6). In a study of 34 histologically proven FNHs, Yen et al.55 found men, and when present, are usually found in men with predispos-
that CEUS had the highest sensitivity (97.1%) in detection of the ing risk factors such as anabolic steroid usage, diabetes or type 1
spoke wheel enhancement or central scar compared with colour glycogen storage disorders.
Doppler US/power Doppler US (40%), contrast-enhanced CT or Pathologically, hepatic adenoma is a well-circumscribed mass
MRI (40%), hepatic angiography (50%) and liver scintigraphy (0%). composed of sheets of cells that closely resemble hepatocytes that
Janica et al.56 observed that the spoke wheel sign was detected by are arranged in plates separated by sinusoids.62 Bile ducts and
CEUS in 100% of FNHs in a study of 26 patients. CEUS is therefore portal tracts are absent and Kupffer cells if present are reduced both
an important diagnostic tool for detecting and confirming the pres- in number and functionality. Large tortuous arteries and dilated
ence of FNH with performance at least on par or even superior to thin-walled veins are often present, which denotes the hypervascu-
other available imaging options. lar nature of the tumour. Poor connective tissue support predis-
poses adenomas to haemorrhage. As a tumour capsule is often
absent or incomplete, haemorrhage may lead to spread into the
Hepatic adenoma liver or rupture into the peritoneal cavity. The risk of haemorrhage
is related to the size of the adenoma and is present in about 4050%
Adenoma is a benign hepatic tumour with an annual incidence of of tumours.63 Macroscopic fat deposition may occur in adenomas
34 per 100000 adult patients and is most commonly encountered as the cells accumulate lipid and glycogen. Adenomas also calcify
in young women on the oral contraceptive pill.57 It has an over- in about 515% of cases. Rarely, malignant transformation into
whelming female preponderance with a female to male ratio of 10:1 hepatocellular carcinoma has been reported in adenomas, mainly
and occurs most frequently in the 2030-year-old age group.58 It is in larger tumours >10cm in size.59 Surgical resection is recom-
a solitary lesion in 7080% of cases and has an average size of mended, particularly for larger adenomas, due to the risk of haem-
810cm.59 Adenomas are typically found in a subcapsular location orrhage and malignant transformation.63
143
CHAPTER 10 Focal liver lesions/echo enhancing agents and the liver
B C
144
Benign focal liver lesions
A B
C D
Hepatic abscess
Figure 10.6 Focal nodular hyperplasia in 3D CEUS in the three
orthogonal planes (1, 2 and 3) and the 3D reconstruction Pyogenic and amoebic abscess represent the majority of hepatic
demonstrating the characteristics of the FNH (4). abscesses detected worldwide. Both diseases have an excellent
prognosis if treated early but are potentially fatal if left undiag-
nosed. US is the first-line imaging investigation for infected patients
who may present with non-specific clinical and laboratory findings.
The sonographic appearance of hepatic adenoma is non-specific Familiarity with the disease process and pertinent sonographic
as it may be hyperechoic, isoechoic, hypoechoic or of mixed echo- findings facilitates prompt diagnosis and treatment.
genicity.62 Uncomplicated adenomas may have a homogeneous Pyogenic abscess is a localised collection of pus with destruction
appearance while presence of fat, intra-tumoral haemorrhage or of involved hepatic parenchyma and stroma, caused by a bacterial
necrosis will lead to a heterogeneous internal appearance. In pathogen.69 At histopathology, the abscess cavity shows multiple
general, increased echogenicity is seen in tumours with fat or intra- locules, usually filled with thick purulent material and lined by a
tumoral haemorrhage and posterior acoustic shadowing is detected fibrous tissue wall.70 Depending on the evolutionary stage of the
in calcified lesion. Colour and power Doppler US may demonstrate abscess, there may be suppuration, liquefaction or fibrosis and the
peripheral peri-tumoral and intra-tumoral vessels. Several authors edges of the cavity are lined by a chronic inflammatory infiltrate.
have demonstrated a continuous venous waveform in adenomas, The most common organisms responsible are Escherichia coli and
which may potentially aid in differentiation from malignant Klebsiella pneumoniae, although there is a polymicrobial source in
tumours such as hepatocellular carcinoma (HCC), which show a more than 50% of infected patients. The usual route of bacterial
pulsatile waveform pattern.64,65 However, these studies were done seeding is by haematogenous dissemination (via the portal vein or
on larger lesions with a mean diameter of >5cm. In smaller lesions, hepatic artery) or via the biliary tract from ascending cholangitis.
the utility of colour and power Doppler US is limited due to techni- Infection can also occur by direct extension from adjacent organs.
cal difficulties in obtaining reproducible signals. Common clinical conditions that predispose to pyogenic abscess
On CEUS, hepatic adenoma is typically hyper-enhancing in the include acute appendicitis, acute diverticulitis, trauma and surgery.
arterial phase and may be iso-enhancing with respect to the back- Amoebic abscess is caused by the protozoan Entamoeba histolytica
ground liver on the portal venous and late phase66,67 (Fig. 10.7). and the usual mode of transmission is via the faecaloral route. The
Atypical of a benign hepatic tumour, some adenomas may also liver is the most common extraintestinal organ involved (in 8.5% of
show portal phase non-enhancement or washout.68,69 Persistent cases) with spread to the liver from the gastrointestinal tract via the
focal non-enhancement on all vascular phases is also seen in areas portal vein.70 Amoebic abscess is most prevalent in the developing
of intra-tumoral haemorrhage or necrosis. Clinically, distinction of world where it is endemic in parts of Africa, the Far East, and in
adenoma from FNH is important as these pathologies generally Central and South America. Worldwide it affects about 10% of the
occur in the same patient cohort, i.e. young women of reproductive population.70 Histologically, there is scant inflammatory reaction
age, and whilst FNHs are typically leave alone lesions, adenomas at the margins and a shaggy fibrin layer. Haemorrhage into
should be treated more aggressively. In a CEUS study of 62 patients the abscess can lead to a pasty material known as anchovy paste.
with 43 FNHs and 19 adenomas, Kim et al.68 found that FNH is The abscess may be purulent if involved by secondary bacterial
predicted on the basis of arterial phase centrifugal filling and stel- infection.
late vascularity while adenomas were less reliably predicted on the The clinical presentation for both these abscess types is highly
basis of centripetal or mixed filling without stellate vascularity. The variable. The classic triad of right upper quadrant pain, fever and
145
CHAPTER 10 Focal liver lesions/echo enhancing agents and the liver
A B C
Figure 10.8 Abscess. Large non-enhancing lesion in the right lobe in the late phase with enhancing septum (A); another abscess with
enhancing pseudo-capsule and segmental normal liver parenchymal hyperperfusion in the arterial phase (B) and non-enhancement of the
bulk of the abscess in the late phase (C).
jaundice may be present in some patients. However, many patients gain were more prevalent in hepatic abscesses to a statistically
present with non-specific clinical findings such as nausea, vomiting, significant degree. Oleszczuk-Raszke et al.77 found that (1) pyogenic
diarrhoea, malaise and weight loss. In general, patients with abscess was more likely to have an irregular honeycomb content
amoebic abscess tend to be more acutely unwell than those with and ill-defined margins while amoebic abscess was more likely to
pyogenic abscess. Laboratory markers such as white cell count and be a sharper defined lesion with a peripheral halo; (2) both abscess
liver functions tests (e.g. serum bilirubin, transaminases, alkaline types may contain central liquefaction but this was more common
phosphatase) are usually deranged in hepatic abscess. Blood cul- in amoebiasis; (3) multiplicity was more common in amoebic
tures are positive in patients with pyogenic abscess in only 50% of abscess and when present this was likely to be contiguous; and (4)
cases. Immunoassays are positive in amoebiasis in over 90% of amoebic abscess was slower to heal than pyogenic abscess and
cases but may be normal in the early stage of infection (within the more likely to develop echogenic changes. Sonographic findings in
first week) before an appreciable immunological response can be patients undergoing treatment for amoebic abscess can be confus-
mounted.70 Definitive diagnosis requires US-guided abscess aspira- ing and may worsen (lesions may increase in number and/or size)
tion and culture of the infected contents. Standard treatment even when the patient is improving clinically.71,78 Treated lesions
involves abscess drainage by US-guided percutaneous catheter can become anechoic or calcified or persist as cystic appearing
placement and a course of appropriate antimicrobial therapy. foci.71,78,79 Clinical management should be tailored according to the
The sonographic appearance of pyogenic abscess is highly vari- clinical status of the patient rather than the imaging findings.71,79
able and depends on the pathological stage of the infection.71,72 The CEUS contributes to the imaging analysis of hepatic abscess by
abscess can appear solid in the early stage prior to the onset of increasing lesion conspicuity and so improving detection and char-
parenchymal necrosis.72 At this stage, sonographic features may acterisation (Fig. 10.8). An abscess is typically detected as a lesion
overlap with those of other focal hepatic pathologies such as liver with an enhancing rim and a persistent hypoechoic central compo-
tumours.73 As the evolutionary stage progresses, liquefaction occurs nent.80 Pulsatile vessels may be seen in the rim or along the internal
and the abscess will appear increasingly fluid with a mixed echo- septa. In comparison to conventional US, the abscess geometry is
genic appearance seen.72 At a later stage, as the abscess matures better appreciated on CEUS with sharper boundaries seen between
with central liquefaction, it will appear predominantly cystic. His- the normal liver parenchyma and the outer wall of the abscess; and
tologically, at this stage, most abscesses are multiloculated with between the inner wall of the abscess and the liquefactive/necrotic
locules communicating with each other.72 As the majority of infected center80 (Fig. 10.9). CEUS can also detect changes in the adjacent
patients present at this late stage, pyogenic abscess is most fre- liver parenchyma that may not be visualised on conventional US.
quently detected as multiloculated cystic hepatic lesions. Due to the Transient arterial hypervascularity due to reactive hyperaemia, a
cystic contents, posterior acoustic enhancement may be detected on peripheral hypovascular area due to oedema or defective venous
sonography. Internal echoes are frequently seen within the cystic perfusion, and flow reversal in the adjacent portal vein have been
contents as a result of internal debris from necrosis. The abscess reported.8082
typically has well-defined but irregularly shaped thin walls.71 Gas- CEUS can be used to differentiate liver abscess from hepatic
containing abscesses (such as those caused by K. pneumoniae and malignancy. Kim et al.83 studied the morphological characteristics
Clostridium) may demonstrate intense internal echogenicity with of pyogenic hepatic abscesses and hypovascular liver malignancies
posterior reverberation artefact. Colour Doppler interrogation may in 24 patients with 16 abscesses and 22 neoplasms. The study found
show flow around the periphery of the abscess and within its paren- that distinguishing features suggesting pyogenic abscess include a
chymal septations. The majority of pyogenic abscesses resolve to coalescent appearance, a sharp boundary to the necrotic cavity, and
normal parenchyma within 18 weeks following treatment.74 In a lack of internal enhancement. Conversely, the study found that
small proportion of cases, residues remain which may calcify. malignant neoplasms generally had ill-defined borders, a variable
Typical sonographic features of amoebic abscess are: (1) absence degree of internal tumour enhancement, and were typically less
of significant wall echoes, (2) round or oval shape, (3) lower echo- complex morphologically.
genicity than normal liver with fine homogeneous low level internal
echoes at high US gain setting, (4) contiguity with the liver capsule75
and (5) posterior acoustic enhancement. Studies have shown that Hepatic steatosis
amoebic and pyogenic abscess cannot be reliably distinguished
based on sonographic appearances alone.76,77 However, Ralls et al.76 Hepatic steatosis is commonly seen in the Western world, affecting
found that two sonographic signs (1) round or oval shape and (2) about 1015% of the general population.84 It is characterised by
hypoechoic appearance with fine homogeneous echoes at high US elevated triglyceride accumulation within the liver, as a result of a
146
Benign focal liver lesions
A B
Figure 10.9 Abscess in the arterial (A) and portal phase (B) showing enhancement of capsule with non-enhancement of the fluid
content.
variety of predisposing factors.8587 The most common aetiological fossa, adjacent to the left portal vein, the porta hepatis, adjacent to
factors associated with development of hepatic steatosis are exces- the falciform ligament and in subcapsular areas. On conventional
sive alcohol consumption, diabetes, obesity and hyperlipidaemia. US, areas of focal fat sparing appear hypoechoic against the echo-
Less often, hepatic steatosis is secondary to viral hepatitis, drugs genic background of hepatic steatotic. A geographic margin
(e.g. steroids and chemotherapy agents) and nutritional and dietary (abruptly angled) and absence of mass effect on adjacent liver
abnormalities. Triglyceride accumulation within hepatocytes occurs parenchyma and vessels is typical. Colour Doppler ultrasound may
as a result of defects in hepatocellular lipid metabolism. Macro- be useful in demonstrating a normal vascular distribution in
scopically, the steatotic liver has a yellowish coloration and may be affected areas with no evidence of vessel displacement. On CEUS,
enlarged.88 Microscopically, lipid vacuoles are seen within involved focal fat sparing is isoechoic to the rest of the liver parenchyma on
hepatocytes and this enables the severity of steatosis to be quanti- all vascular phases (arterial/portal/late phase)95,96 (Fig. 10.10).
fied based on the proportion of hepatocytes that contain fat
inclusions (mild <30%, moderate 3060%, severe >60%).88 Lipid
accumulation is non-uniform in the early stage and has a geo- Focal steatosis
graphic bias with hepatoctyes situated close to central veins more This is less common than focal fatty sparing. The pathogenesis is
susceptible than those situated close to portal triads.84 At an uncertain but abnormal accumulation of fat may occur as a result
advanced stage, a more uniform liver involvement is typically seen. of ischaemia due to decreased portal venous blood flow or decreased
Generalised hepatic steatosis is visualised sonographically as a delivery of unknown substances via the portal vein.88 A key factor
homogeneous increase in liver echogenicity, which exceeds that of is related to increased insulin load in portal blood. Focal steatosis
renal cortex and spleen. Poor depth penetration leading to reduced occurs in similar locations to focal fat sparing such as the gallblad-
appreciation of hepatic architecture is also typically present as a der fossa, adjacent to the falciform ligament, the porta hepatis and
result of the increased attenuation of US waves in hepatic steatosis subcapsular locations. This is because both conditions are related
compared to normal hepatic parenchyma. Steatosis, particularly to venous anomalies in those areas of the liver. Focal steatosis is
when there is non-uniform liver involvement, dramatically increases hyperechoic to the background liver and typically has a geographic
the complexity of conventional sonographic interpretation.8991 outline. Focal steatosis does not exhibit mass effect on the adjacent
Lesions that conform to a nodular shape can be misdiagnosed as liver parenchyma or vessels. On CEUS, focal fat is isoechoic to the
neoplasms.89,90 Detection and characterisation of other pathologies rest of the liver parenchyma on all vascular phases (arterial/portal/
can be compromised as a consequence of loss of typical sonographic late phase). A study by Liu et al.94 found that contrary to the norm,
features that enable pattern recognition, due to image distortion the enhancement pattern of focal steatosis may exhibit hypo-
from the steatotic background.91,92 enhancement in the arterial phase (in 11 of 25 lesions in the study),
Several patterns of non-uniform hepatic steatosis have been rec- which may reflect unusual blood supply and/or histological
ognised on imaging.93,94 These include: (1) focal fat sparing in a changes.
generalised fatty liver, (2) focal steatosis, (3) multifocal steatosis, (4)
lobar or segmental steatosis and (5) perivascular steatosis. Focal fat
sparing and focal/multifocal steatosis can mimic other focal liver Multifocal steatosis
pathologies on imaging, and are discussed below. This is a rare presentation of focal fatty infiltration, which can
mimic metastatic disease particularly when it has a nodular con-
Focal fat sparing figuration.97 Correct diagnosis is challenging, especially in patients
with known malignancy. Multifocal steatosis appears as multifocal
The pathogenesis of this condition is uncertain, but a disturbance areas of increased echogenicity compared to the background liver.
in portal flow has been suggested.88,94 As lipid delivery to the liver Clues to its presence include lack of mass effect, and stability over
from the gastrointestinal tract is via the portal venous system, a time. On CEUS, multifocal steatosis is isoechoic to the rest of the
geographic reduction of portal flow (due to third hepatic inflow liver parenchyma on all phases (arterial/portal/late phase).
from aberrant venous supply) to part of the liver is hypothesised to
spare hepatocytes in that area from steatosis.88 Typically locations In all these cases of non-uniform hepatic steatosis, a confident diag-
for focal fat sparing include segment IV around the gallbladder nosis can be made on CEUS based on an enhancement pattern
147
CHAPTER 10 Focal liver lesions/echo enhancing agents and the liver
A B
which is identical to that of background liver. CEUS also improves haematomas due to the haematocrit effect. Internal septations,
the detection and characterisation of liver neoplasms that coexist in which float freely during real-time scanning and which do not show
the steatotic liver as these lesions may be diagnosed based on rec- vascularity on colour Doppler US interrogation, are a recognised
ognised enhancement patterns, which remain unaltered.92,95 finding. Serial US will show a change in size and appearance of the
haematoma with time. Eventually, over a period of months, the
Liver haematoma haematoma will resolve due to regeneration of liver tissue, but a
residual scar or cystic space may persist. On CEUS, haematoma is
hypoechoic on all vascular phases. Haematomas secondary to intra-
Liver haematoma is most commonly caused by blunt abdominal
tumoral haemorrhage in a pre-existing hepatic neoplasm will show
trauma, with the liver being the second frequent abdominal organ
avascularity of the haematoma juxtaposed with the vascular pattern
injured during blunt trauma (after the spleen). The liver is suscep-
of the underlying tumour. CEUS is a useful supplement to conven-
tible to trauma due to its large size (the largest intra-abdominal
tional US in the assessment of trauma patients, with studies showing
organ), its relatively fixed position in the abdomen and its proxim-
superior detection of solid organ injuries with CEUS compared to
ity to bony structures such as ribs and spine. Other predisposing
conventional US.101,102 Liver lacerations typically appear as well-
causes for liver haematoma include surgery, liver biopsy, coagu-
defined hypoechoic linear or branched areas while contusions
lopathy, intra-tumoral haemorrhage and pregnancy. Hepatic
appears as ill-defined hypoechoic areas without clearly defined
haematomas are also frequently found in newborns at perinatal
margins these are best appreciated on the portal venous phase103
autopsy, but are usually small, subcapsular in location and clini-
(Fig. 10.11). Active haemorrhage is identified as an extravasation of
cally silent.98 It is postulated that the delicate hepatic capsule and
microbubbles into the haematoma and suggests a more clinically
its connections to the collagen along the sinusoids provide the
significant injury. Performance of CEUS may almost approach that
pathogenesis of these haematomas in neonates.98
of contrast CT in the assessment of trauma patients, and CEUS may
Haematomas may have variable shapes and echogenicity. Sub-
have a role in the triage of trauma patients who cannot undergo CT
capsular haematomas typically have a lentiform shape which con-
due to haemodynamic instability but who could have a bedside
forms to the outer contour of the liver capsule. Intraparenchymal
ultrasound examination in the emergency unit.101 In addition, CEUS
haematomas are typically spherical with irregular walls but may
could be used in the follow-up of hospitalised patients with known
also follow given anatomical structures resulting in a more starlike
solid organ injuries who are managed conservatively and who
configuration.99 The ultrasound appearance of haematoma depends
cannot be easily moved to the CT suite.101
on the severity of the bleed and the timing of the scan relative to
the onset of bleeding.100 Acute and subacute haematomas appear
homogeneous and hyperechoic (due to multiple acoustic interfaces Rare benign lesions
as a result of the fibrin and erythrocytes in the haematoma), whereas
in chronic cases, the haematoma appears more cystic with internal The findings on conventional US and CEUS of several documented
echoes due to clot liquefaction.100 Fluidfluid levels can be seen in rare focal liver lesions are discussed.
148
Benign focal liver lesions
A B
Hepatic angiomyolipoma iso-enhancement. In the late phase, all lesions showed iso-
enhancement. Zheng and Kudo106 demonstrated on CEUS that the
Angiomyolipoma (AML) is a mesenchymal tumour containing efferent vessel in two cases of hepatic AML was the hepatic vein,
varying proportions of three elements mature adipose tissue, confirmed by conventional angiography and CT angiography. The
smooth muscle and thick-walled blood vessels. It is classified his- authors postulated that this haemodynamic finding may be an
tologically into mixed, lipomatous, myomatous and angiomatous important characteristic of hepatic AMLs and may facilitate the
types.104,105 It is an extremely rare tumour of the liver and is usually differential diagnosis from other focal hepatic tumours such as
diagnosed postoperatively or by autopsy. Hepatic angiomyolipoma HCC where the main drainage vessel is the portal vein.
can be diagnosed preoperatively according to the following find-
ings: (1) hypervascular nature on imaging suggestive of vascular
proliferation within the tumour, (2) imaging findings of intra- Hepatic lipoma
tumoral fat and (3) positive actin and HMB-45 stains on biopsy
specimens which confirms smooth muscle component.106109 On con- Histologically this lesion is composed of mature adipose tissue.104,105
ventional US, AML may show increased echogenicity secondary to On conventional US, hepatic lipomas appear as well-defined uni-
presence of intra-tumoral fat. However, the fat content within formly hyperechoic lesions.112 These lesions may or may not show
AMLs varies ranging from 5% to 90% and can lead to atypical acoustic shadowing on US. Xu et al.111 found a liver lipoma that
imaging appearances.106 Fat-poor AMLs can therefore appear as showed inhomogeneous hyper-enhancement in the arterial phase
hypo- or isoechoic lesions. In these cases, evaluation of the haemo- with iso-enhancement on the portal venous and late phases.
dynamic characteristics of the hypervascular tumour is more useful
for diagnosis. Colour Doppler imaging can reveal avid tumour
vascularity and pulsatile flow.110 In a study of 2209 focal liver
Intrahepatic biliary cystadenoma
lesions using CEUS, Xu et al.111 reported the enhancement pattern Biliary cystadenoma is a rare cystic neoplasm of the liver and
of four biopsy-proven hepatic AMLs. All lesions showed rapid accounts for less than 5% of all cystic lesions of the liver, with fewer
heterogeneous (n = 1) or homogeneous (n = 3) hyper-enhancement than 200 cases reported globally.113 Histologically, the tumour is a
during the arterial phase with enhancement commencing 1016 multiloculated cystic lesion lined by mucus-secreting cuboidal or
seconds after contrast injection. Intra-lesional and peri-lesional columnar epithelium with an accompanying dense cellular ovarian
arteries were present in all cases. During the portal phase, half the like stroma.114 The tumour usually presents in middle-aged women
cases showed slight hyper-enhancement and the other half showed with a mean age of 50 years and with a great variability in size
149
CHAPTER 10 Focal liver lesions/echo enhancing agents and the liver
ranging from 1.5 to 30cm.115 The majority of patients are asympto- lesion and iso-enhancement in the other lesion during the arterial
matic but large tumours can present with a palpable mass and cause phase, associated with washout in both lesions during the portal
symptoms. The tumour is slow growing but is postulated to be and late phases.111
premalignant with risk of malignant transformation as high as
30%.116 Biliary cystadenoma has a tendency to recur following sur-
gical excision. On conventional US, cystadenoma appears as a well- Hepatic sarcoidosis
defined anechoic cystic mass with echogenic septations and/or Hepatic or splenic sarcoid granulomas are found in 4070% of
papillary infoldings.104,111 Xu et al.111 reported a case of cystadenoma patients with sarcoidosis.128 Liver involvement is usually not appre-
that showed hyper-enhancement of the cystic wall, internal septa- ciable on imaging but when identified the most commonly observed
tions and an intracystic solid portion during the arterial phase with pattern is non-specific textural heterogeneity and hepatomegaly.129
contrast washout in these areas during the portal and late phases. Conventional US may demonstrate normal or increased liver echo-
Lin et al.,117 in a blinded reader study on the diagnostic performance genicity, hepatomegaly, coarsening of liver texture with or without
of CEUS for complex cystic focal lesions, found two cases of histo- discrete nodules (which can be of variable echogenicity), focal cal-
logically proven cystadenomas; they appeared as a well-defined cifications and contour irregularities.111,128,130 Hepatic sarcoidosis
unilocular or multilocular cystic mass which rarely contained mural showed hypo-enhancement on CEUS in all phases.111
or septal nodules. On CEUS, the tumour showed septal enhance-
ment in the arterial phase and hypo-enhancement during the portal
venous and late phases. Solitary necrotic hepatic nodule
This is a very rare benign lesion of uncertain aetiology. The patho-
Biliary epithelial dysplasia of genesis is probably multifactorial and could be related to patholo-
gies such as parasitic infection, trauma or sclerosing haemangiomas.131
the intrahepatic bile duct Histologically, the mass shows a uniform complete necrotic core
This is a premalignant lesion that arises from the epithelium of the with a dense hyalinised fibrous capsule containing elastin fibres
intrahepatic bile duct.118 Xu et al.111 found one histologically proven with inflammatory cells.132 On conventional US, the solitary necrotic
lesion which was slightly hyperechoic and located within a dilated nodule is usually hypoechoic or a target lesion with a hyperechoic
bile duct on conventional US; on CEUS, the lesion showed homo- centre.111 No enhancement is seen on CEUS on all vascular
geneous enhancement during the arterial phase with washout in phases.111,133
the portal venous and late phases. Sonographically, the lesion is
difficult to separate from an intrahepatic cholangiocarcinoma.
MALIGNANT FOCAL LIVER LESIONS
Hepatic inflammatory pseudo-tumour
Inflammatory pseudo-tumour is a benign hepatic mass consisting Liver metastasis
of inflammatory cells and fibrous stroma on histological examina-
tion.119 The aetiology is unclear but it is postulated to be secondary The liver is a frequent site for metastasis from the gastrointestinal
to an inciting hepatic infection.120 The lesion may have variable tract cancers and is one of the most common clinical requests for
non-specific appearances on imaging studies. The mass may be well abdominal US imaging. Metastatic disease of the liver is about 20
defined or poorly defined, have variable echogenicity (hypo- or times more common than any of the primary hepatic neoplasms. It
hyperechoic or mixed), may contain multiple septa, and can have is a sign of advanced tumour stage and implies a very poor prog-
posterior acoustic enhancement.121,122 Inflammatory pseudo-tumour nosis. In the Western world, colorectal cancer accounts for 1416%
can be hypo- or hypervascular. Ding et al.123 found that all four of cancer deaths in men and women respectively with approxi-
lesions in their study showed hypo-enhancement throughout all mately 25% of patients having liver involvement at the time of
phases on CEUS. Xu et al.111 had seven lesions in their study, which initial presentation and up to 50% will develop hepatic metastases
showed a mixture of hyper-, iso- or hypo-enhancement, either during the course of their disease.134,135 For patients with colorectal
homogeneous or heterogeneous in the arterial phase with all lesions hepatic metastases, surgical resection is the treatment of choice with
showing hypo-enhancement in the portal venous and late phases. 1020% of patients being candidates for potentially curative resec-
Due to non-specific imaging appearances, diagnosis of inflamma- tion; resection is indicated if there is no unresectable extrahepatic
tory pseudo-tumour can be difficult and may require biopsy. disease, if liver deposits can be resected with a free clearance margin
of 1cm and if there is adequate liver reserve. The 5-year survival
rates vary from 25 to 40%.136,137 Seventy-five per cent of those who
Peliosis hepatis undergo liver resection will develop recurrence and of these, the
This is a rare benign vascular lesion characterised by sinusoidal liver is involved in 50%. For metastases from other primary malig-
dilatation and blood-filled hepatic spaces. Various aetiological nancies such as pancreatic cancer, hepatic involvement signifies
factors have been described including infectious agents such as poor prognosis and only palliative treatment can be offered.
Bartonella and HIV, malignancies such as HCC, renal and cardiac Hepatic metastases typically appear as multiple focal discrete
transplantation, diabetes, drugs such as steroids and oral contracep- lesions in 90% of cases, but solitary lesions may also occur.100 Diffuse
tives and toxins such as arsenic and polyvinyl chloride.124 It is idi- infiltrative hepatic involvement may be seen in breast cancer or
opathic in 50% of cases. The pathogenesis is unknown but possible lymphoma. On conventional ultrasound, a metastasis may appear
causes include increased sinusoidal pressure, disappearance of hypoechoic, hyperechoic or of mixed echogenicity and some look
normal parenchyma by hepatocyte necrosis, and sinusoidal wall like target lesions.138 These appearances are non-specific in deter-
weakening.111,125 On conventional US, peliosis hepatis demonstrates mining the primary tumour. CEUS appearance of metastasis is vari-
variable echogenicity relative to the surrounding liver and may able depending on the size and vascularity of the tumour and the
have internal vascularity on colour Doppler US imaging.126,127 The degree of necrosis. Metastases of the same cellular type (e.g. colon)
lesion is typically hyperechoic but can show iso-, hypo- or mixed may vary in their enhancement characteristics and metastases of
echogenicity due to the variety of its possible histological features different cellular types (breast and colon) may produce identical
as well as the possibility of additional haemorrhage. Perinodular appearances.139,140 Hepatic metastases from colon and lung carcino-
and intranodular vascularity can be seen on colour Doppler US mas had previously been described as being hypovascular.
imaging. Two histologically proven lesions had previously been However, on continuous scanning at low MI using non-linear
reported, which showed homogeneous hyper-enhancement in one imaging modes, these lesions usually show some peri-tumoral
150
Malignant focal liver lesions
Figure 10.12 Metastasis. Mixed echogenic tumour at baseline (A) showing rim enhancement in the arterial (B) and portal (C) phases
and complete filling defect in the late phase (D).
vessels with central necrosis or homogeneous enhancement during surrounding liver with improved delineation13 (Fig. 10.13). In the
the arterial phase; during the portal phase, they typically appear as case of breast and colonic metastases, there may be a combination
hypoechoic filling defects surrounded by a brighter liver paren- of both hyper- and hypovascular lesions; some of the hypervascular
chyma and rim enhancement (Fig. 10.12).13 For lesions that are lesions may become isoechoic to surrounding liver parenchyma
hyperechoic at baseline, there is a characteristic reversal of the during the arterial phase but can still be recognised by virtue of the
echogenicity to become hypoechoic in the portal and late phases. microbubbles haphazard movement within the hypervascular
Smaller colorectal liver metastases may show a more uniform lesions. During delayed imaging with sinusoidal/liver-specific
display of the intra-lesional vessels during the arterial phase; agents, both hyper- and hypovascular metastases characteristically
however, during the portal phase, the liver parenchyma enhances appear as hypoechoic lesions with or without rim enhancement in
and the metastases may appear as echo-poor filling defects with or a background of echogenic liver.13
without rim enhancement. In contrast, hypervascular metastases Conventional US is particularly poor for detecting metastases
(such as the carcinoids, islet cell, melanoma, breast, renal or thyroid that are small (especially <1cm in size) or isoechoic compared to
malignancies) become markedly hyperechoic during the arterial surrounding liver parenchyma.141 CEUS has improved detection of
phase. In the portal phase, these hypervascular lesions may become liver metastases compared to conventional US based on published
isoechoic to adjacent liver parenchyma and the contrast agent literature.142146 In a study comparing conventional versus CEUS in
washes out of the lesions gradually to become hypoechoic to the the detection of liver metastases, the average number of confirmed
151
CHAPTER 10 Focal liver lesions/echo enhancing agents and the liver
A B
metastases increased from 3.06 to 5.42 following contrast adminis- subcapsular lesions and lesions adjacent to the ligamentum teres in
tration; the sensitivity for detecting individual metastases signifi- patients who had had adjuvant chemotherapy.
cantly improved from 63% to 91%. More importantly sub-centimetre
lesions were identified in over 92% of confirmed cases following
contrast compared with 54% at baseline.147 In a multicentre study
of 123 patients evaluating conventional US versus CEUS for the Improved detection of liver metastases
detection of liver metastases, similar results were observed with the with contrast-enhanced intraoperative
sensitivity for detection of individual lesions improving signifi-
cantly from 71% to 87% following contrast administration. Further-
US (CE-IOUS)
more the specificity also improved significantly from 60% to 88%; More recently, we assessed the value of CE-IOUS in 60 consecutive
in a small subgroup of patients CEUS also showed more metastases patients undergoing liver resection of metastases. The technique for
in 32% of patients than did contrast-enhanced CT.143 In a subse- IOUS and CE-IOUS is as described above.144 Metastases identified
quent multicentre study of 157 patients, off-site blinded readers on CT and/or MR, IOUS and CE-IOUS were counted, sized and
showed improved sensitivity for detection of individual lesions mapped according to the Couinaud classification on a liver sche-
from 38% to 67% following contrast injection, and the characterisa- matic chart for each modality and in real-time for all the sono-
tion of the lesions was also improved with none of the metastases graphic examinations. Benign cysts were not included in the counts.
showing contrast uptake in the late phase.148 Compared with The excised liver segments or lobes were sectioned at pathology to
contrast-enhanced helical CT scan, CEUS was shown to detect more obtain a true pathologic gold standard of the lesions. Correlation
metastases in 12%, equal number in 74% and fewer in 14% of the with resection/biopsy histopathology findings was also carried out.
83 patients presenting with fewer than five lesions.149 There was no Changes in surgical management following CE-IOUS compared
significant difference in the accuracy between contrast-enhanced with those made after IOUS were documented (e.g. abandoned
helical CT and CEUS. More recently Konopke and colleagues resection, more extensive resection, limited resection or combined
showed that CEUS significantly improved the sensitivity of US resection with radio-frequency ablation, etc.).
from 56.3% to 83.8% in the detection of liver lesions in a prospective A total of 107 lesions were identified on histopathology findings
study of 108 patients suspected of having liver metastases of biopsies and resected tissues and of these 103 were confirmed
using histology and intraoperative US as the reference standard.150 metastases and 4 haemangiomas. The number of correctly identi-
CEUS led to the improved detection of sub-centimetre lesions, fied metastases on CT/MRI combined, IOUS and CE-IOUS was 79,
152
Malignant focal liver lesions
84 and 101, respectively. There was a statistically significant increase location of liver metastases as a complement to contrast-
in the number of detected metastases on CE-IOUS compared with enhanced CT and/or MRI.
IOUS and also with combined CT/MRI (p = 0.029 and p = 0.047, 3. CEUS should be used routinely in the surveillance of
respectively). No statistical difference was observed in the number oncology patients.
of metastases detected between IOUS and combined CT/MRI (p =
0.53). For CT/MRI, IOUS and CE-IOUS, the sensitivity was 76.7%,
81.5% and 96.3%, respectively; accuracy was 73.8%, 78.5% and
96.3%, respectively; the positive predictive value was 95.2%, 95.5% Hepatocellular carcinoma
and 98.0%, respectively. The mean (SD) size of the lesions identi-
fied on CT/MRI/IOUS combined and CE-IOUS was 2.73 (1.46) cm
and 1.71 (1.57) cm, respectively. The median size of the additional Incidence
lesions identified on CE-IOUS was 0.8cm. The smallest metastasis Hepatocellular carcinoma (HCC) is a malignant neoplasm com-
identified was 4mm in diameter. Of the 60 patients, CE-IOUS was posed of cells with hepatocellular differentiation.152 It is the most
not performed in 3 patients, 2 patients had peritoneal metastases at common primary liver malignancy, the fifth most frequent cancer
exploration, and 1 patient had widespread metastases in a back- type and third most frequent cause of cancer-related deaths glo-
ground of fatty liver on the basis of IOUS. In 40 of the remaining bally.153 More than half a million new cases are diagnosed yearly
57 patients, there was no alteration in the surgical management; with an age-adjusted worldwide prevalence of 5.514.9 per 100000
CE-IOUS detected no additional lesion in 37 patients; in 2 cases population.154 In some parts of Asia, HCC is the leading cause of
there were additional lesions but they did not entail any extended death from cancer. In the developed world, the incidence of HCC
resection or adjunctive surgical manoeuvres; in another patient, one has increased in the past two decades largely attributable to hepa-
of the lesions was wrongly diagnosed on IOUS and CT as metasta- titis C virus infection.155 In the United States, the average annual
sis and was accurately identified as a benign haemangioma on age-adjusted incidence of HCC increased from 1.3 per 100000 in
CE-IOUS. In contrast, new information identified on CE-IOUS 19811983 to 3 per 100000 in 19961998 with a 25% increase between
alone altered the surgical plan in the remaining 17 of 57 patients 1993 and 1998.156 In more than 80% of cases, HCC occurs in the cir-
(29.8%); additional hepatic metastases were detected in 11 cases rhotic liver, and in these patients HCC constitutes the leading cause
(19.3%), which extended to a tri-segmentectomy in 3 cases, addi- of death.154 HCC is up to 16 times more common in patients with
tional non-segmental wedge resection in 2 patients and radio-fre- cirrhosis than in those without cirrhosis (annual incidence 26.6%
quency ablations of the additional lesions in 6 cases, as an adjunct in cirrhotics and 0.4% in non-cirrhotics).154 In patients with cirrhosis,
to the planned hepatic lobectomy. Prior to radio-frequency ablation the incidence of HCC at 5 years may exceed 25%.157
all additional lesions were biopsied and confirmed as metastasis;
all biopsies and radio-frequency ablations were performed using
CE-IOUS guidance. In 2 patients (3.5%) there were fewer lesions Screening and surveillance of HCC
than identified on preoperative imaging scans and could not be
confidently excluded on IOUS alone, which resulted in alteration Early tumour detection while it is still at a low grade and is ame-
in the original surgical plan from right hepatectomy to excision of nable to curative treatment is the hallmark of a successful screening
three segments in one and removal of segment VII/VIII plus a programme. Screening and surveillance for HCC remains a clinical
metastasectomy in the other. CE-IOUS also confirmed presence of challenge. Despite the lack of concrete evidence of any true survival
an arteriovenous malformation in one patient (1.8%), which was benefit or cost-effectiveness, it is now becoming widely accepted
not identified on IOUS and was previously diagnosed as apparent among hepatologists and endorsed by the World Health Organiza-
solitary metastasis on CT; CE-IOUS also accurately diagnosed a tion that it should be routine in the management of patients with
solitary benign haemangioma with characteristic peripheral nodular end-stage liver disease. Nevertheless some of the rationales for
enhancement with progressive filling-in over the vascular and late screening and surveillance are compelling.
phases in 2 patients (3.5%) which were wrongly identified as metas- The worldwide incidence of HCC is increasing but more notice-
tasis on CT and IOUS. Previously planned resections were therefore ably in North America and Europe; it is now believed that the rise
not carried out. In one case the tumour margin could only be clearly in the latter continents, which is progressively affecting younger
visualised on CE-IOUS to be too close to the inferior vena cava for patients, is mainly due to the rise in hepatitis C viral infection,
resection and it was ablated instead. New findings on CE-IOUS whilst the rates associated with alcoholic cirrhosis and hepatitis B
alone also altered IOUS/CT/MRI hepatic staging in 35.1% (20 of virus infection have remained stable.158 The disease is extremely
57) of patients. lethal, with median survival rates of untreated symptomatic cases
In many centres, hepatic ultrasonography remains the primary ranging between 4 and 6 months. Even for patients with small
imaging modality of choice in imaging the liver for suspected tumours there is a significant mortality as less than 50% will survive
metastases from primary tumours such as: breast, melanoma, 5 years despite undergoing apparently curative resection.
oesophagus, stomach, pancreas and lung. This practice is merely The target population for screening and surveillance for HCC is
historical, readily available and cheap (compared to CT or MR) and readily identifiable. Chronic hepatitis B and C virus infections are
is usually triggered by the patients abnormal liver function tests or well recognised to increase the risk of HCC. In Europe, approxi-
raised tumour markers; the identification of liver metastasis is also mately 28% of liver cancer has been attributed to chronic hepatitis
used as a prognostic indicator of poor outcome. For these tumour B virus infection and 21% to hepatitis C virus infection,159 but the
types, in contrast to colorectal cancer, global detection of hepatic risk is greatest in the presence of co-infection with both hepatitis B
metastasis, i.e. whether metastasis is present or not, is the primary and C virus; male sex and alcohol abuse are also significant risk
goal rather than the actual number and localisation of the metas- factors.160 Cirrhosis is another major risk factor irrespective of the
tasis as liver resection is usually not an option. In that context, aetiology. The annual risk of developing HCC in cirrhosis ranges
CEUS should be implemented for improved detection.151 The rec- between 1% and 6%.161,162 The risk is higher in patients with cirrhosis
ommendations of the European Federation of Societies for Ultra- caused by viral infection compared with non-viral causes. However,
sound in Medicine and Biology (EFSUMB) regarding use of CEUS patients with cirrhosis as a result of genetic haemochromatosis also
for liver metastases are:13 have high rates of HCC. In a prospective study of 152 patients with
haemochromatosis (homozygotes) by Fargion et al.,163 of those with
1. CEUS should be performed to rule out liver metastasis unless liver cirrhosis 29% developed HCC whilst none of those without
conventional US shows clear evidence of the lesions. cirrhosis developed HCC; age over 55 years, presence of HBsAg
2. CEUS should be used in selected cases, when clinically and alcohol abuse increased the relative risk of HCC by 13.3-, 4.9-
relevant for treatment planning, to assess the number and and 2.3-fold, respectively.
153
CHAPTER 10 Focal liver lesions/echo enhancing agents and the liver
In contrast, the estimated incidence of HCC in patients with nodule is less than 2cm, diagnosis can be made using non-invasive
primary biliary cirrhosis is 2.4%.164 The development of HCC criteria (if biopsy is not an option), which have been defined as: (a)
appears to be restricted to patients with stage III/IV disease and radiological criteria: two coincidental imaging techniques showing
the incidence is 5.9% in that category. The male sex has a significant arterial hypervascularisation for lesions over 2cm; (b) combined
impact on disease outcome; the incidence of HCC in female patients criteria: one imaging modality showing arterial hypervascularisa-
is low compared to male patients (4.1% versus 20%). In the presence tion associated with AFP levels over 400ng/mL. Biopsy may be
of advanced disease the incidence for male compared to female another option in some centres, but remains controversial; in some
patients is even higher (45.4% versus 8.3%). The reason for the North American and European centres, biopsy would prelude
increased risk of HCC development in male compared to female hepatic resection or transplant because of risk of tumour seeding
cirrhotic patients with primary biliary cirrhosis is unclear. It has along the needle track. Furthermore a negative biopsy of a lesion
been suggested that this may be the result of increased incidence of visible on imaging techniques in a cirrhotic liver does not necessar-
underlying risk aetiologies such as alcohol abuse and chronic hepa- ily rule out malignancy completely. Therefore within the context of
titis B carriage in males. However, in the study report of Jones the cirrhotic patient, HCC can be diagnosed non-invasively using
et al.,164 such confounding aetiological factors including hepatitis the above-mentioned criteria. Ultrasound is widely accepted to be
B and C, alcoholic liver disease and haemochromatosis have been adequate in screening for hepatomas. Clearly there are several
excluded, which therefore confirms that the risk for HCC is truly stages in this algorithm whereby the use of USCAs might be more
increased in males. The incidence of hereditary causes of cirrhosis effective namely (a) in the 6-monthly recalls to improve detection,
such as Wilsons disease, alpha-1-antitypsin deficiency, galactosae- (b) the characterisation of the lesions measuring less than 2cm and
mia, type IV glycogen storage disease, tyrosinaemia, OslerWeber (c) as the second modality in demonstrating the hypervascularity
Rendu syndrome and familial cirrhosis and autoimmune cirrhosis of the lesion in the non-invasive diagnosis of HCC.
is not clearly established but is presumably much lower than the
above-mentioned well-recognised aetiologies.
Whilst cirrhosis is a major risk factor irrespective of aetiology, up Regenerating nodules, dysplastic
to 56% of patients presenting with HCC have previously undiag-
nosed cirrhosis.165 Cirrhosis may be easily diagnosed by any cross- nodules and HCC
sectional imaging modality if characteristic features such as nodular Cirrhosis is characterised by destruction of normal hepatic architec-
hepatic contour, ascites and/or varices are present. Conventional ture, which is replaced by fibrosis and a spectrum of nodules
US has a sensitivity of 4387.7% and a specificity of 79.9100% for ranging from benign regenerative nodules to HCC.172,173 The devel-
diagnosing cirrhosis, with the most widely accepted signs of disease opment of HCC is postulated to be due to a multistep process of
being (1) enlargement of the caudate lobe with an increased caudate carcinogenesis.174,175 This involves progression from regenerative
to right lobe ratio, (2) superficial nodularity best appreciated on nodule to low-grade dysplastic nodule to high-grade dysplastic
high-frequency US probes and (3) a coarse parenchymal echo nodule to dysplastic nodule with foci of HCC to overt HCC. Pro-
pattern.166 However, in the early stages of the disease, it may be gression along this path is characterised by cytological and archi-
impossible to differentiate between stage III fibrosis and cirrhosis. tectural changes. These entities show overlap in imaging appearances
If the presence of cirrhosis alone were to be used to define the target on conventional US, making accurate differentiation almost impos-
population, these patients would not have been recruited into the sible. A study by Bennett et al.176 of 200 patients with cirrhosis who
screening or surveillance programme. Zaman et al.165 also showed underwent conventional US followed by liver transplantation
that those patients with occult cirrhosis were predominantly within 90 days concluded that sonography has poor sensitivity for
HBsAg-seropositive. Therefore patients with chronic viral hepatitis detecting dysplastic nodules (patient sensitivity 4.8% and lesion
as well as those with overt cirrhosis have to be included in any sensitivity 1.6%) and HCC (patient sensitivity 29.6% and lesion
screening or surveillance programme. sensitivity 20.5%).
Serum alpha-fetoprotein levels (AFP) and conventional ultra- CEUS has an important role in characterising nodules in the cir-
sonography have been the most commonly used screening tests for rhotic liver, as the vascular supply to the nodule and thus its
HCC. The ideal screening tests should also have high sensitivity enhancement pattern may allow the differentiation of HCC from
and specificity. The performance of AFP has been poor in that other focal lesions. As part of the stepwise progression of carcino-
respect with a sensitivity of 3964%, a specificity of 7691% and a genesis in a cirrhotic nodule, there is progressive loss of portal
positive predictive value of 932%.167169 In addition, rise in levels venous supply and development of new arterial vessels, which
of AFP is not specific for HCC and it may also increase transiently, become the dominant supply in overt HCC.177 This arterial neo-
persistently or intermittently with flares of active hepatitis. In con- angiogenesis is the hallmark of HCC and the key to imaging diag-
trast, within the context of screening healthy HBsAg carriers as well nosis.178,179 In general, non-neoplastic nodules have a predominantly
as cirrhotic patients, ultrasound has been shown to have a sensitiv- portal venous supply while HCC has a predominantly hepatic arte-
ity of 71% and 78%, respectively, specificity of 93% but with a posi- rial supply. HCC typically demonstrates washout in the portal
tive predictive value of 14% and 73%, respectively.167,169 These could venous or late phase due to decreased or absent portal venous
be improved further with the administration of a USCA. in-flow.
Previous reported surveillance intervals ranged between 3- and
12-month intervals and it is now generally accepted that the inter-
vals should be 6 months taking into account reported median Regenerative nodule
tumour doubling time, which is about 117 days.170 There are as yet
no studies to determine the best recall policy; however, at the con- This is defined histologically as a hepatocellular nodule containing
sensus meeting of the European Association for the Study of Liver portal tracts surrounded by fibrous septa in a liver involved by
in Barcelona in 2000,171 it had been suggested that cirrhotic patients cirrhosis or other severe disease.172 These nodules may be micron-
should undergo 6-monthly ultrasound and AFP levels assessment; odular (3mm), macronodular (>3mm) or mixed type. Rarely,
patients who have no nodule on US but have increasing AFP levels regenerating nodules can measure several centimetres in size and
should have spiral CT of their liver performed; for those patients mimic a neoplasm.172 The blood supply to the regenerative nodule
with a nodule of less than 1cm, 3-monthly ultrasound is recom- is predominantly from the portal vein, with minimal contribution
mended on the basis that these lesions are far too small to charac- from the hepatic artery. These nodules typically appear hypoechoic
terise accurately and at least 50% of these sub-centimetre lesions on conventional US. On CEUS, these nodules show hypo- or iso-
will not be HCC; patients with a nodule of over 2cm should have enhancement in the arterial phase and iso-enhancement in the
AFP levels over 400ng/mL and CT, MRI or angiography evidence portal venous and late phases compared to the background liver180
of lesion hypervascularity before HCC can be confirmed.171 If the (Fig. 10.14).
154
Malignant focal liver lesions
B
A
Flow within HCC is typically high velocity on Doppler and the flow venous phase washout (72 of 74, 97%). On continuous low MI
may have low resistance due to arterial-venous shunting within the scanning with contrast-enhanced pulse inversion harmonic
tumour.100 On CEUS, the enhancement pattern of HCC is related to (PIH) imaging, chaotic peri-tumoral and intra-lesional tortuous
the degree of the histological differentiation194 (Fig. 10.16). Jang corkscrew/s shaped vessels may be clearly depicted in the arte-
et al.194 performed a retrospective study of 112 consecutive patients rial phase when the lesions become hyperechoic (Fig. 10.17). The
with 112 histologically proven HCCs (23 well differentiated, 77 authors depicted dysmorphic intra-tumoral arteries in the majority
moderately differentiated, and 12 poorly differentiated) comparing of HCCs (81 of 112, 72%). In contrast, well-differentiated and poorly
the arterial and portal venous phase enhancement patterns on differentiated HCCs may give atypical appearances on CEUS (Figs
CEUS with the degree of histological differentiation. The authors 10.18, 10.19 and 10.20). In their study Jang et al.194 found that some
found that moderately differentiated HCC, which accounted for the well-differentiated HCCs demonstrated arterial phase iso- or
majority of cases, showed a classic enhancement pattern of hetero- hypovascularity (9 of 23 lesions, 39%) and iso-vascularity through-
geneous arterial hypervascularity (74 of 77 lesions, 96%) and portal out the portal phase (9 of 9, 100%), postulated to reflect decreased
normal hepatic arterial flow without significant development of
neoplastic arteries and with preservation of portal venous flow. In
poorly differentiated HCCs, the authors found early washout (7 of
9 lesions, 78%) within 90 seconds. A possible explanation for early
washout of poorly differentiated HCCs may derive from its total
lack of similarity to normal hepatocytes and its architecture. While
the majority of HCCs in the study demonstrated washout in the
portal venous or late phase (up to 5 minutes post contrast injection),
9% demonstrated no washout and of these 78% (7 of 9 lesions) were
well-differentiated HCCs.
A B
Cholangiocarcinoma
Cholangiocarcinoma (CC) is the second most common primary
hepatic cancer, representing 30% of all primary hepatic neo-
plasms,195 and accounts for about 3% of all gastrointestinal cancers
globally.196 It has an incidence of 12 cases per 100000 population197
with the peak prevalence in the seventh decade of life and a slight
male preponderance.198 CCs arise from bile duct epithelium and are
adenocarcinomas in 9095% of cases.199 Histologically, tumours are
C D usually associated with extensive intra-lesional fibrosis. Sixty to
seventy per cent of CCs arise at the bifurcation of the hepatic ducts
Figure 10.15 Dysplastic nodule. Hyperechoic lesion at baseline (Klatskin tumours), 2030% at the distal common bile duct, while
(A) which is hypo-enhancing in the arterial phase (B), and iso- 510% are peripheral (occurring distal to the second order bile
enhancing in both portal (C) and late (D) phases. duct branches) and arise from intrahepatic ducts of the liver
B
A
B
A
A B C D
Figure 10.18 Multiple small hepatomas, which are hypoechoic at baseline (A) showing hyper-enhancement in the arterial phase (B),
iso-enhancement in the portal venous phase (C) and washout in the late phase (D).
parenchyma.200,201 Intrahepatic CCs such as hilar and peripheral the CC type. Periductal infiltrating CCs are difficult to detect sono-
forms can be classified according to their growth characteristics as graphically due to small size as well as perceptual difficulties as
periductal-infiltrating (most common), intraductal or mass-forming they can appear isoechoic or show only mild textural inhomogene-
types.202 ity compared to the surrounding liver. Mural and periductal soft
Conventional US is the first-line imaging modality in this patient tissue thickening or focal irregularities of the bile ducts may occa-
cohort as patients usually present at a late stage when signs and sionally be appreciated.204 In longstanding cases due to obstruction,
symptoms suggestive of biliary obstruction such as jaundice or lobar atrophy and resultant crowding of bile ducts and blood
deranged liver function tests trigger an imaging investigation. US vessels is seen.205 Due to the propensity for local invasion, these
is highly sensitive for confirming bile duct dilatation, localising the tumours may infiltrate adjacent vessels, with portal venous involve-
site of obstruction and excluding gallstones as a potential cause.203 ment detected on conventional US with colour Doppler imaging in
On US, dilatation of the intrahepatic bile ducts that converge on the 50% of cases.206 Intraductal tumours may show wall thickening or
liver hilum is the most common finding in patients with Klatskin resemble polypoidal masses but are difficult to appreciate on
tumours. Other findings depend on the growth characteristics of imaging due to small size. Mass-forming CCs appear as a solid
157
CHAPTER 10 Focal liver lesions/echo enhancing agents and the liver
A B
mass with irregular borders and variable echogenicity on conven- interrogation of the tumour in the various vascular phases. On low
tional US with no specific imaging features. Small CCs often appear MI CEUS, intrahepatic CCs typically demonstrate peripheral irreg-
hypo- or isoechoic while larger CCs are generally inhomogeneous ular rim-like enhancement during the arterial phase and hypo-
with mixed echogenicity.100 Small satellite nodules neighbouring enhancement during the late phase.13,53,209211 Three other reported
the primary tumour are a recognised finding. Ancillary findings patterns of arterial enhancement are also seen on CEUS for
that may aid diagnosis if present include peri-lesional bile duct intrahepatic CCs.209 Chen et al.209 retrospectively studied 40
dilatation (seen in up to 30% of cases) and capsular retraction.207 pathologically proven intrahepatic CCs in 40 patients who
Khalili et al.208 found that detection and staging of hilar CCs were underwent both CEUS and triphasic CT. The authors found that
improved by the use of a first-generation US contrast agent (Levo- in the arterial phase, intrahepatic CCs demonstrated (i) peripheral
vist) in the post-vascular phase of US compared with conventional irregular rim-like enhancement (47.5%), (ii) diffuse heterogeneous
US. Similar data using second-generation USCAs with low MI tech- hyper-enhancement (22.5%), (iii) diffuse homogeneous hyper-
nique are lacking although it is reasonable to assume similar if not enhancement (12.5%) and (iv) diffuse heterogeneous hypo-
superior results as more information can be obtained by real-time enhancement (17.5%). The arterial phase patterns on CEUS
158
Malignant focal liver lesions
A B
A B
Figure 10.21 Cholangiocarcinoma, which appears as a filling defect in the portal venous (A) and late phases (B) associated with biliary
dilatation.
correlated well with those on contrast-enhanced CT. The authors This finding may relate to pathological changes that occur as the
postulated that the different enhancement patterns may relate to tumour increases in size such as compression of central vessels
different pathological components in the tumour.209,212 Concentra- resulting in central hypovascularity or necrosis.213
tion of tumour cells in the lesion periphery with fibrosis in the On portal venous and late phase scanning, the vast majority of
lesion centre may give rise to the peripheral rim-like enhancement intrahepatic CCs demonstrate washout on CEUS13,53,209211
pattern seen in the majority of intrahepatic CCs. Tumour may show (Fig. 10.21). These findings are discordant with contrast-enhanced
diffuse enhancement if the major component is tumour cells and CT, which generally shows tumour iso- to hyper-enhancement in
there is no central fibrosis. When there is abundant fibrous stroma, the late phase.209,210 This difference may be explained by considering
the tumour may show arterial hypo-enhancement. The authors also the different properties of the CT and US contrast media. USCAs
found that the enhancement pattern correlated with tumour size are purely intravascular agents with no flow outside the vascular
smaller lesions had a trend towards homogeneous hyper-enhance- bed whereas CT contrast agents have both an intra- and extravas-
ment while larger tumours showed variable enhancement patterns. cular distribution with flow into the interstitium to reach an
159
CHAPTER 10 Focal liver lesions/echo enhancing agents and the liver
equilibrium state.214,215 Therefore, in the late post-contrast phase, the hypovascular metastases showing some degree of mild peripheral
fibrous component of the tumour will appear hypo-enhancing on rim-like arterial enhancement with rapid washout and subsequent
CEUS and hyper-enhancing on contrast-enhanced CT. hypoechogenicity in the portal venous and late phases with pro-
The enhancement pattern of intrahepatic CCs may overlap those gressive increase in lesion conspicuity234 (Fig. 10.22).
of HCC and metastases with potential for misdiagnosis. Diffuse
hyper-enhancement in the arterial phase followed by portal venous
and late phase washout can be seen in both HCC and intrahepatic Rare malignant lesions
CCs. Hypovascular metastases, especially from adenocarcinomas
of the gastrointestinal tract, may show peripheral rim-like enhance-
ment similar to that of intrahepatic CCs.216,217 In these cases, the Fibrolamellar hepatocellular carcinoma
background clinical history (such as the presence of underlying Fibrolamellar HCC is a rare primary hepatic malignancy first
primary malignancy, hepatitis virus infection, etc.), relevant labora- described by Edmonson in 1956.235 Clinical, pathological and
tory data (such as elevation of serum AFP and other serum tumour imaging studies have established it as a distinct entity from conven-
markers), pertinent additional imaging findings (such as evidence tional HCC by its morphology and biological behaviour.236,237 Clini-
of metastatic disease elsewhere in the body, morphological evi- cally, fibrolamellar HCC occurs in young patients while the majority
dence of cirrhosis or associated peri-lesional biliary dilatation) may of cases of conventional HCC are diagnosed in patients older than
be useful discriminating factors. 40 years of age. The disease has a unimodal distribution, beginning
in late adolescence, with a peak incidence at 24.813 years.238 It has
Hepatic lymphoma no sex bias but is more common in white people. The typical risk
factors for conventional HCC such as cirrhosis, viral hepatitis,
excessive alcohol consumption and metabolic disease are generally
Liver involvement by lymphoma usually occurs in the context of
absent in patients with fibrolamellar HCC. Serum tumour markers
the presence of lymphomatous tissue elsewhere in the body (sec-
such as AFP are typically not elevated. Histologically, the disease
ondary hepatic lymphoma). Primary hepatic lymphoma is very
is composed of well-differentiated malignant hepatocytes with
rare, with approximately 100 cases reported worldwide. In com-
deeply eosinophilic and granular cytoplasm due to the presence of
parison, secondary hepatic lymphoma is not uncommon. It occurs
numerous mitochondria associated with thick fibrous lamellae
in approximately 314% of newly diagnosed cases, whereas at
throughout the tumour.239 Prognosis is better for fibrolamellar HCC
autopsy; it is found in 5080% of patients with Hodgkins or non-
than conventional HCC with increased length of survival observed,
Hodgkins lymphoma.218,219 Conditions associated with an increased
even after adjusting for age of cancer diagnosis and other demo-
risk for development of lymphoma include HIV/AIDS, hepatitis C,
graphic data.240
organ transplantation and immunosuppression. Liver involvement
On imaging fibrolamellar HCC usually appears as a solitary well-
in patients with AIDS-related non-Hodgkins lymphoma has been
defined lobulated mass (in 8090% of cases) with an average size
reported to occur in 2645% of cases.220222 A recent meta-analysis
of 912cm (ranges from 520cm).241 It has a central scar in 2071%
revealed that hepatitis C virus (HCV) prevalence in patients with
of cases, which is typically large and may be broad or stellate,
non-Hodgkins lymphoma was 15%, as opposed to 1.5% in the
eccentric or central.241 Calcifications are typical and occur in 3568%
general population and 2.9% in patients with other haematological
of cases and may be punctate, nodular or stellate and are usually
malignancies, implying a causative role of HCV in non-Hodgkins
located near the tumour centre.241 Unlike FNH, calcification within
lymphoma.223 Post-transplant lymphoproliferative disorder (PTLD)
the central scar of a fibrolamellar HCC is a relatively common
is a serious condition that occurs in 210% of all organ transplant
finding. On conventional US, the tumour has a variable echotexture
recipients as a result of chronic immunosuppression,224 which leads
with mixed echogenicity found in 60% of cases with predominance
to an unregulated expansion of lymphoid proliferation. The disor-
of hyperechoic or isoechoic components.242 On US the central scar
der ranges from plasma cell hyperplasia through premalignant
is typically hyperechoic but US is less successful in demonstrating
polymorphic B cell proliferation to malignant monoclonal lym-
central scars, with 3360% of scars detected at US compared to CT
phoma.225 In most cases, the disorder results from EbsteinBarr
and pathological analysis.243 The central scar in FNH is typically
virus induced B-cell lymphoproliferation unopposed by the hosts
hypervascular while in fibrolamellar HCC it is typically hypovas-
pharmacologically suppressed T-cell system. The abdomen is the
cular but may show mild gradual contrast enhancement in the late
most common site involved by PTLD (may be the only site involved
phase. Fan et al.244 described a case of fibrolamellar HCC imaged
in up to 50% of cases) and the liver the most common abdominal
with CEUS. This demonstrated rapid tumour enhancement in the
organ affected.226,227
arterial phase with abnormal vessels of septum distribution seen
There are three established morphological patterns of hepatic
followed by washout in the portal venous phase. The rarity of this
lymphoma involvement: (i) solitary hepatic mass, (ii) multifocal
tumour and paucity of cases studied by CEUS does not permit more
nodules, and (iii) diffuse infiltrative disease.228 Primary hepatic lym-
detailed evaluation of its enhancement features on CEUS.
phoma (usually non-Hodgkin type) most commonly presents as a
solitary mass in 5560% of cases.229 Secondary hepatic lymphoma
most commonly presents with multiple nodular liver masses in the Epithelioid haemangioendothelioma
context of lymphadenopathy elsewhere in the body. Diffuse infiltra-
tive involvement is the most infrequent of the three types and has This is a rare malignant vascular hepatic tumour characterised by
the worst prognosis. A fourth type of extremely rare hepatic lym- the epithelioid appearance of its neoplastic cells, which accounts for
phoma involvement has also been reported. There are three case its name.245 It originates from vascular endothelial cells and spindle
reports of lymphoma presenting as a periportal mass tracking into cells. It should not be confused with infantile haemangioendothe-
the liver; two cases were identified on contrast-enhanced CT218,230 lioma, which is a separate entity and is histologically benign and
and one case on CEUS.231 On conventional US, hepatic lesions are occurs exclusively in infants and young children and resolves spon-
typically hypoechoic, which is thought to be related to the uniform taneously in many cases. Prognosis in epithelioid haemangioen-
cellularity of lymphoma without significant background stroma.232 dothelioma is variable and unpredictable. While 20% of patients die
Posterior acoustic enhancement, typically less than that of a cyst, within the first 2 years after presentation, another 20% have
may also be seen due to the uniformity of the tumour.100 Lesions extended survival of 528 years, regardless of whether they undergo
may also appear almost anechoic and septated and mimic abscesses, treatment. Metastatic disease does not preclude a long survival.246
appear nearly isoechoic relative to hepatic parenchyma, or be Epithelioid haemangioendotheliomas are often multiple and
hypoechoic with a central echogenic focus and mimic metastatic peripherally located and can cause capsular retraction secondary to
disease.233 On CEUS, liver infiltrates of lymphoma behave like tumour desmoplasia.233 The lesions may coalesce over time. Lesions
160
References
A
B
are typically hypoechoic, which correlates with the central core of septations of the cystic lesion and thick coarse calcifications are
myxoid stroma. The combination of hypoechoic coalescent periph- suggestive of cystadenocarcinoma as these are rare in cystade-
eral hepatic masses with capsular retraction is highly suggestive of noma.247 CEUS may reveal wall and septal enhancement during the
diagnosis.232 On CEUS, the mass typically shows irregular intra- arterial phase, with mural or septal nodule enhancement. During
tumoral vessels and diffuse or peripheral hypervascularity during the portal and late phases, contrast washout is seen.117
the arterial phase and rapid washout in the portal venous phase,
especially in the peripheral zone compared to the central zone.233 REFERENCES
The entire lesion shows washout eventually on CEUS whereas on
CT or MRI, the peripheral zone enhancement persists or enlarges 1. Quaia E, Calliada F, Bertolotto M, et al. Characterization of focal liver
gradually over time. Similar to cholangiocarcinoma, this tumour lesions with contrast specific US modes and a sulfur hexafluoride-
filled microbubble contrast agent: diagnostic performance and
has a rich fibrous stroma and the discordance between findings on
confidence. Radiology 2004;232(2):420430.
CEUS and contrast-enhanced CT and MRI can be attributed to the 2. Reinhold C, Hammers L, Taylor CR, et al. Characterization of focal
different properties of the contrast media. Quaia et al.1 found a case hepatic lesions with duplex sonography: findings in 198 patients. AJR
of a histologically proven low-grade malignant epithelioid haeman- Am J Roentgenol 1995;164:11311135.
gioendothelioma, which had an atypical enhancement pattern sug- 3. Lee MG, Auh YH, Cho KS, et al. Color Doppler flow imaging of
gestive of a benign lesion. On conventional US and colour Doppler hepatocellular carcinomas: comparison with metastatic tumours and
imaging, the tumour appeared hypoechoic with a peripheral vessel. hemangiomas by three step grading colour hues. Clin Imaging
On CEUS, there was homogeneous tumour contrast enhancement 1996;20:199203.
during the arterial and portal venous phases with persisting 4. Van Leeuwen MS, Noordzij J, Feldberg MA, et al. Focal liver lesions:
characterization with triphasic CT. Radiology 1996;201:327336.
enhancement present in the late phase. The two reviewers in the
5. Balci NC, Semelka RC. Contrast agents for MR imaging of the liver.
study erroneously categorised this lesion as being benign. Radiol Clin North Am 2005;43(5):887898.
6. Lencioni R. Impact of European Federation of Societies for
Ultrasound in Medicine and Biology (EFSUMB) guidelines on the use
Biliary cystadenocarcinoma of contrast agents in liver ultrasound. Eur Radiol 2006;16:1610.
Biliary cystadenoma is a rare malignant cystic neoplasm that may 7. Albrecht T, Hohmann J, Oldenburg A, et al. Detection and
arise de novo or be the end product of malignant degeneration in characterization of liver metastases. Eur Radiol 2004;14(Suppl 8):
2533.
a benign biliary cystadenoma. It cannot be confidently separated
8. Leen E, Moug S, Horgan PG. Potential impact and utilization of
from biliary cystadenoma on imaging due to overlap of imaging ultrasound contrast media. Eur Radiol 2004;14(Suppl 8):1624.
findings and so surgical excision is generally recommended for 9. Brannigan M, Burns P, Wilson S. Blood flow patterns in focal liver
both pathologies. On US, biliary cystadenoma usually presents as lesions at microbubble enhanced US. Radiographics 2004;24:921
a multiloculated cystic mass. Mural nodularity within the wall or 935.
161
CHAPTER 10 Focal liver lesions/echo enhancing agents and the liver
10. Leen E, Angerson WJ, Yarmenitis S, et al. Multi-centre clinical study fatty infiltration: an atypical sonographic appearance. Gastrointest
evaluating the efficacy of SonoVue (BR1), a new ultrasound contrast Radiol 1989;14:262264.
agent in Doppler investigation of focal hepatic lesions. Eur J Radiol 38. Kim KW, Kim AY, Kim TK, et al. Hepatic hemangiomas with
2002;41(3):200206. arterio-portal shunts: sonographic appearances with CT and MRI
11. Leen E, Ceccotti P, Kalogeropoulou C, et al. Prospective multicentric correlation. AJR Am J Roentgenol 2006;187(4):406414.
trial evaluating a novel method of characterizing focal liver lesions 39. Kim KW, Kim TK, Han JK, et al. Hepatic hemangiomas: spectrum of
using contrast enhanced sonography. AJR Am J Roentgenol US appearances on grey scale, power Doppler, and contrast
2006;186(6):15511559. enhanced US. Korean J Radiol 2000;1:191197.
12. Faccioli N, DOnofrio M, Comai A, Cugini C. Contrast enhanced 40. Quaia E, Bartolotta TV, Midiri M, et al. Analysis of different contrast
ultrasonography in the characterization of benign focal liver lesions: enhancement patterns after microbubble based contrast agent
activity-based cost analysis. Radiol Med 2007;112(6):810820. injection in liver hemangiomas with atypical appearance on baseline
13. Albrecht T, Blomley M, Bolondi L, et al. Guidelines for the use of scan. Abdom Imaging 2006;31:5964.
contrast agents in ultrasound. January 2004. Ultraschall Med. 41. Bartolotta TV, Taibbi A, Galia M, et al. Centrifugal (inside out)
2004;25(4):249256. enhancement of liver hemangiomas: A possible atypical appearance
14. Kono Y, Steinbach GC, Peterson T, et al. Mechanism of parenchymal on contrast enhanced US. Eur J Radiol 2007;64:447455.
enhancement of the liver with a microbubble based US contrast 42. Ungermann L, Elias P, Zizka J, et al. Focal nodular hyperplasia: spoke
medium. Radiology 2002;224:253257. wheel arterial pattern and other signs on dynamic contrast enhanced
15. Becher H, Burns PN. A handbook of contrast echocardiography. ultrasonography. Eur J Radiol 2007;63:290294.
Heidelberg: Springer; 2000. 43. Luciani A, Kobeiter H, Maison P, et al. Focal nodular hyperplasia of
16. Blomley MJ, Eckersley RJ. Functional ultrasound methods in the liver in men: is presentation the same in men and women? Gut
oncological imaging. Eur J Cancer 2002;38(16):21082115. 2002;50:877880.
17. Ackerman NB. The blood supply of experimental liver metastases. IV. 44. Nguyen BN, Flejou JF, Terris B, et al. Focal nodular hyperplasia of the
Changes in vascularity with increasing tumour growth. Surgery liver: a comprehensive pathologic study of 305 lesions and
1974;75(4):589596. recognition of new histologic forms. Am J Surg Pathol 1999;23:
18. Wilson SR, Burns PN. Microbubble contrast for radiological imaging: 14411454.
2. Applications. Ultrasound Q 2006;22(1):1518. 45. Kuo YH, Wang JH, Lu SN, et al. Natural course of hepatic focal
19. Ramnarine KV, Kyriakopoulou K, Gordon P, et al. Improved nodular hyperplasia: a long term follow up study with sonography.
characterization of focal liver tumours: dynamic power Doppler J Clin Ultrasound 2009;37:132137.
imaging using NC100100 echo-enhancer. Eur J Ultrasound 46. Wanless IA, Mawdsley C, Adams R. On the pathogenesis of
2000;11(2):95104. focal nodular hyperplasia of the liver. Hepatology 1985;5(6):
20. Bauer A, Blomley M, Leen E, et al. Liver-specific imaging with SHU 11941200.
563A: diagnostic potential of a new class of ultrasound contrast 47. Buetow PC, Pantongrag-Brown L, Buck JL, et al. Focal nodular
media. Eur Radiol. 1999;9(Suppl 3):S349352. hyperplasia of the liver: radiologicpathologic correlation.
21. Vilgrain V, Boulos L, Vullierme MP, et al. Imaging of atypical Radiographics 1996;16:369388.
hemangiomas of the liver with pathological correlation. 48. Wang LY, Wang JH, Lin ZY, et al. Hepatic focal nodular hyperplasia:
Radiographics 2000;20(2):379397. findings on colour doppler ultrasound. Abdom Imaging 1997;22:
22. Ros PR. Computed tomographypathologic correlations in hepatic 178181.
tumors. In: Ferrucci JT, Mathiew DG, editors. Advances in 49. Uggowitzer M, Kugler C, Machan L, et al. Power doppler imaging
hepatobiliary radiology. St Louis: CV Mosby; 1990:75108. and evaluation of the resistive index in focal nodular hyperplasia of
23. Mergo PJ, Ros PR. Benign lesions of the liver. Radiol Clin North Am the liver. Abdom Imaging 1997;22:268273.
1998;36:319331. 50. Goldberg BB, Hilpert PL, Burns PN, et al. Hepatic tumours: signal
24. Gandolfi L, Leo P, Solmi L, et al. Natural history of hepatic enhancement at Doppler US after injection of a contrast agent.
haemangiomas: clinical and ultrasound study. Gut 1991;32:677680. Radiology 1990;177:713717.
25. Takayasu K, Makuuchi M, Takayama T. Computed tomography of a 51. Numata K, Tanaka K, Mitsui K, et al. Flow characteristics
rapidly growing hepatic hemangioma. J Comput Assist Tomogr of hepatic tumours at colour Doppler sonography: correlation
1990;14:143145. with arteriographic findings. Am J Roentgenol 1993;160:
26. Gibbs JF, Litwin AM, Kahlenberg MS. Contemporary management of 515521.
benign liver tumors. Surg Clin North Am 2004;84(2):463480. 52. Kamal IR, Liapi E, Fishman EK. Focal nodular hyperplasia: lesion
27. Caseiro-Alves F, Brito J, Araujo AE, et al. Liver haemangioma: evaluation using 16 MDCT and 3D CT angiography. AJR Am J
common and uncommon findings and how to improve the Roentgenol 2006;186:15871596.
differential diagnosis. Eur Radiol 2007;17:15441554. 53. Xu HX, Liu GJ, Lu MD, et al. Characterization of focal liver lesions
28. Blondet A, Ridereau- Zins C, Michalak S, et al. Multiple using contrast enhanced sonography with a low mechanical index
pedunculated liver hemangiomas presenting with volvulus. J Radiol mode and a sulfur hexafluoride filled microbubble contrast agent.
2007;88(6):891894. J Clin Ultrasound 2006;34:261272.
29. Tran-Minh VA, Gindre T, Pracros JP, et al. Volvulus in a pedunculated 54. Dietrich CF, Schuessler G, Trojan J, et al. Differentiation of focal
hemangioma of the liver. AJR Am J Roentgenol 1991;156(4):866867. nodular hyperplasia and hepatocellular adenoma by contrast
30. Gibney RG, Hendin AP, Cooperberg PL. Sonographically detected enhanced ultrasound. Br J Radiol 2005;78:704707.
hepatic hemangiomas: absence of change over time. AJR Am J 55. Yen YH, Wang JH, Lu SN, et al. Contrast enhanced ultrasonographic
Roentgenol 1987;149:953957. spoke wheel sign in hepatic focal nodular hyperplasia. Eur J Radiol
31. Taboury J, Porcel A, Tubiana JM, Monnier JP. Cavernous 2006;60:439444.
hemangiomas of the liver studied by ultrasound: enhancement 56. Janica J, Wojciech S, Dolorzycki S, et al. Contrast enhanced,
posterior to a hyperechoic mass as a sign of hypervascularity. wide band phase inversion power Doppler imaging of hepatic
Radiology 1983;149:781785. focal nodular hyperplasia. Hepato-Gastroenterology 2004;51:
32. Hosten N, Puls R, Bechstein WO, Felix R. Focal liver lesions: Doppler 705708.
ultrasound. Eur Radiol 1999;9:428435. 57. Reddy KR, Schiff ER. Approach to a liver mass. Semin Liver Dis
33. Perkins AB, Imam K, Smith WJ, Cronan JJ. Colour and power 1993;13:423435.
Doppler sonography of liver hemangiomas: a dream unfulfilled? 58. Faria SC, Iyer RB, Rashid A, Whitman GJ. Hepatic adenoma. AJR Am
J Clin Ultrasound 2000;28:159165. J Roentgenol 2004;182:1520.
34. Kim TK, Han JK, Kim AY, et al. Hepatic hemangiomas using a 59. Federle MP, Jeffrey RB, Desser TS, et al. Diagnostic imaging:
sonographic contrast agent (Levovist) and power Doppler abdomen. Salt Lake City, UT: Amirsys, 2004;110112.
ultrasonography. J Ultrasound Med 1999;18:737743. 60. Baum JK, Bookstein JJ, Holtz F, Klein EW. Possible association
35. Moody AR, Wilson SR. Atypical hepatic hemangioma: a suggestive between benign hepatomas and oral contraceptives. Lancet
sonographic morphology. Radiology 1993;188:413417. 1973;2:926929.
36. Dietrich CF, Mertens JC, Braden B, et al. Contrast enhanced 61. Edmondson HA, Henderson B, Benton B. Liver cell adenomas
ultrasound of histologically proven liver hemangiomas. Hepatology associated with use of oral contraceptives. N Engl J Med
2007;45:11391145. 1976;294:470472.
37. Marsh JI, Gibney RG, Li DK. Hepatic hemangioma in the presence of 62. Hussain SM, van den Bos IC, Dwarkasing RS, et al. Hepatocellular
162
References
adenoma: findings at state of the art magnetic resonance imaging, hepatic fatty infiltration: a cause of hepatic pseudomass in ultrasound
ultrasound, computed tomography and pathologic analysis. examination. Rocz Akad Med Bialyms 1996;41:499504.
Eur Radiol 2006;16:18731886. 91. Kim KW, Kim MJ, Lee SS, et al. Sparing of fatty infiltration around
63. Leese T, Farges O, Bismuth H. Liver cell adenomas: A 12 year focal hepatic lesions in patients with hepatic steatosis: sonographic
surgical experience from a specialist hepato-biliary unit. Ann Surg appearance with CT and MRI correlation. AJR Am J Roentgenol
1988;208:558564. 2008;190:10181027.
64. Numata K, Tanaka K, Mitsui K, et al. Flow characteristics of 92. Bartolotta TV, Taibbi A, Galia M, et al. Characterization of hypoechoic
hepatic tumours at colour Doppler sonography: correlation focal hepatic lesions in patients with fatty liver: diagnostic
with arteriographic findings. AJR Am J Roentgenol 1993;160: performance and confidence of contrast enhanced ultrasound. Eur
515521. Radiol 2007;17:650661.
65. Bartolozzi C, Lencioni R, Paolicchi A, et al. Differentiation of 93. Dong BW, Chen MH, Li JG, et al. Further study on sonographic
hepatocellular adenoma and focal nodular hyperplasia of the liver: patterns of non uniform fatty liver. Chin J Ultrasonogr
comparison of power Doppler imaging and conventional colour 1993;2:62.
Doppler sonography. Eur Radiol 1997;7:14101415. 94. Liu LP, Dong BW, Yu XL, et al. Evaluation of focal fatty infiltration of
66. Dietrich CF, Ignee A, Trojan J, et al. Improved characterization of the liver using color doppler and contrast enhanced sonography.
histologically proven liver tumours by contrast enhanced J Clin Ultrasound 2008;36:560566.
ultrasonography during the portal venous and specific late phases of 95. Wang ZL, Tang J, Weskott HP, et al. Undetermined focal liver lesions
SHU 508A. Gut 2004;53:401405. on grey scale ultrasound in patients with fatty liver: characterization
67. Wilson SR, Burns PN. An algorithm for the diagnosis of focal liver with contrast enhanced ultrasound. J Gastroenterol Hepatol
masses using microbubble contrast enhanced pulse inversion 2008;23:15111519.
sonography. AJR Am J Roentgenol 2006;186:14011412. 96. Nicolau C, Vilana R, Catala V, et al. Importance of evaluating all
68. Kim TK, Jang HJ, Burns PN, et al. Focal nodular hyperplasia and vascular phases on contrast enhanced sonography in the
hepatic adenoma: differentiation with low mechanical index contrast differentiation of benign from malignant focal liver lesions. AJR Am J
enhanced sonography. AJR Am J Roentgenol 2008;190:5866. Roentgenol 2006;186:158.
69. Barreda R, Ros PR. Diagnostic imaging of liver abscesses. Crit Rev 97. Kroncke TJ, Taupitz M, Kivelitz D, et al. Multifocal nodular fatty
Diagn Imaging 1992;33:2958. infiltration of the liver mimicking metastatic disease on CT: imaging
70. Mortele KJ, Segatto E, Ros PR. The infected liver: radiologic- findings and diagnosis using MR imaging. Eur Radiol 2000;10:
pathologic correlation. Radiographics 2004;24:937955. 10951100.
71. Benedetti NJ, Desser TS, Brooke Jeffrey R. Imaging of hepatic 98. Singer D, Neave C, Oyer C, et al. Hepatic subcapsular hematomas in
infections. Ultrasound Q 2008;24:267278. fetuses and neonatal infants. Pediatr Dev Pathol 1999;2:215220.
72. Hui JYH, Yang MKW, Cho DHY, et al. Pyogenic liver abscesses 99. Scholmerich J, Volk BA. Differential diagnosis of anechoic/
caused by Klebsiella pneumoniae: US appearances and aspiration hypoechoic lesions in the abdomen detected by ultrasound. J Clin
findings. Radiology 2007;242(3):769776. Ultrasound 1986;14:339353.
73. Ryan RS, Al-Hashimi H, Lee MJ. Hepatic abscesses in elderly patients 100. Li D, Hann LE. A practical approach to analyzing focal lesions in the
mimicking metastatic disease. Ir J Med Sci 2001;170:251253. liver. Ultrasound Q 2005;21(3):187200.
74. Sudhamshu KC, Sharma D. Long term follow up of pyogenic 101. McGahan JP, Horton S, Gerscovich EO, et al. Appearances of solid
liver abscess by ultrasound. Eur J Radiol 2009, doi:10.1016/j. organ injury with contrast enhanced sonography in blunt abdominal
ejrad.2009.01.017 (in press). trauma: preliminary experience. AJR Am J Roentgenol 2006;187:
75. Ralls PW, Meyers HI, Lapin SA, et al. Grey scale ultrasonography of 658666.
hepatic amoebic abscess. Radiology 1979;132:125129. 102. Valentino M, Serra C, Zironi G, et al. Blunt abdominal trauma:
76. Ralls PW, Barnes PF, Radin DR, et al. Sonographic features of amebic emergency contrast enhanced sonography for detection of solid
and pyogenic abscesses: A blinded comparison. AJR Am J organ injuries. AJR Am J Roentgenol 2006;186:13611367.
Roentgenol 1987;149:499501. 103. Valentino M, Serra C, Pavlica P, Barozzi L. Contrast enhanced
77. Oleszczuk-Raszke K, Cremin BJ, Fisher RM, et al. Ultrasonic features ultrasound for blunt abdominal trauma. Semin Ultrasound CT MRI
of pyogenic and amoebic hepatic abscesses. Pediatr Radiol 2007;28(2):130140.
1989;19:230233. 104. Horton KM, Bluemke DA, Hruban RH, et al. CT and MR imaging
78. Landay MJ, Setiawan H, Hirsch G, et al. Hepatic and thoracic of benign hepatic and biliary tumours. Radiographics 1999;19:
amoebiasis. AJR Am J Roentgenol 1980;135(3):449454. 431451.
79. Ralls PW, Quinn MF, Boswell WD Jr, et al. Patterns of resolution in 105. Prasad SR, Wang H, Rosas H, et al. Fat containing lesions of the liver:
successfully treated hepatic amoebic abscess: sonographic evaluation. radiologic-pathologic correlation. Radiographics 2005;25:321331.
Radiology 1983;149(2):541543. 106. Zheng RQ, Kudo M. Hepatic angiomyolipoma: identification of an
80. Catalano O, Sandomenico F, Raso MM, Siani A. Low mechanical efferent vessel to be hepatic vein by contrast enhanced harmonic
index contrast enhanced sonographic findings of pyogenic hepatic ultrasound. Br J Radiol 2005;78:956960.
abscesses. AJR Am J Roentgenol 2004;182:447450. 107. Kudo M, Okuno T, Tomita S, et al. Hepatic angiomyolipoma
81. Mendez RJ, Schiebler ML, Outwater EK, Kressel HY. Hepatic preoperatively diagnosed by imaging. J Gastroenterol Hepatol
abscesses: MR imaging findings. Radiology 1994;190:431436. 1993;8:483488.
82. Miller MA, Balfe DM, Middleton WD. Peripheral portal venous 108. Chang JC, Lee YW, Kim HJ. Preoperative diagnosis of
blood flow alterations induced by hepatic masses: evaluation with angiomyolipoma of the liver. Abdom Imaging 1994;19:546548.
color and pulsed Doppler sonography. J Ultrasound Med 109. Ahmadi T, Itai Y, Takahashi M, et al. Angiomyolipoma of the liver:
1996;15:707713. significance of CT and MR dynamic study. Abdom Imaging
83. Kim KW, Choi BI, Park SH, et al. Pyogenic hepatic abscesses: 1998;23:520526.
distinctive features from hypovascular hepatic malignancies on 110. Yen YH, Wang JH, Lu SN, Changchien CS. Contrast enhanced
contrast enhanced ultrasound with SH U 508A; early experience. ultrasonography in hepatic angiomyolipoma. J Ultrasound Med
Ultrasound Med Biol 2004;30(6):725733. 2005;24:855859.
84. Hamer OW, Aguirre DA, Casola G, et al. Fatty liver: imaging patterns 111. Xu HX, Xie XY, Lu MD, et al. Unusual benign focal liver lesions.
and pitfalls. Radiographics 2006;26:16371653. Findings on real time contrast enhanced sonography. J Ultrasound
85. Karcaaltincaba M, Akhan O. Imaging of hepatic steatosis and fatty Med 2008;27:243254.
sparing. Eur J Radiol 2007;61:33. 112. Sonsuz A, Ozdemir S, Akdogan M, et al. Lipoma of the liver. Z
86. Siegelman ES, Rosen MA. Imaging of hepatic steatosis. Semin Liver Gastroenterol 1994;32:348350.
Dis 2001;21:71. 113. Teoh AYB, Ng SSM, Lee KF, Lai PBS. Biliary cystadenoma and other
87. Danet IM, Semelka RC, Braga L. MR imaging of diffuse liver disease. complicated cystic lesions of the liver: diagnostic and therapeutic
Radiol Clin North Am 2003;41:67. challenges. World J Surg 2006;30:15601566.
88. Valls C, Iannacconne R, Alba E, et al. Fat in the liver: diagnosis and 114. Edmondson HA. Tumours of the liver and intrahepatic bile ducts. In:
characterization. Eur Radiol 2006;16:22922308. Atlas of tumour pathology, fasc. 25, first series. Washington DC:
89. Zezos P, Tatsi P, Nakos A, et al. Focal fatty liver sparing lesion Armed Forces Institute of Pathology; 1958.
presenting as a pseudotumour: case report. Acta Gastroenterol Belg 115. Del Poggio P, Buonocore M. Cystic tumours of the liver: a practical
2006;69:323326. approach. World J Gastroenterol 2008;14(23):36163620.
90. Palakow J, Ladny JR, Krejza J. Focal solitary hypoechoic area in 116. Devaney K, Goodman ZD, Ishak KG. Hepatobiliary cystadenoma
163
CHAPTER 10 Focal liver lesions/echo enhancing agents and the liver
hepatic cirrhosis: risk for hepatocellular carcinoma. Radiology and fine needle biopsy. Abdom Imaging 2006;31:537544.
2003;226:691697. 193. Morin SHX, Lim AKP, Cobbold JFL, Taylor-Robinson SD. Use of
167. Pateron D, Ganne N, Trinchet JC, et al. Prospective study of screening second generation contrast enhanced ultrasound in the assessment of
for hepatocellular carcinoma in Caucasian patients with cirrhosis. J focal liver lesions. World J Gastroenterol 2007;13(45):59635970.
Hepatol 1994;20:6571. 194. Jang HJ, Kim TK, Burns PN, Wilson SR. Enhancement patterns of
168. Oka H, Tamori A, Kuroki T, et al. Prospective study of alpha- hepatocellular carcinoma at contrast US: comparison with histologic
fetoprotein in cirrhotic patients monitored for development of differentiation. Radiology 2007;244(3):898906.
hepatocellular carcinoma. Hepatology 1994;19:6166. 195. Khalili K, Wilson SR. The biliary tree and gallbladder. In: Rumack
169. Sherman M, Peltekian, KM, Lee C. Screening for hepatocellular CM, Wilson SR, Charboneau JW, Johnson JM, editors. Diagnostic
carcinoma in chronic carriers of hepatitis B virus: incidence and ultrasound. 3rd edn. St Louis: Elsevier Mosby; 2005:171212.
prevalence of hepatocellular carcinoma in a North American urban 196. Vauthey JN, Blumgart LH. Recent advances in the management of
population. Hepatology 1995;22:432438. cholangiocarcinomas. Semin Liver Dis 1994;14:109114.
170. Sheu JC, Chen DS, Sung JL, et al. Hepatocellular carcinoma in the 197. Shaib YH, El-Serag HB, Davila JA, et al. Risk factors of intrahepatic
early stage. Radiology 1985;155:463467. cholangiocarcinoma in the United States: a case control study.
171. Bruix J, Sherman M, Llovet JM, et al. Clinical management of Gastroenterology 2005;128:620626.
hepatocellular carcinoma. Conclusions of the Barcelona 2000 EASL 198. Shaib Y, El-Sherag HB. The epidemiology of cholangiocarcinoma.
Conference. J Hepatol 2001;35:421430. Semin Liver Dis 2004;24:115125.
172. Willatt JM, Hussain HK, Adusumilli S, Marrero JA. MR imaging of 199. Ishak KG, Anthony PP, Sobin LH. Histological typing of tumours of
hepatocellular carcinoma in the cirrhotic liver: challenges and the liver. WHO International Histological Classification of Tumours.
controversies. Radiology 2008;247(2):311330. Berlin: Springer Verlag; 1994.
173. Ito K, Mitchell DG. Imaging diagnosis of cirrhosis and chronic 200. Nakeeb A, Pitt HA, Sohn TA, et al. Cholangiocarcinoma: a spectrum
hepatitis. Intervirology 2004;47(35):134143. of intrahepatic, perihilar and distal tumours. Ann Surg 1996;224:
174. Coleman WB. Mechanisms of human hepatocarcinogenesis. Curr Mol 463473.
Med 2003;3(6):573588. 201. Khan SA, Thomas HC, Davidson BR, Taylor-Robinson SD.
175. Efremidis SC, Hytiroglou P. The multistep process of Cholangiocarcinoma. Lancet 2005;366:13031314.
hepatocarcinogenesis in cirrhosis with imaging correlation. Eur 202. Liver Cancer Study Group of Japan. The general rules for the clinical
Radiol 2002;12(4):753764. and pathological study of primary liver cancer. 4th edn. Tokyo:
176. Bennett GL, Krinsky GA, Abitbol RJ, et al. Sonographic detection of Kanehra; 2000.
hepatocellular carcinoma and dysplastic nodules in cirrhosis: 203. Saini S. Imaging of the hepatobiliary tract. N Engl J Med
correlation of pretransplantation sonography and liver explant 1997;336:18891894.
pathology in 200 patients. AJR Am J Roentgenol 2002;179:7580. 204. Choi JY, Kim MJ, Lee JM, et al. Hilar cholangiocarcinoma: role of
177. Matsui O. Imaging of multistep human hepatocarcinogenesis by CT preoperative imaging with sonography, MDCT, MRI, and direct
during intraarterial contrast injection. Intervirology cholangiography. AJR Am J Roentgenol 2008;191:14481457.
2004;47(35):438447. 205. Bloom CM, Langer B, Wilson SR. Role of US in the detection,
178. Marrero JA, Hussain HK, Nghiem HV, et al. Improving the prediction characterization and staging of cholangiocarcinoma. Radiographics
of hepatocellular carcinoma in cirrhotic patients with an arterially 1999;19:11991218.
enhancing liver mass. Liver Transpl 2005;11(3):281289. 206. Hann L, Greatrex KC, Bach AM, et al. Cholangiocarcinoma at the
179. Torimura T, Ueno T, Kin M, et al. Overexpression of angiopoietin 1 hepatic hilum: sonographic findings. AJR Am J Roentgenol
and angiopoietin 2 in hepatocellular carcinoma. J Hepatol 1997;168:985989.
2004;40(5):799807. 207. Chen MF. Peripheral cholangiocarcinoma (cholangiocellular
180. Quaia E, DOnofrio M, Cabassa P, et al. Diagnostic value of carcinoma): clinical features, diagnosis and treatment. J Gastroenterol
hepatocellular nodule vascularity after microbubble injection for Hepatol 1999;14:11441149.
characterizing malignancy in patients with cirrhosis. AJR Am J 208. Khalili K, Metser U, Wilson SR. Hilar biliary obstruction: preliminary
Roentgenol 2007;189:14741483. results with Levovist enhanced sonography. AJR Am J Roentgenol
181. Theise ND, Schwartz M, Miller C, Thung SN. Macroregenerative 2003;180:687693.
nodules and hepatocellular carcinoma in 44 sequential adult liver 209. Chen LD, Xu HX, Xie XY, et al. Enhancement patterns of intrahepatic
explants with cirrhosis. Hepatology 1992;16(4):949955. cholangiocarcinoma: comparison between contrast enhanced
182. Krinsky GA, Lee VS. MR imaging of cirrhotic nodules. Abdom ultrasound and contrast enhanced CT. Br J Radiol 2008;81:881889.
Imaging 2000;25(5):471482. 210. DOnofrio M, Vecchiato F, Cantisani V, et al. Intrahepatic peripheral
183. Mitchell DG, Rubin R, Siegelman ES, et al. Hepatocellular carcinoma cholangiocarcinoma (IPCC): comparison between perfusion
within siderotic regenerative nodules: appearances as a nodule ultrasound and CT imaging. Radiol Med 2008;113:7686.
within a nodule on MR images. Radiology 1991;178(1):101103. 211. Li R, Guo Y, Hua X, et al. Characterization of focal liver lesions:
184. Hepatocelullar carcinoma. In: Ishak KG, Goodman ZD, Stocker JT. comparison of pulse inversion harmonic contrast enhanced
Atlas of tumour pathology: tumours of the liver and intrahepatic bile sonography with contrast enhanced CT. J Clin Ultrasound
ducts. Third series, fascicle 31. Armed Forces Institute of Pathology 2007;35(3):109117.
2001:199230. 212. Ros PR, Buck JL, Goodman ZD, et al. Intrahepatic
185. Harvey CJ, Albrecht T. Ultrasound of focal liver lesions. Eur Radiol cholangiocarcinoma: radiologic-pathologic correlation. Radiology
2001;11:15781593. 1988;167:689693.
186. Ebara M, Ohto M, Shinagawa T, et al. Natural history of minute 213. Zhang Y, Uchida M, Abe T, et al. Intrahepatic peripheral
hepatocellular carcinoma smaller than three centimeters complicating cholangiocarcinoma: comparison of dynamic CT and dynamic MRI.
cirrhosis. A study in 22 patients. Gastroenterology 1986;90:289298. J Comput Assist Tomogr 1999;23:670677.
187. Itoh K, Nishimura K, Togashi K, et al. Hepatocellular carcinoma: MR 214. DOnofrio M, Rozzanigo U, Masinielli BM, et al. Hypoechoic focal
imaging. Radiology 1987;164:2125. liver lesions: characterization with contrast enhanced
188. Okabe M. Patho-morphological studies on hepatocellular carcinoma: ultrasonography. J Clin Ultrasound 2005;33:164172.
a study on a mechanism of capsule formation and septum formation 215. Burns PN, Wilson SR. Focal liver masses: enhancement patterns on
of tumour nodule. Acta Hepatol Jpn 1979;20:144156. contrast enhanced images concordance of US scans with CT scans
189. Okuda K, Musha H, Nakashima Y, et al. Clinicopathological features and MR images. Radiology 2006;242:162174.
of encapsulated hepatocellular carcinoma: a study of 26 cases. Cancer 216. Dietrich CF. Characterization of focal liver lesions with
1977;40:12401245. contrast enhanced ultrasonography. Eur J Radiol 2004;51(Suppl):
190. Takayasu K, Arii S, Ikai I, et al. Prospective cohort study of S917.
transarterial chemoembolization for unresectable hepatocellular 217. Furuse J, Nagase M, Ishii H, Yoshino M. Contrast enhancement
carcinoma in 8510 patients. Gastroenterology 2006;131(2):461469. patterns of hepatic tumours during the vascular phase using coded
191. Amitrano L, Guardascione MA, Brancaccio V, et al. Risk factors and harmonic imaging and Levovist to differentiate hepatocellular
clinical presentations of portal vein thrombosis in patients with carcinoma from other focal lesions. Br J Radiol 2003;76:385392.
cirrhosis. J Hepatol 2004;40(5):736741. 218. Coakley FV, OReily EM, Schwartz LH, et al. Non-Hodgkin
192. Tarantino L, Francica G, Sordelli I, et al. Diagnosis of benign and lymphoma as a cause of intra-hepatic periportal low attenuation on
malignant portal vein thrombosis in cirrhotic patients with CT. J Comput Assist Tomogr 1997;21:726728.
hepatocellular carcinoma: colour Doppler US, contrast enhanced US, 219. Soyer P, Beers BV, France TT, et al. Hodgkins and non-Hodgkins
165
CHAPTER 10 Focal liver lesions/echo enhancing agents and the liver
hepatic lymphoma: sonographic findings. Abdom Imaging Characterization and detection. Ultrasound Q 2006;22:1929.
1993;18:339343. 234. Catalano O, Nunziata A, Lobianco R, Siani A. Real-time harmonic
220. Townsend RR, Laing FC, Jeffrey RB Jr, Bottles K. Abdominal contrast material-specific US of focal liver lesions. Radiographics
lymphoma in AIDS: evaluation with US. Radiology 1989;171(3): 2005;25:333349.
719724. 235. Edmonson HA. Differential diagnosis of tumours and tumour
221. Radin DR, Esplin JA, Levine AM, Ralls PW. AIDS related non- like lesions in infancy and childhood. AMA J Dis Child 1956;91(2):
Hodgkins lymphoma: abdominal CT findings in 112 patients. 168186.
AJR Am J Roentgenol 1993;160(5):11331139. 236. Criag JR, Peters RL, Edmondson HA, Omata M. Fibrolamellar
222. Nyberg DA, Jeffrey RB Jr, Federle MP, et al. AIDS related carcinoma of the liver: a tumour of adolescents and young adults
lymphomas: evaluation by abdominal CT. Radiology 1986;159(1): with distinctive clinico-pathologic features. Cancer 1980;46:372379.
5963. 237. Vecchio FM. Fibrolamellar hepatocellular carcinoma of the liver: a
223. Gisbert JP, Garcia-Buey L, Pajares JM, Moreno-Otero R. Prevalence distinct entity within hepatocellular tumours a review. Appl Pathol
of hepatitis C virus infection in B-cell non-Hodgkins lymphoma: 1988;6:139148.
systematic review and meta-analysis. Gastroenterology 2003;125: 238. Torbenson M. Review of the clinicopathological features of
17231732. fibrolamellar carcinoma. Adv Anat Pathol 2007;14(3):217223.
224. Burney K, Bradley M, Buckley A, et al. Post transplant 239. Craig JR. Fibrolamellar carcinoma: clinical and pathologic features.
lymphoproliferative disorder: a pictorial review. Australas Radiol In: Okuda K, Tabor E, eds. Liver cancer. New York: Churchill
2006;50:412418. Livingstone; 1997:255262.
225. Nalesnik MA. The diverse pathology of post-transplant 240. El-Serag HB, Davila JA. Is fibrolamellar carcinoma different from
lymphoproliferative disorders: the importance of a standardized hepatocellular carcinoma? A US population based study. Hepatology
approach. Transpl Infect Dis 2001;3:8896. 2004;39(3):798803.
226. Pickhardt PJ, Siegel MJ. Abdominal manifestations of post 241. Blachar A, Federle MP, Ferris JV, et al. Radiologists performance in
transplantation lymphoproliferative disorder. AJR Am J Roentgenol the diagnosis of liver tumours with central scars by using specific CT
1998;171:10071013. criteria. Radiology 2002;223:532539.
227. Pickhardt PJ, Siegel MJ. Posttransplantation lymphoproliferative 242. Friedman AC, Lichtenstein JE, Goodman ZD, et al. Fibrolamellar
disorder of the abdomen: CT evaluation in 51 patients. Radiology hepatocellular carcinoma. Radiology 1985;157:583587.
1999;213:7378. 243. McLarney JK, Rucker PT, Bender GN, et al. Fibrolamellar carcinoma
228. Gazelle GS, Lee MJ, Hahn PF, et al. US, CT, and MRI of primary of the liver: radiologic-pathologic correlation. Radiographics
and secondary liver lymphoma. J Comput Assist Tomogr 1994;18: 1999;19:453471.
412415. 244. Fan ZH, Chen MH, Dai Y, et al. Evaluation of primary malignancies
229. Noronha V, Shafi NQ, Obando JA, Kummar S. Primary non- of the liver using contrast enhanced sonography: correlation with
Hodgkins lymphoma of the liver. Crit Rev Oncol/Hematol pathology. AJR Am J Roentgenol 2006;186:15121519.
2005;53:199207. 245. Weiss SW, Enzinger FM. Epithelioid hemangioendothelioma: a
230. Park KY, Yu JS, Yoon SW, et al. Burkitts lymphoma representing vascular tumour often mistaken for a carcinoma. Cancer 1982;50:
periportal infiltrating mass on CT. Yonsei Med J 2004;45:723726. 970981.
231. Low G, Leen E. Diagnosis of periportal hepatic lymphoma with 246. Buetow PC, Buck JL, Ros PR, Goodman ZD. Malignant vascular
contrast-enhanced ultrasonography. J Ultrasound Med 2006;25: tumours of the liver: radiologic-pathologic correlation. Radiographics
10591062. 1994;14:53166.
232. Wilson SR. The liver. In: Rumack CM, Wilson SR, Charboneau JW, 247. Korobkin M, Stephens DH, Lee JKT, et al. Biliary cystadenoma and
editors. Diagnostic ultrasound. 3rd edn. St Louis, MO: Elsevier cystadenocarcinoma: CT and sonographic findings. AJR Am J
Mosby; 2005:126135. Roentgenol 1989;153:507511.
233. Jang HJ, Kim TK, Wilson SR. Imaging of malignant liver masses:
166
CHAPTER
Percussionpalpation approach
LIVER BIOPSY 167
Technique 167 The percussionpalpation approach is sometimes referred to as the
Percussionpalpation approach 167 blind approach. Percutaneous LB is usually performed with the
Image-guided approach 167 patient in the supine position, close and parallel to the edge of
Type of needle 168 the bed, with the patients right hand positioned behind the head.5
The quality of the specimen 168 Caudal percussion is helpful in selecting the site for the biopsy over
Indications 169 the hemithorax between the anterior and midaxillary lines, until an
Diagnosis 169 intercostal space is reached where dullness is maximal at the end
Prognosis 169 of expiration. The intercostal space below this point is used. Local
Treatment 169
infiltration with lidocaine 12% (without adrenaline) is usually per-
Patient management 170
Complications 170 formed to ensure that this area is well anaesthetised. The total
length of time required to pass the biopsy needle into and then
RADIOFREQUENCY ABLATION 171 remove it from the liver is usually 23 seconds. The specimen is
Technique 171 then discharged from the needle into a 10% formaldehyde
Principles 171 solution.5
The role of imaging 172
Indications 172
Complications 174
Clinical results 174
Treatment of hepatocellular carcinoma 174
Image-guided approach
Treatment of colorectal hepatic metastases 175 The LB can be performed under imaging control or guidance using
US, computed tomography or magnetic resonance imaging. US is
the most common imaging modality used because it is readily and
widely available, simple, the least costly and does not expose the
patient to radiation. When US is used in obtaining the LB, it is done
either immediately before (site marking) or throughout the entire
procedure (real-time).2,3 Local infiltration with lidocaine 12%
(without adrenaline), as mentioned above, is usually performed.
Prebiopsy US helps to detect focal hepatic tumours (benign or
LIVER BIOPSY malignant), cysts, ascites, intrahepatic biliary dilatation or hepatic
anatomical variation. For focal hepatic lesions, it is an accepted
Liver biopsy (LB), and thus histological assessment of the liver, has standard of practice that image guidance is used in order to guide
been used as a method for diagnosing parenchymal liver diseases and direct the LB.6,7 Although right lobe biopsy is the usual biopsy
since the mid-1940s, well before the development of the sophisti- site in patients with diffuse disease, the choice of where to biopsy
cated imaging techniques and sensitive blood tests now routinely the liver using imaging guidance varies according to the operator.
used to improve diagnostic accuracy.1 Although these non-invasive The intercostal approach does not usually require an extreme
techniques have in many instances replaced liver histology, LB breath hold. This approach is associated with a small risk of inter-
remains an essential tool in the diagnosis and management of costal artery puncture, which can be minimised by inserting the
parenchymal liver diseases.2 Moreover, the use of LB is increasing needle over the cephalad rather than the caudad aspect of the rib.
with the advent of liver transplantation and the progress being Although the intercostal approach is typically closer to the costo-
made in antiviral therapeutic agents. While blind percutaneous phrenic sulci, the lung can be easily avoided because it is readily
needle biopsy is the traditional technique, the use of ultrasound visible as an echogenic structure on US.2
(US) guidance has increased considerably. Histological assessment
can be performed even on a focal liver lesion, when a patients n Ultrasound-assisted approach. This approach is sometimes also
overall clinical picture, together with imaging features, are not suf-
referred to as site marking. The US is performed immediately
ficient to establish a diagnosis. Image guidance is needed whenever
before the LB, an optimal site is identified on the skin, and the
biopsy has to be performed on a focal liver lesion.2 All LB tech-
distance from the skin to any large hepatic vessels or ducts is
niques require specific training to ensure appropriate-sized speci-
measured. In this way, a reasonably precise measurement of
men retrieval and the lowest rate of complications.
the depth needed to be reached by the biopsy needle is
determined2,3 (Fig. 11.1).
Technique n Ultrasound-guided approach. Under real-time US guidance, the
liver and biopsy needle are imaged throughout the procedure.
Currently, there are three techniques for performing an LB: percu- This is usually achieved by utilising an automated biopsy
taneous, transjugular and laparoscopic. The percutaneous LB can device that can be operated with one hand while the US
be performed blind, US guided or US assisted24 (Table 11.1). probe is held with the other hand.3,8 US-guided approach is
167
CHAPTER 11 Biopsy technique and RF ablation
Figure 11.1 US-assisted liver biopsy. The right liver lobe is Figure 11.2 US-guided liver biopsy. The focal liver lesion in
visualised with US with an intercostal approach. A peripheral portion segment VII is visualised at US, with an intercostal approach. A
of the liver, not including major vessels, is chosen to perform 20-gauge spring-loaded automated cutting needle in placed within
US-assisted liver biopsy and the needle path is planned (dotted the lesions under US guidance.
line).
US, ultrasound.
The quality of the specimen
The quality of LB specimen is usually determined by length, width,
fragmentation and complete portal tracts (CPTs).17 The concept of
the quality of an LB specimen has recently emerged as a critical
factor in the assessment of the grade and stage of the liver disease
needed whenever a mass lesion biopsy has to be performed in patients with chronic viral hepatitis. Nowadays, the number of
(Fig. 11.2). Manolakopoulos et al., in a retrospective study, CPTs is considered to be crucial for reliable grading and staging,
showed that the US-assisted approach is as safe as US-guided and it is generally accepted that an optimal LB specimen is
approach and both obtained adequate specimens for defined as being 2025mm long and/or containing more than
histological diagnosis.9 11 CPTs.1820
168
Liver biopsy
Patient management and may lead to mortality. Severe bleeding (requiring hospitalisa-
tion, the likelihood of transfusion, or even radiological intervention
Currently, LB is typically undertaken on an outpatient or same or surgery) has been estimated to occur in between 1 in 2500 and 1
day basis. Indications for, benefits, risks and alternatives of LB in 10000 biopsies after an intercostal percutaneous approach for
have to be discussed with the patient. Written informed consent diffuse, non-focal, liver disease. Less severe bleeding, defined as
should be obtained prior to LB.2 that sufficient to cause pain or reduced blood pressure or tachycar-
Pre-biopsy testing includes measurement of the complete blood dia, but not requiring transfusion or intervention, occurs in approx-
count, including platelet count, prothrombin time (PT)/interna- imately 1 in 500 biopsies. Mortality after LB is usually related to
tional normalised ratio (INR). In some institutions the activated haemorrhage. Despite a wide variation in the literature, the most
partial thromboplastin time and/or cutaneous bleeding time at a commonly quoted mortality rate is less than or equal to 1 in 10000
suitable juncture prior to the biopsy are requested. A prothrombin liver biopsies.14,15,17,28,31,4448
time ratio (normal time/patients time) >50% and a platelet count A large retrospective multicentric study demonstrated that 61%
higher than 50000/L are required to keep the risk of bleeding at of the complications appeared in the first 2 hours after the biopsy,
an acceptably low level.2 82% in the first 10 hours and 96% in the first 24 hours after biopsy.14
Usual daily activities may be undertaken up until the day preced- Some studies showed that the rate of complications is similar in
ing liver biopsy. Following the procedure, patients are encouraged outpatients and inpatients.15,49
to rest quietly. Many physicians recommend that patients who live Differences in complication rates, either minor or major, have
more than 1 hour travelling distance by car from the centre remain been reported between the blind and US-guided LB. The mortality
close by that evening, in case of potential late complication. rate from blind LB is 0.010.1%.14,15,44 The use of US guidance can
However, in the absence of an evident complication or significant prevent inadvertent puncture of other organs or large intrahepatic
pain that necessitates use of potent analgesia, there should be no vessels. US may also reduce the incidence of major complications
restriction upon return to work the following day. Patients are such as haemorrhage, bile peritonitis, pneumothorax, etc. Caturelli
discouraged from lifting weights for a minimum of 24 hours, et al. have shown that, when compared with a historical control
because this may increase intra-abdominal pressure and in theory group from within their institution, there was an overall statistically
could facilitate bleeding from the puncture site.2 significant decrease in complications when US was used (0.53%
An important issue surrounds management of antiplatelet (i.e. versus 2.1% in the historical control group, p < 0.05).50 Moreover, it
aspirin, ticlodipine, clopidogrel, IIb/IIIa receptor antagonists, non- has been demonstrated that US-guided LB causes significantly less
steroidal anti-inflammatory drugs) and/or anticoagulant drugs biopsy pain and significantly less pain-related morbidity.50,51
(i.e., warfarin) before and after the time of liver biopsy. According The relationship between LB complications and the number of
to the American Association for the Study of Liver Diseases needle passes is well documented.15 The frequency of complications
antiplatelet medications should be discontinued several to 10 days increases with the number of passes performed at a rate of 26.4%,
before liver biopsy. Antiplatelet therapy may be restarted 4872 with one pass versus 68% with two or more passes (p < 0.001).28
hours after liver biopsy. Even anticoagulant medications should be A recent meta-analysis of best available evidence concludes that
discontinued prior to liver biopsy. Warfarin should generally be the use of US-guided biopsy is superior to blind needle biopsy. The
discontinued at least 5 days prior to liver biopsy. Heparin and odds ratios of the controlled studies showed that blind needle
related products should be discontinued 1224 hours prior to biopsy carried a higher risk for major complications, post-biopsy
biopsy. Warfarin may be restarted the day following liver pain and biopsy failure.3
biopsy.2,40,41 When a malignant focal liver lesion is biopsied, the procedure is
Routine placement of an intravenous cannula prior to the proce- associated with a risk of tumour spread usually along the biopsy
dure is practised in many facilities as a precaution should there be track.52,53 Although potentially a devastating complication, espe-
significant pain and/or bleeding after the procedure.2 cially in transplant candidates where immunosuppression may
Once liver biopsy has been accomplished, the patient then rests predispose to seeded tumour growth, this risk is almost certainly
quietly and is carefully observed by experienced nursing staff. The overstated in earlier literature. For example, in a recent retrospec-
patient is often placed in the right lateral decubitus position (to tive study of patients undergoing image-guided biopsy of a lesion
allow the liver to rest against the lateral abdominal wall and thereby suspicious for HCC, HCC was diagnosed by biopsy in 74 (63%) of
limit bleeding), although this is largely performed as a result of 118 cases, and an additional 10 were found to have HCC on follow-
longstanding clinical practice.42 The risk of bleeding is greatest up; no patient developed evidence of tumour spread along the
immediately after liver biopsy; thus, it is recommended that patients needle track.54 Biopsy and/or aspiration of infectious lesions is gen-
be observed carefully over the first 23 hours after biopsy.31,43 erally safe. It has been suggested that the presence of an echinococ-
cal cyst (hydatid disease) represents an absolute contraindication to
biopsy because it is known that piercing of an echinococcal cyst
Complications may be associated with fatal anaphylaxis. However, available data
suggest that careful aspiration of these lesions with 19-gauge
The reported complications range from minor (pain and transient to 22-gauge needles is relatively safe. Nevertheless, if suspected,
hypotension) to major, including (a) haemorrhage (intraperitoneal, some consideration and preparation for possible anaphylaxis is
intrahepatic, haemothorax); (b) perforation of the gallbladder or the warranted.55
colon; (c) pneumothorax; and (d) intrahepatic arteriovenous fistula.
Significant bleeding and bile peritonitis are serious complications
Complications of liver biopsy
Bleeding peritoneal, intraparenchymal and thoracic.
Pre-biopsy testing
Bile peritonitis.
Blood count, including a platelet count. Damage to colon or gallbladder.
Prothrombin time. Pneumothorax.
Antiplatelet medications stopped for several to 10 days prior to Arteriovenous fistula.
biopsy. Mortality related to bleeding 1:10000.
Warfarin stopped for 5 days prior to biopsy. Overall complication rate 0.52.0% depending on technique.
Heparin stopped for 1224 hours prior to biopsy. Ultrasound-guided biopsy causes less pain and has the lowest
Corrective measures may be needed if a biopsy is urgent. complication rate.
170
Radiofrequency ablation
A B
Figure 11.4 US-guided RF ablation. A: A multi-tined expandable needle is inserted and deployed within an HCC nodule. B: Following
the activation of the RF generator, a hyperechoic cloud appears at the site of treatment.
A B
C D
Figure 11.5 Initial evaluation of tumour response to RF ablation with contrast-enhanced US. A: Pre-treatment contrast-enhanced
US obtained in the arterial phase shows the small HCC lesion as a hypervascular nodule. B-mode low-mechanical index image is shown in
the right side of the image; the contrast-specific mode during the arterial phase is shown in the left side. B: The tumour is treated with RF
ablation under US guidance. C: At the end of the procedure, a hyperechoic cloud covering the tumour as well as a cuff of surrounding
liver parenchyma is seen on US. D: Contrast-enhanced US study performed at the end of the procedure shows the ablation zone as a
non-enhancing area completely covering the tumour. Periablation enhancement is also seen, representing reactive hyperaemia.
from other primary cancers, promising initial results have been coagulation status. A prothrombin time ratio (normal time/patients
reported in the treatment of breast and endocrine tumours. The time) >50% and a platelet count higher than 50000/L are required
number of lesions should not be considered an absolute contrain- to keep the risk of bleeding at an acceptably low level. The tumour
dication to RF ablation if successful treatment of all metastatic staging protocol must be tailored to the kind of malignancy. In
deposits can be accomplished. Nevertheless, most centres preferen- patients with HCC, the detection of the nodule by ultrasound is
tially treat patients with four or fewer lesions. Tumour size is of usually followed by multidetector spiral computed tomography or
utmost importance to predict the outcome of RF ablation. Imaging dynamic magnetic resonance, following the recommendations of
studies underestimate the size of metastatic deposits. Therefore, the the American Association for the Study of Liver Diseases.32 In
target tumour should not exceed 3cm in longest axis to ensure patients with liver metastases tumour staging protocol should
complete ablation with most of the currently available devices.56 include abdominal US and spiral computed tomography or dynamic
A careful clinical, laboratory and imaging assessment has to be magnetic resonance imaging of the abdomen. Chest computed tom-
performed in each individual patient by a multidisciplinary team ography and positron emission tomography (or positron emission
to evaluate eligibility for percutaneous ablation. Laboratory tests tomography computed tomography) may be required to exclude
should include measurement of serum tumour markers, such as or confirm extrahepatic locations of metastatic disease.56
alpha-fetoprotein for HCC and carcinoembryonic antigen for color- Pre-treatment imaging must carefully define the location of each
ectal metastases, as well as a full evaluation of the patients lesion with respect to surrounding structures. Lesions located along
173
CHAPTER 11 Biopsy technique and RF ablation
the surface of the liver can be considered for RF ablation, although cases in a multicentre survey75 and in 1 (0.5%) of 187 cases in a
their treatment requires adequate expertise and may be associated single-institution series.78 Lesions with subcapsular location and an
with a higher risk of complications. Thermal ablation of superficial invasive tumoral pattern, as shown by a poor differentiation degree,
lesions that are adjacent to any part of the gastrointestinal tract seem to be at higher risk for such a complication.79
must be avoided because of the risk of thermal injury to the gastric
or bowel wall. The colon appears to be at greater risk than the Clinical results
stomach or small bowel for thermally mediated perforation. Gastric
complications are rare, probably owing to the relatively greater wall Most early clinical research with RF ablation was conducted in the
thickness of the stomach or the rarity of surgical adhesions along framework of feasibility studies, aimed at demonstrating the local
the gastrohepatic ligament. The mobility of the small bowel may effect and the safety of the procedure.8082 More recently, the clinical
also provide it with greater protection compared with the relatively efficacy of RF ablation has been evaluated in the treatment of HCC
fixed colon. The use of special techniques such as intraperitoneal and colorectal hepatic metastases.
injection of dextrose to displace the bowel can be considered in
such instances.73 Treatment of lesions adjacent to the hepatic hilum
carries a risk of thermal injury to the biliary tract. This tumour loca- Treatment of hepatocellular carcinoma
tion represents a relative contraindication to RF ablation. In expe-
The therapeutic effect of RF ablation in HCC has been assessed by
rienced hands, thermal ablation of tumours located in the vicinity
studies that evaluated the outcome of treatment at the histological
of the gallbladder was shown to be feasible, although associated in
level and by randomised or cohort studies that investigated the
most cases with self-limited iatrogenic cholecystitis.74 Thermal abla-
long-term survival outcomes of treated patients. Histological data
tion of lesions adjacent to hepatic vessels is possible, since flowing
from explanted liver specimens in patients who underwent RF abla-
blood usually protects the vascular wall from thermal injury: in
tion showed that tumour size and presence of large (3mm or more)
these cases, however, the risk of incomplete treatment of the neo-
abutting vessels significantly affect local treatment effect. Complete
plastic tissue close to the vessel may increase because of the heat
tumour necrosis was pathologically shown in 83% of tumours
loss by convection.62
<3cm and 88% of tumours in a non-perivascular location.83 Com-
parison with percutaneous ethanol injection (PEI) in five ran-
Complications domised trials8488 has shown that RF ablation had higher local
anticancer effect than PEI, leading to a better local control of the
Early major complications associated with RF ablation occur in disease (Table 11.3). The two European trials failed to show a sta-
2.23.1% of patients and include intraperitoneal bleeding, liver tistically significant difference in overall survival between patients
abscess, intestinal perforation, pneumo/haemothorax and bile duct who received RF ablation and those treated with PEI.84,88 However,
stenosis and tumour seeding (0.5%); the procedure mortality rate is survival advantages were identified in three Asian studies.8587
0.10.5%.7577 The minor complication rate ranges from 5% to 8.9%. These data were recently pooled in two independent meta-analyses
The most common causes of death are sepsis, hepatic failure, colon and the survival benefit for patients with small HCC submitted to
perforation and portal vein thrombosis (particularly in patients sub- RF ablation was confirmed.89,90 Therefore, RF ablation appears as
mitted to RF ablation with a surgical approach and Pringle manoeu- the preferred percutaneous treatment for patients with early-stage
vre), while the most common complications are intraperitoneal HCC on the basis of a more consistent local tumour control and
bleeding, hepatic abscess, bile duct injury, hepatic decompensation better survival outcomes.
and grounding pad burns. Minor complications and side effects are Recently, the long-term survival outcomes of RF ablation-treated
usually transient and self-limiting.7577 An uncommon late compli- patients were reported (Table 11.4) and were useful to elucidate
cation of RF ablation can be tumour seeding along the needle track. factors influencing patient prognosis.78,9195 The severity of the
In patients with HCC, tumour seeding occurred in 8 (0.5%) of 1610 underlying cirrhosis and occurrence of new lesions represent the
Table 11.3 Randomised studies comparing RF ablation and PEI in the treatment of early-stage HCC
a
Includes initial treatment failure (incomplete response) and late treatment failure (local recurrence/progression).
174
Radiofrequency ablation
Table 11.4 Studies reporting long-term survival outcomes of patients with early-stage HCC who underwent
percutaneous RF ablation
SURVIVAL (%)
Author No. of patients 1 year 3 years 5 years
Lencioni et al.78
Child A, 1 HCC <5cm or 3 <3cm 144 100 76 51
1 HCC <5cm 116 100 89 61
Child B, 1 HCC <5cm or 3 <3cm 43 89 46 31
Tateishi et al.91
Naive patientsa 319 95 78 54
Non-naive patientsb 345 92 62 38
Cabassa et al.92 59 94 65 43
Choi et al.93
Child A, 1 HCC <5cm or 3 <3cm 359 NA 78 64
Child B, 1 HCC <5cm or 3 <3cm 160 NA 49 38
Takahashi et al.94
Child A, 1 HCC <5cm or 3 <3cm 171 99 91 77
Hiraoka et al.95
ChildPugh AB 105 NA 88 59
a
Patients who received RF ablation as primary treatment.
b
Patients who received RF ablation for recurrent tumour after previous treatment including resection, ethanol injection, microwave ablation and transarterial
embolisation.
NA, not available.
been reported (Table 11.5).69,70,101105 In particular, in three series 12. Lindor KD, Bru C, Jorgensen RA, et al. The role of ultrasonography
including patients with five or fewer lesions, each 5cm or less in and automatic-needle biopsy in outpatient percutaneous liver biopsy.
diameter, the 5-year survival rate ranged from 24% to 44% at 5 Hepatology 1996;23:10791083.
13. Sherman K, Goodman Z, Sullivan S, Farris-Young S. Liver biopsy in
years.69,101,103 When RF ablation was performed in patients with
cirrhotic patients. Am J Gastroenterol 2007;102:789793.
small (<4cm), solitary hepatic colorectal metastases, 40% 5-year 14. Piccinino F, Sagnelli E, Pasquale G, Giusti G. Complications following
survival rate was demonstrated.106 These figures are substantially percutaneous liver biopsy. A multicentre retrospective study on
higher than those obtained with any chemotherapy regimens and 68,276 biopsies. J Hepatol 1986;2:165173.
provide indirect evidence that RF ablation therapy improves sur- 15. McGill DB, Rakela J, Zinsmeister AR, Ott BJ. A 21-year experience
vival in patients with limited hepatic metastatic disease. This con- with major haemorrhage after percutaneous liver biopsy.
clusion is supported by the interim analysis of a randomised Gastroenterology 1990;99:13964000.
controlled trial comparing chemotherapy plus RF ablation to chem- 16. Forssell PL, Bonkowsky HL, Anderson PB, Howell DA. Intrahepatic
otherapy alone in colorectal cancer metastatic to the liver. hematoma after aspiration liver biopsy. A prospective randomized
Recent studies analysed the role of RF ablation with respect to trial using two different needles. Dig Dis Sci 1981;26:631635.
17. Bravo AA, Sheth SG, Chopra S. Liver biopsy. N Engl J Med
surgical resection. In one study, patients with colorectal metastases
2001;344:495500.
isolated to the liver were treated with hepatic resection, RF ablation 18. Bedosa P, Dargere D, Paradis V. Sampling variability of liver fibrosis
plus resection, RF ablation only, or chemotherapy only. Overall in chronic hepatitis C. Hepatology 2003;38:14491457.
survival for patients treated with RF ablation plus resection or RF 19. Colloredo G, Guido M, Sonzogni A, Leandro G. Impact of liver
ablation only was greater than for those who received chemother- biopsy size on histological evaluation of chronic viral hepatitis: the
apy only. However, overall survival was highest after resection: smaller the sample, the milder the disease. J Hepatol 2003;39:239244.
4-year survival rates after resection, RF ablation plus resection, and 20. Cholongitas E, Senzolo M, Standish RA, et al. A systemic review of
RF ablation only were 65%, 36%, and 22%, respectively.107 In another the quality of liver biopsy specimens. Am J Clin Pathol
2006;125:710721.
paper, the outcome of patients with solitary colorectal liver metas-
21. Demetris AJ, Ruppert K. Pathologists perspective on liver needle
tasis treated by surgery or by RF ablation did not differ: the survival biopsy size. J Hepatol 2003;39:275277.
rate at 3 years was 55% for patients treated with surgery and 52% 22. Rocken C, Meier H, Klauck S, et al. Large-needle biopsy versus
for those who underwent RF ablation.108 Other authors used RF thin-needle biopsy in diagnostic pathology of liver diseases. Liver
ablation instead of repeated resection for the treatment of liver 2001;21:391397.
tumour recurrence after partial hepatectomy.109 The potential role 23. Petz D, Klauck S, Rohl FW, et al. Feasibility of histological grading
of performing RF ablation during the interval between diagnosis and staging of chronic viral hepatitis using specimens obtained by
and resection as part of a test-of-time management approach was thin needle biopsy. Virchows Arch 2003;442:238244.
investigated.110 Eighty-eight consecutive patients with colorectal 24. Gazelle GS, Haaga JR, Rowland DY. Effect of needle gauge, level of
anticoagulation, and target organ on bleeding associated with
liver metastases who were potential candidates for surgery were
aspiration biopsy. Work in progress. Radiology 1992;183:
treated with RF ablation. Among the 53 patients in whom complete 509513.
tumour ablation was achieved after RF treatment, 98% were spared 25. Plecha DM, Goodwin DW, Rowland DY, et al. Liver biopsy: effects of
surgical resection because they remained free of disease or because biopsy needle caliber on bleeding and tissue recovery. Radiology
they developed additional metastases leading to unresectability. No 1997;204:101104.
patient in whom RF treatment did not achieve complete tumour 26. Farrell RJ, Smiddy PF, Pilkington RM, et al. Guided versus blind liver
ablation became unresectable due to the growth of the treated biopsy for chronic hepatitis C: clinical benefits and costs.
metastases. J Hepatol 1999;30:580587.
27. Cadranel JF, Rufat P, Degos F. Practices of transcutaneous liver
biopsies in France. Results of a retrospective nationwide study.
Gastroenterol Clin Biol 2001;25:7780.
REFERENCES 28. Cadranel JF, Rufat P, Degos F. Practices of liver biopsy in France:
results of a prospective nationwide survey. For the Group of
1. Sherlock S. Aspiration liver biopsy, technique and diagnostic Epidemiology of the French Association for the Study of the Liver
application. Lancet 1945;2:397401. (AFEF). Hepatology 2000;32:477481.
2. Rockey DC, Caldwell SH, Goodman ZD, et al. Liver biopsy. 29. Riley 3rd TR. How often does ultrasound marking change the liver
Hepatology 2009;49:10171044. biopsy site? Am J Gastroenterol. 1999;94:33203322.
3. Al Knawy B, Shiffman F. Percutaneous liver biopsy in clinical 30. Maharaj B, Bhoora IG. Complications associated with percutaneous
practice. Liver Int 2007;27:11661173. needle biopsy of the liver when one, two or three specimens are
4. Grant A, Neuberger J. Guidelines on the use of liver biopsy in taken. Postgrad Med J 1992;68:964967.
clinical practice. British Society of Gastroenterology. Gut 31. Firpi RJ, Soldevila-Pico C, Abdelmalek MF, et al. Short recovery time
1999;45(Suppl. 4):IV1IV11. after percutaneous liver biopsy: should we change our current
5. Hegarty JE, Williams R. Liver biopsy: techniques, clinical practices? Clin Gastroenterol Hepatol 2005;3:926929.
applications, and complications. Br Med J 1984;288:12541256. 32. Bruix J, Sherman M. Management of hepatocellular carcinoma.
6. Buscarini L, Fornari F, Bolondi L, et al. Ultrasound-guided fine- Hepatology 2005;42:12081236.
needle biopsy of focal liver lesions: techniques, diagnostic accuracy 33. Strader DB, Wright T, Thomas DL, Seeff LB. Diagnosis, management,
and complications. A retrospective study on 2091 biopsies. J Hepatol and treatment of hepatitis C. Hepatology 2004;39:11471171.
1990;11:344348. 34. Lok AS, McMahon BJ. Chronic hepatitis B. Hepatology
7. Sbolli G, Fornari F, Civardi G, et al. Role of ultrasound guided fine 2007;47:507539.
needle aspiration biopsy in the diagnosis of hepatocellular 35. Heathcote EJ. Management of primary biliary cirrhosis. The
carcinoma. Gut 1990;31:13031305. American Association for the Study of Liver Diseases practice
8. Nazarian LN, Feld RI, Herrine SK, et al. Safety and efficacy of guidelines. Hepatology 2000;31:10051013.
sonographically guided random core biopsy for diffuse liver disease. 36. Smith AD. Recurrence of the original liver disease. In: Killenberg PG,
J Ultrasound Med 2000;19:537541. Clavien PA, editors. Medical care of the liver transplant patient. 3rd
9. Manolakopoulos S, Triantos C, Bethanis S, et al. Ultrasound-guided edn. Oxford: Blackwell; 2006. p. 419438.
liver biopsy in real life: comparison of same-day pre-biopsy versus 37. Demetris AJ, Adeyi O, Bellamy CO, et al. Liver biopsy interpretation
real-time ultrasound approach. J Gastroenterol Hepatol for causes of late liver allograft dysfunction. Hepatology
2007;22:14901493. 2006;44:489501.
10. Adams T, Lewis JH. Percutaneous liver biopsy. Clin Perspectives 38. Rockey DC. Non-invasive assessment of liver fibrosis and portal
Gastroenterol 2002;2:117121. hypertension with transient elastography. Gastroenterology
11. Colombo M, Del Ninno E, de Franchis R, et al. Ultrasound assisted 2008;134:814.
percutaneous liver biopsy: superiority of the Tru-Cut over the 39. Takahashi H, Ono N, Eguchi Y, et al. Evaluation of acoustic radiation
Menghini needle for diagnosis of cirrhosis. Gastroenterology force impulse elastography for fibrosis staging of chronic liver
1988;95:487489. disease: a pilot study. Liver Int 2009 Oct 27. [Epub ahead of print]
176
References
40. Eisen GM, Baron TH, Dominitz JA, et al. Guideline on the 66. Ahmed M, Liu Z, Lukyanov AN, et al. Combination radiofrequency
management of anticoagulation and antiplatelet therapy for ablation with intratumoral liposomal doxorubicin: effect on drug
endoscopic procedures. Gastrointest Endosc 2002;55:775779. accumulation and coagulation in multiple tissues and tumour types
41. Madura JA, Rookstool M, Wease G. The management of patients on in animals. Radiology 2005;235:469477.
chronic coumadin therapy undergoing subsequent surgical 67. Goldberg SN, Charboneau JW, Dodd III GD, et al. Image-guided
procedures. Am Surg 1994;60:542546. tumour ablation: proposal for standardization of terms and reporting
42. Hyun CB, Beutel VJ. Prospective randomized trial of post-liver criteria. Radiology 2003;228:335345.
biopsy recovery positions: does positioning really matter? J Clin 68. Llovet JM, Di Bisceglie AM, Bruix J, et al; Panel of Experts in
Gastroenterol 2005;39:328332. HCC-Design Clinical Trials. Design and endpoints of clinical
43. Beddy P, Lyburn I, Geoghegan T, et al. Outpatient liver biopsy: a trials in hepatocellular carcinoma. J Natl Cancer Inst 2008;100:
prospective evaluation of 500 cases. Gut 2007;56:307. 698711.
44. Perrault J, McGill DB, Ott BJ, Taylor WF. Liver biopsy: complications 69. Lencioni R, Crocetti L, Cioni D, et al. Percutaneous radiofrequency
in 1000 inpatients and outpatients. Gastroenterology 1978;74: ablation of hepatic colorectal metastases. Technique, indications,
103106. results, and new promises. Invest Radiol 2004;39:599689.
45. Stone MA, Mayberry JF. An audit of ultrasound guided liver 70. Gillams AR, Lees WR. Radio-frequency ablation of colorectal liver
biopsies: a need for evidence-based practice. Hepatogastroenterology metastases in 167 patients. Eur Radiol 2004;4:22612267.
1996;43:432434. 71. Lencioni R, Crocetti L, Cioni R, et al. Response to radiofrequency
46. Janes CH, Lindor KD. Outcome of patients hospitalized for ablation of pulmonary tumours: a prospective, intention-to-treat,
complications after outpatient liver biopsy. Ann Intern Med multicentre clinical trial (the RAPTURE study). Lancet Oncol
1993;118:9698. 2008;9:621628.
47. Myers RP, Fong A, Shaheen AA. Utilization rates, complications and 72. Berber E, Pelley R, Siperstein AE. Predictors of survival after
costs of percutaneous liver biopsy: a population-based study radiofrequency thermal ablation of colorectal cancer metastases to the
including 4275 biopsies. Liver Int 2008;28:705712. liver: a prospective study. J Clin Oncol 2005;23:13581364.
48. Knauer CM. Percutaneous biopsy of the liver as a procedure for 73. Rhim H, Dodd III GD, Chintapalli KN, et al. Radiofrequency thermal
outpatients. Gastroenterology 1978;74:101102. ablation of abdominal tumours: lessons learned from complications.
49. Douds AC, Joseph AE, Finlayson C, Maxwell JD. Is day case liver Radiographics 2004;24:4145.
biopsy underutilised? Gut 1995;37:574575. 74. Chopra S, Dodd III GD, Chanin MP, Chintapalli KN. Radiofrequency
50. Caturelli E, Giacobbe A, Facciorusso D, et al. Percutaneous biopsy in ablation of hepatic tumours adjacent to the gallbladder: feasibility
diffuse liver disease: increasing diagnostic yield and decreasing and safety. AJR Am J Roentgenol 2003;180:697701.
complication rate by routine ultrasound assessment of puncture site. 75. Livraghi T, Solbiati L, Meloni MF, et al. Treatment of focal liver
Am J Gastroenterol 1996;91:13181321. tumours with percutaneous radio-frequency ablation: complications
51. Pasha T, Gabriel S, Therneau T, et al. Cost-effectiveness of encountered in a multicentre study. Radiology 2003;26:441451.
ultrasound-guided liver biopsy. Hepatology 1998;27:12201226. 76. De Baere T, Risse O, Kuoch V, et al. Adverse events during
52. Durand F, Regimbeau JM, Belghiti J, et al. Assessment of the benefits radiofrequency treatment of 582 hepatic tumours. AJR Am J
and risks of percutaneous biopsy before surgical resection of Roentgenol 2003;181:695700.
hepatocellular carcinoma. J Hepatol 2001;35:254258. 77. Bleicher RJ, Allegra DP, Nora DT, et al. Radiofrequency ablation in
53. Liu YW, Chen CL, Chen YS, et al. Needle tract implantation of 447 complex unresectable liver tumours: lessons learned. Ann Surg
hepatocellular carcinoma after fine needle biopsy. Dig Dis Sci Oncol 2003;10:5258.
2007;52:228231. 78. Lencioni R, Cioni D, Crocetti L, et al. Early-stage hepatocellular
54. Bialecki ES, Ezenekwe AM, Brunt EM, et al. Comparison of liver carcinoma in cirrhosis: long-term results of percutaneous image-
biopsy and noninvasive methods for diagnosis of hepatocellular guided radiofrequency ablation. Radiology 2005;234:961967.
carcinoma. Clin Gastroenterol Hepatol 2006;4:361368. 79. Llovet JM, Vilana R, Bru C, et al. Barcelona Clinic Liver Cancer
55. Khuroo MS, Wani NA, Javid G, et al. Percutaneous drainage (BCLC) Group. Increased risk of tumour seeding after percutaneous
compared with surgery for hepatic hydatid cysts. N Engl J Med radiofrequency ablation for single hepatocellular carcinoma.
1997;337:881887. Hepatology 2001;33:11241129.
56. Crocetti L, DeBaere T, Lencioni R. Quality improvement guidelines 80. Lencioni R, Goletti O, Armillotta N, et al. Radiofrequency thermal
for radiofrequency ablation of liver tumours. Cardiovasc Intervent ablation of liver metastases with a cooled-tip electrode needle: results
Radiol 2009 [Epub ahead of print]. of a pilot clinical trial. Eur Radiol 1998;8:12051211.
57. Bruix J, Sherman M, Llovet JM, et al. EASL Panel of Experts on HCC. 81. Curley SA, Izzo F, Delrio P, et al. Radiofrequency ablation of
Clinical management of hepatocellular carcinoma. Conclusions of unresectable primary and metastatic malignancies: results in 123
theBarcelona-2000 EASL conference. European Association for the patients. Ann Surg 1999;230:18.
Study of the Liver. J Hepatol 2001;35:421430. 82. Wood TF, Rose DM, Chung M, et al. Radiofrequency ablation of 231
58. Stang A, Fischbach R, Teichmann W, et al. A systematic review on unresectable hepatic tumours: indications, limitations, and
the clinical benefit and role of radiofrequency ablation as treatment complications. Ann Surg Oncol 2000;7:593600.
of colorectal liver metastases. Eur J Cancer 2009 [Epub ahead of 83. Lu DS, Yu NC, Raman SS, et al. Radiofrequency ablation of
print]. hepatocellular carcinoma: treatment success as defined by histologic
59. Goldberg SN, Gazelle GS, Mueller PR. Thermal ablation therapy for examination of the explanted liver. Radiology 2005;234:954960.
focal malignancies: a unified approach to underlying principles, 84. Lencioni R, Allgaier HP, Cioni D, et al. Small hepatocellular
techniques, and diagnostic imaging guidance. ALR Am J Roentgenol carcinoma in cirrhosis: randomized comparison of radiofrequency
2000;174:323331. thermal ablation versus percutaneous ethanol injection. Radiology
60. Dodd III GD, Frank MS, Aribandi M, et al. Radiofrequency thermal 2003;228:235240.
ablation: computer analysis of the size of the thermal injury created 85. Lin SM, Lin CJ, Lin CC, et al. Radiofrequency ablation improves
by overlapping ablations. AJR Am J Roentgenol 2001;177:777782. prognosis compared with ethanol injection for hepatocellular
61. Pennes HH. Analysis of tissue and arterial blood temperatures in the carcinoma < or =4 cm. Gastroenterology 2004;127:17141723.
resting human forearm. J Appl Physiol 1948;1:93122. 86. Shiina S, Teratani T, Obi S, et al. A randomized controlled trial of
62. Lencioni R, Crocetti L, Pina MC, Cioni D. Percutaneous image- radiofrequency ablation versus ethanol injection for small
guided radiofrequency ablation of liver tumours. Abdom Imaging hepatocellular carcinoma. Gastroenterology 2005;129:122130.
2009 34:547556. 87. Lin SM, Lin CJ, Lin CC, et al. Randomised controlled trial comparing
63. Rossi S, Garbagnati F, Lencioni R, et al. Percutaneous radio-frequency percutaneous radiofrequency thermal ablation, percutaneous ethanol
thermal ablation of nonresectable hepatocellular carcinoma after injection, and percutaneous acetic acid injection to treat
occlusion of tumour blood supply. Radiology 2000;217:119126. hepatocellular carcinoma of 3 cm or less. Gut 2005;54:11511156.
64. Lencioni R, Crocetti L, Petruzzi P, et al. Doxorubicin-eluting 88. Brunello F, Veltri A, Carucci P, et al. Radiofrequency ablation versus
bead-enhanced radiofrequency ablation of hepatocellular carcinoma: ethanol injection for early hepatocellular carcinoma: a randomized
a pilot clinical study. J Hepatol 2008;49:217222. controlled trial. Scand J Gastroenterol 2008;43:727735.
65. Goldberg SN, Saldinger PF, Gazelle GS, et al. Percutaneous tumour 89. Orlando A, Leandro G, Olivo M, et al. Radiofrequency thermal
ablation: increased necrosis with combined radio-frequency ablation ablation vs. percutaneous ethanol injection for small hepatocellular
and intratumoral doxorubicin injection in a rat breast tumour model. carcinoma in cirrhosis: meta-analysis of randomized controlled trials.
Radiology 2001;220:420427. Am J Gastroenterol 2009;104:514524.
177
CHAPTER 11 Biopsy technique and RF ablation
90. Cho YK, Kim JK, Kim MY, et al. Systematic review of randomized 100. Helmberger T, Holzknecht N, Schopf U, et al. Radiofrequency
trials for hepatocellular carcinoma treated with percutaneous ablation ablation of liver metastases. Technique and initial results. Radiologe
therapies. Hepatology 2009;49:453459. 2001;41:6976.
91. Tateishi R, Shiina S, Teratani T, et al. Percutaneous radiofrequency 101. Solbiati L, Livraghi T, Goldberg SN, et al. Percutaneous radio-
ablation for hepatocellular carcinoma. Cancer 2005;103:1201 frequency ablation of hepatic metastases from colorectal cancer:
1209. long-term results in 117 patients. Radiology 2001;221:159166.
92. Cabassa P, Donato F, Simeone F, et al. Radiofrequency ablation of 102. Machi J, Oishi AJ, Sumida K, et al. Long-term outcome of
hepatocellular carcinoma: long-term experience with expandable radiofrequency ablation for unresectable liver metastases from
needle electrodes. AJR Am J Roentgenol 2006;185:S316S321. colorectal cancer: evaluation of prognostic factors and effectiveness in
93. Choi D, Lim HK, Rhim H, et al. Percutaneous radiofrequency first- and second-line management. Cancer J 2006;12:318326.
ablation for early-stage hepatocellular carcinoma as a first- line 103. Jackobs TF, Hoffmann RT, Trumm C, et al. Radiofrequency ablation
treatment: long-term results and prognostic factors in a large of colorectal liver metastases: mid-term results in 68 patients.
single-institution series. Eur Radiol 2007;17:684692. Anticancer Res 2006;26:671680.
94. Takahashi S, Kudo M, Chung H, et al. Initial treatment response is 104. Sorensen SM, Mortensen FV, Nielsen DT. Radiofrequency ablation of
essential to improve survival in patients with hepatocellular colorectal liver metastases: long-term survival. Acta Radiol
carcinoma who underwent curative radiofrequency ablation therapy. 2007;48:253258.
Oncology 2007;72:S98S103. 105. Veltri A, Sacchetto P, Tosetti I, et al. Radiofrequency ablation of
95. Hiraoka A, Horiike N, Yamashita Y, et al. Efficacy of radiofrequency colorectal liver metastases: small size favorably predicts technique
ablation therapy compared to surgical resection in 164 patients in effectiveness and survival. Cardiovasc Intervent Radiol
Japan with single hepatocellular carcinoma smaller than 3 cm, along 2008;31:948956.
with report of complications. Hepatogastroenterology 106. Gillams AR, Lees WR. Five-year survival following radiofrequency
2008;55:21712174. ablation of small, solitary, hepatic colorectal metastases. J Vasc Interv
96. Livraghi T, Meloni F, Di Stasi M, et al. Sustained complete response Radiol 2008;19:712717.
and complications rates after radiofrequency ablation of very early 107. Abdalla EK, Vauthey JN, Ellis LM, et al. Recurrence and outcomes
hepatocellular carcinoma in cirrhosis: is resection still the treatment following hepatic resection, radiofrequency ablation, and combined
of choice? Hepatology 2008;47:8289. resection/ablation for colorectal liver metastases. Ann Surg
97. Chen MS, Li JQ, Zheng Y, et al. A prospective randomized trial 2004;239:818825.
comparing percutaneous local ablative therapy and partial 108. Oshowo A, Gillams A, Harrison E, et al. Comparison of resection and
hepatectomy for small hepatocellular carcinoma. Ann Surg radiofrequency ablation for treatment of solitary colorectal liver
2006;243:321328. metastases. Br J Surg 2003;90:12401243.
98. Solbiati L, Goldberg SN, Ierace T, et al. Hepatic metastases: 109. Elias D, De Baere T, Smayra T, et al. Percutaneous radiofrequency
percutaneous radio-frequency ablation with cooled-tip electrodes. thermoablation as an alternative to surgery for treatment of liver
Radiology 1997;205:367373. tumour recurrence after hepatectomy. Br J Surg 2002;89:752756.
99. De Baere T, Elias D, Dromain C, et al. Radiofrequency ablation of 100 110. Livraghi T, Solbiati L, Meloni F, et al. Percutaneous radiofrequency
hepatic metastases with a mean follow-up of more than 1 year. AJR ablation of liver metastases in potential candidates for resection: the
Am J Roentgenol 2000;75:16191625. test-of-time approach. Cancer 2003;97:30273035.
178
CHAPTER
A principal plane divides the liver into right and left lobes of
PORTAL VEIN 179 almost equal size. On the visceral surface of the liver this plane is
Anatomy and scanning techniques 179 denoted by a line that runs from the gallbladder fossa through the
Normal findings 179
porta hepatis to the inferior vena cava. The right lobe (Couinaud
Portal hypertension 180
Pathophysiology 180
segments V, VI, VII and VIII) is supplied by the right portal vein
Ultrasound findings in portal hypertension 181 and the left lobe (segments II, III and IV) is supplied by the left
Portal vein flow changes 181 portal vein (Fig. 12.1). Segment I (caudate lobe) receives supply
Change in portal vein calibre 182 from both left and right portal venous branches.1
Splenomegaly 182 A curved array 3.56MHz probe is suitable for imaging the
Changes in hepatic arterial flow in portal hypertension 182 liver and portal vein supplemented with colour and spectral
Portosystemic collaterals (varices) 182 Doppler. The portal vein can be imaged subcostally pointing
Management of portal hypertension 185 posterocephalad or by a right intercostal approach pointing
Surgical portosystemic shunts 185
medially. These approaches give good views of the portal vein,
Transjugular intrahepatic portosystemic shunt (TIPS) 186
Portal vein occlusion 188
hepatic artery and common bile duct. The left lateral decubitus
Portal vein aneurysm 189 position provides good views of the portal vein at the porta hepatis.
Portal vein gas 189 In this position a longitudinal oblique section demonstrates the
portal vein and its relationship to the hepatic artery and common
HEPATIC ARTERY 189 bile duct.
Anatomy and scanning techniques 189
Colour and spectral Doppler is used to document normal hepato-
Normal findings 189
Hepatic artery aneurysms 192
petal flow (towards the liver). Any reversal of flow away from the
Hereditary haemorrhagic telangiectasia (HHT) 192 liver (hepatofugal) is pathological. The main, right and left portal
vein branches can be best imaged by using a right oblique approach
HEPATIC VEINS 192 through the ribs, so that the course of the vein is towards the probe
Anatomy and scanning technique 192 and an angle of less than 60 with the beam is obtained, providing
Normal anatomical variations 193
a good Doppler signal.
Hepatic venous waveforms 194
Hepatic venous outflow obstruction 194
At the porta the hepatic artery crosses anterior to the main portal
Hepatic veno-occlusive disease 195 vein with the bile duct anteriorly (Fig. 12.2). A common normal
Hepatic venous waveforms in cardiac and pulmonary disease 195 variant (1015%) is seen when the artery lies anterior to the duct
Hepatic vein transit times 197 (Fig. 12.3).
Peliosis hepatis 197
Normal findings
PORTAL VEIN
The diameter of the portal vein is variable and is usually about
10mm. The portal vein diameter is measured as it passes anterior
Anatomy and scanning techniques to the inferior vena cava (IVC). The diameter increases with deep
inspiration, postprandially and with posture. A diameter of greater
The portal vein provides approximately 70% of the livers blood than 13mm in the supine position during quiet respiration is taken
supply. The portal vein is formed at the confluence of the splenic as abnormal.
vein and superior mesenteric vein posterior to the neck of the pan- The mean velocity in the portal vein is 1220cm/s but there is
creas. It then passes posterior to the pancreatic head and first part wide variation due to prandial state, position, exercise, respiration
of duodenum to the liver hilum via the hepatoduodenal ligament. and cardiac activity. When discussing portal and hepatic venous
The main portal vein enters the liver at the porta hepatis (liver flow the term periodicity refers to velocity variation due to cardiac
hilum) lying posterior to the hepatic artery and bile duct (the bile activity and phasicity refers to respiratory induced changes. The
duct lying anterolaterally and the hepatic artery lying anteromedi- term pulsatility should only be reserved for arterial flow. Portal
ally). It divides into the main right and left branches before pene- venous flow velocity is usually uniform. Minor phasicity may be
trating the liver, although there is some variation in this. The right seen due to respiration as well as mild periodicity due to retrograde
branch passes transversely in the liver substance for a few centime- transmission of the A wave from the right atrium via the hepatic
tres before dividing into anterior and posterior branches. The left veins or due to hepatic arterial systolic inflow (Fig. 12.4). These rises
portal vein curves anteriorly giving off branches as it traverses the in pressure result in transient decreases in the antegrade portal
liver. The hepatic arteries and bile ducts follow the same pattern. venous flow, which were present in up to 64% of a normal study
The left main portal vein is joined by the ligamentum teres (obliter- group in one series.2,3 The velocity is reduced in portal hypertension
ated umbilical vein) and ligamentum venosum (obliterated ductus and may be increased in anastomotic stenoses, e.g. liver transplant
venosum) as it enters the left lobe. patients.
179
CHAPTER 12 Vascular disorders of the liver
II
I
III
IVb
VI V
Intrahepatic
Pre-sinusoidal: This is usually due to disease affecting the porta
hepatis such as congenital hepatic fibrosis, sarcoidosis,
lymphoma, schistosomiasis, primary biliary cirrhosis, toxic fibrosis
secondary to arsenic, copper and polyvinyl chloride (PVC)
Sinusoidal: Due to hepatitis, sickle cell anaemia or fatty infiltration
Post-sinusoidal: Alcoholic cirrhosis (commonest); veno-occlusive
disease
Post-hepatic
BuddChiari syndrome
Veno-occlusive disease
Right heart failure
Constrictive pericarditis
Splenomegaly
Splenomegaly is an important sign of portal hypertension. The
spleen is best measured in the coronal plane with a maximum
cephalocaudal measurement of 13cm reliably indicating enlarge-
ment. Splenic size does not correlate well with portal pressure and
splenomegaly can be seen in chronic liver disease independent of
portal hypertension. However, splenomegaly is commonly seen in
portal hypertension and is useful in follow-up in patients with
chronic liver disease.
Figure 12.7 Spectral Doppler of the portal vein in a patient Changes in hepatic arterial flow in
with tricuspid regurgitation due to right ventricular failure. Marked portal hypertension
periodicity is present in the waveform.
Normally the liver receives 70% of its blood supply via the portal
vein and 30% from the hepatic artery. In portal hypertension due
to cirrhosis arterialisation occurs in response to a decrease in portal
venous flow (Fig. 12.5). The hepatic artery becomes dilated and is
easily seen on colour Doppler with spectral Doppler demonstrating
Change in portal vein calibre a significant increase in flow both in the main hepatic artery as well
The diameter of the portal vein is variable but should not be greater as the intrahepatic branches. In addition, arteriovenous shunts form
than 13mm (Fig. 12.8). The diameter increases with deep inspira- at the sinusoidal level shunting blood from the hepatic arteries to
tion, postprandially and with posture. A diameter of greater than the portal vein, resulting in arterialised portal venous blood.
13mm in the fasting state, supine position and during quiet respira-
tion is taken as abnormal. This gives an almost 100% specificity but Portosystemic collaterals (varices)
is less sensitive (56%).14,15 A calibre of over 17mm has been shown
to be 100% predictive for large oesophageal varices.16 However, a With rising portal venous pressure (>15mmHg), anastomoses
normal calibre portal vein does not exclude portal hypertension. between the high-pressure portal circulation and the lower-
Dilatation of the splenic and superior mesenteric veins also occurs pressure systemic system form to shunt blood away from the
in portal hypertension with the upper limit of normal ranging from portal system. The collateral vessels formed are thin walled and
10 to 12mm for these vessels. Dilatation of the splenic vein is associ- prone to rupture. The presence of collaterals is highly indicative of
ated with splenomegaly but it may be difficult to distinguish portal hypertension except in isolated splenic or mesenteric vein
between portal hypertension and increased splenic blood flow (due occlusion.
to the hyperdynamic splanchnic circulation) as aetiologies for the Ultrasound underestimates the extent of portosystemic collater-
dilatation. als, reportedly visualising 6590% of varices.1719 However, the vast
182
Portal vein
majority of described collaterals have been imaged by ultrasound9,17 n Umbilical vein. In utero the umbilical vein carries oxygenated
but only a few groups are regularly identified. blood from the placenta to the left portal vein. This involutes
The potential of large portosystemic collateral vessels to decom- after birth, forming the ligamentum teres in the falciform
press the portal venous system and decrease gastrointestinal haem- ligament. In portal hypertension a paraumbilical vein can
orrhage is controversial. The presence of a large splenorenal shunt dilate and carry blood from the left portal vein to the
has been linked with a reduction in bleeding from gastric varices20 umbilical region where it anastomoses with systemic veins
whilst other studies have not demonstrated a clear protective (superior and inferior epigastric veins) to form a caput
effect.21 The pattern of collateral development can influence direc- medusae. The enlarged umbilical vein is readily seen on
tion of flow in the portal vein. Flow may be reversed in the presence ultrasound, carrying blood away from the liver, as it courses
of a large splenorenal shunt. However, if decompression is mainly deep to the anterior abdominal wall musculature (Figs 12.11
due to a large umbilical vein then flow will be hepatopetal. In this and 12.12). It should be noted that a patent umbilical vein
situation flow may be reversed in the right portal vein and normal may be seen in normal subjects but it is less than 2mm in
direction in the left portal vein since the recanalised umbilical vein diameter and its velocity is not greater than 5cm/s.
arises from the left portal vein. n Splenorenal. These are seen as large tortuous vessels coursing
The common portosystemic anastomotic sites (Fig. 12.9) are: between the splenic hilum, upper pole of the left kidney and
left renal vein (Fig. 12.13).
n Gastric and lower oesophagus. Left gastric varices (also known as n Pericholecystic. These varices occur in the gallbladder wall
coronary vein varices) run from the portal/splenic vein to the especially in portal vein thrombosis, bypassing the
lesser gastric curve and may be seen through the left lobe of thrombosed vessel communicating with the intrahepatic
liver (Fig. 12.10). Short gastric varices run between the spleen portal branches. They can also communicate via subhepatic
and the greater gastric curvature and can be seen on ultrasound collaterals to subcostal veins.
using the spleen as a window. Both groups of varices converge n Pancreatico-duodenal. These varices are difficult to
at the gastro-oesophageal junction and can extend cranially via visualise on ultrasound. They communicate with superior
oesophageal varices to anastomose with the azygos vein and and inferior mesenteric veins as well as the left gastroepiploic
systemic circulation. Oesophageal varices are prone to bleeding veins.
and therefore numerous manoeuvres are available to prevent n Porta hepatis. Varices may be seen around the portal vein
haemorrhage at this site as discussed below. especially if it is thrombosed.
Gastro-oesophageal collaterals
Gastroepiploic
Coronary collaterals:
vein Right
Left
Portal vein
Splenorenal
collateral
Splenic vein
Superior
Umbilical vein mesenteric vein
collateral
Inferior
vena cava
Pancreatico-
duodenal
collaterals
Haemorrhoidal
collaterals
Figure 12.9 Major portosystemic collaterals. (Redrawn from Zwiebel WJ, Pellerito JS. Introduction to Vascular Ultrasonography,
5th edn. Elsevier Saunders, Philadelphia, 2004.)
183
CHAPTER 12 Vascular disorders of the liver
A B
A B
Figure 12.11 Recanalised umbilical vein in a patient with cirrhosis. A: B-mode shows a large vessel below the left lobe of liver.
B: Doppler shows venous blood flow towards the transducer and away from the liver.
184
Portal vein
A B
C D
Figure 12.12 Liver cirrhosis and varices in a 26-year-old woman with cystic fibrosis. A: Colour Doppler shows varices in the left upper
quadrant which, when followed caudally, continued (B) as a vessel (arrow) with flow away from the transducer. This vessel bypassed the
umbilicus. C: In the pelvis the vessel joins the inferior epigastric vein (arrow), which (D) joins the external iliac vein (arrow). There was no
umbilical collateral vessel or caput medusae in this patient. (Courtesy of Professor David Cosgrove.)
A B
Figure 12.13 Splenorenal varices. A: Varices are seen between the spleen and left kidney. B: A large collateral vessel (arrow) is seen
carrying blood away from the probe towards the left renal vein.
Other less common portosystemic anastomotic sites are haemor- therapy, endoscopic techniques (injection sclerotherapy or banding
rhoidal, gonadal, iliolumbar and retrosternal. of oesophageal varices), compression of actively bleeding varices
with a Sengstaken tube, surgical or transjugular intrahepatic porto-
systemic shunts (TIPS).
Management of portal hypertension
Surgical portosystemic shunts
One of the major life-threatening problems in portal hypertension
is bleeding varices. There are a variety of options available to The objective of all shunts is to decompress the portal system to
manage this problem. Management options consist of medical minimise the risk of variceal bleeding. There are numerous types
185
CHAPTER 12 Vascular disorders of the liver
of surgical shunts including portacaval, proximal and distal spleno- stents in the late 1990s brought with them lower complication
renal (Warren shunt), mesocaval and mesoatrial shunts. rates.22 TIPS may be regarded as a palliative procedure in end-stage
Non-selective shunts divert all the portal blood flow into the liver disease. The technique involves connecting the portal system
systemic circulation resulting in decompression of the entire portal to the right hepatic vein via an expandable stent. It avoids surgery
system and therefore varices. One of the simplest procedures to and is safe in severe liver failure. Indications include refractory
perform is the portacaval end-to-side shunt in which the portal vein ascites and varices and it has been shown to significantly reduce
is transected at the liver hilum and anastomosed to the inferior vena rebleeding compared to endoscopic management but at a cost of an
cava. These shunts produce immediate protection from variceal increased rate of encephalopathy.23,24 The majority of variceal bleeds
bleeding but they have a high rate of encephalopathy and may can be managed by endoscopic and medical treatment and TIPS is
worsen liver function. reserved for those who do not respond. It can also be employed
With selective shunts, such as the Warren shunt, liver encepha- prior to liver transplantation or if the patient is a poor surgical risk.
lopathy is less common. The Warren shunt consists of anastomos- The procedure is extremely effective in preventing haemorrhage
ing the splenic vein to the left renal vein. The left gastric vein, from gastro-oesophageal varices, reducing ascites and improving
umbilical vein, right gastroepiploic vein, pancreatic branches and the quality of life in end-stage cirrhosis. Complications include
other collateral vessels are ligated. This approach selectively decom- precipitation of encephalopathy and worsening liver function as the
presses the gastro-oesophageal varices and excludes the gastros- stent results in diversion of blood away from the liver. Other com-
plenic circulation from the rest of the portal system. plications include haemorrhage (Fig. 12.15) (serious intraperitoneal
When there is portal vein thrombosis, surgical shunts cannot be haemorrhage due to laceration of the portal vein or hepatic
performed. In these cases the Sugiura procedure may be performed. artery or puncture of the liver capsule) 12%, death (5%) and
This consists of splenectomy, devascularisation of the stomach and infection (12%).25 Ultrasound has an important role in the evalua-
lower oesophagus along with oesophageal transection to stop flow tion of the hepatic and portal veins pre-procedure as well as the
to the gastro-oesophageal varices and is very effective in preventing post-procedure assessment of shunt function and patency.
haemorrhage from these varices. The procedure is performed under fluoroscopic guidance. A cath-
The surgical shunt itself is usually difficult to directly visualise eter is passed via the internal jugular vein to the inferior vena cava
because of its retroperitoneal location and therefore Doppler is and into the right/middle hepatic vein. A tract is then formed
extremely useful in documenting the secondary changes in portal across the liver connecting the right portal vein with the hepatic
flow. Preoperative assessment of the portal venous system is essen- vein. A metal stent is sited to keep the shunt open. This results in
tial to assess the haemodynamic consequences of the shunt on immediate decompression of varices and improvement of the
portal flow and also to look for shunt stenosis and thrombosis in sequelae of portal hypertension.
the follow-up period. Surgical shunts are now rarely performed and The main problems with TIPS are stent occlusion and stenosis.
have been largely replaced by transjugular intrahepatic portosys- Occlusion or stenosis within the first few weeks is usually due to
temic shunt (TIPS). technical problems with the procedure. Late occlusion or stenosis
is related to neointimal hyperplasia (Fig. 12.16).
Direct portography with portosystemic gradient measurement is
Transjugular intrahepatic portosystemic still the gold standard in the assessment of TIPS function but this
shunt (TIPS) is invasive and utilises ionising radiation and iodinated contrast.
Therefore regular surveillance with ultrasound is used to detect
This minimally invasive procedure was first performed in 1969 but problems earlier to allow interventions such as angioplasty and
only became a widespread clinical application in the 1980s follow- thrombolysis. The 1-year stent patency is approximately 85% with
ing the introduction of metallic stents (Fig. 12.14). These uncovered these interventions, a figure that falls to approximately 50% in
stents were prone to occlusion and stenosis. The use of covered their absence. Despite its widespread use in screening for TIPS
A B
Figure 12.14 Normal transjugular intrahepatic portosystemic shunt (TIPS). A: B-mode shows a normally sited metallic TIPS stent
(arrow). B: Doppler shows a normal pulsatile waveform indicative of a widely patent stent.
186
Portal vein
A B
Figure 12.15 Transjugular intrahepatic portosystemic shunt (TIPS) in a patient with BuddChiari syndrome. A: The ultrasound shows
a large haematoma (thick arrows) adjacent to the stent (thin arrow). B: Computed tomography shows the extent of the haematoma (thick
arrow) adjacent to the stent (thin arrow). Note the heterogeneous liver attenuation and splenomegaly (S) due to BuddChiari syndrome.
A B
Figure 12.16 Transjugular intrahepatic portosystemic shunt (TIPS) stenosis. A: Spectral Doppler shows marked elevated (2.3m/s)
turbulent flow in the stent which had been normal several months earlier after insertion. B: Direct portography showed a mid-stent stenosis
(arrow) presumably due to neointimal hyperplasia. The portosystemic gradient was 21mmHg, which following dilatation reduced to
14mmHg with a good angiographic result (not shown).
dysfunction, Doppler data are inconsistent and its role in surveil- occur immediately after TIPS placement; both portal vein diameter
lance is controversial. The sensitivity and specificity vary widely in and mean velocity may increase, resulting in a marked increase in
the ultrasound detection of shunt dysfunction.2629 portal vein flow volume. Blood flow in the main portal vein is
Assuming a right portal vein to right hepatic vein TIPS, Doppler hepatopetal but flow within the intrahepatic portal veins may be
measurements (velocity, direction of flow and waveform) should hepatofugal. Knowledge of the wide spectrum of normal findings
routinely be performed at the portal venous end, midpoint and following TIPS is essential.
hepatic venous end of the shunt as well as the hepatic vein, main The most common site for stent stenosis is at the junction of the
portal vein and left portal vein. Several haemodynamic changes stent with the hepatic vein. There are several Doppler parameters
187
CHAPTER 12 Vascular disorders of the liver
which can be helpful in diagnosing stent stenosis but comparison In patients with cirrhosis, the reported incidence of portal vein
with the pre-procedure indices is essential. No one Doppler param- thrombosis (PVT) is 520%.3335 With more advanced stages of cir-
eter is sufficiently sensitive to be used in isolation to diagnose ste- rhosis there is a higher risk of PVT than in patients with compen-
nosis but use of several indices may be more helpful.30 Ultrasound sated liver disease.36 Doppler is the most sensitive technique to
contrast agents have been shown to improve sensitivity and spe- detect PVT in cirrhosis, with the prevalence of partial and complete
cificity in the diagnosis of shunt dysfunction.31,32 thrombosis being 1.8% and 4.4%, respectively, in one series.12 The
A shunt velocity of less than 50cm/s is highly suggestive of accuracy is less for branch PVT. PVT is not uncommonly a chance
stenosis. Also local high-velocity flow or areas of turbulence or a finding in cirrhosis and Amitrano etal.36 showed that only 57% of
change in velocity of greater than 100cm/s across the stent are cirrhotic patients with PVT were symptomatic. The presence of
suspicious of stenosis. symptoms depends on whether the thrombus is complete or partial
Stent occlusion is reliably diagnosed by Doppler with a high as well as rate of thrombus development. Clinical presentations of
sensitivity and specificity. However, trickle flow may be missed by PVT include variceal bleeding due to collaterals, refractory ascites
ultrasound and ultrasound contrast agents or formal portography and small bowel ischaemia/infarction.36 In acute thrombosis the
is essential to confirm this. thrombus may be anechoic and it may be difficult to differentiate
from a patent vessel, especially in an attenuating cirrhotic liver (Fig.
12.17). The ultrasound settings should be optimised, with the
Portal vein occlusion Doppler sensitivity set to pick up low flow and the vein axis made
less than 60 to the transducer before diagnosing portal vein throm-
The main causes of portal vein occlusion are due to thrombosis or bosis. A Valsalva manoeuvre may induce hepatofugal flow in a low
tumour invasion. The occlusion may be complete or partial and flow system by transiently increasing portal venous resistance. The
only affect a branch. The most common cause is portal hypertension addition of ultrasound contrast agents or the use of other imaging
due to cirrhosis. modalities may resolve the problem. The thrombus may dilate the
188
Hepatic artery
A B
Figure 12.18 Recanalisation of an old main portal vein thrombosis. A: B-mode shows an echogenic thrombus measured by
callipers. B: Colour Doppler shows flow around the thrombus.
vein. The superior mesenteric and splenic veins should be interro- HEPATIC ARTERY
gated to establish the extent of the thrombus. If these vessels are
not involved with thrombus they are usually dilated and exhibit
slow or reversed flow. As the thrombus matures it becomes more Anatomy and scanning techniques
echogenic and retracts resulting in partial recanalisation (Fig. 12.18).
More frequently cavernous transformation occurs (see below). The common hepatic artery arises from the coeliac axis; after the
False positives occur on ultrasound due to inadequate technique origin of the gastroduodenal artery, it becomes the hepatic artery
or insensitive equipment, low velocity to-and-fro portal flow, which proper. It enters the liver adjacent to the portal vein and then
is difficult to detect with Doppler, and failure to use Doppler in divides into right and left hepatic branches supplying the respective
acute anechoic thrombus. False negatives may be due to the detec- liver lobes. The artery accompanies the portal vein, which together
tion of flow within collateral vessels erroneously mistaken for the with the bile duct forms the portal triad and these terminate at the
main portal vein. acinus. The hepatic artery crosses posterior to the common bile duct
In chronic portal vein thrombosis a network of collateral vessels (CBD) and anterior to the portal vein at the level of the porta hepatis
(cavernous transformation) may develop within a few weeks and provides an important reference point for measuring the CBD
around the thrombosed portal vein (Fig. 12.19). Spectral Doppler (Fig. 12.2). Usually the hepatic artery has divided and so the right
demonstrates portal flow in the vessels of the cavernoma. Portosys- hepatic artery branch is most often imaged as it passes between the
temic and intrahepatic collateral vessels may form in chronic portal bile duct and portal vein. The hepatic artery always lies medial to
vein thrombosis. the common bile duct throughout its course and similar to the right
In malignancies such as hepatocellular carcinoma it is very portal vein, the right branch traverses the liver substance for a few
important to differentiate tumour thrombus from bland thrombus. centimetres before dividing into the anterior and posterior branches,
Massive dilatation of the portal vein (>20mm) is suggestive of while the left branch curves anteriorly, dividing into segmental
tumour but this is not specific. Tumour thrombus can be differenti- branches of the parts of the liver it supplies.
ated from bland thrombus by the presence of an arterial spectral There are numerous vascular anomalies that can occur; the
waveform in the thrombosis (Fig. 12.20). This is important as the common hepatic artery can aberrantly arise from the superior
presence of tumour thrombus carries a grave prognosis and renders mesenteric artery (SMA) in approximately 3% of normal variants
the tumour unresectable. Tumour may extrinsically compress the or alternatively the right hepatic artery may arise from the SMA in
portal vein, resulting in stenosis (Fig. 12.21). 11% or the left hepatic artery is replaced with a branch from the left
gastric artery.37
The hepatic artery only contributes to 25% of the blood supply
Portal vein aneurysm of the liver where it is predominantly supplied by the portal vein.38
This dual supply explains the relatively low prevalence of hepatic
Aneurysm of the portal vein is very rare. It may be seen in portal infarction.
hypertension and infective aetiologies. It is important to differenti- The hepatic artery can be traced from the coeliac axis and is easily
ate it from a hepatic artery aneurysm, which carries a worse visualised in the mid-clavicular line just beneath the costal margin
prognosis. in a longitudinal oblique plane. It is at the porta hepatis where the
hepatic artery crosses between the common bile duct and portal
Portal vein gas vein that the artery is commonly assessed, particularly with respect
to Doppler indices.
Portal venous gas is seen in bowel ischaemia/infarction, ulceration,
gastrointestinal sepsis and bowel obstruction. In these conditions it
has a poor prognosis. However, more recently improved imaging Normal findings
techniques have demonstrated it in more benign conditions such as
pneumatosis coli, obstructive airways disease, iatrogenic enema Doppler ultrasound can provide a quantitative measure of blood
administration, colonoscopy and gastrostomy tubes. Tiny echo- flow to the liver. The hepatic artery commonly demonstrates a
genic foci are seen in the portal vein. Spectral Doppler demonstrates splanchnic waveform on Doppler studies and normal main hepatic
spikes of high signal superimposed on the background portal vein artery peak velocities are variable partly because of the angle of
trace (Fig. 12.22). insonation (Doppler angle) which should be between 45 and 60.
189
CHAPTER 12 Vascular disorders of the liver
A B
190
Hepatic artery
A B
Figure 12.21 Portal vein stenosis in a case of pancreatic carcinoma. A: Doppler from the prehepatic portal vein (proximal to a
stenosis) shows a normal flow pattern. B: A tumour mass (arrow) is seen compressing the portal vein. The peak velocity distal to this site
is elevated (91cm/s) with spectral broadening.
In the fasting state the hepatic artery has a low resistance flow are fragile with an increased propensity to haemorrhage. In the
pattern with a peak systolic velocity of 3040cm/s and a diastolic liver, ultrasound can demonstrate vascular malformations. Ana-
flow of 1015cm/s.39 tomically, three different patterns of abnormal vascular communi-
It is widely accepted that changes in the haemodynamic circula- cations can occur in liver: portal vein to hepatic vein (portovenous),
tion of the liver occur with chronic liver disease where there is an hepatic artery to hepatic vein (arteriovenous) and hepatic artery to
increase in hepatic arterial velocity with increasing fibrosis and portal vein (arterioportal), with the most common being arteriov-
progression to cirrhosis. Owing to the variation in using the velocity enous (Fig. 12.24). Only 58% of patients with these vascular mal-
measurement on its own, many research studies have used the formations are symptomatic. When symptomatic, patients present
resistive index (RI) and being a ratio, it is independent of the with high-output cardiac failure, biliary ischaemia (which, when
Doppler angle. Hepatic artery resistive index (RI) is calculated as severe, can progress to biliary and hepatic necrosis and lead to acute
(Peak systolic velocity End diastolic velocity)/Peak systolic veloc- liver failure), or portal hypertension.4652
ity. Typical values range between 0.7 and 0.8. Acquired arteriovenous fistulae are most commonly traumatic
Previous studies in patients with chronic liver disease have dem- secondary to liver biopsy, transhepatic biliary drainage procedures,
onstrated an increase in hepatic artery RI in chronic liver disease, surgery, neoplasms or rupture of a hepatic, superior mesenteric or
which has been thought to be related to the architectural derange- splenic artery aneurysm.
ment that occurs within the liver with increasing severity of
disease.4043 The reproducibility of such data, however, has been
shown to be unreliable, with varying reports of success from differ-
ent research groups. This is predominantly owing to the fact that HEPATIC VEINS
the RI is affected by many variables such as age and heart rate and
most studies have shown no correlation with histology.44
Anatomy and scanning technique
Hepatic artery aneurysms
The blood from the sinusoids of the liver parenchyma enter the
The common sites of arterial aneurysms in following order are hepatic terminal venules where these unite to form larger veins,
infrarenal aorta, iliac arteries, splenic artery followed by the which can vary in number and position although typically in the
common hepatic artery. Ultrasonic findings demonstrate a hypoe- majority of the population there are three major veins: the right,
choic mass which shows marked turbulent flow on colour Doppler middle and left hepatic veins which empty into the superior part
(Fig. 12.23). The commonest cause is iatrogenic (following biopsy) of the inferior vena cava (IVC). They are best imaged in the trans-
but other causes include trauma, liver transplantation, transarterial verse plane. They are larger in calibre than the portal veins and can
chemo-embolisation, vasculitides (polyarteritis nodosa), sepsis and be differentiated from them by their relatively thin anechoic walls
they have been reported in chronic pancreatitis.45 These aneurysms compared to the brighter thicker walls of the portal triads (contain-
commonly rupture (up to 80%) with catastrophic consequences and ing the portal vein, bile duct and hepatic artery) that are encased
therefore should be treated urgently. by echogenic fibrous walls (extension of Glissons capsule). The
hepatic veins do not have valves. The veins run superiorly and
posteriorly, curving towards the IVC, and the vessel calibre
Hereditary haemorrhagic increases as they approach the IVC.
telangiectasia (HHT) The right hepatic vein lies in the coronal plane and empties sepa-
rately into the IVC 1cm below the diaphragm/right atrium. The
This is an autosomal dominant condition characterised by multiple middle hepatic vein passes from the position of the gallbladder fossa
small aneurysmal telangiectases affecting the skin, mucous mem- and joins the left to form a short common trunk and both empty into
branes, gastrointestinal tract, brain, liver and lungs. These vessels the anterolateral aspect of the IVC but enter separately in 1535%.
A B
Figure 12.23 Hepatic artery pseudoaneurysm secondary to endocarditis. A: Colour Doppler shows an aneurysm arising from the
hepatic artery with turbulent flow in it (arrow). B: A selective coeliac axis angiogram revealed a bilobed pseudoaneurysm (arrow) arising
from the left hepatic artery which was successfully embolised.
192
Hepatic veins
A B
Understanding the portal and venous anatomy is essential in The hepatic veins are generally easily visualised intercostally or
understanding how the liver is divided into segments based on the subcostally. The left and middle hepatic veins are best assessed in
Couinauds classification.1 This system has become widely accepted a transverse oblique plane at the xiphisternum while the right
and is particularly useful when a precise description of the position hepatic vein is best assessed intercostally. Sometimes owing to the
of a lesion is required, particularly with respect to planning surgery. cardiac pulsations, the middle hepatic vein can be assessed in
This system based on the anatomy of the portal and hepatic veins the intercostal plane but should be carefully distinguished from the
is considered more accurate than a biliary segmental approach. The right hepatic vein.
major hepatic veins course between the lobes and segments and all
drain cephalically at confluence with the inferior vena cava (IVC)
as described above. The middle hepatic vein runs within the main Normal anatomical variations
lobar fissure dividing the liver into two main lobes (right and left),
thereby separating segments IIV from segments VVIII (Fig. The variation in branching and presence of accessory veins of the
12.25). The left hepatic vein (LHV) on the other hand runs within hepatic venous system are relatively common. The most common
the left intersegmental fissure dividing the left lobe into medial and accessory vein drains the anterosuperior segment of the right lobe
lateral segments, i.e. separating segments II and III from segment (segment VIII) and is present in approximately 30% of the popula-
IV. Lastly, the right hepatic vein runs in the right intersegmental tion. This accessory vein drains either into the middle or right
fissure dividing the right lobe of the liver into anterior and posterior hepatic vein, the former being more common.53 Small inferior veins
segments, separating segments V and VIII from segments VI and drain from the caudate and medial aspect of the right lobe directly
VII, respectively (Fig. 12.26). The portal vein, on the other hand, into the IVC. This drainage pattern explains the behaviour of the
separates the superior and inferior segments of the liver, i.e. seg- caudate lobe in cirrhosis and the characteristic computed tomogra-
ments II from III, segments IVa from IVb and segments V and VIII phy (CT) enhancement pattern seen in BuddChiari syndrome.
from segments VI and VII. Therefore in general, the portal vein Another venous anomaly is a large accessory right hepatic vein
divides the segments superiorly and inferiorly while the hepatic entering the IVC several centimetres inferior to the main venous
veins separate the anterior from the posterior segments (Fig. 12.1). confluence in 610% of people. Smaller accessory veins of the LHV
193
CHAPTER 12 Vascular disorders of the liver
Hepatic vein
velocity tracing A A
C V C
D
S
occlusion of the lumina of the hepatic veins with or without involve- Hepatic venous waveforms in cardiac
ment of the IVC. and pulmonary disease
BuddChiari syndrome can be either primary or secondary; the
primary type is caused by thrombosis or intrinsic luminal web, and Alteration of the hepatic venous waveform occurs in many cardiac
the secondary type is caused by tumour invasion or extraluminal and pulmonary diseases.
compression. Dilatation of the hepatic veins is a common finding in both condi-
The aetiology of BuddChiari syndrome varies and is most com- tions with increase in the retrograde flow which is most commonly
monly idiopathic (66%) although there is an increased risk with due to tricuspid regurgitation (TR) (Fig. 12.33). In mild TR there is
blood coagulopathies, such as polycythaemia rubra vera, chronic increase in the V wave with attenuation of the S wave. In severe TR
leukaemia, anaemia and paroxysmal nocturnal haemoglobinuria. there is fusion of the S and V waves with systolic reversal of the
Other benign causes include the oral contraceptive pill, pregnancy S wave.
and congenital abnormalities, particularly with obstructing mem- In right ventricular dysfunction, due to pulmonary and cardiac
branes. Extension of tumours into the hepatic veins can also be disease, the A wave amplitude may be increased due to right atrial
caused by tumour extension typically seen with hepatocellular hypertrophy, which with further deterioration is accompanied by
carcinoma (HCC), renal cell carcinoma and adrenocortical attenuation of the S wave followed by tricuspid regurgitative
carcinoma. changes.
195
CHAPTER 12 Vascular disorders of the liver
A B
Figure 12.32 Veno-occlusive disease following bone marrow transplantation. A: The main portal vein is patent but shows reverse
flow. All three main hepatic veins were also patent (not shown). B: Following treatment the portal venous flow normalises in direction.
196
References
Peliosis hepatis
This is a rare disorder where blood-filled cavities of varying sizes
(mm to cm) develop within the liver. It is different from haeman-
giomas where there are portal tracts and stroma within these blood-
filled spaces. The diagnosis can only be confirmed histologically.
There is an association with immunosuppressed patients and those
taking anabolic steroids. Doppler sonography is non-specific and
may show single or multiple masses of varying and heterogeneous
Figure 12.33 Doppler trace showing tricuspid regurgitation. echogenicity66 (Fig. 12.34). The assessment with contrast ultrasound
has not been fully described and anecdotally the lesion can demon-
strate mild enhancement but appears bland.
REFERENCES
1. Couinaud C. Liver anatomy: portal (and suprahepatic) or biliary
segmentation. Dig Surg 1999;16(6):459467.
2. Hosoki T, Arisawa J, Marukawa T, et al. Portal blood flow in
congestive heart failure: pulsed duplex sonographic findings.
Radiology 1990;17:733736.
3. Wachsberg R, Needleman L, Wilson DJ. Portal vein pulsatility in
normal and cirrhotic adults without cardiac disease. J Clin Ultrasound
1995;23:315.
4. Freeny PC. Portal hypertension and hepatic veno-occlusive disease.
Radiology 1986;4:110.
5. Vorobioff J, Bredfeldt JE, Groszmann RJ. Increased blood flow through
the portal system in cirrhotic rats. Gastroenterology 1984;87:11201126.
6. Benoit JN, Womack WA, Hernandez L, Granger DN. Forward and
backward flow mechanisms of portal hypertension. Relative
contribution in the rat model of portal vein stenosis. Gastroenterology
1985;89:10921096.
7. Sikuler E, Groszmann RJ. Interaction of flow and resistance in
maintenance of portal hypertension in a rat model. Am J Physiol
1986;250:205212.
8. Gorg C, Riera-Knorrenschild J, Dietrich J. Pictorial review: colour
Doppler ultrasound flow patterns in the portal venous system. Br J
Radiol 2002;75:919929.
9. Zweibel WJ. Sonographic diagnosis of hepatic vascular disorders.
Semin Ultrasound CT MRI 1995;16:3448.
Figure 12.34 Multiple hypoechoic and hyperechoic rounded 10. Moriyasu F, Nishida O, Ban N, et al. Congestion index of the portal
lesions within the liver with minimal vascularity. These features are vein. AJR Am J Roentgenol 1986;146:735739.
non-specific but biopsy revealed peliosis hepatis. (Courtesy of Dr 11. Rector WG, Hoefs JC, Hossack KF, Everson GT. Hepatofugal flow in
Pilcher.) cirrhosis: observations on hepatic haemodynamics and the nature of
arterioportal communications. Hepatology 1988;8:1620.
12. Gaiani S, Bolondi L, Li Bassi S, et al. Prevalence of spontaneous
hepatofugal portal flow in liver cirrhosis. Clinical and endoscopic
Cannon A waves are seen in atrioventricular dissociation (com- correlation in 228 patients. Gastroenterology 1991;100:160167.
plete heart block) due to atrial systole against a closed tricuspid 13. Ohnishi K, Saito M, Sato S, et al. Direction of splenic venous flow
valve. In atrial fibrillation the A wave is lost. assessed by pulsed Doppler flowmetry in patients with a large
splenorenal shunt. Relation to spontaneous hepatic encephalopathy.
Gastroenterology 1985;89:180185.
Hepatic vein transit times 14. Bolondi L, Gandolfi L, Arienti V, et al. Ultrasonography in the
diagnosis of portal hypertension: diminished response of portal
The advent of contrast ultrasound has allowed functional assess- vessels to respiration. Radiology 1982;142:167172.
ment of the vascularity of the liver. These microbubbles can be used 15. Bolondi L, Mazziotti A, Arienti V, et al. Ultrasonographic study of
as a tracer and the theory is that in the presence of chronic liver portal venous system in portal hypertension and other portosystemic
disease or when there is alteration of the blood flow through the shunt operation. Surgery 1984;95:261269.
16. Cottone M, Sciarrino E, Marceno MP, et al. Ultrasound in the screening
liver, for example in patients with metastases, this causes arteriov-
of patients with cirrhosis with large varices. BMJ 1983;533:287.
enous shunting. Therefore, the time taken for a contrast agent to 17. Lafortune M, Patriquin H, Pomier G, et al. Haemodynamic changes
travel through the liver parenchyma and arrive in the hepatic vein in portal circulation after portosystemic shunts: use of duplex
will be shortened in contrast to normal healthy individuals. There sonography in 43 patients. AJR Am J Roentgenol 1987 149:701706.
has been much research into utilising this technique, particularly 18. Subramanyam B, Balthazar E, Madamba M, et al. Sonography of
197
CHAPTER 12 Vascular disorders of the liver
198
CHAPTER
13 Liver transplantation
Suzanne M. Ryan, Maria E.K. Sellars and Paul S. Sidhu
A B
Figure 13.3 Nodule in cirrhosis. A: A new focal lesion of low reflectivity (arrow) is seen in this patient with cirrhosis. B: A microbubble
contrast-enhanced ultrasound demonstrates that this is a benign regenerative nodule (arrow).
ultrasound, making a definite diagnosis of a de-novo hepatocellular Ultrasound is not reliable in the delineation of more complex
carcinoma on routine B-mode imaging ultrasound unreliable.8 anatomy of the portal vein. Portal venous spectral Doppler ultra-
Hence any new nodule in a patient under surveillance for chronic sound in normal patients should give a continuous, undulating
liver disease should be viewed with suspicion (Fig. 13.3). Ultra- hepatopetal trace, although there is considerable variation in flow
sound for early detection of hepatocellular carcinoma in a screening velocity. In the cirrhotic liver, portal hypertension develops, with
population has sensitivities of 85100%, specificities of 8198%, and the increase in pressure accounting for the ensuing complications.
positive predictive values of 5478%.8 The use of contrast-enhanced Portal velocity and portal venous flow vary inversely with the
ultrasound (CEUS) may help to further characterise the lesions.9,10 hepatic venous pressure gradient.14 Portal hypertension may also
The sensitivity and specificity of CEUS in the diagnosis of HCC result in splenomegaly, which may be readily assessed by ultra-
have been found to be similar to that of contrast-enhanced com- sound and monitored over time. Recanalisation of the umbilical
puted tomography (CECT), with enhancement on the arterial vein in the ligamentum teres may be seen, inferring patency of the
phase, and washout on the portal venous phase, taken as diagnostic portal vein with antegrade flow.
for HCC.11 As many as 25% of lesions <2cm with arterial enhance- Portal venous thrombosis is a common complication of chronic
ment but without venous washout in cirrhotic liver remain stable liver disease, occurring in 510% of patients with end-stage cirrho-
or regress over time and are not HCC.12 sis.15 Although not an absolute contraindication to transplantation,16
preoperative detection is vital as the full extent of any thrombus
needs to be demonstrated for optimal surgical planning.17 B-mode
Other malignancies imaging of thrombus may show the presence of hyper-reflective
Cholangiocarcinoma is seen most commonly as a consequence of material lying within the portal vein, seen as either complete occlu-
primary sclerosing cholangitis, seen on ultrasound as a hyper- to sion or a tongue of thrombus with some surrounding flow. Ultra-
hypoechoic ill-defined mass, usually in the region of the liver sound is both sensitive and specific in the detection of portal venous
hilum, giving rise to dilated intrahepatic ducts. Proven cholangi- thrombosis, with the small proportion of inaccurate investigations
ocarcinoma is a contraindication to transplantation. Fibrolamellar attributed to a diminished flow rate.18 Although CDUS of the portal
hepatocellular carcinoma (FLHCC) is a subtype of HCC, has dis- vein has a reported sensitivity of 87.594.0% compared to indirect
tinct radiographic features and a better prognosis. FLHCC occurs portography, the use of CEUS improves colour and spectral Doppler
primarily in young adults, without any associated cirrhosis or signal in difficult cases.19 Ultrasound is sufficiently accurate, as
elevation of alpha-fetoprotein and is relatively slow growing. On compared to CECT, in predicting portal venous patency for it to be
ultrasound, FLHCC usually presents as a large solitary mixed advocated as the sole means of assessment in patients with no prior
reflective mass within a non-cirrhotic liver. Surface lobulations, surgery.20 Low flow or reversal of flow in the portal vein may be
punctate calcification and a central fibrous scar, similar to that seen better documented with CEUS, a reliable indicator of flow direction
in focal nodular hyperplasia, are evident in the majority of patients.13 (Fig. 13.4).21 Microbubble contrast is reported to improve portal vein
These patients may be candidates for either resection or transplan- visualisation in up to 94% of patients with a suboptimal baseline
tation even with large tumours. The detection of an extrahepatic CDUS examination.19 In equivocal cases either magnetic resonance
tumour with or without hepatic metastases excludes the patient venography (MRV) or alternatively indirect portography should be
from transplantation. performed, but should rarely be needed with the availability of
microbubble contrast enhancement. In patients with HCC, malig-
nant thrombus can be inferred by the presence of enhancement
Preoperative vascular assessment within the thrombus with CEUS whereas absence is more likely in
benign thrombus.22 A venous conduit may be fashioned from the
patent superior mesenteric vein (SMV) to the donor graft; demon-
Portal vein stration of SMV patency is required when portal vein thrombus is
The main portal vein usually bifurcates into the right and left portal seen. However, this is difficult to achieve even with the use of
veins, readily demonstrated by CDUS. The main portal vein may microbubble enhancement, and indirect portography, CECT or
trifurcate with an early branching pattern in the right hepatic lobe. MRV may be necessary.
201
CHAPTER 13 Liver transplantation
Hepatic veins
The main branches of the hepatic vein drain into the IVC. Accessory
right hepatic veins occur in 6% of people and can cause increased
bleeding if unrecognised before surgery. The normal hepatic venous
waveform is triphasic but loss of pulsatility and damping occurs in
conditions of decreased liver compliance (such as cirrhosis) as well
as other causes of raised intra-abdominal pressure such as ascites.23
Occlusion of the venous flow may occur at the level of the post-
sinusoidal vein to the IVC and right atrium in BuddChiari syn-
drome, with CDUS assessment of hepatic venous patency usually
definite in the normal patient.24 Non-visualisation of the veins is not
diagnostic of occlusion and use of microbubble contrast is reported
to improve operator confidence (Fig. 13.5).16 Hepatic venography
remains the reference standard used in diagnosis of hepatic vein
occlusion, demonstrating a spider web appearance due to occlusion
of the hepatic veins.
Figure 13.4 Flow reversal in the portal vein. On the baseline Hepatic artery
colour Doppler ultrasound examination, no flow was seen in the The spectral waveform pattern of the hepatic artery may give indi-
portal vein. With contrast-enhanced ultrasound, contrast is seen to rect clues to ongoing disease changes. For example, in the presence
fill the portal vein (arrow) late and flow in a reversed direction. This of cirrhosis, there is a hyper-dynamic hepatic arterial circulation
confirms portal vein patency, important preoperative information.
B
A
Figure 13.6. Hepatic artery in cirrhosis. The configuration of the Figure 13.7 Occluded transjugular intrahepatic portosystemic
spectral Doppler waveform in the hepatic artery of a patient with shunt. The reflective walls of the stent are seen with no
advanced liver cirrhosis, and a patent portal vein, demonstrates a enhancement of the lumen (arrow) following administration of
high resistive index reflecting the increased stiffness of the liver. microbubble contrast.
Portal-venous shunts
Transjugular intrahepatic portosystemic (TIPS) shunt, the creation
of a shunt between the portal and hepatic venous systems, is a
common procedure in the management of variceal haemorrhage
and intractable ascites secondary to portal hypertension. This is
often a holding measure whilst awaiting transplantation. Unfortu-
nately TIPS stents have a significant rate of stenosis and occlusion
and require frequent monitoring. Clearly therefore, non-invasive
imaging is preferable in this group of patients.26 B-mode imaging
of the TIPS stent will demonstrate a highly echogenic grid pattern,
representing the wall of the stent, through which the internal lumen
often cannot be adequately visualised. The exact range of normal Figure 13.8 Portal vein to inferior vena cava shunt. There is
flow velocity is disputed. Flow velocities in excess of 200cm/sec flow reversal in the portal vein (short arrow) with an enlarged inferior
should be regarded as suspicious for a narrow stent.27 Contrast- vena cava with turbulent flow note (long arrow) in a patient with a
enhanced ultrasound confirms patency of the TIPS stent and will surgical portosystemic shunt.
identify narrowing (Fig. 13.7).28 A suspected TIPS stenosis by any
criteria should be referred for further imaging, either with MRV or
transjugular venography. End-to-side portacaval shunts may be Liver volume assessment
demonstrated with some difficulty by ultrasound, but there are no
data published regarding the accuracy in comparison with direct
Of critical importance in determining the successful outcome of
venography (Fig. 13.8).29
transplantation, particularly with the advent of split liver grafts in
the fields of paediatric and living related donor transplantation, is
Assessment of living related donors the size of the graft used. A donor liver should be no less than 50%
of the size of the replaced native liver, since below this there is a
Ultrasound of the abdomen is routinely performed as part of the risk of hepatic failure postoperatively. Conversely, a graft may be
radiological work-up of living related donors, with visualisation of up to 20% larger than the explanted liver. Grafts above this size
all of the solid organs, in order to confirm their normality, and to may cause compression of the adjacent vascular structures and be
exclude liver parenchyma changes and unsuspected lesions. The poorly perfused. In all cases, mismatches lead to problems in
focus of the examination, however, is the hepatic vasculature, with performing the vascular and biliary anastomoses.30,31 Ultrasound
particular attention paid to the anatomy of the hepatic veins, as this determination of volume can be performed by measuring the cross-
has an influence on choice of resection. In addition to ultrasound, sectional area of the liver as seen on consecutive scans in the sagittal
donors will routinely undergo dual phase CECT of the liver (portal plane at 1cm intervals and adding these together, a technique that
and hepatic venous phases), thus giving the surgeon the maximum has been shown to be both accurate and reproducible.32 However,
possible information with which to plan surgery. this is a time-consuming procedure and has now been superseded
203
CHAPTER 13 Liver transplantation
Suprahepatic vena
cava anastomosis
Coeliac trunk
Portal vein
anastomosis
Figure 13.9 Conventional liver transplantation. Donor-recipient sites for vascular and biliary anastomoses. The gallbladder is normally
removed. (Modified from Sidhu PS and Baxter GM (eds), Ultrasound of Abdominal Transplantation. Thieme, Stuttgart, 2006.)
Graft IVC
immunosuppressive drug therapy, but other complications are vascular complications, particularly hepatic artery thrombosis
unique to the surgical transplantation procedure performed. The (HAT). There is evidence to suggest that routine ultrasound of all
main postoperative complications may be grouped into vascular the hepatic vessels on the first day following liver transplantation
and non-vascular abnormalities.36,37 Clinical and laboratory findings and, subsequently, every 3 days in the early postoperative phase is
are often non-specific, making the clinical diagnosis and manage- beneficial.38 Any clinical change would also prompt immediate
ment of these complications difficult. Ultrasound is normally the ultrasound of the hepatic artery as after transplantation the donor
first line of evaluation in the post-transplant phase, used when there biliary system is entirely dependent on hepatic arterial blood
is clinical evidence of graft dysfunction, or routinely for the early supply, in particular the right hepatic artery.39 In the early postop-
detection of complications before any clinical suspicion of erative period, the spectral Doppler waveform can be quite varia-
abnormality. ble, from the presence of high forward diastolic flow to the absence
of any flow at all in diastole. Absence or reversal of flow in diastole
Normal postoperative ultrasound does not appear to indicate a predisposition for thrombosis in the
immediate postoperative period.40 While absence of any colour or
spectral Doppler flow in the hepatic artery can be suggestive of
Following transplantation the liver appears of normal smooth
thrombosis in the immediate post-transplant period, other factors
homogeneous reflectivity as would a normal liver in any patient.
may contribute to an undetectable hepatic artery signal.16 Reper-
Often during the procedure haemorrhage occurs or residual ascites
fusion oedema may occur within the graft for up to 72 hours post
may be present, with small amounts of free fluid seen, occasionally
transplant, leading to an increased RI, and diminished Doppler
tracking along the falciform ligament (Fig. 13.11). The biliary tree
arterial signal. Furthermore, any cause of oedema or inflammation
is normal, although areobilia may be encountered in patients with
in the transplant may produce a similar result; viral hepatitis or
a fashioned choledochojejunostomy (Roux-en-Y loop). All the
rejection can cause severe oedema that can markedly damp the
vessels (hepatic artery, portal vein, IVC and hepatic veins) should
hepatic artery waveform.41
be patent (Fig. 13.12). Colour and spectral Doppler imaging of the
vessels will confirm patency, with interrogation of the main, left
and right hepatic artery of importance. The normal hepatic artery Hepatic artery thrombosis
should return a low resistance spectral pattern with high forward
velocity in end diastole. The RI of a normal hepatic artery is 0.50.8. The quoted incidence of HAT is 5% of adults and 918% of
The normal acceleration time (from end diastole to the first systolic children.42 HAT is a serious complication with mortality of 50
peak) is less than 0.08 second. The portal vein should demonstrate 58%; re-transplantation is often required and even following
a continuous hepatopetal flow with minor respiratory modulation, re-transplantation mortality remains high at 2730%. Risk factors
with the hepatic waveform demonstrating variation during the for HAT include a significant difference in hepatic artery calibre
cardiac cycle. between the donor and recipient, an arterial conduit, excessive cold
ischaemia time, ABO blood type incompatibility, cytomegalovirus
infection, acute rejection, and previous stenotic lesion of the coeliac
Abnormal postoperative ultrasound axis.42 Clinically, impending or complete occlusion of the hepatic
artery is often indicated by generalised non-specific deterioration
of the liver function tests or a biliary leak.39 If the biliary tree sur-
Vascular complications vives the initial ischaemic event, then biliary strictures may develop,
particularly at the hilum of the left and right ducts.43 This in turn
Hepatic artery may lead to infective complications such as cholangitis and biliary
abscess formation. Hepatic abscess formation is also more common
In the first 2 weeks following liver transplantation, routine colour with chronic ischaemia.44
and spectral Doppler ultrasound plays an important role in the The normal Doppler waveform in the hepatic artery is of a broad
detection of both clinically evident and clinically unsuspected systolic peak, high diastolic velocity and low resistive index. Any
205
CHAPTER 13 Liver transplantation
A
B
A B
Figure 13.15 Liver ischaemia and infarction with hepatic artery thrombosis. A: There are area of altered reflectivity (arrows)
in the liver of this patient with hepatic artery thrombosis (same patient as in Fig. 13.13), suggesting areas of ischaemia and infarction.
B: On contrast-enhanced ultrasound these areas (arrows) are more obvious and likely to be areas of infarction. The liver graft is not
viable and re-transplantation is necessary. The arrowhead points to a subhepatic fluid collection.
reduces the possibility of detecting a raised peak systolic velocity. serial examinations accurately excludes significant hepatic artery
The use of CEUS may be beneficial in patients with HAS, making disease. The diagnosis of HAS may be inferred using ultrasound if
it easier to accurately identify the exact site of the stenosis and to serial hepatic arterial spectral Doppler waveforms show a progres-
identify collateral vessel formation, if present.51 sive reduction in arterial velocity proximal to the site of the stenosis
There are two situations where the diagnosis of HAS should be and the development of the tardus parvus waveform in the absence
made with caution: during surgery using intraoperative Doppler of parenchyma abnormality.
ultrasound, and in the early (<48 hours) postoperative period. Fre- Hepatic artery stenosis and occlusion over a long period may
quently the postoperative low RI will over time return to normal. have less devastating consequences to the liver graft. If the hepatic
Therefore follow-up ultrasound is recommended when a low RI is artery narrows and subsequently becomes occluded graft function
detected in the HA in the presence of normal hepatic function in may be preserved due to the formation of a number of arterial col-
the postoperative period. If clinical suspicion for HAS remains high, laterals. Furthermore, when a choledochojejunostomy is fashioned
a normal ultrasound examination should not prevent CECT angi- in children or adults replacing a recipient common bile duct, the
ography, as HAS may not manifest the tardus parvus Doppler highly vascular jejunal bed allows rapid collateralisation and pro-
ultrasound abnormality.49 However, in the absence of a tardus tects the graft from acute ischaemic complications. In the presence
parvus waveform the HAS is less severe, but nevertheless impor- of a good collateral supply an entirely normal intrahepatic spectral
tant to identify, in order that appropriate clinical management is Doppler waveform may be demonstrated even in the presence of
instituted. A normal hepatic artery spectral Doppler waveform on complete main hepatic artery occlusion. A more common finding
is the damping of the intrahepatic systolic arterial spectral Doppler
waveform with the maintenance of high diastolic spectral Doppler
waveform. Hence the presence of hepatic arterial flow within the
graft must be taken in the clinical context of graft function. Although
late arterial occlusion may be clinically silent, the majority of
patients suffer one or more complications.42
A B
Figure 13.18 Hepatic artery stenosis direct visualisation. A: The primary Doppler ultrasound criterion of arterial stenosis in any
location of the body is a marked focal increase in peak systolic velocity by direct evaluation of the site of the stenosis. In this case a
velocity of 2.10m/s is seen in the transplant hepatic artery in the subhepatic space. B: The angiographic study demonstrates the stenosis
of the hepatic artery (arrow) as seen on the ultrasound examination.
208
Early postoperative ultrasound
A B
C D
Figure 13.19 Hepatic artery pseudo-aneurysm. A: A cystic structure with surrounding soft tissue changes (arrows) close to the site
of the surgical anastomoses in the transplant patient. B: There is colour filling of the central cystic aspect demonstrating the classical
yingyang sign of a pseudo-aneurysm caused by turbulent arterial flow. C: The pseudo-aneurysm (arrow) is identified on the selective
angiographic study. D: The pseudo-aneurysm has been treated successfully with coil embolisation (arrow).
209
CHAPTER 13 Liver transplantation
document portal vein stenosis in the absence of any thrombus.55 prothrombotic state. Acute rejection with diminished portal venous
Percutaneous transhepatic dilatation of the portal vein stenosis may flow has been proposed as a cause of portal vein thrombosis and
be successful.56 However, if this technique fails, patients should may be an important factor in small children with full size liver
be treated by portosystemic shunt or revision of the portal vein grafts.55 Portal vein thrombus may be demonstrated on ultrasound
anastomosis. If adequate collateralisation occurs, with both portal as internal echoes within the portal vein, expansion of the portal
vein stenosis and portal vein thrombosis, graft survival may be vein and loss of colour Doppler signal. Reduction in the hepatic
unaffected. artery RI accompanies portal vein thrombosis and may be a helpful
secondary sign for the determination of portal vein thrombosis (Fig.
13.21). A hepatic artery RI of 0.50 or less, together with an equivocal
Portal vein occlusion finding at portal venous CDUS, is reported to have a specificity of
Portal vein occlusion following liver transplant is uncommon, 100% and a sensitivity of 44% for portal vein thrombosis.57 Eventu-
occurring in less than 2% of patients, more often in children.36,42,53 ally, an acute thrombus becomes anechoic; CDUS may show lack
Portal vein thrombosis is invariably related to technical difficulties: of portal venous flow and CEUS may be used to increase the con-
malalignment with a redundant length of portal vein, leading to fidence in diagnosis.2,15
kinking and stricturing. Other predisposing factors include previ-
ous portal vein shunt surgery, previous portal vein thrombosis and
Portal vein gas
sclerosis, vessel trauma from a portal cannula and underlying
Intraportal venous gas is occasionally seen as echogenic shadowing
within the portal vein, and is a more common finding than previ-
ously recognised. While it may be secondary to necrotic bowel, or
intra-abdominal sepsis, it can also be an incidental finding post liver
transplantation without any long-term consequences.58
Hepatic veins
Occlusion or stenosis of the IVC anastomosis is rare, occurring in
less than 1% of recipients, usually due to technical surgical prob-
lems or as a consequence of compression by a fluid collection.59
Suprahepatic stenosis presents with a clinical picture of acute or
chronic BuddChiari syndrome with ascites, peripheral oedema,
portal hypertension and biopsy evidence of hepatic venous conges-
tion. Infrahepatic stenosis may cause only lower extremity swelling.
A reduction in the calibre of the IVC or hepatic vein, with impaired
flow and resultant pre-stenotic dilatation of the hepatic veins, is an
indirect diagnostic finding of stenosis at CDUS. Direct signs of
stenosis include a focal stricture on B-mode images and turbulent
flow with increased velocity on spectral Doppler ultrasound (Fig.
13.22). Thrombosis of the hepatic vein or IVC may be depicted as
intraluminal echogenic thrombus with no flow on Doppler images.
Figure 13.20 Portal vein stenosis. A focal area of narrowing and Distension of the hepatic veins and IVC may also be demonstrated.
colour turbulence is observed in the portal vein (arrow). A peak A persistent monophasic waveform is a sensitive finding of stenosis
velocity of 127cm/s and a step-up in velocity across the narrowed at spectral Doppler ultrasound, but it is not specific for a substantial
portal vein is suggestive of a portal vein stenosis. hepatic vein stenosis. Any pathological process that changes liver
A B
Figure 13.21 Portal vein thrombosis. A: The portal vein (arrows) demonstrates no colour Doppler flow with an echo-poor thrombus-
filled lumen. The colour Doppler signal is present in the patent hepatic artery. B: The spectral Doppler waveform in the transplant hepatic
artery demonstrates high forward flow in diastole in the same patient as in part A.
210
Early postoperative ultrasound
A B
Figure 13.22 Hepatic vein stenosis. A: There are areas of narrowing and increase in colour Doppler flow (arrows) in two hepatic veins
post-liver transplantation with the piggy-back technique. B: There is complete loss of the normal pulsatility in the hepatic vein as a
consequence of the hepatic vein stenosis.
compliance will alter hepatic vein pulsatility.60 Perioperative ischae- non-invasive diagnostic examination modality to detect liver allo-
mia, vascular catastrophe, rejection and cholangitis may all cause graft rejection, with the main role of radiology to exclude other
damping of the spectral Doppler trace. Although ultrasound can complications prior to a histological diagnosis with liver biopsy.
be diagnostic, inferior vena cavography and pressure studies are
required for the definitive diagnosis. Hepatic vein thrombosis is
rare, as the hepatic veins are not directly involved in a surgical Biliary system
anastomosis. Hepatic vein thrombosis may be seen in those recipi- Biliary complications are an important cause of postoperative mor-
ents who have had a transplant for BuddChiari syndrome, when bidity and mortality in liver transplantation.37 The main complica-
the underlying abnormality recurs.61 tions after liver transplantation are biliary obstruction and bile
A common variation of caval replacement is the piggy-back leakage. The reported incidence of complications has decreased
technique. The three hepatic veins are joined together to form a single from 50% with mortality as high as 30% in early series to a current
large orifice. The blind inferior end of the donor IVC often thrombo- complication rate of less than 20% and a mortality of less than 5%.66
ses and this thrombus may be seen in the blind end of the donor IVC The current surgical practice for biliary reconstruction is end-to-end
on routine ultrasound. Some sources have found the piggy-back anastomosis, where the recipient bile duct may be utilised. However,
technique to be prone to the BuddChiari syndrome, or haemor- if the recipient has an underlying biliary abnormality with an
rhage, but this has not been the experience at our institution.53 insufficient length of a common bile duct, such as in biliary
atresia or sclerosing cholangitis, or when a cut-down graft is trans-
planted, it will be necessary to construct a choledochojejunostomy.
Non-vascular complications Strictures of the bile duct anastomosis are more common after
duct-to-duct reconstruction, occurring in 514% of cases (Fig.
13.23).43,67 Non-anastomotic strictures carry a worse prognosis, rep-
Rejection
resenting a diffuse biliary injury occurring with HAT, prolonged
Following hepatic transplantation, acute rejection is the most cold ischaemia and ABO incompatible donors (Fig. 13.24).68 It is
common serious complication affecting allograft survival, and important that CDUS confirms patency of the hepatic artery when
occurs in more than 30% of patients.62 Treatment, which is usually non-anastomotic strictures are present.
successful, involves manipulation of immunosuppressive drug Bile duct dilatation is unusual in the early postoperative trans-
therapy. Acute rejection is due to an inflammatory cellular infiltrate plant period.69 In non-transplant patients, ultrasound is the accepted
and does not significantly affect the peripheral hepatic vascula- method for detecting biliary duct dilatation.70 However, the sensi-
ture.63 In chronic rejection there is deposition of subintimal foam tivity is lower in liver transplant patients, with a sensitivity of 38
cells, myo-intimal foam cells, myo-intimal hyperplasia, and intimal 46%, and a specificity of 98%.71 Dilatation of the intrahepatic ducts
sclerosis, resulting in progressive arterial narrowing and slow flow has a higher predictive value for diagnosis of biliary obstruction
with subsequent thrombosis.64 Non-anastomotic vascular stenosis, than common bile duct diameter. If bile duct dilatation is suspected
as well as diffuse intrahepatic arterial narrowing, is a feature in clinically, ultrasound nonetheless remains the investigation of
patients with chronic transplant rejection. choice, providing evidence to support the need to proceed to
Ultrasound presents a non-specific profile in acute rejection; there further imaging.
is no correlation between the RI and acute rejection64 and no correla- On ultrasound, in the early postoperative period it is practice to
tion between loss of hepatic artery diastolic flow and acute rejec- measure the common, left and right bile ducts to confirm non-
tion.63 Changes in hepatic arterial and venous velocity profiles dilatation and record the baseline measurement. This is particularly
reflect alteration in hepatic vascular resistance, which is not specific important in cut-down grafts in children, where intrahepatic bile
to rejection; occurring with preservation injury, sepsis and non- duct dimensions are those of adult proportions and early measure-
thrombotic graft infarction.60 An area of decreased reflectivity and ment will avoid an erroneous call of bile duct dilatation. If the bile
attenuation has also been described in the periportal region with ducts increase in size along with biochemical changes or biliary
ultrasound and CECT, respectively, but this has a low sensitivity dilation is persistent for more than 3 months after transplantation,
and specificity in the diagnosis of rejection.65 There is no reliable a biliary system abnormality is invariably present.
211
CHAPTER 13 Liver transplantation
Fluid collections
Abscess formation occurs in approximately 10% of liver transplants
Bile leaks are usually secondary to anastomotic complications. In postoperatively, most of which occur in subphrenic or subhepatic
a review of biliary complications in 1792 patients following liver spaces.74 Ultrasound guidance will allow drainage of any fluid col-
transplant, 50% of bile leaks were due to anastomotic complications lection. Occasionally, fluid collections may be completely obscured
and the remaining leaks were due to HAT (17.2%), leaks at the by bowel gas on ultrasound, with CECT providing the conclusive
T-tube site (31%), and leaks from aberrant ducts.69 The majority of imaging modality. Haematoma formation may be seen in the imme-
bile leaks occur early, within the first thirty days of liver transplan- diate postoperative period and is usually secondary to extensive
tation or at the time of removal of the T-tube, if in position. Diag- intraoperative abdominal bleeding from varices. Haematomas may
nosis of a biliary leak is often difficult without cholangiography. be present at any site, again most commonly in the subphrenic and
Ultrasound can readily detect intra- and extrahepatic bilomas that subhepatic space.37 In the first 3 weeks following liver transplant
occur as a result of post-transplantation bile leaks. However, their the majority of haematomas are composed of clotted blood and
appearance may be indistinguishable from other collections of fluid aspiration is neither necessary nor possible. The development of
in the upper abdomen such as ascites, seroma or haematoma (Fig. new collections in the late postoperative period raises the possibil-
13.25). Subhepatic collections are common in the early post- ity of bile leak as a consequence of HAT, or loculated ascites as a
transplant period. Ultrasound-guided fine-needle aspiration may consequence of portal vein or IVC flow abnormalities.37
confirm the nature of the fluid. Drainage of bile leaks may promote Post transplantation abdominal bleeding occurs in less than 10%
healing of the bile ducts and may save the liver graft.72 of patients and may be due to HAP, breakdown of a vascular
212
Role of ultrasound in long-term follow-up
A B
Figure 13.28 Focal hepatic post-transplant lymphoproliferative disease. A: In this post-transplant patient several focal low
attenuation lesions (arrows) are seen on the arterial phase of the CECT examination. B: On the post-contrast ultrasound a single subtle low
reflective lesion (arrow) demonstrates washout in the late phase but still has some intralesional vascularity identified.
Other extranodal manifestations of abdominal PTLD include peritoneal, retroperitoneal and extraperitoneal lymph nodes may
involvement of the gastrointestinal tract (approximately 30%) with be enlarged. Omental and mesenteric involvement by PTLD is less
the small bowel most frequently involved, splenic involvement in common, seen in about 10% of patients with abdominal disease and
28% of cases manifesting as focal low-reflectivity lesions, splenom- manifesting as an extranodal mass. These may be well circum-
egaly or both, and renal involvement which occurs in less than 20% scribed or infiltrative, representing either primary tumour involve-
of patients (Fig. 13.30).80 Unlike renal lymphoma that arises in the ment or direct extension from an abdominal organ.
non-transplant patient, PTLD kidney involvement tends to be uni-
lateral and unifocal. A solitary round low echogenic lesion without
renal enlargement is the most common manifestation, while diffuse
Renal complications
renal enlargement, which may extend beyond the capsule, occurs Renal insufficiency due to the nephrotoxic effects of the immuno-
less commonly. Abdominal lymph node involvement, seen in suppressive therapy is a common complication and has been
about 20% of patients, appears as non-specific nodal enlargement. reported in up to 25% of paediatric recipients.84 Ultrasound may be
These involved nodes are typically 23cm in diameter but may used to exclude obstruction in patients with deteriorating renal
coalesce to form larger masses with central low attenuating areas function and give information regarding the size and reflectivity of
from necrosis being an uncommon finding. Any combination of the kidneys.
214
Role of ultrasound in long-term follow-up
A B
Figure 13.31 Post-transplant liver abscess. A: Multiple areas of mixed reflectivity (arrows) in a liver transplant patient. B: On the
contrast-enhanced images these areas are seen to be avascular, with irregular borders and septations in keeping with multiple abscesses.
to prevent reinfection with immunoprophylaxis and antiviral abnormality for which recurrence of PSC must be considered. Most
therapy. patients transplanted for PSC will have a choledochojejunostomy
as a consequence of abnormal recipient extrahepatic ducts,
which is prone to a higher incidence of cholangitis and biliary
Hepatocellular carcinoma (HCC) strictures leading to a cholangiopathy similar to PSC. This presents
The histological pattern and degree of differentiation of HCC give difficulty both on cholangiographic and histological methods in
no indication as to the subsequent course of disease, as it is the determining absolute PSC recurrence. Furthermore, patients trans-
preoperative staging of the tumour which indicates the recurrence planted for PSC are known to have a higher incidence of biliary
rate. The lowest recurrence rates occur in small tumours of less than complications, again reflecting the use of a choledochojejunostomy
5cm without evidence of disease spread.94 Tumour recurrence rate reconstruction.
of 7% is seen with tumours less than 5cm and 62% when tumours
are greater than 5cm in size.95 Furthermore, infiltration of regional
lymph nodes or the presence of gross or microscopic vascular inva- PAEDIATRIC LIVER TRANSPLANTATION
sion by tumour at the time of transplantation significantly influ-
ences the prognosis.96 A combination of ultrasound, CECT and
magnetic resonance imaging is accurate at detecting HCC recur- Introduction
rences in the liver transplant. Imaging features for HCC in the
post-transplant liver are similar to those in the pre-transplant liver.
Paediatric liver transplantation is a well-established and effective
Overall, children who have received a liver transplant for primary
treatment option for children with acute or chronic liver disease. In
hepatic malignancy have a better prognosis than adults. The quoted
the United Kingdom approximately 100 children undergo liver
10-year survival rate is 21% in adults and 50% in children.97 The
transplantation annually either as an elective procedure (approxi-
recurrence of HCC in a non-cirrhotic liver transplant should be
mately 85% 5-year survival rate) or as an emergency in the acute
readily detected on ultrasound but there are no available published
setting. Paediatric liver donors are rare and therefore various surgi-
data to confirm this.
cal techniques have been developed to facilitate transplantation
in this group of patients, leading to improved survival and quality
Fibrolamellar HCC of life.
association with infantile polycystic kidney disease and Langerhans situation, instead of removing the whole of the diseased liver, only
cell histiocytosis. part of it is resected. A donor reduced or split lobe is used to replace
the resected lobe. In acute liver failure, once the native right liver
recovers and regenerates, withdrawal of immunosuppression will
Acute liver failure (ALF) cause the atrophy of the transplanted segments.111
Usually secondary to infection, ALF is defined by the presence of
hepatic encephalopathy and coagulopathy within 8 weeks of the
onset of liver disease. Over half of cases are due to non-A-E
Reduced liver transplantation
hepatitis.107 Other causes include paracetamol overdose, mushroom The term liver reduction is used when a liver is cut down to the
poisoning, autoimmune liver failure and metabolic diseases such required size of recipient and the remaining segments are dis-
as neonatal haemochromatosis, tyrosinaemia and Wilsons disease. carded.112 The left lobe (segments I to IV) can be removed, leaving
the right lobe (segments V to VIII) for transplantation, or the right
lobe can be removed and the left lobe transplanted. In both these
Metabolic liver disease cases the IVC is retained with the transplanted lobe, so either caval
Liver transplantation for metabolic diseases is divided into that replacement or piggy-back techniques can be used. A liver can
performed for end-stage liver disease or premalignant change also be reduced to a left lateral segment (segments II and III) by
(including 1-antitrypsin deficiency, Wilsons disease, galactosae- removing the extended right lobe (segments I and IV to VIII); this
mia, protoporphyria, glycogen storage diseases) and that allows an adult liver to be used for a small paediatric recipient. In
performed for major extrahepatic features (including Crigler this case, the IVC of the donor liver cannot be retained with the left
Najjar syndrome, primary familial amyloidosis, homozygous lateral segment and the piggy-back technique has to be used,
hypercholesterolaemia). joining the left hepatic vein of the donor liver to the confluence of
the hepatic veins on the anterior wall of the IVC of the recipient. A
left lateral segment reduction is rarely performed these days as the
Portal hypertension (PHT) right lobe can be used for another recipient, resulting in what is
described as a split liver transplant in which one organ is used for
PHT follows obstruction of the paediatric intra- or extrahepatic
two recipients. Following transplantation, the principal difference
portal venous system. This can be at a hepatic level secondary to
between a reduced graft and a whole organ is that there is a rela-
liver cirrhosis, prehepatic due to thrombosis or rarely posthepatic
tively flat cut surface which has the potential to bleed or leak bile
following obstruction to venous outflow or IVC obstruction.106
(Fig. 13.32).
Portal vein
Common bile anastomosis
duct anastomosis
Hepatic artery
anastomosis
Infrahepatic vena
cava anastomosis
Duodenum
Hepatic artery
218
Paediatric liver transplantation
A B
Figure 13.34 Normal ultrasound appearances in the paediatric patient post liver transplantation. A: The native liver (long arrow)
is slightly more echogenic in comparison with the transplanted auxiliary liver graft (short arrow), which is not always as distinct on the
ultrasound examination. B: The splenic artery (short arrow) is seen arising from the coeliac axis with the patent hepatic artery (long arrow)
coursing towards the split liver transplant in an 18-month-old child. The portal vein (small arrows) is patent.
A B
Figure 13.35 Paediatric hepatic artery thrombosis. A: The portal vein is patent on colour Doppler ultrasound (arrow) but no colour
Doppler signal is present at the site of the hepatic artery (arrowhead) in this patient with a split liver graft. B: Following contrast-enhanced
ultrasound, the occlusion of the hepatic artery is confirmed by absence of any enhancement in the hepatic artery, but with enhancement
seen in the portal vein (arrow).
show a bi- or triphasic waveform pattern due to transmitted cardiac biliary anatomy. Clinical manifestations of early complications are
pulsations.114,115 Variable volumes of free fluid may be seen in the varied and there may be no alteration in the liver biochemistry.
abdomen and pelvis and haematoma at the cut surface of a reduced Post-surgical surveillance ultrasound is therefore important for the
sized graft is common. Spleen length is important in the assessment detection of silent complications and ultimately graft salvage.36,114,116
of portal vein flow and the development of portal hypertension. Routinely at our institution uncomplicated paediatric liver trans-
plant patients are imaged with ultrasound on day 1, day 5 and prior
Ultrasound of complications of paediatric to discharge (usually after 1014 days) with follow-up at 1 month,
3 months, 6 months and then annually thereafter.
liver transplantation
Post-surgical vascular and biliary complications are more common
in children than in adults primarily due to discrepancies in the size
Vascular complications
of the donor and recipient vessels and use of vascular conduits. It Vascular complications usually occur early, the commonest being
is therefore important for the observer to have an understanding of hepatic artery thrombosis, which can occur in up to 18% of paedi-
the surgical techniques used which determine the vascular and atric patients117(Fig. 13.35). Ultrasound may demonstrate no arterial
219
CHAPTER 13 Liver transplantation
spectral or colour Doppler signal although some intrahepatic Portal vein stenosis is rare and usually occurs at the anastomosis
Doppler signal may be detected due to collateralisation from the site. This may be detected on routine follow-up with high-velocity
adjacent vascular choledochojejunostomy. These arterial collaterals turbulent flow in the dilated post-stenotic segment and a decrease
may exhibit a normal or tardus parvus waveform with an RI of <0.5 in the vessel lumen of >50%. A post-stenotic jet with a velocity of
and can go undetected due to the speed at which they develop in >100cm/s is usually pathognomonic36,114 (Fig. 13.37).
the absence of any altered hepatic biochemistry.47 The graft may Inferior vena cava and hepatic vein complications are rare
later demonstrate changes secondary to infarction and bile duct (<1%). These are often suspected clinically as patients present
ischaemia with biliary dilatation. with hepatomegaly, ascites, oedema and pleural effusions and
Hepatic artery stenosis is reported to occur in up to 14% of chil- are usually related to surgical problems at the site of the
dren leading to rejection, biliary ischaemia and hepatic failure.116 anastomosis.36
This usually occurs at the anastomotic site. Spectral Doppler wave-
form demonstrates an accelerated velocity (>200cm/s) with turbu-
lent colour Doppler in the portion of the vessel immediately distal Biliary complications
to the stenosis.36 These are more common than vascular complications, occurring in
Portal vein thrombosis commonly occurs in the extrahepatic up to 30% of patients. Patients who have received a cut-down liver
segment. There is a spectrum of change ranging from non-occlusive may be at increased risk of biliary anastomotic complications, and
filling defects on greyscale imaging to absent flow with reverse flow the altered anatomy makes imaging of these livers difficult (Fig.
in the intrahepatic portal vein branches (Fig. 13.36). 13.38). This group of patients deserves particularly careful monitor-
ing of the intrahepatic duct diameters because in paediatric patients
receiving a left lobe graft from an adult donor, the diameter of the
bile duct will be appropriate for an adult and may be unusually
large for a child. It is therefore important to record the size of the
bile duct in such cases during the early postoperative phase, and
to monitor for any subsequent dilatation. Failure to do this may
give rise to an erroneous diagnosis of biliary dilatation in this
group of patients.
A B
Figure 13.37 Paediatric portal vein stenosis. A: There is an echogenic area of narrowing (arrow) at the site of the portal vein stenosis
in a split liver transplant. B: The spectral Doppler gate is placed at the site of maximum colour Doppler turbulence and the velocity is
measured at 270.4cm/s, in keeping with a pronounced portal vein stenosis.
220
Paediatric liver transplantation
Anastomotic bile leaks are the commonest complication but stric- transplantation.120 Ultrasound is valuable in these patients to estab-
tures following vascular problems, cut surface bile leaks and lish the diagnosis by observing the diaphragm movement during
obstruction due to debris and stones also occur. Intraparenchymal spontaneous respiration. The condition is probably caused by
bilomas, cholangitis and cystic duct remnant mucoceles are rarely damage to the phrenic nerve during clamping of the suprahepatic
reported.118,119 Ultrasound typically demonstrates bile duct dilata- vena cava.
tion, perihepatic or cut surface collections in the case of bile
leaks which are usually amenable to ultrasound-guided drainage
(Fig. 13.39). Fluid in the choledochojejunostomy may masquerade Small bowel complications
as a pathological fluid collection, and care needs to be taken to These typically involve the choledochojejunostomy and include
identify this.115 Roux loop torsion, stasis, intussusception and infarction.121
Hepatoblastoma
Hepatoblastoma is the commonest primary liver tumour in children
under 5 years of age for which transplantation is a recognised treat-
ment. Factors associated with a poor prognosis and disease recur-
rence include previous resection, portal vein invasion by tumour,
multifocal disease, other vascular invasion and the presence of
Figure 13.38 Paediatric bile duct dilatation. Central bile duct extrahepatic disease. Unifocal disease, irrespective of tumour size,
dilatation (between cursors) in a child with a left lateral segment with fetal epithelium on histology is associated with a better
graft who developed a liver hilar anastomotic stricture following outcome whilst the presence of anaplastic cell type has been associ-
portal vein stenosis. ated with a poor prognosis.123
A B
Figure 13.39 Paediatric abdominal collections. A: Anechoic fluid collection (between cursors) adjacent to the cut surface of a left
lateral segment graft. B: Complex septated collection (between cursors) in the upper abdomen representing bilomas or haematoma.
221
CHAPTER 13 Liver transplantation
44. Balan V, Abu-Elmagd K, Demetris AJ. Autoimmune liver diseases. 69. Greif F, Bronsther OL, Van Thiel DH, et al. The incidence, timing and
Recurrence after liver transplantation. Surg Clin North Am management of biliary tract complications after liver transplantation.
1999;79:147152. Ann Surg 1994;219:4045.
45. Katyal S, Oliver JH, Buck DG, Federle MP. Detection of vascular 70. Neimin HL, Mintzer RA. Accuracy of biliary duct ultrasound;
complications after liver transplantation: early experience in conparison with cholangiography. AJR Am J Roentgenol 1977;129:
multislice CT angiography with volume rendering. AJR Am J 979982.
Roentgenol 2000;175:17351739. 71. Kok T, Van der Sluis A, Klein JP, et al. Ultrasound and
46. Sidhu PS, Shaw AS, Ellis SM, et al. Microbubble ultrasound contrast cholangiography for the diagnosis of biliary complications after
in the assessment of hepatic artery patency following liver orthoptic liver transplantation; a comparative study. J Clin
transplantation: role in reducing frequency of hepatic artery Ultrasound 1996;24:103115.
arteriography. Eur Radiol 2004;14:2130. 72. Kaplan S, Zajko AB, Koneru B. Hepatic bilomas due to hepatic artery
47. Hall TR, Diarmid SV, Grant EG, et al. False-negative duplex Doppler thrombosis in liver transplant recipients: percutaneous drainage and
studies in children with hepatic artery thrombosis after liver clinical outcome. Radiology 1990;174:10311035.
transplantation. AJR Am J Roentgenol 1990;154:573575. 73. Evans RA, Raby ND, OGrady J, et al. Biliary complications following
48. Flint EW, Sumkin JH, Zajko AB, Bowen A. Duplex sonography of orthoptic liver transplantation. Clin Radiol 1990;41:190194.
hepatic artery thrombosis after liver transplantation in the 74. Woods RP, Shaw BW, Starzl TE. Extrahepatic complications of liver
cyclosporin era. AJR Am J Roentgenol 1988;151:481483. transplantation. Semin Liver Disease 1985;5:377384.
49. Ryan SM, Sidhu PS. CT of liver transplantation. Appl Radiol 75. Caiado AHM, Blasbalg R, Marcelino ASZ, et al. Complications of liver
2006;35:1021. transplantation: multimodality imaging approach. Radiographics
50. Abbasoglu O, Levy MF, Vodapally MS, et al. Hepatic artery stenosis 2007;27:14011417.
after liver transplantation incidence, presentation, treatment, and 76. Cox KL, Lawerence-Miyasaki LS, Garcia-Kennedy R, et al. An
long term outcome. Transplantation 1997;27:250255. increased incidence of Epstein-Barr virus infection and
51. Sidhu PS, Ellis SM, Karani JB, Ryan SM. Hepatic artery stenosis lymphoproliferative disorders in young children on FK506 after liver
following liver transplantation: significance of the tardus parvus transplantation. Transplantation 1995;59:524529.
waveform and the role of microbubble contrast media in the 77. Younes BS, McDiarmid MG, Martin JH, et al. The effect of
detection of a focal stenosis. Clin Radiol 2002;57:789799. immunosuppression on post-transplant lymphoproliferative disease
52. Marshall MM, Muiesan P, Srinivasan P, et al. Hepatic artery in pediatric liver transplant patients. Transplantation 2000;70:9497.
pseudoaneurysms following liver transplantation: incidence, 78. McCarthy M, Ramage JK, McNair A, et al. The clinical diversity and
presenting features and management. Clin Radiol 2001;56:579587. role of chemotherapy in lymphoproliferative disorder in liver
53. Lerut J, Tzakis A, Bron KM, et al. Complications of venous transplantation recipients. J Hepatol 1997;27:10151021.
reconstruction in human orthotopic liver transplantation. Ann Surg 79. Morrison VA, Dunn DL, Manivel JC, et al. Clinical characteristics of
1987;205:404414. post-transplant lymphoproliferative disorders. Am J Med 1994;97:
54. Hamady M, Rela M, Sidhu PS. Spontaneous resolution of a portal 1424.
vein stenosis over a 21-month period in a split-liver transplant: 80. Pickhardt PJ, Siegel MJ. Abdominal manifestations of post
demonstration by colour Doppler ultrasound, catheter angiography transplantation lymphoproliferative disorder. AJR Am J Roentgenol
and splenic pulp pressures. Eur Radiol 2002;12:22802283. 1998; 171:10071013.
55. Samuel D, Gillet D, Reynes M, Bismuth H. Portal and arterial 81. Pickhardt PJ, Siegel MJ. Post transplantation lymphoproliferative
thrombosis in liver transplantation: a frequent event in severe disorder of the abdomen: CT evaluation in 51 patients. Radiology
rejection. Transplantation Proc 1989;21:22252227. 1999;213:7378.
56. Raby N, Karani JB, Thomas S, et al. Stenoses of vascular anastomoses 82. Navarro F, Pyda P, Pageaux GP, et al. Lymphoproliferative disease
after hepatic transplantation: treatment with balloon angioplasty. after liver transplantation: primary biliary location. Transplant Proc
AJR Am J Roentgenol 1991;157:167171. 1998;30:14861488.
57. Platt JF, Rubin JM, Ellis JH. Hepatic artery resistance changes in 83. Bowen A, Hungate RG, Kaye RD, et al. Imaging in liver
portal vein thrombosis. Radiology 1995;196:9598. transplantation. Pediatr Gastrointest Radiol 1996;34:757778.
58. Chezmar JL, Nelson RC, Bernardino ME. Portal venous gas after 84. McDiarmid SV, Busuttil RW, Ascher NL, et al. FK506 (Tacrolimus)
hepatic transplantation; sonographic detection and clinical compared with cyclosporine for primary immunosuppression after
significance. AJR Am J Roentgenol 1989;153:12031205. paediatric liver transplantation: results from the US multicenter trial.
59. Rossi AR, Pozniak MA, Zarvan NP. Upper inferior vena caval Transplantation 2001;59:530536.
anastomotic stenosis in liver transplant recipients: Doppler US 85. Cattral MS, Langas AN, Wisecarver JL, et al. Survival of graft versus
diagnosis. Radiology 1993;187:387389. host disease in a liver transplant recipient. Transplantation
60. Coulden RA, Britton PD, Farman P, Noble-Jamieson G, Wright DGD. 1994;57:12711274.
Preliminary report: hepatic vein Doppler in the early diagnosis of 86. Holbert BL, Campbell WL, Skolnick ML. Evaluation of the
acute liver transplant rejection. Lancet 1990;336:273275. transplanted liver and postoperative complications. Radiol Clin North
61. Ruckert JC, Ruckert RI, Rudolph B, Muller JM. Recurrence of the Am 1998;33:521540.
BuddChiari syndrome after orthotopic liver transplantation. 87. Nicholson V, Johnson PC. Infectious complications in solid organ
Hepatogastroenterology 1999;46:867871. transplant recipients. Surg Clin North Am 1994; 74:12231245.
62. Demetris JA, Slasky S, Van Thiel DH, et al. Pathology of hepatic 88. Desai SR, Beese RC, Karani JB. Intrahepatic abscess formation
transplantation; a review of 62 adult allograft recipients following adult orthoptic liver transplantation. Br J Radiol
immunosuppressed with a cyclosporine/steroid regimen. Am J 1996;96:200.
Pathol 1985;118:151161. 89. Jamieson NV, Williams R, Calne RY. Liver transplantation for Budd
63. Longley DG, Skolnick ML, Sheahan DG. Acute allograft rejection in Chiari syndrome 19761990. Ann Chir 1991; 45:362365.
liver transplant recipients: lack of correlation with loss of hepatic 90. Hulff G, Todo S, Tzakis AG, et al. Liver transplantation for Budd
artery diastolic flow. Radiology 1988;169:417420. Chiari syndrome. Ann Surg 1990;211:4349.
64. Marder DM, De Marino GB, Sumkin JH, Sheahan DG. Liver 91. Testa G, Crippin JS, Netto GJ, et al. Liver transplantation for hepatitis
transplant rejection: value of the resistive index in Doppler US of C: recurrence and disease progression in 300 patients. Liver Transpl
hepatic arteries. Radiology 1989;173:127129. 2000;6:553561.
65. Kaplan SB, Sumkin J, Campbell WL, et al. Periportal low attenuation 92. OGrady JG, Smith HM, Davies SE, et al. Hepatitis B reinfection after
areas on CT; value as evidence of liver transplant rejection. AJR Am J orthoptic liver transplantation. Serological and clinical implications.
Roentgenol 1989;152:285287. J Hepatol 1992;14:104111.
66. Klein AS, Savador S, Burdick JF, et al. Reduction of morbidity and 93. Davern TJ, Lake JR. Recurrent disease after liver transplantation.
mortality from biliary complications after liver transplantation. Semin Gastrointest Dis 1998;9:86109.
Hepatology 1991;14:818823. 94. McPeake JR, OGrady J, Zaman S, et al. Liver transplantation for
67. Lerut J, Gordon RD, Iwatsuki S, et al. Biliary tract complications in primary hepatocellular carcinoma: tumor size and number determine
human orthoptic liver transplantation. Transplantation 1987;43: outcome. J Hepatol 1993;18:226234.
4751. 95. Imatsuki S, Gordon RD, Shaw BJ, Starzl TE. Role of liver
68. Lopez RR, Bennar KG, Ivanceu K, et al. Management of biliary transplantation in cancer therapy. Ann Surg 1985;202:401407.
complications after liver transplantation. Am J Surg 1992;163: 96. Ismail T, Angrisani L, Gunson BK, et al. Primary hepatic malignancy:
519524. the role of liver transplantation. Br J Surg 1990;77:983987.
223
CHAPTER 13 Liver transplantation
97. Migliazza L, Lopez Santamaria M, Murcia J, et al. Long-term survival 112. de Hemptinne B, Salizzoni M, Tan KC, Otte JB. The technique of liver
expectancy after liver transplantation in children. J Pediatr Surg reduction in orthotopic liver transplantation. Transplant Proc
2000;35:57. 1988;20:508511.
98. El-Gazzaz G, Wong W, El-Hadary MK, et al. Outcome of liver 113. Rela M, Vougas V, Muiesan P, et al. Split liver transplantation. Kings
resection and transplantation for fibrolamellar hepatocellular College Hospital experience. Ann Surg 1998;227:282288.
carcinoma. Transpl Int 2000;13:S406S409. 114. Crossin JD, Muradali D, Wilson SR. US of liver transplants: normal
99. Mackie J, Groves K, Hoyle A, et al. Orthoptic liver transplantation for and abnormal. Radiographics 2003;23:10931114.
alcoholic liver disease: a retrospective analysis of survival and risk 115. Caron KH, Strife JL, Babock DS, Ryckman FC. Left-lobe hepatic
factors predisposing to recidivision. Liver Transpl 2001;7:418427. transplants: spectrum of normal imaging findings. AJR Am J
100. OGrady JG, Polson RJ, Rolles K, et al. Liver transplantation for Roentgenol 1992;159:497501.
malignant disease. Results in 93 consecutive patients. Ann Surg 116. Berrocal T, Parron M, Alvarez-Luque A, et al. Pediatric liver
1988;207:373379. transplantation: a pictorial essay of early and late complications.
101. Garcia RF, Garcia CE, McMaster P, Neuberger J. Transplantation for Radiographics 2006;26:11871209.
primary biliary cirrhosis: retrospective analysis of 400 patients in a 117. Karani JB, Heaton ND. Review. Imaging in liver transplantation.
single center. Hepatology 2001;33:2227. Clin Radiol 1998;53:317322.
102. Gow PJ, Chapman RW. Liver transplantation for primary sclerosing 118. Lorenz JM, Funaki B, Leef JA, et al. Percutaneous transhepatic
cholangitis. Liver 2000;20:97103. cholangiography and biliary drainage in paediatric liver transplant
103. Kelly DA. Current results and evolving indications for liver patients. AJR Am J Roentgenol 2001;176:761765.
transplantation in children. J Pediatr Gastroenterol Nutr 119. OLoughlin EV, Stromon MO, Shun A, et al. Biliary strictures and
1998;27:214221. hepatic artery flow abnormalities in split liver transplants. Pediatr
104. Bisset GS, Strife J, Balistreri WF. Evaluation of children for Transpl 2010;14:121125.
transplantation; value of MR imaging and sonography. AJR Am J 120. Smyrniotis V, Andreani P, Muiesan P, et al. Diaphragmatic nerve
Roentgenol 1990;155:351356. palsy in young children following liver transplantation. Successful
105. Colombo C, Russo MC, Zazzeron L, Romano G. Liver disease in treatment by plication of the diaphragm. Transpl Int 1998;11:281283.
cystic fibrosis. J Pediatr Gastroenterol Nutr 2006;43:S49S55. 121. Gimson AES, Karani JB, Heaton ND. Major biliary tract and vascular
106. Engelmann G, Schmidt J, Oh J, et al. Indications for paediatric liver complications. In: Williams R, Portmann B, Tan KC, editors. The
transplantation. Data from the Heidelberg paediatric liver practice of liver transplantation. London: Churchill Livingstone; 1995.
transplantation program. Nephrol Dial Transplant 2007;22:823828. p. 199209.
107. Lee WS, McKieman P, Kelly DA. Etiology, outcome and prognostic 122. Wilde EW, Moore DJ, Bellah RD. Posttransplantation
indicators of childhood fulminant hepatic failure in the United lymphoproliferative disorder in pediatric recipients of solid organ
Kingdom. J Pediatr Gastroenterol Nutr 2005;40:11601172. transplants: timing and location of disease. AJR Am J Roentgenol
108. Bismuth H, Houssin D. Reduced-sized orthotopic liver graft in 2005;285:13351341.
hepatic transplantation in children. Surgery 1984;95:367370. 123. Koneru B, Flye MW, Busuttil RW, et al. Liver transplantation for
109. Strong R, Lynch S, Ong T, et al. Successful liver transplantation from hepatoblastoma. The American experience. Ann Surg 1991;213:
a living donor to her son. N Engl J Med 2010;322:15051507. 118121.
110. Strong RW, Ong TH, Pillay P, et al. A new method of segmental 124. Ryckman FC, Alonso MH, Busuttil RW, Klintmalm GBG.
orthotopic liver transplantation in children. Surgery 1988;104:104107. Transplantation for primary hepatic malignancy in children.
111. Bartlett A, Rela M. Progress in surgical techniques in paediatric liver In: Transplantation of the liver. Philadelphia: WB Saunders; 1996.
transplantation. Paediatr Transplant 2009;14:3340. p. 216226.
224
CHAPTER
Ducts
NORMAL ANATOMY OF
THE BILIARY TREE Normal variations in the anatomy of the ducts are common. The
point at which the cystic duct joins the common hepatic duct is
The intrahepatic bile ducts run in the portal tracts alongside the particularly variable; usually the ducts unite just beyond the porta
portal vein radicles and hepatic artery branches. At the porta hepatis, but the cystic duct may join the right hepatic duct or the
hepatis, the right and left hepatic ducts join to form the common join may be much lower occasionally within the head of the
227
CHAPTER 14 Gallbladder and biliary tree
Hepatic artery
Usually, the hepatic artery arises from the coeliac axis and runs for
a short distance to the right before turning superiorly. At this point
the artery lies anterior to the portal vein with the common duct to the
right. Just proximal to the porta hepatis the artery branches, and
the right hepatic artery crosses to the right, posterior to the common
hepatic duct before entering the substance of the liver (Fig. 14.10).
In about 15% of subjects, the right hepatic artery passes anteriorly
to the common hepatic duct, and in a smaller proportion (approxi-
mately 5%), the right hepatic artery originates from the superior
mesenteric artery the replaced right hepatic artery and passes
posteriorly to the superior mesenteric vein before turning anteriorly
to the portal vein.8 Colour Doppler ultrasound may be useful in
sorting out the anatomy in these cases,9 although it is usually pos-
sible to identify the vessels by tracing them back to their point of
origin (Fig. 14.11).
Figure 14.1 Right hepatic duct. The normal calibre right hepatic TECHNIQUE AND ULTRASOUND
duct (arrows) is seen anterior to the right branch of the portal vein.
APPEARANCE
The biliary system should be examined after the patient has fasted
not only does this distend the gallbladder with bile to allow
investigation of its lumen, but it helps to reduce the contents of the
stomach and duodenum, which may obscure the common duct and
pancreas.
pancreas itself. The cystic duct may pass medially either posteriorly
In some patients, the posterior wall of the gallbladder is closely
or anteriorly to the common hepatic duct, then curving laterally to
adjacent to the duodenum and distal acoustic shadowing from the
join its medial border.
latter may simulate gallbladder pathology (Fig. 14.12). In such
On ultrasound scans it is not usually possible to recognise the
cases, giving the patient a drink of water usually helps to outline
exact point of union of the cystic and common hepatic ducts, and
the duodenum and display the gallbladder wall more clearly.
it has therefore become accepted convention to refer to the extrahe-
The normal gallbladder in the non-fasted state is contracted and
patic bile duct as the common duct.3
thick walled (Fig. 14.13). This may be indistinguishable from patho-
logical contraction and care should always be taken to ensure that
Gallbladder the patient has adhered to the correct preparation if the gallbladder
is small or not visualised on ultrasound.10
The shape, size and position of the gallbladder are highly variable. The equipment of choice for examination of the gallbladder and
In some cases the gallbladder fossa lies deep within the liver so the biliary tree is a curved array transducer, which allows good acoustic
gallbladder appears to be surrounded by hepatic tissue the so- access both subcostally and intercostally, with an adequate near
called intrahepatic gallbladder. At the other end of the spectrum, field to accommodate superficial gallbladders. A frequency of
the gallbladder may be attached to the porta only at the neck, 56MHz, with a focal zone set at the appropriate depth, generally
forming a very mobile structure which may be found in the right provides sufficiently good resolution to detect even small stones
iliac fossa or even in the pelvic region, depending upon patient within the gallbladder. The penetration at this frequency may,
position. however, not be adequate in large or obese patients, in whom a
In some subjects the fundus of the gallbladder is folded over the lower frequency (34MHz) may be necessary. With the lower fre-
Phrygian cap which can make examination of the lumen diffi- quency the width of the beam is greater and small stones may not
cult.4 Turning the patient onto his/her left side, or even partially be demonstrated due to lack of acoustic shadowing.11 Similarly, if
prone, can unfold the gallbladder, making it more accessible to full the stone is outside the focal zone of the transducer, in the near or
ultrasound interrogation (Figs 14.7 and 14.8). Not infrequently the far fields, acoustic shadowing from a stone may be lost because the
neck of the gallbladder may be elongated, and turned back on itself. beam is wider (see Figs 14.23 and 14.24).12
This may be mistaken for a duct or vessel, or may even be missed A comprehensive examination of the biliary system naturally
altogether. The sonographer must be aware of this anatomical includes the demonstration of both liver and pancreas. The normal
shape in order to reliably exclude gallstones (Fig. 14.8C). intrahepatic bile ducts are rarely visualised during routine scans
Folding of the gallbladder is a common variation which may but it is not uncommon to display the main right and left hepatic
mimic septation. True septa are uncommon, and can be distin- ducts as thin tubular structures running parallel to the main
guished from folding of the gallbladder by scanning in both longi- branches of the portal vein (Fig. 14.1).13
tudinal and transverse planes with the patient supine and in the left An initial survey of the gallbladder with the patient supine, along
decubitus position. Septae can lead to errors in diagnosis when the with the liver and pancreas, is usual. In the majority of patients, the
sonographer reports one portion of the gallbladder as free of stones gallbladder is best imaged with the patient decubitus, as the gall-
and misses a stone in the distal portion (Fig. 14.9).5 Although not bladder flops medially, allowing the sonographer access through
usually considered clinically significant, there is some evidence that the acoustic window of the liver, and unfolding the gallbladder. In
gallbladder septae or folds may delay gallbladder emptying, par- addition, the improved access allows the sonographer to position
ticularly from the distal segment, and that this may be associated the transducer perpendicular to the long axis of the gallbladder,
with abdominal pain.6 allowing a more thorough and confident interrogation. It is helpful
The gallbladder may be totally absent, or there may be double to align the transducer along the long axis of the gallbladder, to
or even triple gallbladders with either a single cystic duct or include neck and fundus, then angling laterally and medially so
with multiple separate cystic ducts these anomalies are extremely that the entire volume of the gallbladder is examined. A subcostal
rare.7 approach may often be possible using suspended deep inspiration
228
Technique and ultrasound appearance
A B
229
CHAPTER 14 Gallbladder and biliary tree
A
B
230
Technique and ultrasound appearance
A B
Figure 14.6 Shadow from neck of gallbladder. A: Acoustic shadow from normal neck of gallbladder. B: Because the gallbladder neck
is parallel (rather than perpendicular) to the beam, sound is attenuated more by the neck wall, causing a shadow.
A B
Figure 14.7 Phrygian cap. A: Patient supine. B: Patient right side raised.
231
CHAPTER 14 Gallbladder and biliary tree
A B
Figure 14.9 Septated gallbladder. Longitudinal scan. Figure 14.10 Normal hepatic artery (arrow) crossing between
common duct (callipers) and portal vein.
232
Technique and ultrasound appearance
A B
Figure 14.13 Normal contracted gallbladder. Normal wall thickness of physiologically contracted (postprandial) gallbladder
A: Longitudinal scan. B: Transverse scan.
to bring the liver down to provide an acoustic window. However, enhancement behind the gallbladder. However, this may not be
an intercostal approach is the most successful technique in the apparent if gas-filled bowel lies immediately posteriorly (Fig.
majority of patients, allowing the gallbladder to be imaged through 14.14). In transverse scans, the gallbladder appears circular, increas-
the right lobe of the liver in quiet respiration, with the minimum of ing in diameter towards the fundus. If possible, the transducer
artefact due to scattering and reverberation from adjacent bowel. should be maintained at right angles to the long axis, as an oblique
The normal gallbladder has an echo-free lumen and is sur- section may give a spurious impression of gallbladder wall thicken-
rounded by a smooth, moderately reflective wall. Since there is little ing (Fig. 14.15).14
attenuation of the ultrasound beam, the time gain compensation The gallbladder must be examined with the patient in at least two
used appropriately for the adjacent liver will result in acoustic different positions if small mobile stones or non-mobile polyps are
233
CHAPTER 14 Gallbladder and biliary tree
Figure 14.14 Shadowing stone versus gas. Posterior to the Figure 14.16 Normal common duct anterior to portal vein. Note
gallbladder neck there is clean shadowing beyond a row of stones how the duct widens as it travels in the free edge of the lesser
(arrowhead). The bowel loop located behind the body and fundus omentum.
of the gallbladder (arrow) transmits a more reverberative dirty
shadow. Posterior enhancement behind the fluid-filled gallbladder
may not be apparent if bowel gas lies against the gallbladder.
relation of the portal vein.15 The lower end of the duct is best
demonstrated on transverse scans through the head of the pancreas
(Fig. 14.17).
A water load may be helpful in allowing visualisation of the
lower end of the common duct by displacing gas from the gastric
antrum and duodenum in the left anterior oblique position, and it
may also act as an acoustic window.
A B
Figure 14.17 Normal common duct in head of pancreas on transverse scans. A: Duct seen within pancreatic head in transverse
scan. B: Duct (callipers) entering the duodenal papilla.
A B
Figure 14.18 Measurement of the common duct. A: Callipers across the walls of a normal calibre common duct. B: Left-hand image
demonstrates over-amplification (too much gain) causing blooming of the echoes in the walls of the duct. This could give rise to inaccurate
measurements. The right-hand image illustrates an accurate duct measurement with the correct gain settings.
4. In the elderly there is a generalised loss of elasticity of the permanently dilated after surgery or non-operative drainage,
tissues and the normal duct diameter increases with or may even increase slightly in diameter.1821 Inflammation
advancing age.18 presumably reduces the elasticity of the duct wall so that it
5. The diameter of the duct is often increased in patients who becomes incapable of recoiling back down, and the resultant
have had a cholecystectomy. Ducts that were normal floppy duct will distend with minimal pressure or volume
preoperatively tend to remain normal postoperatively, while increases as the duct assumes some of the original gallbladder
ducts that were acutely obstructed usually decrease in size reservoir function.22,23
postoperatively following stone removal or drainage
procedure. However, ducts that were chronically dilated Bearing all the above in mind, a useful working rule is that the
or in which there has been chronic infection often remain diameter of the normal common duct as measured on ultrasound
235
CHAPTER 14 Gallbladder and biliary tree
Stones the structure, and the resulting shadow should be sharp and clean
(Fig. 14.22). This is in contradistinction to the shadowing beyond
The prevalence of gallstones in developed societies is approxi- bowel gas, which is caused purely by reflection of sound and is
mately 10%, and as many as two-thirds of gallstone carriers are therefore usually less well defined and dirty due to reverberation
asymptomatic.44,45 But, since the probability of developing biliary artefacts51 a useful practical point in sorting out whether shadows
symptoms for subjects with silent stones has been shown to be only are due to gallstones or to bowel gas. Shadowing beyond a stone is
1525% in 10 years,46 the increasing use of ultrasound in patients not affected by the chemical composition of the stone, the presence
with symptoms that suggest the presence of gallstones will unmask of calcium within the stone, or the shape and surface characteristics
many previously undiagnosed stones and thus create both ethical of the stone,52 but is dependent on the geometric relationship
and economic dilemmas for physicians and health care planners.47 between the ultrasound beam and the stone.53 The beam width
Only around 30% of patients with asymptomatic gallstones eventu- needs to be as small as possible since shadowing will not occur
ally require surgery. unless the stone occupies the full width of the beam (Fig. 14.23).
The standard management for symptomatic gallstones is laparo- Beam width is reduced by focusing and by using transducers of
scopic cholecystectomy, with open surgery being reserved for more higher frequency.
complex cases. Previous experience with medical (dissolution) A further practical consideration concerning the demonstration
therapies has been disappointing, as despite its excellent safety of stones in the gallbladder relates to signal processing methods.54
record there is a high incidence of stone recurrence (up to 60%) and
slow response to treatment.48
Cholescintigraphy, using a 99mTc-labelled derivative of imino-
diacetic acid, is useful as a second-line test for confirmation of cystic
duct obstruction, either when ultrasound has failed to show stones,
or when the origin of the symptoms remains in doubt in the pres-
ence of stones.
The composition, size, shape and number of stones vary widely
from patient to patient, presenting a wide range of ultrasound
appearances.
Classic appearances
The most commonly encountered ultrasound appearance of a stone
in the gallbladder is that of a highly reflective intraluminal structure
which is gravity-dependent and casts an acoustic shadow (Fig.
14.21). When all these features are present, the diagnostic accuracy
is 100%.49 It is useful to analyse each of these ultrasound features
more closely so that the limitations of the method are appreciated,
thus enabling scan technique and machine settings to be adjusted
appropriately.
The size of a structure that can produce an echo from within the
gallbladder lumen is not a limitation since it has been shown that
particles as small as 5 to 10m will produce echoes within bile.50 Figure 14.22 Gallstone shadowing. Transverse scan of
Such tiny particles are not considered to be stones, and do not fulfil gallbladder; clean shadowing from two small stones, which is free
the diagnostic criteria given above since they do not produce acous- from reverberation. Compare with the reverberation from the bowel
tic shadows. behind the gallbladder to the left of the stones.
The production of an acoustic shadow beyond a reflecting struc-
ture depends upon both the absorption and reflection of sound by
A
B D E
i ii iii
A B
Figure 14.24 Tiny stones with acoustic shadowing. A: Longitudinal scan demonstrating the shadow from a row of tiny stones (arrow).
B: The same case with the focal zone set anterior to the stones; note how the shadowing is no longer apparent as the beam is wider at
this level.
Refinement of scanning technique can further improve the accu- reaction. This condition is associated with gallstones in over 95% of
racy rates (to almost 99%), using movement of the patient during cases, but its particular importance lies in the increased incidence of
the study57 to observe differences in movement between bowel gas both gallbladder carcinoma and cholangiocarcinoma (in 10% to 20%
in the duodenum or hepatic flexure and a contracted gallbladder of cases), and prophylactic cholecystectomy is usually advised (see
full of stones. Diagnostic specificity is also aided by the observation section on gallbladder carcinoma).
of the wallechoshadow (WES) triad,58 otherwise known as the
double-arc-shadow sign.59 This complex consists of the reflective
anterior wall of the gallbladder separated by a thin echo-poor rim
Movement/layering/floating of stones
(representing either a small amount of residual bile or an echo-poor Gravity dependence of stones can be demonstrated by moving the
portion of the thickened gallbladder wall) from the reflective ante- patient during the ultrasound examination. Usually this is achieved
rior surface of the stone, which casts a complete acoustic shadow by turning the patient into the left decubitus or right anterior
(Fig. 14.26). oblique positions, but erect scans with the patient sitting or stand-
Persistent acoustic shadowing emanating from the gallbladder ing may also be performed. In this way, previously hidden stones
fossa may also be produced by a porcelain gallbladder, which is the lying in the neck of the gallbladder may come into view and
term given to calcification of the gallbladder wall.60 Wall calcifica- the distinction between polyps and stones is facilitated (Figs 14.27
tion may be the end-result of chronic infection and inflammatory and 14.28).
A B
Figure 14.27 Stone in the gallbladder. A: With the patient supine there is no evidence of any stone. B: A stone comes into view when
the patient is turned right side up.
A B
Figure 14.28 Stone in the fundus. The stone in the gallbladder neck (A, supine) is clearly seen in the fundus of the gallbladder when the
patient is scanned in the erect position (B).
239
CHAPTER 14 Gallbladder and biliary tree
Movement may also help when there are small stones from which are caused by particles 5 to 10m in size, and chemical analysis
it is proving difficult to demonstrate acoustic shadowing. If these revealed that these were mainly calcium bilirubinate granules
stones can be collected into a group then the shadow may become together with some cholesterol crystals.53
more readily visible.61 Echogenic bile may also be due to pus or blood in the bile as a
Similarly, if small stones form a thin layer on the posterior wall result of infection or trauma, or it may be seen in association with
of the gallbladder, the echoes from the stones may be erroneously obvious stones in the gallbladder (Fig. 14.32).64 In these cases, the
ascribed to the wall itself. Shadowing from small stones lying on appearances are incontrovertibly pathological, and when taken in
the posterior wall of the gallbladder may be obscured by the high
reflectivity of the wall itself or of the immediately adjacent bowel
gas, causing a blooming effect (Fig. 14.29). If such stones can be
encouraged either to float across the gallbladder lumen or to clump
together, the shadowing becomes obvious. Good technique, includ-
ing the correct use of frequency, focal zone and gain settings, is
essential in the diagnosis of tiny stones (Fig. 14.30).
Difficulties can sometimes arise when stones float up to the ante-
rior wall so that the gallbladder lumen is not visualised, but once
again, movement of the patient is crucial in avoiding this pitfall
(Fig. 14.31).
Milk of calcium bile (sometimes known as limy bile), where the
bile becomes a thick paste-like material, is another instance where
gravity dependence is an aid to ultrasound diagnosis. The appear-
ances here are predominantly those of echoes and shadowing from
the gallbladder fossa, but layering out of the milk of calcium will
be evident on the erect scans.62,63
Microlithiasis/biliary sludge
Non-shadowing, gravity-dependent echoes within the gallbladder
are variously referred to as biliary sludge or echogenic bile.
Several different pathological and physiological entities can result
in these ultrasound appearances and, since neither of the above
terms specifies a particular cause, there is considerable confusion
about the significance of these findings. Most commonly the echoes Figure 14.29 Layered stones. A layer of small stones on the
represent particles (calcium salts) that have precipitated from the posterior wall is difficult to separate from the wall echoes, but note
bile. In-vitro studies have shown that the echoes in biliary sludge the band of distal shadowing.
A B
Figure 14.30 Technique for small stones: transverse scan of the gallbladder. A: Line density has been increased by reducing the area
of scan, and the frequency has been increased from the normal liver setting. B: The focal zone has been moved alongside the gallbladder
to display the small stones.
240
Pathology of the gallbladder
Figure 14.31 Floating stones. The gallbladder lumen may be Figure 14.32 Stones and echogenic bile. Stones in the neck of
masked by the shadow from stones which float up to the the gallbladder (shadowing) with inspissated bile, or biliary sludge,
anterior wall. filling the gallbladder lumen.
A B
Figure 14.33 Echogenic bile. A: Transverse scan through a gallbladder containing non-shadowing echogenic material in a patient who
had been on intravenous feeding. B: Layering gallbladder sludge in a fasting patient.
conjunction with the patients history, physical signs and other sludge (Fig. 14.35). This may give rise to a diagnostic dilemma
ultrasound features, the diagnosis can be quite specific. since the appearances may mimic a soft tissue mass projecting into
However, echogenic bile may also be seen when there is bile the gallbladder lumen, resulting in a false diagnosis of gallbladder
stasis in the absence of stone disease, and several clinical conditions tumour or polyp (Fig. 14.36).69 Movement of the echoes with gravity
have been associated with this including pregnancy, rapid weight should be the key to differentiating these conditions, but the bile in
loss, parenteral nutrition (Fig. 14.33), octreotide therapy and bone these cases may be thick and viscid so that movement of the echoes
marrow transplant.65 may be imperceptibly slow. A repeat scan with a normal diet in the
Microlithiasis may also be due to pathological biliary obstruction interim should reveal the true nature of the problem.70
or physiological factors, such as gallbladder dysmotility, and can
be associated with biliary colic, acute cholecystitis and, in a minor-
ity of cases, recurrent acute pancreatitis.66 The larger particles are Gallbladder wall thickening
an intermediary step towards the formation of gallstones67 (although
this result is by no means inevitable if biliary sludge is In the fasting state, the normal gallbladder is distended and has a
demonstrated). wall thickness of less than 3mm.71 The normal anterior wall appears
It has been pointed out that some non-shadowing echoes within as a single smooth well-defined reflecting structure and its
the gallbladder are due to slice thickness artefacts. Clues that should thickness can be measured accurately, while the posterior wall can
alert the sonographer to this possibility include non-dependence on be more difficult to measure because this wall is frequently in
receiver gain and lack of change in height of debris between scans contact with air-containing bowel and the end-point is indistinct
performed in transverse and longitudinal planes (Fig. 14.34).68 (Fig. 14.37).
Occasionally non-shadowing echoes within the gallbladder may When the gallbladder contracts in response to a fat-containing
clump together, giving the so-called sludge balls or tumefactive meal or injection of cholecystokinin, the wall becomes thicker72 and
241
CHAPTER 14 Gallbladder and biliary tree
Figure 14.34 False echogenic bile. Slice thickness artefact Figure 14.37 Non-fasting gallbladder. Normal non-fasting
causing echoes within the gallbladder on the left-hand image. gallbladder wall. Longitudinal scan.
The bile is echo-free after slight readjustment of transducer
angulation on the right-hand image.
Figure 14.39 Gallbladder wall in hypoalbuminaemia. Thickened Table 14.1 Causes of gallbladder wall thickening
gallbladder wall in a patient with hypoalbuminaemia but no ascites. Physiological:
Postprandial
Inflammatory disease of the gallbladder:
Acute cholecystitis
Chronic cholecystitis
Sclerosing cholangitis85
AIDS86
the presence of ascites was due to the underlying hypoalbuminae- Crohns disease87
mia with shift of fluid from the intravascular to extravascular space. Non-inflammatory disease of the gallbladder:
Patients with non-portal hypertension ascites, due to malignancy, Adenomyomatosis
are more frequently found to have normal gallbladder wall Carcinoma of gallbladder
Leukaemia
thickness.78,79
Multiple myeloma
Gallbladder wall thickening can be seen in the presence of ascites
Oedema of the gallbladder wall:
even when the serum albumin level is normal and care is taken over Ascites
transducer angulation,80 and in these cases the wall thickening is Hypoalbuminaemia
caused by ascites per se, presumably due to passive diffusion of Heart failure
fluid. A further twist to the tale has been provided by the observa- Portal hypertension
tion that in patients with cirrhosis of the liver, portal hypertension Renal disease
can give rise to thickening of the gallbladder wall congestive Malignant lymphatic obstruction88/lymphoma
cholecystopathy due to venous dilatation in the absence of either Adjacent inflammatory disease:
hypoalbuminaemia or ascites,81 and colour or power Doppler can Acute viral hepatitis
assist in identifying varices of this nature. Alcoholic hepatitis89
The gallbladder wall thickens in response to a wide range of Acute pancreatitis
pathological processes (Fig. 14.40) (see Table 14.1) and is thus a very Pericholecystic abscesses
non-specific sign when used in isolation.82 However, several of the Hepatobiliary schistosomiasis90
conditions listed in Table 14.1 result in other ultrasound findings;
the detection of gallbladder wall thickening may then provide
useful contributory or confirmatory evidence.
Ultrasound signs may, of course, have uses other than purely
diagnostic. In acute viral hepatitis, gallbladder wall thickening has
There is no single ultrasound sign that is specific for the diagnosis
not only been observed,83 but has also been shown to correlate well
of acute cholecystitis; rather there is a range of findings which
with the degree of liver cell necrosis84 and thus carries prognostic
are conveniently discussed as either major or minor signs
implications (Fig. 14.41).
(Table 14.2).
Most studies have indicated that the sensitivity for a major sign
Acute cholecystitis of acute cholecystitis is 8186%, and the specificity is 9498%. The
addition of a minor sign increases the sensitivity of ultrasound to
Most patients presenting with acute cholecystitis undergo laparo- 9098%.92 Not reflected in these figures for sensitivity and specifi-
scopic cholecystectomy, following analgesia, within the first week city is the ability to diagnose non-biliary sources of right upper
of the onset of symptoms.91 This trend for urgent cholecystectomy quadrant pain in as many as 35% of the patients without gall
demands that the diagnosis is made quickly, and therefore for disease.93
patients who present with acute right upper quadrant pain, ultra- Increased thickness of the gallbladder wall (Fig. 14.42) is well
sound is the initial imaging procedure of choice, also enabling a documented in acute cholecystitis,94,95 but as discussed above, it is
search to be made for other causes of the patients pain.43 found in many other conditions, and is thus a minor sign. However,
243
CHAPTER 14 Gallbladder and biliary tree
Major Minor
A B
Figure 14.48 Large pericholecystic abscess (arrows) extending into the liver from the thick-walled gallbladder which is seen to contain
stones. A: Longitudinal scan. B: Transverse scan.
Figure 14.49 Emphysematous cholecystitis. Thickened Figure 14.50 Acalculous cholecystitis. Thickened gallbladder
gallbladder wall containing an area of high reflectivity with distal wall in acalculous cholecystitis.
shadowing due to gas.
increasing use of high-resolution ultrasound in suspected biliary specificity may be improved by ultrasound-guided percutaneous
disease, however, the condition is being diagnosed with increasing aspiration of the gallbladder so that bacteria and/or leukocytes can
frequency and a spectrum of severity is now recognised whereby be detected in the bile,121 but initial enthusiasm for the technique
conservative treatment may be considered in a proportion of has become tempered by the limitation that a negative result does
patients.117 Emphysematous cholecystitis may occur in the absence not exclude acute cholecystitis.122 This is only to be expected when
of gallstones usually in diabetics it is postulated that ischaemia it is remembered that in patients coming to surgery for acute chole-
of the gallbladder wall may be a primary factor in these cases. cystitis, only approximately half have infected bile from which
Acute cholecystitis is acalculous in approximately 510% of all aerobic or anaerobic organisms may be cultured.
patients with acute cholecystitis.118 It frequently occurs as a compli- In patients with acute cholecystitis who are unsuitable for
cation of a prolonged or severe illness such as recent major surgery, surgery, and in whom antibiotics have not been effective, percuta-
burns, sepsis, prolonged hypotension, general debility and diabe- neous gallbladder drainage under ultrasound guidance represents
tes.119 Histologically, the changes in the gallbladder wall are similar an effective, bedside treatment,123 with aspiration being preferred
to calculous cholecystitis, although gangrene and perforation are over cholecystostomy due to its lower complication rate.124
more common in the acalculous variety presumably because of
delayed diagnosis and treatment. The lack of stones and the inabil-
ity to elicit the ultrasonic Murphys sign in a comatose patient Chronic cholecystitis
contribute to the diagnostic difficulty, although thickening of the
gallbladder wall in association with a lack of response of the gall- Chronic cholecystitis, which is associated with recurrent right
bladder to cholecystokinin, distension of the gallbladder and the upper quadrant pain, is almost always found in association with
presence of sludge are helpful signs (Fig. 14.50).120 Diagnostic gallstones although the exact aetiology is unclear and the classic
246
Pathology of the gallbladder
A B
Figure 14.51 Chronic cholecystitis. A: Contracted, thick-walled gallbladder containing stones. B: Irregularly thickened, hyperechoic
gallbladder wall, with stones.
chicken and egg debate continues to rage. Chronic inflammation wall, with intramural diverticula which may be echo-free if they
of the wall is likely to be associated with repeated episodes of contain fluid bile, or highly reflective if they contain bile concre-
(sometimes) subclinical acute cholecystitis, together with mechani- tions. Segmental and eccentric wall thickening may produce mid-
cal abrasion of the gallbladder wall from stones. cavity strictures, and the high-amplitude periluminal foci (due to
In association with the stones there is a chronic inflammatory cell aggregates of solid bile elements in the RokitanskyAschoff sinuses)
infiltrate throughout all the layers of the wall which becomes thick- give a typical diamond ring appearance on transverse sections of
ened with fibrosis in both the subserosal and muscular layers, the gallbladder (Fig. 14.52).129
resulting in overall shrinkage of the viscus and reduction of the The clinical significance of adenomyomatosis of the gallbladder
lumen. In this clinical context, the ultrasonic demonstration of is controversial since it is found in both symptomatic and asymp-
stones in the gallbladder, with or without thickening of the gall- tomatic individuals. However, a significant proportion of patients
bladder wall, is usually taken to be diagnostic (Fig. 14.51). with adenomyomatosis do improve after cholecystectomy, espe-
If the presence of ultrasonically demonstrated gallstones is taken cially if the symptoms were more suggestive of biliary colic than of
as an indicator of chronic gallbladder disease as defined by vague dyspepsia, or if gallstones are found in association with the
surgery, then ultrasound has been found to have a sensitivity adenomyomatosis. Segmental adenomyomatosis, in which the gall-
ranging from 90% to 98%, with specificity consistently in the 94 bladder is effectively divided by a stricture into two compartments,
98% range.92 predisposes to cholecystolithiasis, particularly in the fundal com-
If clinical suspicion persists in the case of a normal ultrasound, partment, due to bile stasis.130
MRCP is useful in identifying stones in the common duct in addi- The strawberry gallbladder of cholesterolosis, another non-
tion to demonstrating possible biliary duct anomalies.125 inflammatory condition of the gallbladder, is the result of the accu-
mulation of lipids in the mucosa of the gallbladder wall. The
Hyperplastic cholecystoses resulting surface nodules are usually less than 1mm in diameter,
which may be difficult to demonstrate on ultrasound, but larger
polypoid excrescences forming cholesterol polyps may also develop.
In some cases of chronic cholecystitis, the lining epithelium of the
These are displayed as small reflective foci attached to the wall of
gallbladder extends between the muscle bundles, giving rise to
the gallbladder which do not exhibit posterior shadowing or mobil-
deeply situated gland-like structures, known as Rokitansky
ity with patient movement (Fig. 14.53).131
Aschoff sinuses. When extensive, these diverticula form numerous
The aetiology of cholesterolosis is not fully understood. It is sug-
gland-like spaces lined by epithelial cells that extend throughout
gested that the mucosal changes might arise simply because of
the gallbladder wall. A focal increase in wall thickness may result
increased cholesterol uptake from bile containing extra cholesterol,
in localised narrowing of the gallbladder lumen, giving rise to the
and a correlation with high serum cholesterol has been demon-
appearance of a stricture. The term cholecystitis glandularis prolif-
strated,132 but this remains controversial and the exact causes are
erans has been applied to such a condition.
complex and likely to be multifactorial.133 Whilst cholecystectomy
However, these hyperplastic changes in the gallbladder wall
is unlikely to benefit patients with vague dyspeptic symptoms, it is
may occur in the absence of either gallstones or inflammatory infil-
likely to help patients in whom the history suggests biliary colic, or
trates, when the condition is known as adenomyomatosis.126 Aden-
when there are associated gallstones.134
omyomatosis is thought to be present in up to 5% of the adult
population,127 and has also been recorded in the paediatric popula-
tion. It is distinct from chronic cholecystitis, and although excessive Polyps
intraluminal pressure has been suggested as the cause, the exact
aetiology remains unclear. Polyps of the gallbladder include pseudo-tumours such as inflam-
The ultrasound features of adenomyomatosis are well recog- matory polyps, cholesterol polyps and adenomyomas, the localised
nised.128 There is diffuse or segmental thickening of the gallbladder form of adenomyomatosis. They are common, and in the absence
247
CHAPTER 14 Gallbladder and biliary tree
A B
248
Pathology of the gallbladder
of accompanying gallstones are probably not clinically significant ultrasound. CT is useful in identifying early signs of malignancy in
if small. large polyps prior to surgery.
The commonest type of true benign neoplasm is the adenoma, Contrast-enhanced ultrasound has been used in helping to dif-
which can be either sessile or papillary and is usually solitary.135 ferentiate gallbladder polyps and carcinomas from sludge balls141
Adenomatous gallbladder polyps have been described in Peutz but as vascularity in the form of contrast uptake is demonstrable in
Jeghers syndrome;136 10% are multiple, and 10% show evidence of the majority of larger lesions,142 and also occurs in different types
carcinoma in situ.137 Intestinal metaplasia can be found in large of polyps, its clinical usefulness is limited (Fig. 14.57).
adenomas and may be a premalignant change138 and, as in the There are other benign neoplasms of the gallbladder including
intestinal tract, it is probably the larger adenomas that undergo fibroma, lipoma, myoma, carcinoid and haemangioma, but they are
malignant transformation. Adenomas are usually incidental find- all extremely rare.143
ings, but they can cause biliary colic.
The typical ultrasound appearance is of a soft tissue mass project- Carcinoma
ing into the gallbladder lumen (Figs 14.54 and 14.55). It remains
fixed to the gallbladder wall despite movement of the patient and
does not cast an acoustic shadow (Fig. 14.56). Because of the prob- Carcinoma of the gallbladder is a highly malignant tumour charac-
ability of an adenoma/carcinoma sequence, cholecystectomy is terised by early metastases and a 5-year survival rate of less than
advisable if the polyp is 10mm or larger, even for asymptomatic 5%.144 although this can be improved in cases of early detection.145
polyps.139 Other risk factors for malignancy include a wide-based, It is the fifth most common malignancy of the gastrointestinal tract,
or sessile polyp, irregularity of the surface, solitary lesions and age and the most common cancer of the biliary tract worldwide, com-
over 50.140 Polyps that show a tendency to enlarge are also at higher prising 13% of all cancers. It affects females four times as com-
risk of malignant transformation, and may be monitored with monly as males, and its prevalence increases with age. There is a
Figure 14.55 Two hyperplastic polyps within the same Figure 14.57 Contrast ultrasound of gallbladder polyps shows
gallbladder. take-up of contrast in the polyps.
249
CHAPTER 14 Gallbladder and biliary tree
high correlation with gallstones (8090%) and chronic cholecystitis, evidence of biliary obstruction, porta hepatis or peripancreatic lym-
suggesting that chronic inflammation of the gallbladder mucosa phadenopathy, or liver metastases.96
may result in a dysplasia which goes on to neoplastic transforma- Although the overall prognosis for this tumour remains bleak
tion. Up to 1.5% of patients undergoing cholecystectomy for stones with a mean survival of less than 5 months from the time of diag-
turn out to have gallbladder carcinoma.146 nosis, ultrasound may facilitate treatment of early and curable car-
Early diagnosis of this tumour is difficult, and frequently not cinomas by the fortuitous detection of tumours in patients who are
made until local spread and metastases have occurred, but the asymptomatic or who have symptoms attributable to the coexistent
ultrasound detection of gallbladder wall irregularities,147 or of a stones.155 In countries where the rate of cholecystectomy for chole-
complex reflective mass obliterating the gallbladder lumen,148 may lithiasis has increased, there has been a corresponding decrease in
enable the diagnosis to be made preoperatively. the mortality from gallbladder carcinoma.156
The various ultrasonic appearances of gallbladder carcinoma149152 As with any other abdominal viscus, blood-borne metastases
have been well described. The most common finding is of a large may find their way to the gallbladder, albeit rarely, and asymmetri-
solid mass filling the gallbladder bed (Fig. 14.58). This appearance cal wall thickening or polypoid intraluminal masses may be
is non-specific, the underlying nature of the mass being implied by indistinguishable from primary gallbladder cancer (Fig. 14.60).157
the lack of visualisation of a separate gallbladder lumen or the pres- Malignant melanoma is the most common source of gallbladder
ence of stones within the mass. The tumour may also be detected metastases although this is rare, and associated with an extremely
as an irregular polypoid mass within the gallbladder lumen, or as poor prognosis.158
irregular thickening of the gallbladder wall which may be focal or
diffuse, or as a combination of the two. In patients with gallbladder
polyps, the risk of malignant transformation is increased in polyps Worms
of 10mm or over, and in patients aged over 50.153 For this reason,
cholecystectomy is advised in such cases. Parasitic infections are common in tropical countries, and may find
Local extension of the tumour into the adjacent liver is also their way into the gallbladder and/or bile ducts, causing biliary
readily identifiable with ultrasound.154 However, CT is still the obstruction, cholangitis or even cholangiocarcinoma. They are
method of choice for staging purposes, particularly in the detection increasingly recognised on ultrasound as worldwide travel exposes
of lymphatic and peritoneal spread. individuals in non-endemic areas to parasites, with a consequent
Approximately 25% of patients with a porcelain gallbladder (cal- improvement in the understanding of the imaging features of
cification of the gallbladder wall) will have associated carcinoma, infestation.
and the lesion may be obscured by the acoustic shadow arising
from the calcified anterior wall. Differentiating a porcelain gallblad-
der from a gallbladder full of stones is important because of this
Ascariasis
high risk of malignancy. With careful scanning, the non-calcified The Ascaris lumbricoides roundworm is the most common parasitic
anterior wall of the gallbladder can be seen in the case of stones,58,59 infestation of the gastrointestinal tract worldwide, and is endemic
while the calcified posterior wall of a porcelain gallbladder may be in the Far East, countries of the former Soviet Union, Latin America
seen, giving diagnostic appearances of a biconvex curvilinear reflec- and Africa. Worldwide it is probably second only to gallstones as
tive structure (Fig. 14.59).60 The development of a carcinoma within a cause of acute biliary symptoms. The adult worm is 1550cm long
a porcelain gallbladder can be detected if there is local or diffuse and some 5mm thick, and lives mainly in the jejunum. It has a
thickening of the gallbladder wall external to the calcified portion, propensity to migrate up into the common bile duct from where it
an eccentric mass arising from the gallbladder wall, or if there is may enter the gallbladder or intrahepatic bile ducts. It may then
A B
Figure 14.58 Carcinoma of the gallbladder producing a large, ill-defined solid mass in the gallbladder fossa note the colour flow
within the mass. A: Longitudinal scan. B: Transverse scan.
250
Pathology of the gallbladder
A B
Figure 14.59 Porcelain gallbladder. A: X-ray showing typical gallbladder wall calcification. B: Transverse scan through the gallbladder
demonstrating calcification of the inner wall.
A B
C D
Figure 14.60 Metastatic deposits (arrows) from an anaplastic lung primary are seen in the gallbladder wall as echo-poor nodules.
A: Longitudinal scan. B: Transverse scans. C: Metastases from malignant melanoma giving rise to a clearly defined, slightly heterogeneous
soft tissue lesion arising from the gallbladder wall, oblique scan and D: transverse scan.
A B
Figure 14.61 Worms in gallbladder. Longitudinal scan (A) and transverse scan (B) showing curved worm in the gallbladder lumen.
252
Bile duct pathology
Ultrasound has been shown to be highly accurate in diagnosing removal of the stone, but may remain baggy and mildly dilated
surgical jaundice, detecting dilatation of the intrahepatic or extrahe- in around 25% of cases.191
patic biliary tree in 8595% of patients with proven obstruction,171177 Dilatation of the intrahepatic bile ducts is usually most appar-
and has a high positive predictive value for obstruction with an ent near the porta hepatis if the obstruction is in the common
incidence of false positive findings of less than 5%. Ultrasound is duct, with dilatation of the left hepatic ducts often being more
also highly accurate at defining the level of obstruction, although noticeable than those in the right lobe in the early stages of
the actual cause may be diagnosed in only about a third of patients. obstruction. The ultrasound appearances of dilated ducts have
Obstruction may occur without duct dilatation (see below) and been variously described as the parallel channel192 and double-
thus there is a false negative rate although, more recently, the barrelled shot-gun193 signs, which depend upon the bile ducts
reported sensitivity for the detection of choledocholithiasis has dilating to become equal to or greater than the diameter of the
increased to over 80%.178,179 These results are attributable to improve- adjacent portal vein branch. (When scanned along their long axes,
ments in equipment and meticulous scanning technique. Further- these structures are seen as two parallel channels, while in cross-
more, the introduction of endoscopic ultrasound has demonstrated section the appearance is apparently reminiscent of looking into a
sensitivities of up to 97% in the detection of CBD stones180 and, double-barrelled shot-gun) (Fig. 14.66). When the parallel chan-
although invasive, has the advantage of improved sensitivity for nels occur in a fatty liver the outer walls may be masked by the
stone detection. In cases of biliary duct dilatation, EUS is also accu- high reflectivity of the liver parenchyma. In this case all that is
rate in diagnosing the cause of obstruction181,182 in cases of stricture, seen is the interface between the vein and duct, giving rise to the
neoplasm and other, extra-ductal causes of obstruction relating to stylet sign (Fig. 14.66B).194 Care should be taken, however, not to
the ampulla and head of pancreas. EUS is considered a safe and confuse biliary duct dilatation with the double channel of a
useful technique for selecting patients for therapeutic ERCP, allow- thrombosed portal vein in portal hypertension, and consequent
ing many patients to avoid the potential complications of a purely increased diameter of the hepatic artery. Careful examination of
diagnostic ERCP.183 the main portal vein should establish if it is thrombosed, and
whether the artery is dilated. Colour Doppler will differentiate
the main artery from the portal vein, but will not, of course, dis-
tinguish a thrombosed portal vein and a dilated bile duct, neither
Bile duct dilatation of which demonstrates flow.
When scanning a patient with dilated intrahepatic ducts, there is
The ultrasound diagnosis of obstructive (surgical) jaundice depends often an immediate overall impression of too many tubes in the
upon the detection of bile duct dilatation. liver. These tubes do not correspond to hepatic arteries or portal
Within the liver, the normal non-dilated small bile ducts are veins, and must be bile ducts (Fig. 14.67).195 The nature of the
difficult to visualise on ultrasound. The larger main right and left branching pattern of the intrahepatic bile duct system is such that
bile ducts can be identified as tubular structures running when dilated, the ducts are seen to converge together, giving a
anterior to and parallel with the right and left branches of the portal characteristic stellate pattern. This is in contradistinction to the
vein and measure up to 2mm in diameter in the non-dilated branching pattern of the portal veins which have a more orderly
system (Fig. 14.65).184,185 The diameter of the normal common duct arrangement whereby the peripheral branches all take origin from
at the porta hepatis should be less than 5mm,186,187 increasing the main right and left branches (Fig. 14.68).196
slightly (less than 6mm) as the duct runs caudally in the free edge Finally, the fluid in the dilated bile ducts is clear bile and
of the lesser omentum188 and within the head of the pancreas. ultrasound is transmitted without attenuation. When, as is usual,
The diameter of the non-obstructed duct does increase with age189 the time gain compensation is set to compensate for the livers
or if there has been previous obstruction.190 The dilated preopera- attenuation, there will be increased through transmission of
tive duct returns to a normal diameter in 75% of patients following sound (enhancement) beyond dilated ducts (Fig. 14.69). This is
A B
Figure 14.65 A: Normal intrahepatic bile duct. Right hepatic duct (arrow) seen running anterior to right branch of portal vein. B: A different
case demonstrating a dilated CBD (callipers) with branching dilated intrahepatic ducts.
254
Bile duct pathology
A B
Figure 14.66 Dilated intrahepatic bile duct. A: Parallel channel or double-barrelled shot-gun sign of dilated ducts. B: Stylet sign; the
linear echo represents the interface between the vein and dilated duct.
A B
Figure 14.68 A: Dilated intrahepatic bile ducts near the periphery of the liver form a stellate branching pattern. B: Colour Doppler
demonstrating the dilated duct (no flow) next to the normal portal vein (in red.).
A B
Figure 14.69 Dilated intrahepatic bile ducts. A: Enhancement beyond dilated ducts. B: Duct dilatation with posterior enhancement
results in a patchy echotexture within liver which can be difficult to interpret.
Figure 14.71
Choledocholithiasis. A:
Distended gallbladder (gb)
due to (B) a stone obstructing
the common duct (CBD)
(arrow). C: Confirmed on
ERCP prior to stone removal.
B 257
CHAPTER 14 Gallbladder and biliary tree
However, whenever duct dilatation is encountered, it is useful to sufficiently to cause duct dilatation, and the temporal lag
assess the degree of distension of the gallbladder as this may offer between onset of obstruction and onset of dilatation.201
a clue to the level of the obstructing lesion. A distended gallbladder 3. The absence of a bile pool around stones in the duct impairs
suggests a low common duct obstruction, while a contracted gall- the ability of the ultrasonographer to spot the stones. The
bladder is consistent with obstruction above the level of the cystic contrast between the reflectivity of solid stone and the
duct insertion. But the possibility of dual pathology must always echo-free nature of fluid bile that is so useful in the diagnosis
be considered, and the gallbladder findings must be regarded as of stones in the gallbladder is not present when the stones are
supportive rather than of primary importance. in direct contact with the highly reflective walls of the duct
and the adjacent gas-containing bowel. A particularly
Choledocholithiasis embarrassing situation can arise when the duct is absolutely
A B
Figure 14.73 Stone in non-dilated duct. A: A stone is present at the lower end of the normal calibre CBD. Note the shadowing from
the stone is difficult to recognise due to the close proximity of bowel. B: MRCP of the same case demonstrating the stone in the non-
dilated duct.
258
Bile duct pathology
full of stones, giving rise to a highly reflective structure with from other intraluminal pathology such as blood clot, tumour
distal acoustic shadowing which is misdiagnosed as bowel or parasitic infection.
gas (Fig. 14.74). 5. Gas in the bile duct may give ultrasound appearances
4. As many as 10% of common duct stones may lack a distal identical to those of stones, i.e. high reflectivity and acoustic
acoustic shadow,220,221 especially when the stones are at the shadowing emanating from within the duct lumen (Fig.
lower end of the duct (Fig. 14.75). This phenomenon may be 14.76), and may obscure the presence of stones. The gas is
due to the differing composition of common duct stones (as usually widely distributed throughout the intrahepatic biliary
compared to gallbladder stones), and indeed some are merely ducts and thus the nature of the problem should be apparent
conglomerations of soft sludge, or to technical factors such as to the sonographer. However, the increasing incidence of
gain settings, transducer frequency and focusing, and endoscopic sphincterotomy severely restricts the usefulness of
reflection/refraction of sound by the curved walls of the duct. ultrasound in searching for retained stones after surgical or
Non-shadowing stones in the duct cannot be distinguished endoscopic procedures.
A B
Figure 14.74 Stones filling the lumen of the common duct (A) casting a posterior acoustic shadow(s). B: Shadows from a row of
stones within the right intrahepatic bile duct.
A B
Figure 14.75 No shadowing from stones within the common duct. A: Stone (arrow) in the lower duct. B: MRCP of patient in A,
confirming stones at the lower end of the duct.
259
CHAPTER 14 Gallbladder and biliary tree
Developments in equipment and transducer technology do clue to a calculous aetiology of biliary obstruction is the dispropor-
permit the demonstration of small stones within minimally dilated, tionate dilatation of the extrahepatic biliary tree in comparison to
or even normal calibre ducts, as long as meticulous scanning tech- the intrahepatic ducts. When this is noted, the search for a calculus
nique is employed. It is important to scan the common duct in both should be even more diligent. However, despite all these efforts,
longitudinal and transverse scan planes (Fig. 14.77), to be prepared approximately 30% of common duct stones will be missed mainly
to employ various patient positions, including decubitus with right due to impaction in the lower end of the common duct where they
side raised (Fig. 14.78), as well as upright and semi-upright posi- are hidden by the duodenum (Fig. 14.79). MRCP and EUS are
tions, and to use water in the stomach and duodenum, all in an helpful in demonstrating ductal stones in the presence of a negative
effort to demonstrate pathology in the common duct. An important percutaneous ultrasound and continuing clinical suspicion.222
A B
Figure 14.77 Stone in the lower end of the common bile duct. A: Stone (with posterior shadowing identified) within the lower end of
common duct. B: Confirmed on MRCP.
260
Bile duct pathology
inspection by the pathologist. It is this latter form of cholangiocar- The ultrasound visibility of these tumours may increase after a
cinoma that presents on ultrasound as biliary dilatation without a biliary stent has been inserted (percutaneous or endoscopic) (Fig.
detectable mass, possibly with some increased reflectivity and 14.83), and it is often then possible to visualise the lesion sufficiently
thickening of the duct wall, and is thus extremely difficult to well to permit ultrasound-guided confirmatory biopsy. However,
diagnose. cholangiocarcinomas have a fibrous nature making it difficult to
obtain samples adequate for cytological confirmation via fine- duct as it traverses the gland prior to entering the duodenal papilla.
needle aspiration, so that a cutting biopsy for a histological sample Acute pancreatitis may cause transient extrahepatic duct dilatation
is often necessary. but usually does not result in intrahepatic duct dilatation (Fig.
Ultrasound may provide additional information in the diagnosis 14.86), whereas the fibrous stricturing of the common duct of
of cholangiocarcinomas, although it tends to under-diagnose chronic pancreatitis may be indistinguishable from malignant
the extent of large lesions. Contrast ultrasound can provide a more disease both on ultrasound and at surgery. Carcinomas of the head
accurate picture of the extent and potential operability of the of the pancreas are characteristically hypoechoic, solid masses into
lesion (Fig. 14.83CE). Direct invasion to involve surrounding struc- which the dilated common duct can be followed (Fig. 14.87). Detec-
tures such as the portal vein, hepatic artery and liver substance, as tion of coexistent pancreatic duct dilatation provides useful con-
well as metastatic spread to regional lymph nodes, are all demon- firmatory evidence of pancreatic pathology, and ultrasonic double
strable on ultrasound (Fig. 14.84). However, the demonstration duct dilatation may be caused by chronic pancreatitis, impacted
of extrahepatic spread is limited with ultrasound, and helical pancreatic and biliary calculi, and ampullary carcinoma, as well as
CT, MRCP and, more recently, PET-CT, can improve the by pancreatic carcinoma. Ultrasound is highly sensitive for duct
accuracy of staging in patients with cholangiocarcinoma prior to dilatation but has less specificity than the ERCP sign of double duct
surgery.239 obstruction, which is almost invariably due to pancreatic carci-
As well as metastasising to the liver, cholangiocarcinomas may noma (Fig. 14.88).
be multifocal and may be indistinguishable from hepatic metastatic Ampullary carcinoma is difficult to identify on ultrasound. The
disease on ultrasound, and from sclerosing cholangitis on cholangi- findings of dilatation of the common duct with a normal head of
ography due to the multiple strictures in the biliary tree. pancreas should raise the suspicion of this tumour, especially if pan-
creatic duct dilatation is also detected. The diagnosis must be
made endoscopically, and it is important that it is not overlooked,
since these tumours often present early with jaundice (due to their
Other tumours obstructing the bile ducts strategic location) and radical surgery may offer a good chance
of cure.
Biliary ducts may be obstructed by intrahepatic tumour, enlarged
lymph nodes at the porta hepatis, carcinoma of the head of the
pancreas and ampullary tumours.
The lymph nodes at the porta hepatis are not usually demonstra- Choledochal cysts
ble on ultrasound scans unless enlarged. Because of their proximity
to the confluence of the right and left hepatic ducts and their dis- Choledochal cysts usually present in children or young adults, and
tribution along the length of the common duct, the bile ducts may are discussed more fully in Chapter 69. The ultrasound appear-
be compressed and obstructed by lymphomatous or metastatic ances are usually of massive cystic dilatation of the extrahepatic
disease in the nodes. The nodal nature of a mass at the porta hepatis common duct, although the main intrahepatic ducts may be
is usually obvious on ultrasound by carefully observing the affected.240243 The underlying anomaly is thought to be an abnor-
interfaces that indicate that the tumour is composed of several mal insertion of the common duct into the distal pancreatic duct,
discrete masses and, whilst it is true that lymphoma usually results resulting in reflux of pancreatic secretions into the common duct
in large nodes that are particularly poorly reflective, biopsy is that cause fibrotic structuring and obstruction to the biliary
required for accurate distinction between lymphoma and metas- tree.244,245 The condition is more common in females and East
tases (most frequently from colon, stomach, pancreas and breast) Asians and presents with jaundice, fever and pain (due to cholan-
(Fig. 14.85). gitis) with a palpable right upper quadrant mass (Fig. 14.89). As
Enlargement of the head of the pancreas, whether due to inflam- well as recurrent cholangitis, complications include stone forma-
mation or malignancy, may compress the lower end of the common tion with progression to biliary cirrhosis and portal hypertension
263
CHAPTER 14 Gallbladder and biliary tree
A B
Figure 14.86 Dilated common duct due to acute pancreatitis. A: Longitudinal scan. B: Transverse scan showing the oedematous,
inflamed pancreas.
A B
Figure 14.87 Dilated common duct due to pancreatic carcinoma. A: Longitudinal scan showing dilated common and hepatic ducts.
B: Transverse scan showing the dilated CBD (arrow) in the head of pancreas with a dilated pancreatic duct (callipers).
and an increased incidence of cholangiocarcinoma. The differential liver substance (Fig. 14.91).249250 These cysts represent non-
diagnosis includes other fluid-filled masses such as hepatic cyst, obstructive saccular dilatation of the intrahepatic biliary tree,251
pancreatic pseudocyst, enteric duplication, hepatic artery aneu- which can be demonstrated on CT, percutaneous cholangiography,
rysm246 and echinococcal disease (Fig. 14.90). Confirmation of the ERCP or MRCP. The extrahepatic bile ducts are usually unaffected.
diagnosis may be obtained from 99mTc-HIDA scintigraphy, when Stones may form within the cysts or dilated ducts, giving rise to
excretion of radioactivity into the cyst will confirm its continuity cholangitis which may progress to the formation of pyogenic liver
with the biliary system. abscesses. There may be an association with renal tubular ectasia
or other forms of cystic disease of the kidney, and there is a rather
uncertain relationship to congenital hepatic fibrosis in which there
Carolis disease is bile duct proliferation and multiple strictures with proximal
cystic dilatation252 also in association with renal cystic disease,
Carolis disease congenital dilatation of the intrahepatic bile usually of the infantile polycystic type. Caroli himself classified the
ducts,247 otherwise known as communicating cavernous ectasia of condition into two types: the pure form without hepatic fibrosis or
the intrahepatic ducts248 is an autosomal recessive disorder in which portal hypertension, and a second type associated with congenital
ultrasound scanning reveals multiple cystic spaces throughout the hepatic fibrosis.253
264
Bile duct pathology
A B
Figure 14.88 Double duct obstruction due to pancreatic carcinoma. A: Dilatation of the common bile duct in the liver. B: Dilatation
of the pancreatic duct (arrow).
A B
Figure 14.89 Choledochal cyst. A: Longitudinal scan (arrow). B: Transverse scan showing aneurysmally dilated common duct with no
intrahepatic duct dilatation. Callipers are shown across the normal calibre proximal duct, leading into the choledochal cyst.
The differential diagnosis includes severe biliary dilatation due resection is appropriate, but in cases of the diffuse form, transplan-
to any of the other causes of biliary obstruction, polycystic disease tation may be considered curative.
of the liver (in which the cysts do not communicate with the bile
ducts or each other) and congenital hepatic fibrosis. Other non-
invasive imaging tests, such as 99mTc-HIDA scanning, may help in
diagnosis,254 but, as alluded to above, it has been speculated that Oriental cholangiohepatitis
Carolis disease, polycystic disease and congenital hepatic fibrosis
are all parts of the same spectrum,255 and hence MRCP or CT may Recurrent pyogenic cholangitis, also known as oriental cholan-
be needed for a specific diagnosis. The condition may sometimes giohepatitis, is endemic in southeast Asia but now occasionally
be lobar, affecting only part of the liver, in which case surgical recognised in Western societies, particularly amongst the Asian
265
CHAPTER 14 Gallbladder and biliary tree
population.256 It is characterised by recurrent attacks of cholangitis, diagnosis, further imaging including MRCP, CT or cholangiogra-
due to peribiliary fibrosis which causes biliary duct strictures, and phy may be needed for full evaluation.
is caused by the adult worms of the Clonorchis sinensis liver fluke
which are ingested by humans in raw freshwater fish. However, the
parasites are not found in all patients with the clinical condition, Biliary ascariasis
and some authorities question the causal relationship.
The ultrasound features consist of massively dilated bile ducts The Ascaris lumbricoides roundworm is an extremely common cause
with multiple strictures, the common duct being most frequently of biliary pathology worldwide. The worms infest the small bowel
involved, followed by left, then right hepatic ducts. The parasites but can migrate up the common bile duct and may enter the gall-
may be identified within the ducts255 and also within the gallblad- bladder and the intrahepatic ducts. Biliary colic is common, while
der.257 There are often bilirubinate stones within the ducts; these are jaundice, ascending cholangitis and parasitic liver abscesses occur
often soft and sludge-like. In most patients there is secondary bacte- occasionally.
rial infection with E. coli in the bile. Gas-forming organisms may The characteristic ultrasound appearance is of single or multiple
result in pneumobilia and there is an increased incidence of cholan- reflective, linear or curved intraductal structures, usually non-
giocarcinoma presumably as a result of chronic irritation leading shadowing. These may produce a spaghetti-like appearance due to
to dysplasia. As the disease progresses, with recurrent attacks of the central echo-free digestive tract of the worm.260,261 Movements
cholangitis, biliary cirrhosis with portal hypertension may result.256 of the worms in the common duct and gallbladder may be observed
All these pathological processes result in a complex ultrasono- using real-time ultrasound (Fig. 14.92).262 The diagnosis is con-
graphic picture,257259 and although ultrasound may be of consider- firmed by isolating the worms or their eggs from the stool, and
able value in screening for the disease and in suggesting the medical treatment is usually effective in eradicating the infestation.
A B
Figure 14.91 Carolis disease. A and B: Cystic dilatation of the biliary tree in a child, subsequently shown to be Carolis disease.
266
References
A B
Figure 14.93 Sclerosing cholangitis. A: Increased reflectivity of intrahepatic portal tracts. B There is irregular mucosal thickening in the
common duct.
267
CHAPTER 14 Gallbladder and biliary tree
22. Glazer GM, Filly RA, Laing FC. Rapid change in caliber of the 48. Konikoff FM. Gallstones approach to medical management. Med
non-obstructed common duct. Radiology 1981;140:161162. Gen Med 2003;5(4):8.
23. Mueller PR, Ferrucci JT, Simeone JF, et al. Observations on the 49. Crade M, Taylor KJW, Rosenfield AT, et al. Surgical and pathologic
distensibility of the common bile duct. Radiology 1982;142:467472. correlation of cholecystosonography and cholecystography. AJR Am J
24. Cooperberg PL, Li D, Wong P, et al. Accuracy of common duct size in Roentgenol 1978;131:227229.
the evaluation of extrahepatic biliary obstruction. Radiology 50. Filly RA, Allen B, Minton MJ, et al. In vitro investigation of the origin
1980;135:141144. of echoes within biliary sludge. J Clin Ultrasound 1980;8:193200.
25. Colecchia A, Sandri L, Bacchi-Reggiani ML, et al. Is it possible to 51. Sommer FG, Taylor KJW. Differentiation of acoustic shadowing due
predict the clinical course of gallstone disease? Usefulness of to calculi and gas collections. Radiology 1980;135:399.
gallbladder motility evaluation in a clinical setting. Am J 52. Carroll BA. Gallstones: in vitro comparison of physical, radiographic
Gastroenterol 2006;101(11):25762581; quiz 2672. and ultrasonic characteristics. AJR Am J Roentgenol 1978;131:
26. Portincasa P, Moschetta A, Colecchia A, et al. Measurements of 223226.
gallbladder motor function by ultrasonography: towards 53. Filly RA, Moss AA, Way LW. In vitro investigation of gallstone
standardization. Dig Liver Dis 2003;35(Suppl 3):S5661. shadowing with ultrasonic tomography. J Clin Ultrasound 1979;7:
27. Pallotta N. Ultrasonography in the assessment of gallbladder motor 255.
activity. Dig Liver Dis 2003;35(Suppl 3):S6769. 54. Jaffe CC, Taylor KJW. The clinical impact of ultrasonic beam
28. Degirmenci B, Albayrak R, Haktanir A, et al. Acute effect of smoking focussing patterns. Radiology 1979;131:469472.
on gallbladder emptying and refilling in chronic smokers and 55. Taylor KJW, Jacobson P, Jaffe CC. Lack of an acoustic shadow on
nonsmokers: a sonographic study. World J Gastroenterol scans of gallstones: a possible artefact. Radiology 1979;131:463464.
2006;12(34):55405543. 56. Callen PW, Filly RA. Ultrasonographic localisation of the gallbladder.
29. Braverman DZ, Johnson ML, Kern F. Effects of pregnancy and Radiology 1979;133:693698.
contraceptive steroids on gallbladder function. N Engl J Med 57. Conrad MR, Leonard J, Landay MJ. Left lateral decubitus sonography
1980;302:362364. of gallstones in the contracted gallbladder. AJR Am J Roentgenol
30. Delamarre J, Capron J-P, Joly J-P, et al. Gallbladder inertia in celiac 1980;134:141144.
disease: ultrasonographic demonstration. Dig Dis Sci 1984;29: 58. MacDonald FR, Cooperberg PL, Cohen MM. The WES triad a
876877. specific sign of gallstones in the contracted gallbladder. Gastrointest
31. Nino-Murcia M, Burton M, Chang P, et al. Gallbladder contractility in Radiol 1981;6:3941.
patients with spinal cord injuries: a sonographic investigation. AJR 59. Ratpopoulos V, DOrsi C, Smith E, et al. Dynamic
Am J Roentgenol 1990;154:521524. cholecystosonography of the contracted gallbladder: the double-arc-
32. Stads S, Venneman NG, Scheffer RC, et al. Evaluation of gallbladder shadow sign. AJR Am J Roentgenol 1982;138:275278.
motility: comparison of two-dimensional and three-dimensional 60. Kane RA, Jacobs R, Katz J, Costello P. Porcelain gallbladder:
ultrasonography. Ann Hepatol 2007;6(3):164169. ultrasound and CT appearance. Radiology 1984;152:137141.
33. Yoon HJ, Kim PN, Kim AY, Lee MG. Three-dimensional sonographic 61. Crow HC, Bartrum RJ, Foote SR. Expanded criteria for the ultrasonic
evaluation of gallbladder contractility: comparison with diagnosis of gallstones. J Clin Ultrasound 1976;4:289.
cholescintigraphy. J Clin Ultrasound 2006;34(3):123127. 62. Love MB. Sonographic features of milk of calcium bile. J Ultrasound
34. Fisher RS, Thistle J, Lembo A, et al. Tegaserod does not alter fasting Med 1982;1:325327.
or meal-induced biliary tract motility. Am J Gastroenterol 63. Chun GH, Deutsch AL, Scheible W. Sonographic findings in milk of
2004;99(7):13421349. calcium bile. Gastrointest Radiol 1982;7:371373.
35. Wilson SA, Gosink BB, van Sonnenberg E. Unchanged size of a 64. Conrad MR, Janes JO, Dietchy J. Significance of low level echoes
dilated common bile duct after a fatty meal: results and significance. within the gallbladder. AJR Am J Roentgenol 1979;132:967972.
Radiology 1986;160:2931. 65. Pazzi P, Gamberini S, Buldrini P, Gullini S. Biliary sludge: the
36. Simeone JF, Butch RJ, Mueller PR, et al. The bile ducts after a fatty sluggish gallbladder. Dig Liver Dis 2003;35(Suppl 3): S3945.
meal: further sonographic observations. Radiology 1985;154:763768. 66. Garg PK, Tandon RK, Madan K. Is biliary microlithiasis a significant
37. Darweesh RMA, Dodds WJ, Hogan WJ, et al. Fatty meal sonography cause of idiopathic recurrent acute pancreatitis? A long-term
for evaluating patients with suspected partial common duct follow-up study. Clin Gastroenterol Hepatol 2007;5(1):7579.
obstruction. AJR Am J Roentgenol 1988;151:6368. 67. Jngst C, Kullak-Ublick GA, Jngst D. Gallstone disease:
38. Amouzal P, Palazzo L, Amouzal G, et al. Endosonography: promising Microlithiasis and sludge. Best Pract Res Clin Gastroenterol
method for diagnosis of extrahepatic cholestasis. Lancet 2006;20(6):10531062.
1989;ii:11951198. 68. Goldstein A, Madrazo BL. Slice thickness artefacts in gray scale
39. McMahon CJ. The relative roles of magnetic resonance ultrasound. J Clin Ultrasound 1981;9:365375.
cholangiopancreatography (MRCP) and endoscopic ultrasound in 69. Anastasi B, Sutherland GR. Biliary sludge ultrasonic appearance
diagnosis of malignant common bile duct strictures: a critically simulating neoplasm. Br J Radiol 1981;54:679681.
appraised topic. Abdom Imaging 2008;33(1):1013. 70. Fakhry J. Sonography of tumefactive biliary sludge. AJR Am J
40. McMahon CJ. The relative roles of magnetic resonance Roentgenol 1982;139:717719.
cholangiopancreatography (MRCP) and endoscopic ultrasound in 71. Engel JM, Deitch EA, Sikkema W. Gallbladder wall thickness:
diagnosis of common bile duct calculi: a critically appraised topic. sonographic accuracy and relation to disease. AJR Am J Roentgenol
Abdom Imaging 2008;33(1):69. 1979;134:907909.
41. Sgouros SN, Bergele C. Endoscopic ultrasonography versus other 72. Finberg HJ, Birnholtz J. Ultrasound evaluation of the gallbladder
diagnostic modalities in the diagnosis of choledocholithiasis. Dig Dis wall. Radiology 1979;133:693698.
Sci 2006;51(12):22802286. 73. Marchal G, Van de Voorde P, Van Dooren W, et al. Ultrasonic
42. Perry KA, Myers JA, Deziel DJ. Laparoscopic ultrasound as the appearance of the filled and contracted normal gallbladder. J Clin
primary method for bile duct imaging during cholecystectomy. Surg Ultrasound 1980;8:439442.
Endosc 2008;22(1):208213. 74. Lewandowski BJ, Winsberg F. Gallbladder wall thickness distortion
43. Health and Policy Committee, American College of Physicians. How by ascites. AJR Am J Roentgenol 1981;137:519521.
to study the gallbladder. Ann Intern Med 1988;109:752754. 75. Laing FC. Gall bladder and bile ducts. In: Rumack CM, Wilson SR,
44. Barbara L. Epidemiology of gallstone disease: the Sirmione Study. Charboneau JW, editors. Diagnostic ultrasound. St Louis: Mosby;
In: Capocaccia L, Ricci G, Angelico F, et al, editors. Epidemiology 1998, p. 175219.
and prevention of gallstone disease. Lancaster: MTP Press; 1984, 76. Sanders RC. The significance of sonographic gallbladder wall
p. 2325. thickening. J Clin Ultrasound 1980;8:143146.
45. GREPCO. Prevalence of gallstone disease in an Italian adult female 77. Fiske CE, Laing FC, Brown TW. Ultrasonographic evidence of
population. Am J Epidemiol 1984;119:796805. gallbladder wall thickening in association with hypoalbuminemia.
46. Gupta SK, Shukla VK. Silent gallstones: a therapeutic dilemma. Trop Radiology 1980;135:713716.
Gastroenterol 2004;25(2):6568. 78. Dayananda L, Moorthy S, Prabhu NK, et al. Diagnostic value of gall
47. Dowling RH. Epidemiology and medical treatment of cholesterol bladder wall thickness in patients with ascites. Ind J Gastroenterol
gallstones: recurrence, post-dissolution management and the future. 2006;25:4445.
In: Capocaccia L, Ricci G, Angelico F, et al, editors. Epidemiology 79. Tsujimoto F, Miyamoto T, Tada S. Differentiation of benign from
and prevention of gallstone disease. Lancaster: MTP Press; 1984, malignant ascites by sonographic evaluation of gallbladder wall.
p. 116128. Radiology 1985:157:503504.
268
References
80. Ralls PW, Quinn MF, Juttner HU, et al. Gallbladder wall thickening: 109. Bergman AB, Neiman HL, Kraut B. Ultrasonographic evaluation of
patients without intrinsic gallbladder disease. AJR Am J Roentgenol pericholecystic abscesses. AJR Am J Roentgenol 1979;132:201203.
1981;137:6568. 110. Madrazo BL, Francis I, Hricak H, et al. Sonographic findings in
81. Saverymuttu SH, Grammatopoulos A, Meanock CI, et al. Gallbladder perforation of the gallbladder. AJR Am J Roentgenol 1982;139:
wall thickening (congestive cholecystopathy) in chronic liver disease: 491496.
a sign of portal hypertension. Br J Radiol 1990;63:922925. 111. Hunter ND, Macintosh PK. Acute emphysematous cholecystitis: an
82. Shlaer WJ, Leopold GR, Scheible FW. Sonography of thickened ultrasonic diagnosis. AJR Am J Roentgenol 1980;134:592593.
gallbladder wall: a non-specific finding. AJR Am J Roentgenol 112. Blaquiere RM, Dewbury KC. The ultrasound diagnosis of
1981;136:337339. emphysematous cholecystitis. Br J Radiol 1982;55:114116.
83. Maudgal DP, Wansborough Jones MH, Joseph AEA. Gallbladder 113. Parulekar SG. Sonographic findings in acute emphysematous
abnormalities in acute infectious hepatitis. Dig Dis Sci cholecystitis. Radiology 1982;145:117119.
1984;29:257260. 114. Bloom RA, Fisher A, Pode D, Asaf Y. Shifting intramural gas: a new
84. Juttner H-U, Ralls PW, Quinn MF, Jenney JM. Thickening of ultrasound sign of emphysematous cholecystitis. J Clin Ultrasound
gallbladder wall in acute hepatitis: ultrasound demonstration. 1984;12:4042.
Radiology 1982;142:465466. 115. Nemcek AA, Gore RM, Vogelzang RL, Grant M. The effervescent
85. Brandt DJ, MacCarty RL, Charbonneau JW, et al. Gallbladder disease gallbladder: a sonographic sign of emphysematous cholecystitis. AJR
in patients with primary sclerosing cholangitis. AJR Am J Roentgenol Am J Roentgenol 1988;150:575577.
1988;150:571574. 116. Bloom RA, Libson E, Lebensart PD, et al. The ultrasound spectrum of
86. Romano AJ, van Sonnenberg E, Casola G, et al. Gallbladder and bile emphysematous cholecystitis. J Clin Ultrasound 1989;17:251256.
duct abnormalities in AIDS: sonographic findings in eight patients. 117. Gill KS, Chapman AH, Weston MJ. The changing face of
AJR Am J Roentgenol 1988;150:123127. emphysematous cholecystitis. BJR 1997;70:986991.
87. McClure J, Banerjee SS, Schofield PS. Crohns disease of the 118. Deitch EA, Engel JM. Acute acalculous cholecystitis: an ultrasonic
gallbladder. J Clin Pathol 1984;37:516518. diagnosis. Am J Surg 1981;142:290292.
88. Carroll BA. Gallbladder wall thickening secondary to focal lymphatic 119. Shuman WP, Rogers JV, Ruydd TG, et al. Low sensitivity of
obstruction. J Ultrasound Med 1983;2:8991. sonography and cholescintigraphy in acalculous cholecystitis. AJR
89. Laudanna AA, Ferreyra NP, Cerri GG, Bettarello A. Thickening of the Am J Roentgenol 1984;142:531534.
gallbladder wall in alcoholic hepatitis verified by ultrasonographic 120. Mirvis SE, Vainright JR, Nelson AW, et al. The diagnosis of acute
examination. Scand J Gastroenterol 1987;22: acalculous cholecystitis: a comparison of sonography, scintigraphy,
521524. and CT. AJR Am J Roentgenol 1986;147:11711175.
90. Cerri GG, Alves V, Magalhaes A. Sonography in hepatobiliary 121. McGahan JP, Walter JR. Diagnostic percutaneous aspiration of the
schistosomiasis. Radiology 1984;153:777. gallbladder. Radiology 1985;155:619622.
91. Johansson M, Thune A, Blomqvist A, et al. Impact of choice of 122. McGahan JP, Lindfors KK. Acute cholecystitis: diagnostic accuracy of
therapeutic strategy for acute cholecystitis on patients health-related percutaneous aspiration of the gallbladder. Radiology 1988;167:
quality of life. Results of a randomized, controlled clinical trial. Dig 669671.
Surg 2004;21:359362. 123. Tsutsui K, Uchida N, Hirabayashi S, et al. Usefulness of single
92. Marton KI, Doubilet P. How to image the gallbladder in suspected and repetitive percutaneous transhepatic gallbladder aspiration for
cholecystitis. Ann Intern Med 1988;109:722729. the treatment of acute cholecystitis. J Gastroenterol 2007;42(7):
93. Laing FC, Federle MP, Jeffrey RB, Brown TW. Ultrasonic evaluation 583588.
of patients with acute right upper quadrant pain. Radiology 124. Chopra S, Dodd GD 3rd, Mumbower AL, et al. Treatment of acute
1981;190:449455. cholecystitis in non-critically ill patients at high surgical risk:
94. Handler SJ. Ultrasound of gallbladder wall thickening and its relation comparison of clinical outcomes after gallbladder aspiration and after
to cholecystitis. AJR Am J Roentgenol 1979;132:581585. percutaneous cholecystostomy. AJR Am J Roentgenol 2001;176(4):
95. Marchal GJF, Casaer M, Baert AL, et al. Gallbladder wall sonolucency 10251031.
in acute cholecystitis. Radiology 1979;133:429433. 125. De Waele E, Op de Beeck B, De Waele B, Delvaux G. Magnetic
96. Kane RA. The biliary system. In: Kurtz AB, Goldberg BB, editors. resonance cholangiopancreatography in the preoperative assessment
Gastrointestinal ultrasonography. New York: Churchill Livingstone; of patients with biliary pancreatitis. Pancreatology 2007;7(4):
1988, p. 75137. 347351.
97. Sherman M, Ralls PW, Quinn M, et al. Intravenous cholangiography 126. Berk RN, van der Vegt JH, Lichtenstein JE. The hyperplastic
and sonography in acute cholecystitis: prospective evaluation. AJR cholecystoses: cholesterolosis and adenomyomatosis. Radiology
Am J Roentgenol 1980;135:311313. 1983;146:595601.
98. Clain A. Hamilton Baileys physical signs in clinical surgery. 14th ed. 127. Stunell H, Buckley O, Geoghegan T, et al. Imaging of
Bristol: Wright; 1967. adenomyomatosis of the gall bladder. J Med Imaging Radiat Oncol
99. Ralls PW, Halls J, Lapin SA, et al. Prospective evaluation of the 2008;52(2):109117.
sonographic Murphy sign in suspected acute cholecystitis. J Clin 128. Raghavendra BN, Subramanyam BR, Balthazar EJ, et al. Sonography
Ultrasound 1982;10:113115. of adenomyomatosis of the gallbladder: radiologic-pathologic
100. Ralls PW, Colletti PM, Lapin SM, et al. Real time sonography in correlation. Radiology 1983;146:747752.
suspected acute cholecystitis. Radiology 1985;155:767. 129. Fowler RC, Reid WA. Ultrasound diagnosis of adenomyomatosis of
101. Yamashita H, Hachisuka Y, Kotegawa H, et al. The blood flow the gallbladder: ultrasonic and pathological correlation. Clin Radiol
velocity in the wall of the gallbladder is an indicator of the degree of 1988;39:402406.
inflammation in acute cholecystitis. Hepatogastroenterology 130. Nishimura A, Shirai Y, Hatakeyama K. Segmental adenomyomatosis
2006;53(72):819822. of the gallbladder predisposes to cholecystolithiasis. J Hepatobiliary
102. Dinkel HP, Kraus S, Heimbucher J, et al. Sonography for selecting Pancreat Surg 2004;11(5):342347.
candidates for laparoscopic cholecystectomy, a prospective study. 131. Price RJ, Stewart ET, Foley WD, Dodds WJ. Sonography of polypoid
AJR Am J Roentgenol 2000;174:14331439. cholesterolosis. AJR Am J Roentgenol 1982;139:1197.
103. Jeffrey RB, Laing FC, Wong W, Callen PW. Gangrenous cholecystitis: 132. Khairy GA, Guraya SY, Murshid KR. Cholesterolosis. Incidence,
diagnosis by ultrasound. Radiology 1983;148:219221. correlation with serum cholesterol level and the role of laparoscopic
104. Wales LR. Desquamated gallbladder mucosa: unusual sign of cholecystectomy. Saudi Med J 2004;25(9):12261228.
cholecystitis. AJR Am J Roentgenol 1982;139:810811. 133. Strmsten A, von Bahr S, Bringman S, et al. Studies on the
105. Sood BP, Kalra N, Gupta S, et al. Role of sonography in the diagnosis mechanism of accumulation of cholesterol in the gallbladder mucosa.
of gallbladder perforation. J Clin Ultrasound 2002;30(5):270274. Evidence that sterol 27-hydroxylase is not a pathogenetic factor.
106. Simeone JF, Brink JA, Mueller PR, et al. The sonographic diagnosis of J Hepatol 2004;40(1):813.
acute gangrenous cholecystitis: importance of the Murphy sign. AJR 134. Planells Roig M, Bueno Lled J, Sanahuja Santaf A, Garca Espinosa
Am J Roentgenol 1989;152:289290. R. Quality of life (GIQLI) and laparoscopic cholecystectomy
107. Kane RA. Ultrasonographic diagnosis of gangrenous cholecystitis and usefulness in patients with gallbladder dysfunction or chronic
empyema of the gallbladder. Radiology 1980;134:191194. non-lithiasic biliary pain (chronic acalculous cholecystitis). Rev Esp
108. Jenkins M, Golding RH, Cooperberg PL. Sonography and computed Enferm Dig 2004;96(7):442446, 446451.
tomography of haemorrhagic cholecystitis. AJR Am J Roentgenol 135. Carter SJ, Rutledge J, Hirsch JH. Papillary adenoma of the
1983;140:11971198. gallbladder: ultrasonic demonstration. J Clin Ultrasound 1978;6:433.
269
CHAPTER 14 Gallbladder and biliary tree
136. Foster DR, Foster DBE. Gallbladder polyps in Peutz-Jeghers 167. Tanaka K, Shimada M, Hattori M, et al. Sjogrens syndrome with
syndrome. Postgrad Med J 1980;56:373376. abnormal manifestations of the gallbladder and central nervous
137. Niv Y, Kosakov K, Shcolnik B. Fragile papilloma (papillary system. J Pediatr Gastroenterol Nutr 1985;4:148151.
adenoma) of the gallbladder. A cause of recurrent biliary colic. 168. Dietrich CF, Chichakli M, Hirche TO, et al. Sonographic findings of
Gastroenterology 1986;91:9991001. the hepatobiliary-pancreatic system in adult patients with cystic
138. Kozuka S, Kurashina M, Tsubone M, et al. Significance of intestinal fibrosis. J Ultrasound Med 2002;21(4):409416.
metaplasia for the evolution of cancer in the biliary tract. Cancer 169. Chaudry G, Navarro OM, Levine DS, Oudjhane K. Abdominal
1984;54:22772285. manifestations of cystic fibrosis in children. Pediatr Radiol
139. Sun XJ, Shi JS, Han Y, et al. Diagnosis and treatment of polypoid 2006;36(3):233240.
lesions of the gallbladder: report of 194 cases. Hepatobiliary Pancreat 170. Lunderquist A. The radiology of jaundice. Clin Gastroenterol
Dis Int 2004;3(4):591594. 1989;3:387406.
140. Myers RP, Shaffer EA, Beck PL. Gallbladder polyps: epidemiology, 171. Taylor KJW, Rosenfield AT. Grey scale ultrasonography in the
natural history and management. Can J Gastroenterol 2002;16(3): differential diagnosis of jaundice. Arch Surg 1977;112:820825.
187194. 172. Sample WF, Sarti DA, Goldstein LI, et al. Gray-scale ultrasonography
141. Numata K, Oka H, Morimoto M, et al. Differential diagnosis of of the jaundiced patient. Radiology 1978;128:719725.
gallbladder diseases with contrast-enhanced harmonic gray scale 173. Vallon AG, Lees WR, Cotton PB. Gray-scale ultrasonography in
ultrasonography. J Ultrasound Med 2007;26(6):763774. obstructive jaundice. Gut 1979;20:5154.
142. Inoue T, Kitano M, Kudo M, et al. Diagnosis of gallbladder diseases 174. Koenigsberg M, Wiener SN, Walzer A. Accuracy of sonography in
by contrast-enhanced phase-inversion harmonic ultrasonography. the differential diagnosis of obstructive jaundice: a comparison with
Ultrasound Med Biol 2007;33(3):353361. cholangiography. Radiology 1979;133:157165.
143. Majeski JA. Polyps of the gallbladder. J Surg Oncol 1986;32:1618. 175. Dewbury KC, Joseph AEA, Hayes S, Murray C. Ultrasound in
144. Lai CH, Lau WY. Gallbladder cancer a comprehensive review. the evaluation and diagnosis of jaundice. Br J Radiol 1979;52:
Surgeon 2008;6(2):101110. 276280.
145. Misra MC, Guleria S. Management of cancer gallbladder found as a 176. Wild SR, Cruikshank JG, Fraser GGM, et al. Grey-scale
surprise on a resected gallbladder specimen. J Surg Oncol ultrasonography and percutaneous transhepatic cholangiography in
2006;93(8):690698. biliary tract disease. BMJ 1980;281:15241526.
146. Lai CH, Lau WY. Gallbladder cancer a comprehensive review. 177. Haubek A, Pedersen JH, Buscharth F, et al. Dynamic sonography in
Surgeon 2008;6(2):101110. the evaluation of jaundice. AJR Am J Roentgenol 1981;136:
147. Olken SM, Bledsoe R, Newmark H. The ultrasonic diagnosis of 10711074.
primary carcinoma of the gallbladder. Radiology 1978;129:481482. 178. Caddy GR, Tham TC. Gallstone disease: symptoms, diagnosis and
148. Crade M, Taylor KJW, Rosenfield AT, et al. The varied ultrasonic endoscopic management of common bile duct stones. Best Pract Res
character of gallbladder tumour. JAMA 1979;241:21952196. Clin Gastroenterol 2006;20(6):10851101.
149. Yeh H-C. Ultrasonography and computed tomography of carcinoma 179. Lindsell DRM. Ultrasound imaging of pancreas and biliary tract.
of the gallbladder. Radiology 1979;133:167173. Lancet 1990;335:390393.
150. Dalla Palma L, Rizzatto G, Pozzi-Mucelli RS, Bazzocchi M. Grey scale 180. Ney MV, Maluf-Filho F, Sakai P, et al. Echo-endoscopy versus
ultrasonography in the evaluation of carcinoma of the gallbladder. endoscopic retrograde cholangiography for the diagnosis of
Br J Radiol 1980;53:662667. choledocholithiasis: the influence of the size of the stone and
151. Yum HY, Fink AH. Sonographic findings in primary carcinoma of diameter of the common bile duct. Arq Gastroenterol 2005;42(4):
the gallbladder. Radiology 1980;134:693696. 239243.
152. Ruiz R, Teyssou H, Fernandez N, et al. Ultrasonic diagnosis of 181. Songr Y, Temuin G, Sahin B. Endoscopic ultrasonography in the
primary carcinoma of the gallbladder: a review of 16 cases. J Clin evaluation of dilated common bile duct. J Clin Gastroenterol
Ultrasound 1980;8:489495. 2001;33(4):302305.
153. Lee KF, Wong J, Li JC, Lai PB. Polypoid lesions of the gallbladder. 182. Garrow D, Miller S, Sinha D, et al. Endoscopic ultrasound: a
Am J Surg 2004;188(2):186190. meta-analysis of test performance in suspected biliary obstruction.
154. Bach AM, Loring LA, Hann LE, et al. Gallbladder cancer: can Clin Gastroenterol Hepatol 2007;5(5):616623.
ultrasonography evaluate extent of disease? J Ultrasound Med 183. Tse F, Liu L, Barkun AN, et al. EUS: a meta-analysis of test
1998;17:303309. performance in suspected choledocholithiasis. Gastrointest Endosc
155. Koga A, Yamauchi S, Izumi Y, Hamanaka N. Ultrasonographic 2008;67(2):235244.
detection of early and curable carcinoma of the gallbladder. Br J Surg 184. Dewbury KC. Visualisation of normal biliary ducts with ultrasound.
1985;72:728730. Br J Radiol 1980;53:774780.
156. Diehl AK, Beral V. Cholecystectomy and changing mortality from 185. Bressler EL, Rubin JM, McCracken S. Sonographic parallel channel
gallbladder cancer. Lancet 1981;ii:187189. sign: a reappraisal. Radiology 1987;164:343346.
157. Phillips G, Pochaczevsky R, Goodman J, et al. Ultrasound patterns of 186. Cooperberg PL. High resolution real time ultrasound in the
metastatic tumours in the gallbladder. J Clin Ultrasound 1982; evaluation of the normal and obstructed biliary tract. Radiology
10:379. 1978;129:477480.
158. Marone U, Carac C, Losito S, et al. Laparoscopic cholecystectomy 187. Cooperberg PL, Li D, Wong P, et al. Accuracy of common hepatic
for melanoma metastatic to the gallbladder: is it an adequate surgical duct size in the evaluation of extrahepatic biliary obstruction.
procedure? Report of a case and review of the literature. World J Radiology 1980;135:141144.
Surg Oncol 2007;5:141. 188. Parulekar SG. Evaluation of common bile duct size. Radiology
159. Lim JH. Parasitic diseases in the abdomen: imaging findings. Abdom 1979;133:703707.
Imaging 2008;33(2):130132. 189. Wu C-C, Ho Y-H, Chen C-Y. Effect of ageing on common bile duct
160. Das CJ, Kumar J, Debnath J, Chaudhry A. Imaging of ascariasis. diameter: a real time sonographic study. J Clin Ultrasound
Australas Radiol 2007;51(6):500506. 1984;12:473.
161. Lim JH, Mairiang E, Ahn GH. Biliary parasitic diseases including 190. Ruddell WSJ, Ashton MG, Lintott DJ, Axon ATR. Endoscopic
clonorchiasis, opisthorchiasis and fascioliasis. Abdom Imaging retrograde cholangiography and pancreatography in investigation of
2008;33(2):157165. post-cholecystectomy patients. Lancet 1980;i:444447.
162. Rana SS, Bhasin DK, Nanda M, Singh K. Parasitic infestations of the 191. Csendes A, Csendes P, Burdiles P, et al. Behavior of the common bile
biliary tract. Curr Gastroenterol Rep 2007;9(2):156164. duct diameter before and 12 years after choledochostomy for
163. Braverman DZ, Johnson ML, Kern F Jr. Effects of pregnancy and cholecystolithiasis and choledocholithiasis. A prospective study.
contraceptive steroids on gallbladder function. N Engl J Med J Gastrointest Surg 2007;11(10):12941297.
1980;302:362. 192. Weill F, Eisencher A, Zeltner F. Ultrasonic study of the normal and
164. Kane RA. Ultrasonographic evaluation of the gallbladder. Crit Rev dilated biliary tree: shot-gun sign. Radiology 1978;127:221.
Diagn Imaging 1982;17:107. 193. Conrad MR, Landay MJ, Janes JO. Sonographic parallel channel sign
165. Singh S, Kansra S. Kawasaki disease. Natl Med J India 2005;18(1): of biliary tree enlargement in mild to moderate obstructive jaundice.
2024. AJR Am J Roentgenol 1978;130:279.
166. Mateen MA, Saleem S, Rao PC, et al. Ultrasound in the diagnosis of 194. Ingram C, Joseph AEA. The stilette sign: the appearance of dilated
typhoid fever. Indian J Pediatr 2006;73(8):681685. ducts in the fatty liver. Clin Radiol 1989;40:257258.
270
References
195. Laing FC, London LA, Filly RA. Ultrasonographic identification of 223. Carroll BA. Biliary cystadenoma and cystadenocarcinoma: gray scale
dilated intrahepatic bile ducts and their differentiation from portal ultrasound appearance. J Clin Ultrasound 1978;6:337340.
venous structures. J Clin Ultrasound 1978;6:90. 224. Bondstam S, Kivilaakse EO, Standetskjold-Nordenstam C-GM, et al.
196. Taylor KJW, Rosenfield AT, De Graaff CS. Anatomy and pathology of Sonographic diagnosis of a bile duct polyp. AJR Am J Roentgenol
the biliary tree as demonstrated by ultrasound. In: Taylor KJW, editor. 1980;135:610611.
Diagnostic ultrasound in gastrointestinal disease. Clinics in 225. Stanley J, Vujic I, Schabel SI, et al. Evaluation of biliary cystadenoma
diagnostic ultrasound. Edinburgh: Churchill Livingstone; 1979, and cystadenocarcinoma. Gastrointest Radiol 1983;8:245258.
p. 103121. 226. Marchal G, Gelin J, Van Steenbergen WV, et al. Sonographic
197. Muhletaler CA, Gerlock AJ, Fleischer AC, James AE. Diagnosis of diagnosis of intraluminal bile duct neoplasm; a report of 3 cases.
obstructive jaundice with non-dilated bile ducts. AJR Am J Gastrointest Radiol 1984;9:329333.
Roentgenol 1980;134:11491152. 227. Patel T. Worldwide trends in mortality from biliary tract
198. Thomas JL, Zornoza J. Obstructive jaundice in the absence of malignancies. BMC Cancer 2002;2:10.
sonographic biliary dilatation. Gastrointest Radiol 1980;5:357360. 228. Davila JA, El-Serag HB. Cholangiocarcinoma: the other liver cancer
199. Beinart C, Efremidis S, Cohen B, Mitty HA. Obstruction without on the rise. Am J Gastroenterol 2002;97:31993200.
dilatation. JAMA 1981;245:353356. 229. Wise C, Pilanthananond M, Perry BF, et al. Mechanisms of biliary
200. Greenwald RA, Pereiras R, Morris SJ, Schiff ER. Jaundice, carcinogenesis and growth. World J Gastroenterol 2008;14(19):
choledocholithiasis, and a non-dilated common duct. JAMA 29862989.
1978;240:19831984. 230. Klatskin G. Adenocarcinoma of the hepatic duct at its bifurcation
201. Fried AM, Bell RM, Bivins BA. Biliary obstruction in a canine model: within the porta hepatis. Am J Med 1965;38:241256.
sequential study of the sonographic threshold. Invest Radiol 231. Dillon E, Peel ALG, Parkin GJS. The diagnosis of primary bile duct
1981;16:317319. carcinoma (cholangiocarcinoma) in the jaundiced patient. Clin Radiol
202. Carroll BA, Oppenheimer DA. Sclerosing cholangitis: sonographic 1981;32:311317.
demonstration of bile duct wall thickening. AJR Am J Roentgenol 232. Meyer DG, Weinstein BJ. Klatskin tumors of the bile ducts:
1982;139:1016. sonographic appearance. Radiology 1983;148:803804.
203. Vaishali MD, Agarwal AK, Upadhyaya DN, et al. Magnetic resonance 233. Subramanyam BR, Raghavendra BN, Balthazar EJ, et al. Ultrasonic
cholangiopancreatography in obstructive jaundice. J Clin features of cholangiocarcinoma. J Ultrasound Med 1984;3:405.
Gastroenterol 2004;38(10):887890. 234. Marchan L, Muller NL, Cooperberg PL. Sonographic diagnosis of
204. Filippone A, Ambrosini R, Fuschi M, et al. Clinical impact of MR Klatskin tumors. AJR Am J Roentgenol 1986;147:509.
cholangiopancreatography in patients with biliary disease. Radiol 235. Gibson RN, Yeung E, Thompson JN, et al. Bile duct obstruction;
Med (Torino) 2003;105(12):2735. radiologic evaluation of level, cause and tumour resectability.
205. Weinstein DP, Weinstein BJ, Brodmerkel GJ. Ultrasonography of Radiology 1986;160:4347.
biliary tract dilatation without jaundice. AJR Am J Roentgenol 236. Karstrup S. Ultrasound diagnosis of cholangiocarcinoma at the
1979;132:729734. confluence of the hepatic ducts (Klatskin tumours). Br J Radiol
206. Weinstein BJ, Weinstein DP. Biliary tract dilatation in the non- 1988;61:987990.
jaundiced patient. AJR Am J Roentgenol 1980;134:899. 237. Yeung EYC, McCarthy P, Gompertz RH, et al. The ultrasonographic
207. Glazer GM, Filly RA, Laing FC. Rapid change in calibre of the appearances of hilar cholangiocarcinoma (Klatskin tumours). Br J
non-obstructed common duct. Radiology 1980;140:161162. Radiol 1988;61:991995.
208. Scheske GA, Cooperberg PL, Cohen MM, et al. Dynamic changes in 238. Kruskal JB, Kane RA. Correlative imaging of malignant liver tumors.
the caliber of the major bile ducts, related to obstruction. Radiology Semin Ultrasound CT MR 1992;13(5):336354.
1980;135:215216. 239. Kim JY, Kim MH, Lee TY, et al. Clinical role of 18F-FDG PET-CT in
209. Mueller PR, Ferrucci JT Jr, Simeone JF. Observations on the suspected and potentially operable cholangiocarcinoma: a
distensibility of the common bile duct. Radiology 1982;142:467472. prospective study compared with conventional imaging. Am J
210. Mahour GH, Wakim KG, Soule EH, et al. Structure of the common Gastroenterol 2008;103(5):11451151.
bile duct in man. Ann Surg 1967;166:9194. 240. Filly RA, Carlsen EN. Choledochal cyst: report of a case with specific
211. Schein CF, Beneventano TC. Choledochal dynamics in man. Surg ultrasonographic findings. J Clin Ultrasound 1979;4:710.
Gynecol Obstet 1968;126:591596. 241. Reuter K, Raptopoulos VD, Cantelmo N, et al. The diagnosis of a
212. Sauerbrei EE, Cooperberg PL, Gordon P, et al. The discrepancy choledochal cyst by ultrasound. Radiology 1980;136:437438.
between radiographic and sonographic bile duct measurements. 242. Han BK, Babcock DS, Gelfand MH. Choledochal cyst with bile duct
Radiology 1980;137:751755. dilatation; sonography and 99mTc IDA cholescintigraphy. AJR Am J
213. Clain A. Hamilton Baileys physical signs in clinical surgery. 14th ed. Roentgenol 1981;136:10751079.
Bristol: Wright. 1967. 243. Kangarloo H, Sarti DA, Sample WF, et al. Ultrasonographic spectrum
214. Laing FC, Jeffrey RB, Wing VW. Improved visualisation of of choledochal cysts in children. Pediatr Radiol 1980;9:15.
choledocholithiasis by sonography. AJR Am J Roentgenol 244. Kimura K, Ohto M, Ono T, et al. Congenital cystic dilatation of the
1984;143:949952. common bile duct: relationship to anomalous pancreaticobiliary
215. Dong B, Chen M. Improved sonographic visualisation of ductal union. AJR Am J Roentgenol 1977;128:571577.
choledocholithiasis. J Clin Ultrasound 1987;15:185190. 245. Jona JZ, Babitt DP, Starshak RJ, et al. Anatomic observations and
216. Rickes S, Treiber G, Mnkemller K, et al. Impact of the operators etiologic and surgical considerations in choledochal cyst. J Pediatr
experience on value of high-resolution transabdominal ultrasound in Surg 1979;14:315320.
the diagnosis of choledocholithiasis: a prospective comparison using 246. Filly RA, Freimanis AK. Thrombosed hepatic artery aneurysm
endoscopic retrograde cholangiography as the gold standard. Scand J report of a case diagnosed echographically. Radiology
Gastroenterol 2006;41(7):838843. 1970;97:629630.
217. Way LW, Sleisenger MH. Biliary obstruction, cholangitis, and 247. Caroli J, Spoupaut R, Kossakowski J, et al. La dilatation polykistique
choledocholithiasis. In: Sleisenger MH, Fordtran JS, editors. congenitale des voies biliaires interhepatiques: essai de classification.
Gastrointestinal disease. Philadelphia: WB Saunders; 1983, Sem Hop 1958;34:488495.
p. 13891403. 248. Mujahed Z, Glenn F, Evans J. Communicating cavernous ectasia of
218. Glenn F. Postcholecystectomy choledocholithiasis. Surg Gynecol the intrahepatic bile ducts (Carolis disease). AJR Am J Roentgenol
Obstet 1972;134:249252. 1971;113:2126.
219. Laing FC, Jeffrey RB. Choledocholithiasis and cystic duct obstruction: 249. Bass EM, Funston MR, Shaff MI. Carolis disease: an ultrasound
difficult ultrasonographic diagnosis. Radiology 1983;146:475479. diagnosis. Br J Radiol 1977;50:366369.
220. Kane RA. The biliary system. In: Kurtz AB, Goldberg BB, editors. 250. Mittelstaedt CA, Volberg FM, Fischer GJ, et al. Carolis disease:
Gastrointestinal ultrasonography. Clinics in diagnostic ultrasound. sonographic findings. AJR Am J Roentgenol 1980;134:585587.
Edinburgh: Churchill Livingstone; 1988, p. 75137. 251. Yonem O, Bayraktar Y. Clinical characteristics of Carolis disease.
221. Dewbury KC, Smith CL. The misdiagnosis of common bile duct World J Gastroenterol 2007;13(13):19301933.
stones with ultrasound. Br J Radiol 1983;56:625630. 252. Rosenfield AT, Siegel NJ, Kappelman NB, Taylor KJW. Gray scale
222. Ledro-Cano D. Suspected choledocholithiasis: endoscopic ultrasound ultrasonography in medullary cystic disease of the kidney and
or magnetic resonance cholangio-pancreatography? A systematic congenital hepatic fibrosis with tubular ectasia: new observations.
review. Eur J Gastroenterol Hepatol 2007;19(11):10071011. AJR Am J Roentgenol 1977;129:297303.
271
CHAPTER 14 Gallbladder and biliary tree
253. Caroli J. Diseases of intrahepatic bile ducts. Isr J Med Sci 259. Federle MP, Cello JP, Laing FC, Jeffrey RB. Recurrent pyogenic
1968;4:213215. cholangitis in Asian immigrants. Radiology 1982;143:151.
254. Imai Y, Watanabe MD, Kondo Y, Nakanishi MD. Carolis disease: its 260. Schulman A, Loxton AJ, Heydenrych JJ, Abdurahman KE.
diagnosis with non-invasive methods. Br J Radiol 1981;54:526528. Sonographic diagnosis of biliary ascariasis. AJR Am J Roentgenol
255. Morikawa P, Ishida H, Niizawa M, et al. Sonographic features of 1982;139:485489.
biliary clonorchiasis. J Clin Ultrasound 1988;16:655658. 261. Al Absi M, Qais AM, Al Katta M, et al. Biliary ascariasis: the value of
256. Mori T, Sugiyama M, Atomi Y. Gallstone disease: management of ultrasound in the diagnosis and management. Ann Saudi Med
intrahepatic stones. Best Pract Res Clin Gastroenterol 2006;20(6): 2007;27(3):161165.
11171137. 262. Cerri GC, Leite GJ, Simoes JB, et al. Ultrasonographic evaluation of
257. Lim JH, Ko YT, Lee DH, Kim SY. Clonorchiasis: sonographic findings ascaris in the biliary tract. Radiology 1983;146:753754.
in 59 proved cases. AJR Am J Roentgenol 1989;152:761764. 263. Doyle TCA, Roberts-Thomson IC. Radiological features of sclerosing
258. Ralls PW, Colletti PM, Quinn MF, et al. Sonography in recurrent cholangitis. Australas Radiol 1983;27:163.
oriental pyogenic cholangitis. AJR Am J Roentgenol 1981;136:1010.
272
CHAPTER
15 Intraoperative ultrasound
Steven Kennish and Jane A. Smith
used to scan organs such as the pancreas and bile ducts, when good routinely available in IOUS transducers, enabling vascular patency
line density can be achieved throughout the field. Curved arrays to be established during transplant and resection, and allowing
are particularly useful for liver scanning when a wider field of view thrombus to be located during surgical resection procedures.
is required. Many electronic linear arrays have a beam steering Transducers with pulse inversion harmonic imaging capability
facility which allows the field of view to be converted into a trap- are required for contrast-enhanced IOUS (CE-IOUS).
ezoid shape for hepatic imaging. The design of a laparoscopic ultrasound probe is constrained by
T-shaped or side-fire probes are specifically designed for scan- the 1011mm diameter of a standard laparoscopic port, through
ning organs such as the liver where access to the dome may be which access to the abdominal cavity is gained (Fig. 15.3). Neverthe-
limited even after surgical mobilisation. Ergonomic design allows less, laparoscopic probes have benefited from the technological
a comfortable grip between the fingers (Fig. 15.2). End-fire probes improvements that have allowed the miniaturisation of established
can also be used when more space is available within the abdominal high performance linear and curved array transducers. A penalty
cavity, or when larger resection specimens are removed and is paid in terms of a reduced field of view, but longer crystal lengths
scanned separately. Doppler imaging functions are also now (up to 4cm) help reduce the scanning times of larger organs.12 As
with standard transducers, broadband probes which operate at
57MHz are useful for organs such as the liver, and probes of
7.510MHz are suited to imaging the common bile duct, pancreas
and kidneys. Modern laparoscopic probes are designed to be flex-
ible to assist with maintenance of good organ surface contact.
Technique
Scanning technique is tailored to the target organ and the individual
patient, and it is always advisable to review preoperative imaging,
Figure 15.1 IOUS using a curved array high-frequency Figure 15.3 A laparoscopic US probe with a linear array
transducer. The liver with the middle hepatic vein is demonstrated. configuration. The probe is flexible in two planes by manipulating
A metastasis is breaching the vein wall. the control at the handle.
B C
A D
Figure 15.2 IOUS probes. A: T probe. B: I shaped array. C: an end-firing array. D: A curved array particularly useful for hepatic
scanning with access to the dome of the liver. E: The back of the curved array is shaped to take the sonographers fingers.
274
Clinical applications
A B
Figure 15.4 IOUS, liver. A: The surface moisture of the organs enables the IOUS probe to be placed directly onto the surface of the liver.
B: A small surface metastasis, not demonstrated preoperatively, is palpated and demonstrated on IOUS.
or have it available on a viewing screen within theatre. It is impor- A split-screen viewing system with laparoscopic ultrasound
tant to have easily accessible, suitable preset programmes in the images side by side laparoscopic camera views of the intra-
machine, which incorporate all the basic image optimisation func- abdominal probe position is advised. This is said to help prevent
tions, as once scrubbed up, it may be difficult to optimise the image iatrogenic organ damage from overzealous probe manipulation.12
unless a second ultrasound colleague is present. A methodical approach to scanning with a laparoscopic probe
For most open surgical IOUS procedures it is sufficient to put a consists of numerous arching sweeps with the pivot fixed at the
sterile probe cover over the clean probe. Sterile gel should be put port site. This can be time-consuming compared to conventional
inside the cover first, and the probe placed into the cover taking open IOUS, but the benefits of an overall shorter operation time and
care to smooth any air bubbles from the probe face. As most probe faster patient recovery must be borne in mind. Laparoscopic ultra-
covers tend to be relatively short, a second, sterile laparoscopic- sound is perhaps an area where the surgeon is at an advantage over
style cover, which is longer and open at both ends, can be placed his or her radiological colleague. Competent laparoscopic instru-
over the whole, allowing the cable to be covered and keeping the ment manipulation necessitates an operator learning curve. The
area sterile. surgeon will be comfortable with this technique, but a number of
The whole organ or region in question must be adequately training simulators and courses are available to the enthusiastic
imaged. A methodical approach is recommended with a slow sonologist.14
sweeping motion over the organ surface in a controlled manner. It A further consideration with laparoscopic ultrasound is the
is sensible to overlap areas with scanning sweeps and to image both necessity for probe sterilisation, as unlike IOUS, the probe comes
in sagittal and transverse planes.1,10 Specific attention can be given into direct contact with the patient. A number of sterilisation agents
to any lesions encountered, and image capture may be used for are discussed in the literature, including ethylene oxide gas, low-
documentation and audit purposes. Contrast administration and/ temperature hydrogen peroxide gas and glutaraldehyde solution.1,8
or biopsy may be used to assist diagnosis, and ablation is among A suitable bath long enough to accommodate the probe and cable
the options available for treatment. Specific reference to vascular is required, and care should be taken to avoid contact between the
anatomy is vital for the operating surgeon, and the Couinaud clas- plug and cleaning fluid.
sification for liver segmentation is used.
IOUS can be seen as an extension of the bimanual examination
of the organ, especially when considering the liver and pancreas
(Fig. 15.4). Indeed studies have demonstrated that palpation alone CLINICAL APPLICATIONS
can identify surface lesions missed by IOUS.3,13 This results from a
recognised limitation, whereby near-field lesions just below the
liver capsule surface are inadequately imaged due to compression Liver
by the probe, or poor near-field focusing. Bathing the organ surface
with sterile degassed saline can overcome this problem by utilising IOUS is most commonly performed to assess the liver during
the water standoff principle.1 However, the natural moisture found planned resection for primary or metastatic disease. It has a useful
coating the abdominal organs is usually sufficient to provide acous- role in allowing targeted biopsy guidance if questionable lesions
tic coupling (Fig. 15.4) and modern probes with good near-field are encountered, and guiding thermal ablation procedures as part
focusing have improved the demonstration of near-field lesions. In of treatment. It is also used to assess adult livingrelated donor
cases when a tiny lesion can be palpated but not adequately visu- liver, and is invaluable for providing vascular anatomical
alised on IOUS, scanning from underneath the liver whilst identify- information to provide an operative roadmap for the surgical team
ing the lesion with a finger is useful. This can bring the lesion into (Fig. 15.5).
the focal zone of the transducer, making location more successful. Colorectal cancer is the third most common malignancy after
Laparoscopic ultrasound lacks the advantage of direct organ pal- breast and lung cancer, in the United Kingdom, a picture that
pation, compounded by a lack of tactile stimulus feedback from the mirrors much of the Western world.15 Surgical resection is the only
laparoscopic probe, and relies solely on imaging. The planes of scan current hope of cure, with 5-year survival in up to 45% of patients.16
are limited by the laparoscopic port and the flexibility of the probe. Only 1020% of patients with colorectal metastases to the liver will
For small structures, such as ducts or superficial pancreatic nodules, be suitable for resection, although newer surgical techniques and
a water standoff may be beneficial for assessing the near field. chemotherapeutic regimes have helped increase the numbers of
275
CHAPTER 15 Intraoperative ultrasound
A B
C D
Figure 15.6 A: A metastasis close to the hepatic vein is planned for ablation. B: The ablation probe is guided to the lesion using IOUS.
C: The tines of the RF ablation probe are deployed in the lesion. D: Small reflective air bubbles are discharged during the ablation process.
276
Clinical applications
worth considering the delay between preoperative imaging and plan in just 411.5% of patients.5,23 However, many studies fail to
IOUS. Gaps of over 6 weeks are not unusual in some studies.19 It take into account the operator and training dependence of ultra-
may be that this delay accounts for the emergence of some of the sound, and the possible differences in ultrasound detection rates of
smaller lesions, rather than a true superiority of IOUS over preop- different qualities and ages of ultrasound equipment, all of which
erative imaging. Nevertheless, this makes an important case for the have a potential impact on the accuracy of IOUS. Nevertheless,
use of IOUS in cases where delays between preoperative imaging almost all comparative imaging studies conclude by advocating
and surgery cannot be avoided. IOUS as the ultimate determinant of liver lesion quantity, charac-
Surgical planning is clearly dependent on preoperative imaging, teristics and anatomical location.
and the emphasis on improving preoperative imaging is motivated It is foreseeable that with continued improvements to MRI, the
by the desire to avoid offering patients a laparotomy, only to dis- now minimal to moderate improved detection rate of IOUS over
cover that the volume of hepatic or extrahepatic disease encoun- preoperative imaging will diminish further. The danger, however,
tered precludes an attempt at curative resection. The evolution of is that this will become a self-fulfilling prophecy, with non-
laparoscopic assessment does not solve this problem, as a general sonologists using IOUS with the sole purpose of identifying MRI-
anaesthetic and procedure is still obviously best avoided if unneces- detected lesions, for characterisation and demonstration of anatomical
sary. Significant progress has been made with improved lesion relations. To prevent this scenario a dedicated complete survey of the
detection for both CT and MRI over the past 20 years. liver by an experienced sonologist is advocated for every case.
CT during arterial portography (CTAP) has been demonstrated to Almost all liver lesions missed on preoperative imaging are less
have a liver metastasis pick-up rate comparable to IOUS, with a sen- than 1.5cm in diameter.20 High-resolution IOUS improves the
sitivity rate between 80 and 97%.2022 However, it is relatively inva- detection rate at this range, but is by no means perfect. Substantial
sive, with recognised risks of arterial dissection, groin haematoma recurrence rates after partial resection indicate that small metas-
and pseudoaneurysm formation. It also suffers from a high false posi- tases are still missed by IOUS.24 When considering the sensitivity
tive rate, which has the potential to overstage disease and potentially and specificity of various imaging modalities, careful consideration
deny a patient a curative resection, and it has now been largely must be given to the reference standard. This should be a detailed
replaced by improvements in MRI techniques and hardware. histopathological examination of the resected specimen. It will
MRI is easy to perform, does not involve radiation and is non- often be apparent, however, that resection specimens are laminated
invasive, if you discount the peripheral intravenous injection of transversally in slices of 5mm thickness for microscopic examina-
contrast medium. It has been shown to be as good at detecting liver tion.24 Lesions smaller than 5mm in diameter may still be missed
metastases as CTAP with a lower false positive rate.22 There has by histopathological examination.
been some interest as to whether (with improved MRI scanner Recently, ultrasound contrast agents have been found to improve
hardware and techniques) the improved detection of lesions with the detection rate of metastases intraoperatively, in particular sub-
IOUS still holds true. A relatively recent paper acknowledging centimetre lesions.
improved preoperative MRI indicated that IOUS still provided Exciting early results have shown CE-IOUS to be significantly
additional useful information for 47% of patients undergoing more sensitive (96.1%) than CT/MRI (76.7%) and conventional
hepatic resection.17 Surgical strategy was altered in 18% of patients IOUS (81.5%) in detecting liver metastases with histopathology
based on IOUS findings alone. Identification of sub-centimetre as a reference standard.7 Ultrasound contrast agents are micro
metastatic lesions, lesion characterisation and demonstration of bubbles of air or low solubility gas such as perfluorocarbons and
vascular anatomy are cited as major areas to which IOUS contrib- sulphur hexafluoride. Metastases show variable contrast take-up
utes. Other groups comparing preoperative MRI and IOUS have in the arterial phase of contrast injection, but are universally
shown less impressive differences, with IOUS changing the surgical hypo-enhancing in the sinusoidal phase (Fig. 15.7). Persistent
A B
Figure 15.7 A: Contrast-enhanced US demonstrates the hypo-enhancing nature of a metastasis during the sinusoidal phase of injection.
Small, sub-centimetre lesions can now be seen (arrows). B: The normal background liver parenchyma has taken up contrast to become
hyperechoic, increasing the contrast resolution between the three metastases (arrows) and normal liver.
277
CHAPTER 15 Intraoperative ultrasound
A B
Figure 15.8 A: A small metastasis (arrow) is almost isoechoic with the background liver. B: The sonographers fingers (F) palpate a small
isoechoic metastasis (arrows) to locate it prior to guided open ablation.
A B
Figure 15.10 A: During liver transplant, the main hepatic artery is established as patent with colour Doppler following anastomosis.
B: Spectral trace of the artery demonstrating normal flow.
Pancreas
Islet cell tumours with endocrine activity can present with pro-
found clinical features when tumour volume is still very small.
Insulinomas with recurrent episodes of hypoglycaemia and gastri-
nomas with refractory peptic ulcer disease are prime examples.
Small tumours may be radiologically occult, with up to 50% of
insulinomas and gastrinomas not showing up on preoperative
imaging.30 Even recent studies have demonstrated a disappointing
sensitivity of 63.9% for insulinoma location with modern multislice
CT.31 Once again, IOUS has been advocated as an extension of
Figure 15.11 The normal head of pancreas during open
bimanual palpation at open surgery (Fig. 15.11), and successful
surgery, with the normal common bile duct (arrow).
location of tumours in up to 96.7% of patients has been demon-
strated.31 Most islet cell tumours are hypoechoic with respect to
surrounding pancreatic tissue. Their hypervascular nature allows
power and colour Doppler imaging to assist in localisation.9 IOUS
also allows for the detailed assessment of peripancreatic tissues and Biliary tree
regional lymph nodes for metastatic disease. A comprehensive
survey is required because islet cell tumours are frequently Enthusiasts of laparoscopic US suggest that its use to visualise the
multiple. extrahepatic biliary tree can exclude common bile duct stones and
Results for laparoscopic US localisation of islet cell tumours have prevent iatrogenic duct injury (Fig. 15.12).33 Bile duct injury was a
not been as promising, and conversion to open procedures has been particular concern with the original learning curve for laparoscopic
deemed necessary for a significant minority of cases. This probably cholecystectomy seen in the 1990s, when an increase in this particu-
emphasises the benefits of careful bimanual palpation of the pan- larly troublesome complication was seen. Laparoscopic US is useful
creas and surrounding duodenum, and also perhaps the inherent as, apart from the lack of radiation involved, it allows anatomical
difficulty of laparoscopic pancreatic surgery. delineation prior to tissue dissection. However, most surgeons still
Endoscopic ultrasound (EUS) has been shown to have an islet cell seem more comfortable with on-table cholangiography (OTC). An
tumour detection rate of up to 88%, outperforming CT and MRI as OTC requires visual identification of anatomy based on the camera
preoperative imaging.32 Lesions within the body and tail of the view alone, and considerable tissue dissection is required to get to
pancreas are naturally more difficult to detect with EUS than those the point of cystic duct cannulation and fluoroscopy. It is possible
in the head of the gland. Conventional open IOUS is still the gold for a bile duct injury to occur during this period of pre-OTC laparo-
standard imaging modality because pancreatic head lesions are still scopic dissection.
better dealt with by open surgery, and real-time imaging is invalu- Certainly, avoiding ionising radiation is sensible, and colour
able to the surgeon. Doppler imaging may be useful in identifying the cystic artery. The
279
CHAPTER 15 Intraoperative ultrasound
Intraoperative ultrasound
IOUS provides dynamic real-time imaging for the assessment of
predominantly solid-organ oncological disease.
Direct transducer contact with the organ/s of interest allows
higher-frequency scanning than used for percutaneous
ultrasound, and produces high-resolution images.
IOUS is the gold-standard imaging modality for assessing the
liver during resection for primary cancer and metastatic disease.
IOUS demonstrates greater sensitivity than preoperative imaging
modalities for detecting small lesions.
Improvements in preoperative computed tomography and
magnetic resonance imaging have reduced the impact of IOUS
on surgical planning, although IOUS still retains an improved
detection rate.
IOUS facilitates the real-time assessment of vascular anatomy
and surgical dissection planes.
Laparoscopic IOUS is used to image the liver and other organs
as an adjunct to minimally invasive surgery.
Contrast-enhanced IOUS has shown some early promise of
Figure 15.12 Laparoscopic US of the common bile duct seen improved liver lesion detection over conventional IOUS.
through a fluid-filled duodenum.
A B
Figure 15.13 A: Transplant kidney on IOUS. B: Power Doppler demonstrates good perfusion of the kidney.
learning curve for laparoscopic US of the bile ducts is admittedly part) for the loss of opportunity to palpate organs of interest as
slow, however, and it has been shown that this technique cannot traditionally open procedures become laparoscopic. There is
completely replace OTC. Unclear visualisation of the bile duct, already evidence to support the use of conventional IOUS for open
equivocal determination of bile duct stones, poor anatomical dem- nephron-sparing surgery for smaller hereditary renal cancers.34 The
onstration and technical difficulties with the equipment have all impact of CT-guided RFA on this kind of work is perhaps becoming
been cited as reasons to proceed to OTC.33 apparent. Partial adrenalectomy and nephrectomy are guided by
Most patients with a clinical or biochemical suspicion of intra- laparoscopic US.35,36 Conventional IOUS with colour Doppler
ductal stones will have had preoperative magnetic resonance imaging is useful for assessing the vasculature of transplant kidneys
cholangiopancreatography (MRCP) or endoscopic retrograde (Fig. 15.13).
cholangiography (ERCP), where stones can be removed or a sphinc-
terotomy can be performed. Some surgeons still advocate OTC or
laparoscopic US, however, especially if there has been a delay REFERENCES
between MRCP or ERCP and surgery.
1. Kruskal JB, Kane RA. Intraoperative US of the liver: techniques and
clinical applications. Radiographics 2006;26:10671084.
2. Clarke MP, Kane RA, Steele Jr G, et al. Prospective comparison of
Urology preoperative imaging and intraoperative ultrasonography in the
detection of liver tumours. Surgery 1989;106:849855.
Surgeons are becoming ever more willing to embrace laparoscopic 3. Boutkan H, Luth W, Meyer S, et al. The impact of intraoperative
US, particularly because it is seen as a compensation (at least in ultrasonography of the liver on the surgical strategy of patients with
280
References
gastrointestinal malignancies and hepatic metastases. Eur J Surg Oncol 20. Soyer P, Levesque M, Elias D, et al. Detection of liver metastases from
1992;18:342346. colorectal cancer: comparison of intraoperative US and CT during
4. Kane RA, Hughes LA, Cua EJ, et al. The impact of intraoperative arterial portography. Abdom Gastrointest Radiol 1992;183:541544.
ultrasonography on surgery for liver neoplasms. J Ultrasound Med 21. Nomura K, Kadoya M, Ueda K, et al. Detection of hepatic metastases
1994;13(1):16. from colorectal carcinoma: comparison of histopathologic features of
5. Sahani DV, Kalva SP, Tanabe KK, et al. Intraoperative US in patients anatomically resected liver with results of preoperative imaging. J Clin
undergoing surgery for liver neoplasms: comparison with MR Gastroenterol 2007;41(8):789995.
imaging. Radiology 2004;232:810814. 22. Vogl TJ, Schwarz W, Blume S, et al. Preoperative evaluation of
6. Koffron AJ, Auffenberg G, Kung R, Abecassis M. Evaluation of 300 malignant liver tumours: comparison of unenhanced and SPIO
minimally invasive liver resections at a single institution, less is more. (Resovist)-enhanced MR imaging with biphasic CTAP and
Ann Surg 2007;246:385394. intraoperative US. Eur Radiol 2003;13:262272.
7. Leen E, Ceccotti P, Moug SJ, et al. Potential value of contrast-enhanced 23. Cerwenka H, Raith J, Bacher H, et al. Is intraoperative
intraoperative ultrasonography during partial hepatectomy for ultrasonography during partial hepatectomy still necessary in the age
metastases, an essential investigation before resection? Ann Surg of magnetic resonance imaging? Hepatogastroenterology 2003;50(53):
2006;243:236240. 15391541.
8. Torzilli G, Palmisano A, Del Fabbro D, et al. Contrast-enhanced 24. Fioole B, de Haas RJ, Wicherts DA, et al. Additional value of contrast
intraoperative ultrasonography during surgery for hepatocellular enhanced intraoperative ultrasound for colorectal liver metastases. Eur
carcinoma in liver cirrhosis: is it useful or useless? A prospective J Radiol 2008;67:169176.
cohort study of our experience. Ann Surg Oncol 2007;14(4): 25. Albrecht T, Hohmann J, Oldenburg A, et al. Detection and
13471355. characterisation of liver metastases. Eur Radiol Suppl 2004;14(8):
9. Kane RA. Intra-operative ultrasound. In: Cosgrove DO, editor. Clinical 2533.
ultrasound: abdominal and general. 2nd ed. Edinburgh: Churchill 26. Siosteen AK, Elvin A. Intra-operative uses of contrast-enhanced
Livingstone; 2000. p. 143164. ultrasound. Eur Radiol Suppl 2004;14(8):8795.
10. Coti MA, Kaloma F, de Oliveira ML, et al. Patient variability in 27. Torzilli G, Olivari N, Moroni E, et al. Contrast-enhanced intraoperative
intraoperative ultrasonographic characteristics of colorectal liver ultrasonography in surgery for hepatocellular carcinoma in cirrhosis.
metastases. Arch Surg 2008;143(1):2934. Liver Transpl 2004;10(21):3438.
11. Silas AM, Kruskal JB, Kane RA. Intraoperative ultrasound. Radiol Clin 28. Buell JF, Thomas MT, Rudich S, et al. Experience with more than
North Am 2001;39(3):429448. 500 minimally invasive hepatic procedures. Ann Surg 2008;248(3):
12. Ganguli S, Kruskal JB, Brennan DD, Kane RA. Intraoperative 475486.
laparoscopic ultrasound. Radiol Clin North Am 2006;44(6):925935. 29. Lai EC, Tang CN, Ha JP, et al. The evolving influence of laparoscopy
13. Jarnagin WR, Bach AM, Winston CB, et al. What is the yield of and laparoscopic ultrasonography on patients with hepatocellular
intraoperative ultrasonography during partial hepatectomy for carcinoma. Am J Surg 2008;196(5):736740.
malignant disease? J Am Coll Surg 2001;192(5):577583. 30. Zeiger MA, Shawker TH, Norton JA. Use of intraoperative
14. Gurusamy KS, Aggarwal R, Palanivelu L, Davidson BR. Virtual reality ultrasonography to localize islet cell tumors. World J Surg 1993;17:
training for surgical trainees in laparoscopic surgery. Cochrane 448454.
Database Syst Rev 2009;21(1):CD006575. 31. Roland CL, Lo CY, Miller BS, et al. Surgical approach and
15. UK Bowel Cancer Incidence Statistics. Cancer Research UK. perioperative complications determine short-term outcomes in patients
http://info.cancerresearchuk.org/cancerstats/types/bowel/ with insulinoma: results of a bi-institutional study. Ann Surg Oncol
incidence/ 2008;15(12):35323537.
16. Malik HZ, Prasad KR, Halarzun KJ, et al. Preoperative prognostic 32. Liu H, Peng C, Zhang S, et al. Strategy for the surgical management of
score for predicting survival after hepatic resection for colorectal liver insulinomas: analysis of 52 cases. Dig Surg 2007;24:463470.
metastases. Ann Surg 2007;246(5):806814. 33. Machi J, Johnson JO, Deziel DJ, et al. The routine use of laparoscopic
17. Conlon R, Jacobs M, Dasgupta D, Lodge JPA. The value of ultrasound decreases bile duct injury: a multicenter study. Surg
intraoperative ultrasound during hepatic resection compared with Endosc 2009;23(2):384388.
improved preoperative magnetic resonance imaging. Eur J Ultrasound 34. Choyke PL, Pavlovich CP, Daryanan KD, et al. Intraoperative
2003;16:211216. ultrasound during renal parenchymal sparing surgery for hereditary
18. Gaitini D, Kopelman D, Soudak M, et al. Impact of intraoperative renal cancers: a 10-year experience. J Urol 2001;165:397400.
sonography on resection and cryoablation of liver tumours. J Clin 35. Ukimura O, Okihara K, Kamoi K, et al. Intraoperative ultrasonography
Ultrasound 2001;29(5):265272. in an era of minimally invasive urology. Int J Urol 2008;15:673680.
19. Guimaraes CM, Correia MM, Baldisserotto M, et al. Intraoperative 36. Cheng SP, Saunders BD, Gauger PG, Doherty GM. Laparoscopic
ultrasonography of the liver in patients with abdominal tumors. partial adrenalectomy for bilateral pheochromocytomas. Ann Surg
Journal of Ultrasound Med 2004;23:15491555. Oncol 2008;15(9):25062508.
281
CHAPTER
16 Pancreas
Zahir Amin
and it now has a useful role for problem-solving and guided aspira-
INTRODUCTION tions and biopsies.3,10,11 Therefore, ultrasound still has an important
complementary role in evaluating pancreatic pathology.
Major technological advances in all of the imaging modalities have
changed their roles in pancreatic imaging.13 Computed tomogra-
phy (CT) and magnetic resonance imaging (MRI) are the principal
modalities used to evaluate pancreatic pathology.3,4 If clinical sus- ANATOMY (Figs 16.1, 16.2)12,13
picion for pancreatic pathology is high, then CT is often the initial
test requested rather than ultrasound, because of a significant false The pancreas is a retroperitoneal organ in the anterior pararenal
negative rate for detecting pancreatic pathology with ultrasound. space, and develops embryologically from the fusion of dorsal and
However, transabdominal ultrasound is still frequently the first ventral buds. It usually lies in a slightly oblique transverse position
imaging modality to detect or infer (if dilated common bile duct) at around the level of the first or second lumbar vertebra, but its
pancreatic pathology. Although the deep posterior position of the exact position and size are variable. It is divided into a head, neck,
pancreas can result in poor or suboptimal ultrasound views because body and tail region.
of overlying bowel gas or in large patients,5 when the pancreas is The head of the pancreas lies most caudally and sits just anterior
well seen ultrasound can be a powerful imaging tool for detecting to the inferior vena cava and inferior to the portal vein. It lies adja-
and characterising pancreatic pathology.6 With modern ultrasound cent to the duodenal loop, with the first part of duodenum lying
machines, high quality images of the pancreas can be acquired, superolaterally, the second part laterally and third part inferiorly.
ultrasound contrast medium is available for enhancement,7,8 and The uncinate process extends from the medial, inferior and poste-
the image detail may be comparable or superior to CT or MRI.9 rior part of the head of pancreas and lies posterior to the superior
Endoscopic ultrasound is being increasingly used and usually gives mesenteric vessels. The neck of the pancreas is usually thinner than
very high quality and detailed images of the pancreas although a the rest of the gland and lies anterolateral to the portal vein/supe-
relatively invasive test, there is greater availability and expertise, rior mesenteric vein (SMV) confluence, and just posterior to the
285
CHAPTER 16 Pancreas
A B C
Figure 16.1 Embryological development of the pancreas. A: The dorsal and ventral buds of the pancreas are initially separate.
B: In the 5-week embryo the ventral bud has migrated around the duodenum to lie close to the dorsal bud. C: By week 6, the two buds
fuse. The main pancreatic duct is derived from the distal part of the dorsal bud and the proximal part of the ventral bud. The duct connecting
the dorsal bud to the duodenum usually degenerates.
head of pancreas and a larger main dorsal duct extending from the
Pancreatic imaging
accessory papilla to the pancreatic tail14,15 in incomplete pancreas
Pancreatic imaging has improved along with major technological divisum a thin branch just connects dorsal and ventral ducts.15 Most
advances. patients with pancreas divisum are asymptomatic but some patients
CT and MRI are the principal imaging modalities for assessing the may have stenosis and partial obstruction at the accessory papilla,
pancreas. resulting in poor drainage which may cause acute or chronic pan-
Conventional US still has a significant false negative rate for creatitis or pancreatic type pain.16 Annular pancreas can also occur
detecting pancreatic pathology because of its deep posterior with failure of dorsal/ventral fusion, and the ventral pancreas then
position. partially encases and narrows the second part of duodenum.17
However, when the pancreas is well seen, US may give better
detail than CT and MRI.
Endoscopic US is increasingly available and provides very high
quality and detailed pancreatic images. SCANNING TECHNIQUE
US has an important complementary role in evaluating pancreatic
pathology. These include conventional transabdominal ultrasound, endo-
scopic ultrasound and intraoperative/laparoscopic ultrasound.
With all these techniques, the texture, size and contour of the pan-
creas should be evaluated, and the pancreatic duct, distal common
bile duct, splenic/superior mesenteric/portal veins, and the coeliac
axis/superior mesenteric artery identified.
pylorus; the groove for the gastroduodenal artery separates the
head and neck of the pancreas. The body of the pancreas lies in the
midline posterior to the gastric antrum/body or left lobe of liver Transabdominal ultrasound
and anterior to the splenic vein. The tail of the pancreas extends
laterally to the splenic hilum, anterior to the splenic vein, which is Although the image of the pancreas that can be obtained has
a main anatomical landmark. improved considerably over recent years with improvements in
The gastroduodenal artery arises from the common hepatic machine and transducer technology, the technique, skill and per-
artery and runs along the anterior lateral margin of the neck and sistence of the ultrasonographer is the most important aspect of
head of the pancreas. The common bile duct crosses the anterior good pancreatic ultrasound. This will also depend on patient size,
surface of the portal vein to the right of the hepatic artery, and depth of the pancreas and overlying bowel gas. However, even in
passes behind the first part of duodenum to run inferiorly and large patients, it can be worthwhile trying to image the pancreas
posteriorly within the head of pancreas. The right hepatic artery since with transducer pressure, good views of the pancreas are still
may arise from the superior mesenteric artery, and so may be seen possible with ultrasound (Fig. 16.3).
passing close to the undersurface of the head of pancreas this is Patient fasting prior to abdominal ultrasound ensures an empty
an important variant for the surgeon planning a resection of the stomach, allowing compression and apposition of the walls of the
pancreatic head. The splenic artery is very tortuous and runs along gastric antrum and visualisation of the body and neck of the pan-
the superior margin of the body and tail of the pancreas. creas (Fig. 16.2A). Water or a solution containing cellulose particles
The main pancreatic duct (Wirsung) runs along the length of the or simethicone can be given to the patient to fill the stomach and
gland from the ampulla and tapers towards the pancreatic tail. In provide an acoustic window to the pancreas18 (Fig. 16.4). A gradual
4050% of cases an accessory duct (Santorini) may be present, increase in transducer pressure may displace gas-filled bowel
passing laterally from the main duct in the head of pancreas to an loops, with the image nearly always improving during the ultra-
accessory papilla in the duodenum just above the level of the sound examination (Fig. 16.5).
ampulla. In 510% of the population the dorsal and ventral parts of Optimising ultrasound views of the pancreas varies between
the pancreas fail to completely fuse, resulting in complete or incom- patients but includes transverse, longitudinal and angled oblique
plete pancreas divisum with a small ventral duct in the separate scans. Techniques to further improve the images include scanning
286
Scanning technique
GA
SV
SMV SMA
D2 P
A
IVC A
IVC Sp
A
B
St
SMV
CA
SV
D
C
D
CBD
E F
Figure 16.2 Normal pancreas. A: The pancreatic head (P) lies anterior to the inferior vena cava (IVC), posterior to the gastric antrum (GA)
and medial to the second part of duodenum (D2). Both the gastroduodenal artery (short arrow) and common bile duct are shown (long arrow).
B: More superior view showing the neck, body and part of the tail of pancreas posterior to the left lobe of liver with a normal thin pancreatic
duct just visible (arrows). C: The pancreatic tail is seen lying anterior to the splenic vein (SV). D: Sagittal view of the body of pancreas posterior
to the liver and anterior to the SMV. The hepatic artery is seen (arrow). E: More lateral oblique sagittal view of the head of pancreas (P),
showing the CBD, portal vein (PV) and also the pancreatic duct (arrow). F: Inferior head of pancreas close to the ampulla. The pancreatic duct
(arrow) is anterior to the CBD, close to the duodenum (D), appearances suggestive of pancreas divisum. A, aorta; IVC, inferior vena cava; SMV,
287
superior mesenteric vein; SV, splenic vein; SMA, superior mesenteric artery; CA, coeliac axis; Sp, spine, St, stomach.
CHAPTER 16 Pancreas
A B
Figure 16.3 Large patient. A: Head of pancreas seen as a deep echogenic structure just lateral to the mesenteric vessels (arrows).
B: More superiorly the echogenic body of pancreas is outlined (arrows).
A B
Figure 16.5 Compression ultrasound. A: Poor view of head of pancreas (P) before transducer pressure. B: Improved image of
pancreatic head after transducer pressure.
Sp
SV T
A B
Figure 16.6 Pancreatic tail. A: Pancreatic tail (T) seen through the spleen (Sp), lying anterior to the splenic vein (SV) and artery (arrow).
B: In a younger patient the tail appears more hypoechoic.
289
CHAPTER 16 Pancreas
A B
Figure 16.7 Harmonic imaging. A: Mucinous cystic neoplasm in tail of pancreas with eccentric wall thickening (arrows). B: With
harmonic imaging there is reduced noise and a sharper image, with clearer solid/fluid differentiation.
A B
Figure 16.8 Colour Doppler. A: Small cyst in the neck of pancreas (between cursors) of similar echogenicity to adjacent vessels.
B: Colour Doppler allows differentiation of cyst and vessels.
allow colour Doppler to differentiate vessels from cystic lesions. fine-needle aspiration (FNA)/biopsy after the patient has been
The linear array probe allows needle-guided aspirations and biop- imaged less invasively by CT or MRI10,27 (Fig. 16.12). Since EUS is
sies (Fig. 16.10). A balloon over the transducer tip can be distended often performed at more specialist referral centres, a common
with water to improve acoustic contact between transducer and gut problem is that CT or MRI is not available at the time of the
wall. The close proximity between pancreas and stomach/duode- EUS, and this inevitably makes the test less useful. EUS is best
nal wall means that high frequencies can be used to get detailed viewed as complementary to CT and/or MRI.27,28 There are still
high-resolution images of the pancreas and pancreatic duct down limited training centres for EUS, and learning pancreatic EUS
to under 1mm (Fig. 16.11). The range of frequencies available are is considerably more difficult and demanding compared to
usually 512MHz, the lower frequency allowing greater depth of oesophageal EUS.22,29
imaging away from the gut wall, up to about 7cm. Increasingly, with high quality US/CT/MRI, EUS is used as an
After passing the echo-endoscope into the stomach and duode- interventional tool for biopsy of lesions adjacent to the oesophagus,
num, the air is removed during slow withdrawal. Gentle tip angula- stomach and duodenum, or for guided drainage of adjacent collec-
tion and rotation is used to optimise views of the pancreas. The tions such as pseudocysts, or for coeliac axis block.10,26,27 Although
uncinate process is seen from the third part of the duodenum; most very high sensitivities have been reported for EUS FNA, the number
of the head of pancreas from the second part of the duodenum and of false negatives and inadequate samples can be relatively high,
the body and tail of pancreas can be visualised through the stomach resulting in the biopsy being repeated either by EUS or under US
(Fig. 16.11). or CT guidance.30
Although occasionally used as a primary diagnostic/assessment, Miniprobes are also available these are tiny transducers fixed
EUS is best used for targeted problem-solving or for EUS to the tip of thin 24mm diameter catheters. They are not very
290
Scanning technique
c c
Intraoperative ultrasound
High-frequency linear array probes (7.510MHz), covered with a
sterile plastic sheath and held against the pancreas at laparotomy,
provide very good images of the pancreas and pancreatic duct.32
Transducers at the tip of laparoscopes are also being increasingly
used to provide high quality images33 (Fig. 16.13). Filling the lesser
sac with fluid may improve more superficial resolution. The need
Figure 16.10 EUS. Linear array probe with balloon over the tip of for the presence of a radiologist during intraoperative scanning is
the transducer and aspiration needle shown through the working diminishing, since many surgeons using these techniques have
channel of the echo-endoscope. been trained in their use.
291
CHAPTER 16 Pancreas
PD
A B
Figure 16.12 EUS ampullary mass. A: Small mass (arrows) at the ampulla not seen on CT, blocking and dilating the pancreatic duct
(PD). B: Needle (arrow) inserted into the mass between the bile duct stent and blocked pancreatic duct, for aspiration cytology.
292
Acute pancreatitis
Scanning techniques
US assessment of the pancreas should include its parenchymal in older patients.42 The margins of the pancreas are usually well
texture, size and contour, the pancreatic and bile ducts, the defined but lobulated.
coeliac axis, portal vein and superior mesenteric vessels. If the pancreas is well seen on ultrasound then the main pancre-
Good technique, experience and persistence of the atic duct is usually visible in the neck/body region (Figs 16.11A and
ultrasonographer all contribute in the assessment of the pancreas 16.17). The size of the duct increases with age, up to a maximum of
with US. 3mm;43; up to age 30 years the mean duct diameter has been
Even in large patients, transducer compression can result in good reported as 1.5mm, and in those over 80 years the mean diameter
US views of the pancreas. is 2.3mm.44 However, duct diameters of up to 5mm may be seen
Pancreatic US views can be improved by filling the stomach with in elderly people.41
water, alterations in patient breathing and position, harmonic Ultrasound assessment of the pancreatic duct following secretin
imaging, and colour Doppler to define the vessels. (1iu/kg) stimulation has been reported.44,45 In one study, younger
Contrast-enhanced US has a limited role in pancreatic US it patients duct increased from 1.6mm to 3.1mm, and older patients
may be useful in characterising the nature of a pancreatic mass if from 1.9mm to 3.5mm.44 A suboptimal response suggests pancre-
well seen. atic insufficiency and a greater duct dilatation suggests obstruction
of the duct. However, ultrasound assessment after secretin stimula-
tion will only be used occasionally in most centres if the patient is
unable to have secretin-stimulated magnetic resonance cholangio-
pancreatography (MRCP) or even CT, since these tests will usually
give better and more consistent images of the pancreatic duct as
The main indications for intraoperative scanning are detection of well as duodenal secretions.
small insulinomas and intraductal papillary mucinous tumours, Pancreas divisum is usually a difficult diagnosis to make on
and defining the anatomy and position of the pancreatic duct ultrasound but may be suggested if the pancreatic duct is dilated
during duct drainage procedures.34,35 and can be followed from the body/neck to its insertion into the
duodenum separate from the common bile duct (CBD), cranial and
ventral to the ampulla (where CBD inserts). However, the often thin
communication between dorsal and ventral pancreatic ducts will
NORMAL APPEARANCES not be seen on ultrasound, so the diagnosis of divisum can only be
suggested rather than confirmed (Fig. 16.2F).
The normal size of the pancreas is variable, and measurements are A relatively common normal variant is a hypoechoic posterior
not usually made; more important than actual size of the pancreas head/uncinate process of pancreas, due to focal fatty sparing of the
is any focal or diffuse change in echogenicity or duct calibre. ventral pancreas46 (Fig. 16.18). Although it can mimic a mass, there
However, the presence of parenchymal atrophy is important. The is no duct dilatation or real mass effect and the diagnosis can
maximum measurement of the head of pancreas is about 2.5cm, usually be made on ultrasound. It has been reported to be present
the neck <1cm, the body 1.5cm, and the tail 3.5cm. The normal in 3040% of patients having abdominal US,47 and up to 75% of
tail of pancreas can appear focally enlarged and is not infrequently patients undergoing EUS.48
called abnormal if well seen on ultrasound (Fig. 16.14).
The pancreas is typically homogeneous, and slightly more echo-
genic than liver.36 The echogenicity is related to the degree of fat
deposition37 and is variable; younger patients tend to have a hyp- ACUTE PANCREATITIS
oechoic pancreas and older patients have a hyperechoic pancreas
with increased fat replacement38 (Figs 16.6 and 16.15); the latter also
occurs in obesity, with steroid ingestion, in Cushings syndrome General considerations
and with cystic fibrosis.39,40 The pancreas can be as echogenic as
retroperitoneal fat in up to 35% of cases.41 The parenchyma may be Acute pancreatitis is acute inflammation of the pancreas with acute
heterogeneous with hyperechoic stranding (Fig. 16.16), especially abdominal pain and raised serum amylase or lipase, the latter
293
CHAPTER 16 Pancreas
A B
Figure 16.15 Pancreas. A: Normal hypoechoic pancreatic body/tail. B: Normal echogenic pancreas.
Aetiology Pathophysiology
Gallstones are the commonest cause (in about 50% of cases), includ- This is not clearly understood, but several factors initiate inflamma-
ing occult stones, microlithiasis and sludge.49 Alcohol is the second tion.54 These include overdistension of the pancreatic duct (by
commonest cause, in 2025% of cases.52,53 Other causes include obstruction or reflux of bile/duodenal contents), alcohol (protein
raised lipids, hypercalcaemia, endoscopic retrograde cholangiopan- plugs form in ducts) and other toxins, hypertriglyceridaemia and
creatography (ERCP), trauma, viral infections, and various hypercalcaemia.55 The end result is a release of activated and
drugs.49,52 In 2025% of cases no cause is found and these are destructive pancreatic enzymes into the pancreas and surrounding
labelled idiopathic.52 tissues. This may lead to changes ranging from mild interstitial
294
Acute pancreatitis
D
V
A B
Figure 16.18 Ventral pancreas. A: Hypoechoic ventral pancreas (arrows) in the posterior head of pancreas. B: EUS from the third part
of the duodenum showing a hypoechoic ventral pancreas (V) posterior to the superior mesenteric artery and an echogenic dorsal head of
pancreas (D).
Normal appearances associated with traumatic necrosis, abscess and fistulas.57 Blunt
abdominal injuries result in disruption in the vulnerable neck of
The normal size of the pancreas is variable, any alteration in pancreas region, with the duct tearing where it is compressed
echogenicity or duct dilatation being more important in assessing against the aorta and spine this is the commonest cause of pan-
pathology. creatitis in children, and distal pancreatectomy is usually required
The echogenicity of the pancreas increases with age, with if there is complete duct disruption.58
increased fat replacement.
The pancreatic duct diameter also increases with age mean
diameter 1.5mm in patients under 30 years, and 2.3mm in Clinical features
patients over 80 years. Duct diameters up to 5mm have been Typical presentation is with acute epigastric pain and elevated pan-
reported in elderly patients without associated pancreatic creatic enzymes. Mild pancreatitis occurs in 7080% of cases and
pathology. causes minimal organ dysfunction with rapid resolution of symp-
Pancreas divisum occurs in 510% of the population and may be toms.59 Severe pancreatitis occurs in 2030% and is associated with
suggested on US if the dorsal duct is dilated and followed to the severe systemic disturbance and an early toxic phase and later
duodenum with a separate insertion from the bile duct, cranial septic complications. The serum amylase rise may be transient and
and ventral to the ampulla. unrecorded, and the diagnosis may be unclear even if there is
A hypoechoic posterior head/uncinate process of pancreas severe pancreatitis. Various clinical scoring systems can be used to
occurs due to focal fatty sparing of the ventral pancreas, predict severity of an episode of acute pancreatitis, although there
may mimic a mass, and is reported in 3040% of patients is still a need for a more objective early measure of severity.49,52 A
having abdominal US and in as many as 75% of patients C-reactive protein of greater than 150mg/L at 48 hours also pre-
undergoing EUS. dicts a severe attack.52,60
Around 2035% of patients with gallstone pancreatitis will have
gallstone-related morbidity within 6 months,61,62 so early cholecys-
tectomy is indicated; if the patient is unfit for surgery endoscopic
sphincterotomy is indicated.52
pancreatitis to severe pancreatic or peripancreatic necrosis, as well Mortality rates after acute pancreatitis are dependent on inten-
as release of toxins into the systemic circulation.55 Pancreatic paren- sive care and radiological monitoring with active treatment of com-
chymal necrosis is maximal at 23 days after the acute onset of plications, most serious of which are infected necrosis and arterial
attack. Vascular damage occurs by direct effect of pancreatic bleeding/pseudoaneurysm formation. In patients with pancreatic
enzymes, necrosis and infection, and can lead to venous thrombo- necrosis, mortality is about 10% with sterile necrosis and 25% with
sis, acute arterial or venous haemorrhage, or pseudoaneurysm infected necrosis.63
formation.
In patients with pancreas divisum, gallstone pancreatitis affects Role of ultrasound
only the relatively small ventral pancreas. Drainage via the acces-
sory papilla may be impaired and so this may predispose to pan- CT is the technique of choice in evaluating patients with suspected
creatitis in patients with divisum, but this is controversial.49 or established acute pancreatitis. However, US is often the initial
Traumatic pancreatitis usually results in duct disruption and a test in patients presenting with abdominal pain it may be possible
parenchymal defect, and a large pseudocyst often forms.56 Penetrat- to assess the abnormal pancreas and any fluid collections, but views
ing injuries can result in disruption at any point, and may be may be limited with ileus and pain/tenderness (Fig. 16.19).3
295
CHAPTER 16 Pancreas
A B
Figure 16.19 Acute pancreatitis. A: Pain and extensive bowel gas because of an ileus limited US views of the pancreas but a small
amount of free fluid was seen adjacent to the liver, supporting some acute intra-abdominal inflammation. B: CT in the same patient shows
some fluid and stranding around the pancreatic tail. Note the distended air-filled bowel anteriorly, highlighting the reason for the poor
US views.
A B
Figure 16.20 Mild acute pancreatitis. A: Slightly enlarged, oedematous and hypoechoic body of pancreas. B: Focal pancreatitis with an
ill-defined hypoechoic mass in the head of pancreas and slight dilatation of the pancreatic duct.
Therefore CT is indicated if there is still clinical concern and US Once the diagnosis of acute pancreatitis is established, any dete-
unhelpful. US has a critical role in detecting gallstones, and should rioration is imaged with CT (or MRI), but US can be used inter
be repeated if no stones are initially detected.52 Biliary dilatation mittently and may allow adequate views and assessment of
will be seen on US if the distal CBD is obstructed, and CBD stones collections.
may be visible with US. A very useful and underused role of US is in assessing how much
EUS may detect tiny stones or microlithiasis as a cause of acute fluid or solid component is present within a pseudocyst, allowing
pancreatitis.64 Although some authors suggest EUS after the first a decision on whether further drainage of any liquid component is
attack of acute pancreatitis,65 there is not enough evidence to needed.66
support this. However, patients with recurrent idiopathic pan- US or EUS can be used prior to endoscopic cystgastrostomy to
creatitis should have EUS.52 EUS is as accurate as and safer than assess the gut/pseudocyst wall thickness and the presence of any
ERCP for the detection of CBD stones.52 intervening blood vessels, particularly venous collaterals.66
296
Acute pancreatitis
A B
D
C
Figure 16.21 Severe acute pancreatitis. A: Disruption of pancreatic parenchyma in the body/tail of pancreas (long arrow), adjacent fluid
and solid necrosis (short arrows). B: Corresponding CT showing the disrupted pancreas (arrow) and the peripancreatic necrosis tracking
around the pancreatic tail, spleen and left kidney. C: Enlarged, disorganised pancreatic tail (arrows) with tiny pockets of fluid/oedema and
variable echogenicity of fat necrosis. D: Similar findings around the left kidney.
Contrast-enhanced US has been reported to be useful in patients Hypoechoic change may be diffuse or focal, the latter mimicking
with acute pancreatitis,67 but there are problems with consistently a tumour mass (Fig. 16.20B). The pancreatic duct is usually com-
imaging the whole pancreas in these patients, which is a significant pressed and thin, and may not be visible, but if there is a focal mass,
drawback to its practical value in this situation.3 there may be some mass effect resulting in slight dilatation of the
duct beyond the mass.
Appearances on ultrasound
Severe pancreatitis
Ultrasound views are likely to be more limited because of increased
Mild pancreatitis tenderness and ileus. Views of the head and tail of pancreas are
The pancreas may appear normal, enlarged, hypoechoic (less than sometimes possible from the flanks. The abnormalities that may be
liver echogenicity) and oedematous (Fig. 16.20). Reduction in seen include free fluid, a hypoechoic bulky gland, and possible
parenchymal echogenicity results in increased visibility of duct parenchymal disruption. Peripancreatic fluid/collections accumu-
wall, and thin septations separating lobules may also be seen. There late in the lesser sac and/or track down the flanks. Fat necrosis and
may be oedema/fluid around pancreas and/or around the liver solid inflammatory change are common findings on CT, but are
and spleen and in the flanks. CT is less sensitive at showing subtle difficult to see well on ultrasound and usually appear as solid areas
changes within the pancreas, but much more sensitive at defining of increased and decreased echogenicity and associated with tiny
change in the peripancreatic fat (Fig. 16.19B). pockets of fluid echogenicity (Fig. 16.21).
297
CHAPTER 16 Pancreas
Figure 16.22 Pseudocysts. A: Large pseudocyst arising from the pancreatic tail, some internal echoes and a slightly irregular and thick
margin. B: EUS of a large pseudocyst with thick nodular septa and nodules attached to the wall. The main differential diagnosis was of a
mucinous cystic neoplasm, but analysis of aspirated fluid showed absence of mucin, high amylase and low tumour markers, making a
pseudocyst much more likely. C: Although this pseudocyst appeared cystic on CT, US showed it was mainly solid with small cystic
components a drain was inserted but very little fluid aspirated as suggested by the US appearance. D: In another patient, a pseudocyst
was drained and follow-up CT suggested a residual cyst, but EUS showed there was mainly solid material within it.
298
Acute pancreatitis
Infection
Causes of infection after acute pancreatitis include infected pseu-
docyst/abscess, infected pancreatic necrosis and infected peripan-
Biliary obstruction
creatic necrosis (Fig. 16.24). An abscess occurs 24 weeks after onset US should easily detect any biliary dilatation, and if gallstones are
of acute pancreatitis and is typically well defined with a thick wall, present or suspected, urgent ERCP is indicated. Transient swelling
hypo- or anechoic centre and often containing bright echoes which of the pancreatic head can lead to an oedematous CBD stricture, but
may indicate pus, air or necrotic tissue debris. Necrosis may become this can later lead to a more fibrotic stricture. There is a risk of
infected in about 10% of patients with acute pancreatitis, but in up cholangitis, so if the liver function tests are obstructive then biliary
to 80% with severe necrotising pancreatitis;68 this peaks at 3 weeks stenting is appropriate.
GB
GB
A B
Figure 16.23 Phlegmon. A: CT showing large low-density collection anterior to the head of pancreas, thought to be cystic, but of slightly
increased density compared to the adjacent gallbladder. B: US showed this to be a solid heterogeneous inflammatory mass. GB,
gallbladder.
299
CHAPTER 16 Pancreas
Gastrointestinal tract obstruction and initial procedure implies a significant persistent communication
with the main pancreatic duct. ERCP and pancreatic stent is indi-
renal obstruction cated initially, and surgery may need to be considered.
These may be seen as sequelae of acute pancreatitis; they usually
resolve with time and without intervention.
Infected necrosis
Suspected infected necrosis should be aspirated for culture.70 If pus
Intervention is aspirated, then a radiological drain usually follows. However,
consideration should be given to necrosectomy, although this is not
mandatory as previously reported.52
Pseudocyst aspiration/drainage A common scenario in practice is that some (varying proportion)
This can be performed by direct puncture, or by a transgastric solid necrosis that does not initially drain becomes more infected
approach with US and/or fluoroscopic guidance (Fig. 16.26). EUS after the drain has been inserted and then liquefies and drains very
guidance can also be used for endoscopic transgastric aspiration slowly (may be weeks to months) usually requiring further drains,
and drainage. Drainage is indicated if the patient is symptomatic changes and upsizing. The infected cavity may evacuate from the
or the cyst is infected or enlarging. Continued drainage after the drain, or fistulation occurs into adjacent gastrointestinal (GI) tract.
300
Chronic pancreatitis
A B
Figure 16.25 Pseudoaneurysm. A: Arterial phase CT showing pseudoaneurysm (arrow) surrounded by thrombus in the head of
pancreas, not initially recognised. B: US 1 week later showed an echo-poor and heterogeneous corresponding focal area, but no colour
Doppler flow (arrow). The pseudoaneurysm had spontaneously thrombosed, confirmed on repeat CT.
Figure 16.26 Drainage of pseudocyst. A: US-guided insertion of a pigtail catheter into a pseudocyst. B: High-frequency US used to
guide a needle through the gastric antrum (arrows) into a pseudocyst (P). The tract is then dilated before insertion of a pigtail catheter.
The drain can be cut within the stomach at a later date to allow continued internal drainage. C: EUS-guided aspiration of a pseudocyst
posterior to the gastric wall.
Ultrasound and EUS Figure 16.27 Focal chronic pancreatitis. Hypoechoic mass in
the head of pancreas, around a bile duct stent (arrow), in a patient
Ultrasound has the advantage over CT of allowing detailed views known to have chronic pancreatitis. Several biopsies from this mass
of the pancreatic parenchyma when it is visualised, and many revealed fibrosis only, and no progression on follow-up CT scans.
302
Chronic pancreatitis
papers have been written about the changes in the echotexture of to tumour calcification (Fig. 16.29). Intraductal calculi are protein
the pancreatic parenchyma in chronic pancreatitis.3,8082 A normal aggregates with calcium carbonate deposits, and their echogenicity
echotexture may be seen in up to 40% of patients with chronic increases with increasing calcium content. Non-calcified intraductal
pancreatitis, mainly in the early stages. However, the echogenicity protein plugs are usually not detectable, but may be seen on high-
of the pancreas usually increases in chronic pancreatitis due to a frequency US and/or with harmonic imaging as echogenic foci
combination of increased fat and fibrosis, but this is also seen in without acoustic shadowing (Fig. 16.30).
obese and older patients.6,38,4142 Therefore, on its own this ultra- The presence of duct dilatation and irregularity may also be seen
sound change is not helpful. Similarly, volume assessment is dif- on ultrasound of patients with chronic pancreatitis. Any pseudo-
ficult and subjective, and parenchymal atrophy is non-specific. Foci cysts detected further support a diagnosis of chronic pancreatitis.
of increased and decreased gland echogenicity are said to be more A pancreatic duct diameter of greater than 3mm is considered
specific for chronic pancreatitis,83 but again this is more reliable as pathological.83 It is the most easily identified US sign in chronic
a supportive sign. pancreatitis with a sensitivity of 6070% and specificity 8090%.6
Ultrasound detection of pancreatic intraductal calcification is However, it may be normal, especially in the early stages of chronic
highly suggestive of chronic pancreatitis6,84 (Fig. 16.28), although pancreatitis, and duct dilatation may be secondary to an obstructing
any focal cluster of calcification associated with a mass may be due lesion, or an intraductal papillary mucinous neoplasm (IPMN).
A B
C D
Figure 16.28 Chronic pancreatitis. A: Small echogenic foci in the body of pancreas around a slightly dilated pancreatic duct (arrows).
B: Corresponding CT showing numerous small calcifications and an irregular and dilated pancreatic duct. C: Dilated pancreatic duct
containing large stones, and marked parenchymal atrophy. D: Cyst in the head of pancreas, dilated pancreatic duct and parenchymal
atrophy in a patient with longstanding chronic pancreatitis.
303
CHAPTER 16 Pancreas
A B
Figure 16.29 Chronic pancreatitis mass. A and B: Hypoechoic masses around calcifications in patients with known chronic
pancreatitis; in A biopsy and follow-up were in keeping with benign change, but in B biopsy showed adenocarcinoma.
A B
Figure 16.32 Autoimmune pancreatopathy. A: Enlarged hypoechoic head of pancreas with a plastic bile duct stent (arrows).
B: Enlarged body of pancreas with a slightly irregular duct (arrows). C: CT showing typical enlarged pancreatic tail with a rim of low
density fibrosis. D: ERCP showing typical appearance of an irregular pancreatic duct.
305
CHAPTER 16 Pancreas
CBD
A B
Figure 16.33 Cancer-dilated ducts. A: Dilated CBD down to a small obstructing mass (arrows). B: Dilated pancreatic duct and
parenchymal atrophy secondary to an obstructing mass (arrows).
A B
m a
cbd
smv
v t
A B
ha
PV
Figure 16.36 Venous involvement. A: Tumour (t) just touching SMV (v) but echogenicity around vessel preserved. B: Sagittal US
showing loss of echogenicity between tumour (t) and portal vein superiorly (arrows), although this is preserved with the SMV (smv)
anteriorly. C: Colour Doppler showing tumour encasing and narrowing the portal vein (PV), partially encasing the hepatic artery (ha), and
308 further tumour encasing the SMA (arrows). D: Colour Doppler demonstrating complete occlusion of the portal vein (arrow).
Pancreatic tumours
extent may be impossible on US since the mass is then almost iso- these are often small (Fig. 16.38) and better seen on CT than US. The
echoic to normal pancreas. Ultrasound contrast media may be presence of ascites suggests peritoneal metastases, the latter occa-
helpful in this situation, and the tumour may be better shown as a sionally seen on ultrasound.
hypovascular mass than on post-contrast CT scans6,94 (Figs 16.9C Endoscopic ultrasound detects smaller lesions not seen on US,
and 16.35). The sensitivity of US tumour detection is 7298%, and and also gives better staging/assessment of portal vein/SMV
specificity greater than 90%.6 However, overall contrast-enhanced involvement2,3 (Fig. 16.39). Much has been written comparing EUS
CT is more sensitive than contrast-enhanced US in tumour detec- with CT and other imaging modalities for detection and staging of
tion,6 and CT is also more objective with consistently better images. pancreatic masses, but many of these studies are heavily biased in
Tumour size is important to record since it may have prognostic favour of EUS. EUS performs best as a complementary technique
value; masses under 2cm not surprisingly have a more favourable for problem-solving after the operator has studied the cross-
outlook.95 sectional images it is an invasive technique which should not be
Assessment of the local extent of the tumour should be made, used on its own for evaluating pancreatic tumours since it does
and whether there is invasion into the stomach and duodenum not perform well if the operator is blinded to the results of
gastric distension with fluid suggests gastroduodenal stricturing. other imaging studies.96
Posterior extension into retroperitoneal fat occurs early and tumour
tracks along perineural sheaths and lymphatics. The mesenteric
vessels, portal vein and main arterial branches should be assessed
for any vessel encroachment, encasement or occlusion by tumour.
If the tumour is in contact with the portal vein or SMV it is not
necessarily invading these structures any loss of echogenicity of
the vessel wall suggests invasion (Fig. 16.36). Any tumour contact
Pancreatic tumours adenocarcinoma
with the hepatic artery, superior mesenteric artery (SMA) and
coeliac axis suggests vessel involvement (Fig. 16.37). More obvious 90% of pancreatic tumours are ductal adenocarcinomas with a
signs of vascular involvement are direct tumour extension into poor prognosis due to metastases and local vascular invasion.
vessel lumen, complete encasement, vessel distortion and narrow- The differential diagnosis of a solid focal pancreatic mass also
ing, and vessel occlusion. Colour flow US can be very helpful in includes focal pancreatitis, NET, lymphoma and metastases.
defining the vessels, and more clearly showing a strictured segment. Contrast-enhanced US may differentiate between vascular and
Acute vascular thrombosis may be difficult to diagnose on greyscale non-vascular masses, but gives similar information to contrast-
US if the thrombus is very hypoechoic, and so colour flow US can enhanced CT and MRI.
also be useful in clarifying this. Doppler US may show high velocity US or EUS may detect a pancreatic mass if none is seen on CT
jets through strictured segments and turbulent flow beyond this, or MRI, so can be useful for problem-solving in suspected
but in practice the greyscale and colour flow information allows pancreatic neoplasms.
adequate vascular assessment. Lymphadenopathy may occur, and Surgery for pancreatic cancer has become more aggressive, and
this is seen usually around the pancreaticoduodenal region, hepa- although metastases and arterial encasement precludes surgery,
toduodenal region and around the coeliac axis. Slightly enlarged portal venous involvement can be dealt with by venous grafts.
reactive nodes are common after bile duct stent insertion, but sig- US or EUS may define the extent of portal venous involvement if
nificantly enlarged abdominal nodes are likely to be involved (Fig. CT/MRI are inconclusive.
16.38). The liver should be carefully assessed for any metastases;
A B
Figure 16.37 Arterial involvement. A: Sagittal view of a pancreatic tumour involving the inferior margin of the hepatic artery (long arrow)
and the anterior inferior wall of the portal vein (short arrow). B: Encasement and narrowing of the coeliac axis (arrow) and its main
branches by a large pancreatic body tumour, the narrowed vessels well seen with colour Doppler.
309
CHAPTER 16 Pancreas
T T
A B
Figure 16.38 Nodes and liver metastases. A: Pancreatic head tumour (T) with a large adjacent lymph node (N). B: Pancreatic tumour
(T) surrounding a biliary stent, and two metastases at the edge of the adjacent left lobe of liver (arrows).
A B
P
SCA
B
A
D
C
Figure 16.40 Serous cystadenoma. A: Well-defined, heterogeneous and mainly solid-looking mass (SCA) in the pancreatic head and
neck with a few tiny cysts. The pancreatic body (P) was echogenic. Large cyst (L) is seen in the liver. B: Corresponding T2-weighted MR
image with a bright T2 lesion indicating it is cystic, with a central signal void in keeping with a scar. C: Cystadenoma seen on EUS with
detailed view of small cysts of variable size and an echogenic stroma. D: Following microbubble contrast enhancement, a larger
cystadenoma (arrows) shows moderate enhancement, some calcification and larger cysts. Enhancing liver (L) is also seen.
311
CHAPTER 16 Pancreas
imaging features are present. The decision to biopsy or resect is Solid pseudopapillary neoplasm
made based on the ultrasound/CT/MR features: only typical
serous cystadenomas are observed on follow-up imaging; others This is a rare low-grade malignant tumour, usually occurring in
are resected or followed up usually after biopsy confirmation of the young women.105,106 It occurs more frequently in the head of pan-
diagnosis.99101 creas, and appears on imaging as a large well-defined heterogene-
ous mass with solid and cystic elements there are typically
finger-like projections of pseudopapillary excrescences. It may be
Mucinous cystic neoplasm completely cystic if there is extensive necrosis of haemorrhage.
Fluidfluid debris may be seen, and there may be calcification in
This was previously called macrocystic adenoma. It may be malig-
the periphery of the mass. It is generally hypovascular following
nant or have a high risk of malignant change, and so is resected if
contrast medium injection, but any solid tissue within it does
the diagnosis is made or suspected. It usually occurs in women
enhance. It may appear solid on ultrasound.
aged 3050 years, mostly in the margin of the body/tail of pancreas.
It may be unilocular or multilocular and the cysts are typically
>2cm. The cysts are lined by columnar epithelium and contain
mucin, which may result in fine echoes on US. There may be Cystic neoplasms
nodular or papillary projections and septations on US; the wall is
usually thick and may be calcified (Fig. 16.7 and 16.41). When Cystic pancreatic neoplasms include serous cystadenomas,
there is malignant change, there may be metastases to the nodes mucinous cystic neoplasm, IPMN, solid pseudopapillary
and liver. neoplasm, cystic NETs and cystic metastases.
This neoplasm has a much better prognosis than ductal adeno- Serous cystadenomas are benign lesions with multiple <2cm
carcinoma following surgical resection.102 cysts, and may appear as an echogenic mass if the cysts are tiny
(<2mm).
Mucinous cystic neoplasms may be uni- or multilocular, and the
Intraductal papillary mucinous cysts are typically >2cm. Nodular projections or septations may
neoplasms (IPMN) be seen on US.
IPMNs produce mucin which distends the duct and the papilla.
These are characterised by proliferation of pancreatic ductal epithe- They may be main duct type or branch duct type, the latter
lium and excessive production of mucin. They may be main duct presenting as a cystic mass without significant main duct
type, branch duct type, or a combined type. They are benign or dilatation.
low-grade malignant neoplasms, but foci of aggressive cancer may Small incidental pancreatic cysts are being increasingly detected,
form and become invasive.103 and may be due to a small pseudocyst, serous cystadenoma,
There is usually very dilated, non-strictured MPD containing mucinous cystic neoplasm, or IPMN. If the cyst is <3cm,
mucin (may be reflective on ultrasound) (Fig. 16.42A,B). ERCP typi- unilocular and asymptomatic, then it is very likely to be benign
cally shows a patulous papilla with mucin extruding, and this is and can be followed up on imaging. Septations or solid
diagnostic; there may be filling defects on a pancreatogram due to components warrant further investigation such as EUS FNA for
mucin or mural nodules. The branch type is due to cystic ectasia of tumour markers and cytology.
a side branch and is seen as a cyst communicating with the MPD,
which is not usually dilated (main differential diagnosis is pseudo-
cyst) (Fig. 16.42C,D). There is a good prognosis with long-term
survival after pancreatectomy. Resection is usually performed for
main duct IPMN, but is more controversial for branch duct type, Management of cystic pancreatic lesion
which can usually be managed with follow-up imaging and resected
if they cause symptoms, become >3cm in size, associated with dila- This is an increasingly common problem in view of improved
tation of the main pancreatic duct, or if they contain mural nodules.104 imaging resulting in a greater number of cystic pancreatic lesions
being detected (Fig. 16.43).
The commonest causes to consider are pseudocyst, serous cysta-
denoma, mucinous cystic neoplasm and IPMN.
If there is a clear history of pancreatitis and the imaging features
are consistent with a pseudocyst, then it is usually reasonable to
manage as such, with either follow-up or drainage. However, con-
sideration should be given to the possibility of pancreatitis occur-
ring secondary to a cystic neoplasm. If there is a cluster of tiny cysts
in an echogenic stroma, then it may be reasonable to treat as a
serous cystadenoma and follow up with imaging unless the patient
is symptomatic.
All patients with pancreatic cysts should be assessed clinically,
serum tumour markers measured, and then considered for detailed
thin section multislice CT, MRI with MRCP (to look for any obvious
communication with duct), and EUS with cyst fluid analysis.100
Assessment should be of cyst size, septations, calcification,
mural/intracystic nodules and communication with the
pancreatic duct.107
EUS morphology is of limited use in view of significant inter- and
intra-observer variability.108 However, fluid viscosity (?mucin) and
a raised CEA (or CA19.9) are useful in predicting a premalignant
or malignant cyst; abnormal cytology is rarely seen.107,109
Cysts which are symptomatic, multilocular (solid components
and thick wall), with raised tumour markers or mucin, or abnormal
Figure 16.41 Mucinous cystic neoplasm. EUS showed a large cytology, should be considered for surgical resection.107,109 Small
cyst with a slightly irregular and thickened wall (arrow). unilocular cysts are nearly always benign, but the presence of
312
Pancreatic tumours
Figure 16.42 IPMN. A: Dilated pancreatic duct (arrow) and cyst (c) in head of pancreas. B: Corresponding ERCP, this patient had
pancreas divisum and the accessory papilla was open and had mucus extruding from it, which is diagnostic of an IPMN. Opacification
showed mobile filling defects (arrow) in large branch connecting to main duct, in keeping with mucus. C: Lobulated cyst (arrows) in
pancreatic head without main duct dilatation. D: Corresponding MRI (T2-weighted sequence) with cyst (c) and non-dilated pancreatic
duct (arrow).
septations, although not diagnostic of malignancy, is associated whether they secrete excess hormones leading to specific clinical
with borderline or in-situ malignancy in 20% of cases.110 syndromes.113,114 Most solitary tumours occur sporadically, but mul-
Small asymptomatic cysts, <3cm, with no suspicious features on tiple NETs usually occur in familial multiple endocrine neoplasia
imaging or EUS aspirate, may be followed up. These will be the (MEN) type 1.115 The commonest functioning tumours are insulino-
majority of incidental pancreatic cysts. Follow-up of these lesions mas (5060%) and gastrinomas (20%), and because of the symptoms
has not been clearly defined, but suggested to be for at least 4 years caused they present early and are usually small. Most (90%) insuli-
since the growth rate of small cystic neoplasms is usually very nomas are benign, single, intrapancreatic and <2cm at presenta-
slow;109,111 a repeat FNA should be considered if there is change in tion.113 Malignant insulinomas (about 10%) are usually >3cm and
cyst morphology/size or clinical circumstances.109 Size criteria about a third have metastases at time of diagnosis.6 Gastrinomas
alone are insufficient, since a significant number of cysts <3cm are are often small (40% are <1cm) and multiple and about 60% are
malignant or mucinous.112 malignant they produce excessive gastrin, resulting in increased
gastric acid and peptic ulcers (ZollingerEllison syndrome).110,112
They are more difficult to localise than insulinomas, and are more
Neuroendocrine tumours (NETs) often extra-pancreatic. They are typically located in the gastrinoma
triangle, a region defined by the junction of the cystic duct/CBD,
Pancreatic neuroendocrine tumours arise from the islet cells, and junction of the second and third portions of the duodenum, and
may be functioning (85%) or non-functioning (15%) depending on junction of head/neck of pancreas. About 2530% of NETs of the
313
CHAPTER 16 Pancreas
A B
Figure 16.43 Incidental cysts. A: Thin-walled 1.6cm cyst at junction of body/tail of pancreas. EUS aspirate showed clear fluid with low
tumour markers. B: 2cm cyst identified on CT, but EUS showed irregular outline and solid components, and aspiration revealed mucin
and raised tumour markers. Pathology after resection showed an IPMN.
A B
C D
Figure 16.44 Neuroendocrine tumours. A: Incidental hypoechoic NET extending anterior to an echogenic pancreas, surrounded by
some hypoechoic intra-abdominal fat and against the undersurface of an echogenic liver. B: Corresponding CT showing marked arterial
phase enhancement of tumour (arrows). C: EUS showing a hypoechoic nodule just visible within a hypoechoic pancreatic tail. D: EUS FNA
confirmed a NET.
8090% for detecting small NETs (Fig. 16.13), which may then be as hypoechoic focal or diffuse pancreatic enlargement (Fig. 16.47).
possible to resect laparoscopically.120 Features that should increase suspicion for pancreatic lymphoma
Non-functioning NETs are well defined on US and usually easy include: pancreatic duct not significantly dilated despite the pres-
to see because of their size at presentation. They often have areas ence of a large mass; no significant parenchymal atrophy; and
of necrosis, haemorrhage or calcification, and so are heterogeneous enlarged nodes below the level of the renal hilum.122 Biopsy is
on US (Fig. 16.46). Larger lesions may show cystic degeneration. An important if pancreatic lymphoma is suspected since most cases
irregular or ill-defined margin is suggestive of malignancy.116 respond well to chemotherapy.123
Figure 16.45 NETs on EUS. A: Hypoechoic insulinoma. B: Extra-pancreatic gastrinoma, relatively echogenic. C: Cystic extra-pancreatic
gastrinoma. D: Corresponding EUS views of thickened gastric folds, in keeping with hypergastrinaemia.
316
Pancreatic tumours
A B
Figure 16.46 Large NET. A: Large mass arising from tail of pancreas (arrow). B: Corresponding CT with pancreatic tail mass (arrow) and
numerous cystic liver metastases.
A B
Figure 16.47 Lymphoma. A: Focal mass in pancreatic tail in HIV-positive patient; biopsy showed this to be lymphoma. B: Large mass in
head of pancreas (m) with multiple adjacent enlarged nodes (arrows).
A B
Figure 16.48 Metastases. A and B: Focal hypervascular mass (arrows) in pancreatic tail several years after resection of a renal cancer. 317
EUS FNA confirmed a renal cancer metastasis.
CHAPTER 16 Pancreas
Complications
The complication rate for pancreatic biopsy is low, theoretically
greater for percutaneous targeted biopsies compared to EUS
guidance.
For percutaneous biopsies, the minor complication rate is up to 5%,
Figure 16.49 Biopsy. Echogenic needle tract (arrows) through mainly post-procedure pain, and the major complication rate is about
pancreatic head mass close to plastic stent. 1% including bleeding, duodenal perforation and abscess.128,129,131
318
Pancreatic transplantation
PV
IVC Aorta S
a
v
SMV
A B
Figure 16.50 Pancreatic transplant. A: Diagram showing duodenovesical anastomosis (arrow). The donor aortic segment (a) containing
the coeliac axis and SMA is attached to the recipient common iliac artery, and the donor portal vein (v) is attached to the common iliac
vein. B: Diagram showing duodeno-jejunal anastomosis (arrow) with venous drainage into the recipient SMV. B, bladder; D, donor
duodenum attached to pancreas; IVC, inferior vena cava; PV, portal vein; S, stomach; SMV, superior mesenteric vein.
319
CHAPTER 16 Pancreas
Pancreatic transplantation
Pancreatic transplantations are being increasingly performed with
low mortality and 1-year graft function rates of up to 84%.
Pancreatic and renal transplants are often combined in diabetic
patients with end-stage nephropathy.
The preferred technique is the donor duodenum (with pancreas)
anastomosed to the recipient jejunum and venous flow to the
SMV, rather than duodenum to bladder and venous flow to iliac
vein as was originally done. This reduces complications.
Graft dysfunction is often asymptomatic, and so regular
monitoring is needed. Biochemical markers and US features of
rejection are non-specific, and surveillance US-guided biopsy of
the graft is often used.
US is the main modality in the initial imaging assessment of
pancreatic transplants, and may show collections or vascular
problems.
US views of the pancreatic transplant may be poor because of
adjacent bowel gas and/or a small transplant. CT or MRI may be
needed for further evaluation.
320
References
14. Quest L, Lombard M. Pancreas divisum: opinio divisa. Gut 43. Ikeda M, Sato T, Morozumi A, et al. Morphologic changes in the
2000;47(3):317319. pancreas detected by screening ultrasonography in a mass survey,
15. Kamisawa T, Tu Y, Egawa N, et al. Clinical implications of incomplete with special reference to main duct dilatation, cyst formation and
pancreas divisum. JOP 2006;7(6):625630. calcification. Pancreas 1994;9:508512.
16. Kamisawa T, Tu Y, Egawa N, et al. Pancreas divisum in 44. Glaser J, Stienecker K. Does aging influence pancreatic response in
pancreaticobiliary maljunction. Hepatogastroenterology the ultrasound secretin test by impairing hydrokinetic exocrine
2008;55(81):249253. function or sphincter of Oddi motor function. Dig Liver Dis
17. Zyromski NJ, Sandoval JA, Pitt HA, et al. Annular pancreas: dramatic 2000;32(1):2528.
differences between children and adults. J Am Coll Surg 45. Osawa S, Kataoka K, Sakagami J, et al. Relation between
2008;206(5):10191025. morphologic changes in the main pancreatic duct and exocrine
18. Abu-Yousef MM, El-Zein Y. Improved US visualization of the pancreatic function after a secretin test. Pancreas 2002;25(1):1219.
pancreatic tail with simethicone, water, and patient rotation. 46. Atri M, Nazarnia S, Mehio A, et al. Hypoechogenic embryologic
Radiology 2000;217:780785. ventral aspect of the head and uncinate process of the pancreas: in
19. Hohl C, Schmidt T, Honnef D, et al. Ultrasonography of the pancreas vitro correlation of US with histopathologic findings. Radiology
2. Harmonic imaging. Abdominal Imaging 2007;32:150160. 1994;190(2):441444.
20. Bertolotto M, DOnofrio M, Martone E, et al. Ultrasonography of the 47. Coulier B. Hypoechogenic aspects of the ventral embryonic cephalic
pancreas 3. Doppler imaging. Abdominal Imaging 2007;32:161170. pancreas: a large prospective clinical study. J Belge Radiol
21. Uomo G. Ultrasound elastography. A possible improvement of the 1996;79(3):120124.
paraphernalia of pancreatic imaging. JOP 2008;9(5):666667. 48. Savides TJ, Gress FG, Zaidi SA, et al. Detection of embryologic
22. Das A, Mourad W, Lightdale CJ, et al. An international survey of the ventral pancreatic parenchyma with endoscopic ultrasound.
clinical practice of EUS. Gastrointest Endosc 2004;60(5):765770. Gastrointest Endosc 1996;43(1):1419.
23. Lennon AM, Penman ID. Endoscopic ultrasound in cancer staging. 49. Kingsnorth A, OReilly D. Acute pancreatitis. BMJ 2006;332:10721076.
Br Med Bull 2007;84:8198. 50. Srivastava R, Fraser C, Gentleman D, et al. Hyperamylasaemia: not
24. Kahl S, Malfertheiner P. Role of endoscopic ultrasound in the the usual suspects. BMJ 2005;331:890891.
diagnosis of patients with solid pancreatic masses. Dig Dis 51. Beger HG, Rau BM. Severe acute pancreatitis: clinical course and
2004;22:2631. management. World J Gastroenterol 2007;13(38):50435051.
25. Rossi FT. Endoscopic ultrasound. Minn Med 2008;91(6):3841. 52. British Society of Gastroenterology. UK guidelines for the
26. Boujaoude J. Role of endoscopic ultrasound in diagnosis and therapy management of acute pancreatitis. Gut 2005;54(Suppl III):S19.
of pancreatic adenocarcinoma. World J Gastroenterol 53. Gullo L, Migliori M, Pezzilli R, et al. An update on recurrent acute
2007;13(27):36623666. pancreatitis: data from five European countries. Am J Gastroenterol
27. Agarwal B, Krishna NB, Labundy JL, et al. EUS and/or EUS-guided 2002;97:19591962.
FNA in patients with CT and/or magnetic resonance imaging 54. Bhatia M, Wong FL, Cao Y, et al. Pathophysiology of acute
findings of enlarged pancreatic head or dilated pancreatic duct with pancreatitis. Pancreatology 2005;5(23):132144.
or without a dilated common bile duct. Gastrointest Endosc 55. Steinberg W, Tenner S. Acute pancreatitis. N Engl J Med
2008;68(2):237242. 1994;330(17):11981210.
28. Meining A, Dittler HJ, Wolf A, et al. You get what you expect? A 56. Kao LS, Bulger EM, Parks DL, et al. Predictors of morbidity after
critical appraisal of imaging methodology in endosonographic cancer traumatic pancreatic injury. J Trauma 2003;55(5) 898905.
staging. Gut 2002;50:599603. 57. Vasquez JC, Coimbra R, Hoyt DB, Fortlage D. Management of
29. Keafalides PT, Gress F. Simulator training for endoscopic ultrasound. penetrating pancreatic trauma: an 11-year experience of a level-1
Gastrointest Endosc Clin N Am 2006;16(3):543552. trauma center. Injury 2001;32(10):753759.
30. Miura F, Takada T, Amano H, et al. Diagnosis of pancreatic cancer. 58. Mattix KD, Tataria M, Holmes J, et al. Pediatric pancreatic trauma:
HPB (Oxford) 2006;8:337342. predictors of nonoperative management failure and associated
31. De Angelis C, Martini M, Repici A, et al. Instruments and accessories outcomes. J Pediatr Surg 2007;42(2):340344.
for diagnostic endoscopic ultrasound (radial scanning and 59. Beger HG, Rau B, Mayer J, Pralle U. Natural course of acute
miniprobes). Minerva Med 2007;98(4):253260. pancreatitis. World J Surg 1997;21(2):130135.
32. DOnofrio M, Vecchiato F, Faccioli N, et al. Ultrasonography of the 60. Dervenis C, Johnson CD, Bassi C, et al. Diagnosis, objective
pancreas 7. Intraoperative imaging. Abdom Imaging 2007;32(2): assessment of severity, and management of acute pancreatitis:
200206. Santorini consensus conference. Int J Pancreatol 1999;25:195210.
33. Jakimowicz JJ. Intraoperative ultrasonography in open and 61. McCullough LK, Sutherland FR, Preshaw R, Kim S. Gallstone
laparoscopic abdominal surgery: an overview. Surg Endosc pancreatitis: does discharge and readmission for cholecystectomy
2006;20(Suppl 2):S425435. affect outcome? HPB (Oxford) 2003;5(2):9699.
34. Falconi M, Bettini R, Boninsegna L, et al. Surgical strategy in the 62. Gurusamy KS, Samraj K, Fusai G, Davidson BR. Early versus delayed
treatment of pancreatic neuroendocrine tumors. JOP 2006;7(1): laparoscopic cholecystectomy for biliary colic. Cochrane Database
150156. Syst Rev 2008 Oct 8;(4): CD007196.
35. Hayashibe A, Sakamoto K, Shinbo M, et al. A resected case of 63. Dervenis C. Assessments of severity and management of acute
multiple intraductal papillary mucinous tumors of the pancreas with pancreatitis based on the Santorini Consensus Conference report.
US guided ductal branch oriented partial pancreatectomy. JOP 2000;1:178182.
Pancreatology 2005;5:462465. 64. Al-Haddad M, Wallace MB. Diagnostic approach to patients with
36. Wiersema MJ, Wiersema LM. Endosonography of the pancreas: acute idiopathic and recurrent pancreatitis, what should be done?
normal variation versus changes of early chronic pancreatitis. World J Gastroenterol 2008;14(7):10071010.
Gastrointest Endosc Clin N Am 1995;5:487496. 65. Yusoff IF, Raymond G, Sahai AV. A prospective comparison of the
37. Marks V, Filly R, Callen P. Ultrasonic evaluation of normal pancreatic yield of EUS in primary vs. recurrent idiopathic acute pancreatitis.
echogenicity and its relation to fat deposition. Radiology Gastrointest Endosc 2004;60:673678.
1980;137:457459. 66. Baron T. Treatment of pancreatic pseudocysts, pancreatic necrosis,
38. Glaser J, Stienecker K. Pancreas and aging: a study using and pancreatic duct leaks. Gastrointest Endosc Clin N Am
ultrasonography. Gerontology 2000;46(2):9396. 2007;17(3):550579.
39. Gupta A, Arenson A, Mckee J. Effect of steroid ingestion on 67. Rickes S, Uhle C, Kahl S, et al. Echo-enhanced ultrasound:
pancreatic echogenicity. J Clin Ultrasound 1987;15:171174. a new valid initial imaging approach for severe acute pancreatitis.
40. Haber HP. Cystic fibrosis in children and young adults: findings on Gut 2006;55(1):7478.
routine abdominal sonography. AJR Am J Roentgenol 2007;189(1): 68. Al Mofleh IA. Severe acute pancreatitis: pathogenetic aspects and
8999. prognostic factors. World J Gastroenterol 2008;14(5):675684.
41. Martinez-Noguera A, Montserrat E, Torrubia S, et al. Ultrasound of 69. Toouli J, Brooke-Smith M, Bassi C, et al. Guidelines for the
the pancreas: update and controversies. Eur Radiol 2001;11: management of acute pancreatitis. J Gastroenterol Hepatol
15941606 2002;17(suppl):S1539.
42. Rajan E, Clain JE, Levy MJ, et al. Age-related changes in the pancreas 70. Rau B, Pralle U, Mayer JM, Beger HG. Role of ultrasonographically
identified by EUS: a prospective evaluation. Gastrointest Endosc guided fine-needle aspiration cytology in the diagnosis of infected
2005;61(3):401406. pancreatic necrosis. Br J Surg 1998;85:179184.
321
CHAPTER 16 Pancreas
71. Carter CR, McKay CJ, Imrie CW. Percutaneous necrosectomy and pancreas. N Engl J Med 2004;351(12):12181226.
sinus tract endoscopy in the management of infected pancreatic 99. Hung JS, Yang CY, Hu RH, et al. Surgical treatment of pancreatic
necrosis: an initial experience. Ann Surg 2000;232:175180. serous cystadenoma: aggressive for operations but limited resections.
72. McErlean A, Looby S, Lee MJ. Percutaneous ultrasound-guided Pancreas 2007;35(4):358360.
thrombin injection as first-line treatment of pancreatic 100. Scheiman JM. Management of cystic lesions of the pancreas.
pseudoaneurysm. Cardiovasc Intervent Radiol 2007;30:526528. J Gastrointest Surg 2008;12(3):405407.
73. Siddiqi AJ, Miller F. Chronic pancreatitis: ultrasound, computed 101. Belsley NA, Pittman MB, Lauwers GY, et al. Serous cystadenoma of
tomography, and magnetic resonance imaging features. Semin the pancreas: limitations and pitfalls of endoscopic ultrasound-
Ultrasound CT MR 2007;28(5):384394. guided fine-needle aspiration biopsy. Cancer 2008;114(2):102110.
74. Forsmark CE. The diagnosis of chronic pancreatitis. Gastrointest 102. Fernandez-del Castillo C. Mucinous cystic neoplasms. J Gastrointest
Endosc 2000;52:293298. Surg 2008;12(3):411413.
75. Walsh TN, Rode J, Theis BA, Russell RC. Minimal change chronic 103. Burdick JS. Intraductal papillary mucinous neoplasms. Gastrointest
pancreatitis. Gut 1992;33:15661571. Endosc Clin N Am 2008;18(3):523533.
76. Glasbrenner B, Kahl S, Malfertheiner P. Modern diagnostics of 104. Waters JA, Schmidt CM. Intraductal papillary mucinous neoplasm
chronic pancreatitis. Eur J Gastroenterol Hepatol 2002;14(9): when to resect? Adv Surg 2008;42:87108.
935941. 105. Huang H-L, Shih S-C, Chang W-H, et al. Solid-pseudopapillary
77. Wallace MB. Imaging the pancreas: into the deep. Gastroenterology tumor of the pancreas: clinical experience and literature review.
2007;132:484487. World J Gastroenterol 2005;11(9):14031409.
78. Balakrishnan V, Chatni S, Radhakrishnan L, et al. Groove pancreatitis: 106. Choi J-Y, Kim M-J, Kim JH, et al. Solid pseudopapillary tumor of the
a case report and review of the literature. JOP 2007;8(5):592597. pancreas: typical and atypical manifestations. AJR Am J Roentgenol
79. Lee H, Lee JK, Kang SS, et al. Is there any clinical or radiologic 2006;187:W178W186.
feature as a preoperative marker for differentiating mass-forming 107. Edirimanne S, Connor SJ. Incidental pancreatic cystic lesions. World J
pancreatitis from early-stage pancreatic adenocarcinoma? Surg 2008;32(9):20282037.
Hepatogastroenterology 2007;54(79):21342140. 108. Ahmad NA, Kochman ML, Brensinger C, et al. Interobserver
80. Raimondo M, Wallace MB. Diagnosis of early chronic pancreatitis by agreement among endosonographers for the diagnosis of neoplastic
endoscopic ultrasound. Are we there yet? JOP 2004;5(1):17. versus non-neoplastic pancreatic cystic lesions. Gastrointest Endosc
81. Wallace MB, Hawes RH, Durkalski V, et al. The reliability of EUS for 2003;58:5964.
the diagnosis of chronic pancreatitis: interobserver agreement 109. Garcea G, Ong SL, Rajesh A, et al. Cystic lesions of the pancreas. A
among experienced endosonographers. Gastrointest Endosc diagnostic and management dilemma. Pancreatology 2008;8(3):236251.
2001;53:294299. 110. Sahani DV, Saokar A, Hahn PF, et al. Pancreatic cysts 3cm or smaller:
82. Kahl S, Glasbrenner B, Leodolter A, et al. EUS in the diagnosis of how aggressive should treatment be? Radiology 2006;238:912919.
early chronic pancreatitis: a prospective follow-up study. Gastrointest 111. Das A, Wells CD, Nguyen CC. Incidental cystic neoplasms of
Endosc 2002;55(4):507511. pancreas: what is the optimal interval imaging surveillance? Am J
83. Remer EM, Baker MB. Imaging of chronic pancreatitis. Radiol Clin Gastroenterol 2008;103(7):16571662.
North Am 2002;40:12291242. 112. Walsh RM, Vogt DP, Henderson JM, et al. Management of suspected
84. Homma T, Harada H, Koizumi M. Diagnostic criteria for chronic pancreatic neoplasms based on cyst size. Surgery 2008;144(4):677684.
pancreatitis by the Japan Pancreas Society. Pancreas 1997;15: 113. Abboud B, Boujaoude J. Occult sporadic insulinoma: localization and
1415. surgical strategy. World J Gastroenterol 2008;14(5):657665.
85. Sahani DV, Kalva SP, Farrell J, et al. Autoimmune pancreatitis: 114. Jani N, Moser AJ, Khalid A. Pancreatic endocrine tumors.
imaging features. Radiology 2004;233(2):345352. Gastroenterol Clin North Am 2007;36:431439.
86. Zandieh I, Byrne MF. Autoimmune pancreatitis: a review. World 115. Scarsbrook AF, Thakker RV, Wass JAH, et al. Multiple endocrine
J Gastroenterol 2007;13(47):63276332. neoplasia: spectrum of radiologic appearances and discussion of a
87. Okazaki K, Uchida K, Matsushita M, Takaoka M. How to diagnose multitechnique imaging approach. Radiographics 2006;26(2):433451.
autoimmune pancreatitis by the revised Japanese clinical criteria. 116. Power N, Reznek RH. Imaging pancreatic islet cell tumours. Imaging
J Gastroenterol 2007;42(Suppl 18):3238. 2002;14:147159.
88. Deshpande V, Chiocca S, Finkelberg D, et al. Autoimmune 117. Intenzo CM, Jabbour S, Lin HC, et al. Scintigraphic imaging of body
pancreatitis: a systemic immune complex mediated disease. Am J neuroendocrine tumors. Radiographics 2007;27(5):13551369.
Surg Pathol 2006;30:15371545. 118. Anderson MA, Carpenter S, Thompson NW, et al. Endoscopic
89. Lowenfels AB, Maisonneuve P. Epidemiology and risk factors for ultrasound is highly accurate and directs management in patients
pancreatic cancer. Best Pract Res Clin Gastroenterol 2006;20(2): with neuroendocrine tumors of the pancreas. Am J Gastroenterol
197209. 2000;95(9):22712277.
90. Adham M, Mirza DF, Chapuis F, et al. Results of vascular resections 119. Ardengh JC, de Paulo GA, Ferrari AP. EUS-guided FNA in the
during pancreatectomy from two European centres: an analysis of diagnosis of pancreatic neuroendocrine tumors before surgery.
survival and disease-free survival explicative factors. HPB (Oxford) Gastrointest Endosc 2004;60(3):378384.
2006;8(6):465473. 120. Jaroszewski DE, Schlinkert RT, Thompson GB, Schlinkert DK.
91. Lind PA, Isaksson B, Almstrom M, et al. Efficacy of preoperative Laparoscopic localization and resection of insulinomas. Arch Surg
radiochemotherapy in patients with locally advanced pancreatic 2004;139:270274.
carcinoma. Acta Oncol 2008;47(3):413420. 121. Liakakos T, Misiakos EP, Tsapralis D, et al. A role for surgery in
92. Loos M, Kleeff J, Friess H, Buchler MW. Surgical treatment of primary pancreatic B-cell lymphoma: a case report. J Med Case
pancreatic cancer. Ann NY Acad Sci 2008;1138:169180. Reports 2008;2:167.
93. White R, Winston C, Gonen M, et al. Current utility of staging 122. Leite NP, Kased N, Hanna RF, et al. Cross-sectional imaging of
laparoscopy for pancreatic and peripancreatic neoplasms. J Am Coll extranodal involvement in abdominopelvic lymphoproliferative
Surg 2008;206(3):445450. malignancies. Radiographics 2007;27:16131634.
94. Minniti S, Bruno C, Biasiutti C, et al. Sonography versus helical CT in 123. Saif MW, Khubchandani S, Walczak M. Secondary pancreatic
identification and staging of pancreatic ductal adenocarcinoma. J Clin involvement by a diffuse large B-cell lymphoma presenting as acute
Ultrasound 2003;31(4):175182. pancreatitis. World J Gastroenterol 2007;13(36):49094911.
95. Birk D, Fortnagel G, Formentini A, Beger HG. Small carcinoma of the 124. Adsay NV, Andea A, Basturk O, et al. Secondary tumors of the
pancreas. Factors of prognostic relevance. Hepatobiliary Pancreatic pancreas: an analysis of a surgical and autopsy database and review
Surg 1998;5:450454 of the literature. Virchows Arch 2004;444:527535.
96. Rosch T, Dittler HJ, Strobel K, et al. Endoscopic ultrasound criteria 125. David AW, Samuel R, Eapen A, et al. Pancreatic metastasis from renal
for vascular invasion in the staging of cancer of the head of the cell carcinoma 16 years after nephrectomy: a case report and review
pancreas: a blind re-evaluation of videotapes. Gastrointest Endosc of the literature. Trop Gastroenterol 2006;27(4):175176.
2000;52(4):469477. 126. Bachmann J, Michalski CW, Bergmann F, et al. Metastasis of rectal
97. Sidden CR, Mortele KJ. Cystic tumors of the pancreas: ultrasound, adenocarcinoma to the pancreas. Two case reports and a review of
computed tomography, and magnetic resonance imaging features. the literature. JOP 2007;8(2):214222.
Semin Ultrasound CT MR 2007;28(5):339356. 127. Brugge WR. Pancreatic fine needle aspiration: to do or not to do?
98. Brugge WR, Lauwers GY, Sahani D, et al. Cystic neoplasms of the JOP 2004;5(4):282288.
322
References
128. Amin Z, Theis B, Russell RC, et al. Diagnosing pancreatic cancer: 138. Eloubeidi MA, Chen VK, Eltoum IA, et al. Endoscopic ultrasound-
the role of percutaneous biopsy and CT. Clin Radiol 2006;61(12): guided fine needle aspiration biopsy of patients with suspected
9961002. pancreatic cancer: diagnostic accuracy and acute and 30-day
129. Brandt KR, Charboneau JW, Stephens DH, et al. CT- and US-guided complications. Am J Gastroenterol 2003;98:26632668.
biopsy of the pancreas. Radiology 1993;187:99104. 139. Micames C, Jowell PS, White R, et al. Lower frequency of peritoneal
130. Ihse I, Axelson J, Dawiskiba S, Hansson L. Pancreatic biopsy: Why? carcinomatosis in patients with pancreatic cancer diagnosed by
When? How? World J Surg 1999;23:896900. EUS-guided FNA vs. percutaneous FNA. Gastrointest Endosc
131. Di Stasi M, Lencioni R, Solmi L, et al. Ultrasound-guided fine needle 2003;58:690695.
biopsy of pancreatic masses: results of a multicenter study. Am J 140. Schwartz DA, Unni KK, Levy MJ, et al. The rate of false-positive
Gastroenterol 1998;93:13291333. results with EUS-guided fine-needle aspiration. Gastrointest Endosc
132. Mallery JS, Centeno BA, Hahn PF, et al. Pancreatic tissue sampling 2002;56:868872.
guided by EUS, CT/US, and surgery: a comparison of sensitivity and 141. Gruessner AC, Sutherland DE. Pancreas transplant outcomes for
specificity. Gastrointest Endosc 2002;56:218224. United States (US) cases reported to the United Network for Organ
133. Shah SM, Ribeiro A, Levi J, et al. EUS-guided fine needle aspiration Sharing (UNOS) and non-US cases reported to the International
with and without Trucut biopsy of pancreatic masses. JOP Pancreas Transplant Registry (IPTR) as of October, 2000. Clin Transpl
2008;9(4):422430. 2002;4572.
134. Erickson RA, Sayage-Rabie L, Beissner RS. Factors predicting the 142. Gruessner AC, Sutherland DER. Report for the International Pancreas
number of EUS-guided fine-needle passes for diagnosis of pancreatic Transplant Registry-2000. Transplant Proc 2001;33:16431646.
malignancies. Gastrointest Endosc 2000;51:184190. 143. Nikolaidis P, Amin RS, Hwang CM, et al. Role of sonography in
135. Eloubeidi MA, Tamhane A. EUS-guided FNA of solid pancreatic pancreatic transplantation. Radiographics 2003;23:939949.
masses: a learning curve with 300 consecutive procedures. 144. Wong JJ, Krebs TL, Klassen DK, et al. Sonographic evaluation of
Gastrointest Endosc 2005;61:700708. acute pancreatic transplant rejection: morphology Doppler analysis
136. Wiersema MJ, Levy MJ, Harewood GC, et al. Initial experience with versus guided percutaneous biopsy. AJR Am J Roentgenol
EUS-guided trucut needle biopsies of perigastric organs. Gastrointest 1996;166:803807.
Endosc 2002;56:275278. 145. Atwell TD, Gorman B, Larson TS, et al. Pancreas transplants:
137. Nakamura R, Machado R, Amikura K, et al. Role of fine needle experience with 232 percutaneous US-guided biopsy procedures in
aspiration cytology and endoscopic biopsy in the preoperative 88 patients. Radiology 2004;231:845849.
assessment of pancreatic and peripancreatic malignancies. Int J
Pancreatol 1994;16:1721.
323
CHAPTER
Spleen
Simon J. Freeman
17
disease; abnormalities will thus be regularly encountered by most
INTRODUCTION 324 ultrasound practitioners. Whilst ultrasound is not always able to
FUNCTION 324 provide a definitive diagnosis, when combined with clinical, labora-
tory and other imaging information a specific or short differential
EMBRYOLOGY, ANATOMY AND MICROSTRUCTURE 324 diagnosis is usually possible.
EXAMINATION TECHNIQUE 325
Spleen
Portal vein
Splenic vein
Pancreas
Right kidney
Left kidney
Transverse colon
(reflected)
Figure 17.1 Diagrammatic representation of the anatomical relations of the spleen (stomach removed and position indicated by
the dotted lines).
A B
terminating at its confluence with the superior mesenteric vein to space between the sinusoids (open circulation). Transit times
form the portal vein. The lymphatic drainage of the spleen runs through the spleen are much faster for blood passing through the
adjacent to the splenic vessels to nodes around the coeliac axis. The closed system than the open system.
spleen is innervated mainly from sympathetic nerves; referred pain
from the spleen is usually localised to the epigastrium and left
upper quadrant.
Microscopically the spleen has two major components: the red EXAMINATION TECHNIQUE
and white pulps, supported by a fibrous trabecular framework. The
white pulp consists of sheaths of lymphoid cells around splenic A coronal (longitudinal) view of the spleen can usually be obtained
arterioles; in many areas these sheaths are focally enlarged, forming with the patient supine or lying in the right lateral decubitus posi-
lymphoid follicles. The red pulp makes up most of the splenic tion with the transducer in the mid-axillary line; it is often helpful
volume and consists of venous sinusoids and splenic cords. Arteri- to raise the patients left arm. The spleen is examined in its entirety
oles that have passed through the white pulp divide into capillaries through the intercostal spaces in longitudinal and transverse planes
which then terminate either directly into the splenic sinusoids (Fig. 17.2). Scans are performed in suspended respiration and it is
(closed circulation) or alternatively into macrophage-rich cord frequently necessary to try different phases of respiration to achieve
325
CHAPTER 17 Spleen
complete visualisation. Subcostal, anterior and posterior approaches Contrast-specific low acoustic power machine presets are required
are not usually helpful unless the spleen is enlarged. The spleen can which result in almost complete suppression of tissue echoes from
also be examined with endoscopic ultrasound (Fig. 17.3). the splenic parenchyma. Indications for CEUS include:8
The spleen is ideally suited to examination with ultrasound 1. focal splenic or perisplenic lesions (particularly splenunculi)
microbubble contrast agents. Contrast-enhanced ultrasound 2. diffuse inhomogeneity of the splenic parenchyma
(CEUS) examinations are performed in real-time following intra 3. assessment of splenic trauma.
venous injection of second-generation ultrasound contrast media.
Almost all focal splenic pathology is hypovascular relative to
normal splenic tissue; thus abnormalities are evident as echo-poor
defects. CEUS often greatly increases the conspicuity of focal splenic
lesions (Fig. 17.4).9 However, its ability to characterise splenic
masses is less well established.
A B
Figure 17.4 A small echo-poor splenic mass that is poorly appreciated on conventional greyscale ultrasound (A, arrow) but is easily
seen with CEUS (B).
A B
Figure 17.7 A: Tumour in the pancreatic tail (arrow) visualised using the spleen as an acoustic window. B: corresponding CT image.
Splenic size
Clinical examination is imprecise in detecting splenomegaly.
A single longitudinal ultrasound measurement of the spleen
accurately correlates with splenic size.
Assessment of splenic size must pay due regard to the patients
age, sex and body habitus.
The spleen increases in size during normal pregnancy.
A small and hypovascular spleen may indicate functional
hyposplenia.
than 11cm, breadth less than 7cm and thickness less than 5cm.17
Another study found that a length of over 12cm was two standard
Figure 17.8 In this patient with ascites the gastrosplenic deviations above the mean.18 However, a study of normal college
ligament is outlined by ascitic fluid (arrows); the position of the athletes found that 7% had a spleen length of greater than 13cm.19
lesser sac (LS) and stomach (ST) are shown. The weight of the spleen is greater in males, increases with increas-
ing body weight, height and surface area and declines with age after
early adulthood.20 It is difficult therefore to give a single measure-
ment for the upper limit of splenic size that is applicable to all
posterior to the pancreas. The pancreatic tail often lies in the spleno-
patients and the sonologist will need to make a judgement based
renal ligament and can sometimes be well seen using the spleen as
on the patients age, sex and body habitus. As a guide it is often
an acoustic window (Fig. 17.7). In some patients with ascites the
considered that a measurement less than 12cm is normal, 1213cm
gastrosplenic ligament may be visualised (Fig. 17.8).
indeterminate and more than 13cm enlarged.
CEUS studies show avid splenic parenchymal enhancement
The spleen shows a linear increase in size in healthy women
approximately 15 seconds after injection. Initially (arterial phase)
throughout pregnancy21,22 and changes in size of the spleen have
enhancement is inhomogeneous due to differential flow rates
also been documented following abdominal trauma23 and as an
through the open and closed splenic circulation, analogous to the
adaptation to high altitude.24
appearances of normal arterial phase CT. After 3060 seconds (late
Small splenic size (length 7cm, width 3cm) may indicate func-
phase) enhancement becomes homogeneous and persists for 57
tional hyposplenia, particularly if accompanied by absent or
minutes, well beyond blood-pool enhancement, due to microbubble
reduced parenchymal blood flow on colour Doppler or CEUS
accumulation in the spleen (Fig. 17.9).10
examination.1,25 This is a potentially important finding in view of
the association with overwhelming infection.
Splenic size
Physical examination only has 5682% sensitivity for identifying
splenomegaly in comparison with imaging studies.11 Ultrasound is NORMAL VARIANTS AND CONGENITAL
a simple and reliable method for measuring splenic size. Size is ABNORMALITIES OF THE SPLEEN
usually assessed by a single longitudinal length measurement. This
has been shown to have good correlation to actual splenic length,
volume and weight on cadaveric studies and to in-vivo calculations Septation, clefts and notches
of splenic volume.12,13 Area and volume calculations based on 2D
and 3D ultrasound have also been proposed but these more complex Incomplete fusion of the splenic lobules may result in clefts or
measurements are not used in routine clinical practice.1416 notches in the normally smooth superolateral surface (Fig. 17.10);
The spleen reaches maximum size soon after puberty but there these can occasionally be misinterpreted as lacerations in the setting
are conflicting data regarding the normal size of the adult spleen. of abdominal trauma.26 Echogenic septation is sometimes seen
One large study found 95% of subjects had a splenic length of less between splenic lobules (Fig. 17.11).
327
CHAPTER 17 Spleen
A B
Figure 17.9 Normal appearance of the spleen following ultrasound contrast medium injection. A: In the early (arterial) phase
there is inhomogeneous enhancement due to differential circulation in the open and closed systems. B: In the same patient in the late
phase there is uniform enhancement.
Figure 17.10 Large cleft in the superolateral surface of the Figure 17.12 Accessory spleen (arrows) in a typical location
spleen (arrows). medial to the spleen.
Accessory spleens/splenunculi
and splenosis
Accessory spleens (splenunculi) arise due to failure of fusion of one
or more of the splenic lobules. They occur in 1030% of patients on
postmortem studies26 and in approximately 2% more than one may
be present.27 Accessory spleens are most commonly located medial
to the splenic hilum, adjacent to or within the pancreatic tail or
below the spleen (in the splenorenal ligament). Rarely they may be
located elsewhere in the abdomen.28
Sonographically accessory spleens are usually homogeneous,
round, smaller than 2cm in diameter and identical in echogenicity
to the spleen (Fig. 17.12).27 The presence of a vascular pedicle and
vascular supply from the main splenic vessels can frequently be
demonstrated with Doppler ultrasound and are helpful diagnostic
features.29,30 Diagnosis is not usually difficult but errors may arise,
particularly:
1. post splenectomy31
Figure 17.11 Echogenic septation running through the splenic 2. when the accessory spleen is located in the pancreatic tail
parenchyma. (Courtesy of Dr P Allan, Royal Infirmary, Edinburgh, where it may mimic a pancreatic mass32,33
UK.) 3. when the accessory spleen is unusually located
328
Normal variants and congenital abnormalities of the spleen
A B
Figure 17.13 Recurrent littoral cell angioma in an accessory spleen post splenectomy. A: Greyscale image showing a soft tissue
mass in the splenic bed representing a accessory spleen. B: CEUS demonstrates a number of ill-defined hypovascular nodules within the
accessory spleen in the late phase of enhancement (arrows). C: Corresponding CT image showing recurrent nodules of littoral cell
angioma (arrows).
329
CHAPTER 17 Spleen
A B
Figure 17.14 Splenosis following splenectomy. A: Ultrasound. B: CT appearances showing a soft tissue nodule adjacent to the left
kidney representing splenosis (arrow).
A B
Figure 17.15 Wandering spleen in the pelvis mimicking a pathological pelvic mass. A: Transvaginal ultrasound image.
B: Corresponding T2-weighted sagittal MRI image showing the ectopic spleen (arrows) above the uterus. (Courtesy of Dr H.
Andrews, Bristol Royal Infirmary, UK.)
A B
Figure 17.16 Heterotaxy syndrome (polysplenia). In this asymptomatic patient ultrasound demonstrates A: three splenic masses on
the right side of the abdomen, B: midline liver with anomalous drainage of the hepatic veins above the diaphragm. C: Corresponding
CT image.
A B
Figure 17.17 Massive splenomegaly due to myelofibrosis. A: On a standard ultrasound image the spleen is too large for
measurement within the ultrasound sector. B: Extended field of view imaging allows the entirety of the spleen to be imaged and measured.
332
Focal lesions of the spleen
Figure 17.19 Extensive echo-poor retroperitoneal Figure 17.21 NHL with a large nodular deposit.
lymphadenopathy encasing the aorta (AO) in a patient with
lymphoma and splenomegaly.
Figure 17.20 Low-grade NHL showing sparse small echo- Figure 17.22 NHL with bulky disease and infiltration of the
poor nodules. pancreatic tail (arrows).
incidence from the fifth decade and represents a diverse group of 15% of lymphoma patients had an abnormal ultrasound appearance
lymphatic malignancies. NHL is more likely to affect extranodal of the splenic parenchyma.61 Discrete focal lesions may be single or
sites (including the spleen) than HD,54 generally carries a worse multiple and are invariably echo-poor relative to normal spleen;61,62
prognosis and can be broadly divided into low-grade and high- echogenic, calcified or cystic lesions are exceptionally uncommon.
grade groups. Low-grade NHL is usually widely disseminated at Patterns include:
presentation and is a slowly progressive disease; high-grade NHL
more often presents with rapidly progressing localised disease. 1. diffuse alteration of splenic echotexture. This is most
Accurate anatomical staging of disease is important, particularly in commonly seen in HD and low-grade NHL and is often
HD, to select appropriate treatment regimens with a minimum of difficult to appreciate although ultrasound appears to be
toxicity. CT and MRI, rather than ultrasound, are the mainstays of superior to CT in identifying this subtle type of
staging although positron emission tomography CT (PET-CT) is involvement.60,63 CEUS may help accentuate this
now becoming increasingly important. heterogenicity9,64,65
Standard imaging techniques (ultrasound, CT and MRI) have a 2. small nodules (<3cm) are most commonly seen in HD and
low sensitivity in detecting lymphomatous infiltration of the spleen low-grade NHL (Fig. 17.20)
although PET-CT may perform better.57,58 Historically this resulted 3. large nodules (>3cm) are usually a feature of high-grade
in the need for staging laparotomy and splenectomy in many NHL (Fig. 17.21)
patients with HD.59,60 Fortunately modern treatment regimens mean 4. bulky disease, which may extend outside the spleen to
that surgery is no longer recommended and failure to detect splenic involve adjacent organs, is seen in high-grade NHL
involvement does not adversely affect prognosis.55 (Fig. 17.22).
The size of the spleen is not a reliable predictor of lymphomatous
involvement. In up to one-third of patients the spleen will appear In view of the rarity of other splenic masses, detection of a hyp-
normal in size despite infiltration being present. Conversely reac- oechoic rounded mass in the spleen of a patient with known lym-
tive splenomegaly is a common finding; mild to moderate splenic phoma can be regarded as evidence of involvement without the
enlargement without infiltration occurs in approximately 30% of need for biopsy61 although infarction (see below), which is common
patients with HD and 70% of patients with NHL.55 Massive in patients with lymphoma, should be considered when typical
splenomegaly, however, almost always indicates infiltration. lesions are identified. In many patients ultrasound will also be able
A number of parenchymal sonographic abnormalities have been to demonstrate intra-abdominal lymphadenopathy, nodes at the
described in the lymphomatous spleen; in one study approximately splenic hilum indicating splenic involvement (Fig. 17.23).55
333
CHAPTER 17 Spleen
A B
Figure 17.25 Splenic metastases. A: Echo-poor metastases secondary to ovarian cancer; the complex fluid lateral to the spleen is
secondary to pseudomyxoma peritonei. B: Isoechoic metastasis with an echo-poor halo secondary to breast cancer. C: Cystic metastases
secondary to melanoma. (Part C courtesy of Dr P. Allan, Royal Infirmary, Edinburgh UK).
A B
Figure 17.26 Breast metastases. A: Greyscale imaging demonstrates an inhomogeneous splenic parenchyma with an abnormal surface
contour. B: Following ultrasound contrast microbubble administration the metastases are more easily identified.
335
CHAPTER 17 Spleen
A B
Figure 17.27 Splenic angiosarcoma. A: Ultrasound image shows a splenic mass that is predominantly echogenic but with a central
cystic/necrotic component. B: Corresponding CT image showing the splenic mass and hypervascular liver metastases. (Reproduced from
Abbott RM, Levy AD, Aguilera NS, Gorospe L, Thompson WM. Primary vascular neoplasms of the spleen: Radiologic-pathologic
correlation. RadioGraphics 2004;24:1137-1163, provided courtesy of the Armed Forces Institute of Pathology, Washington, DC.)
A B
336 Figure 17.30 Atypical haemangioma. A: Containing small cystic spaces (courtesy of Mrs J. Bates, St James University Hospital, Leeds,
UK). B: Echo-poor haemangiomas (courtesy of Dr S. Elliot. Freeman Hospital, Newcastle, UK).
Focal lesions of the spleen
isoechoic in comparison with the normal spleen (Fig. 17.32).8 Other developmental or neoplastic in nature. Hamartomas are usually
lesions may be hypoechoic in the late phase and therefore impos- solitary and asymptomatic; however, large lesions may present
sible to differentiate from many other splenic lesions.1,9 The typical with a palpable mass or thrombocytopenia/anaemia. Multiple
nodular peripheral enhancement pattern with centripetal filling lesions may be associated with tuberous sclerosis and Wiskott
seen in liver haemangiomas appears to be uncommon.9 For lesions Aldrich syndrome.73 Sonographically the lesions are usually solid,
with atypical features correlative CT, MRI or red-cell scintigraphy well circumscribed of varying but usually increased echogenicity,
may be required. sometimes with internal blood flow on colour Doppler examination
Splenic hamartomas are rare benign tumours composed of (Fig. 17.33).71,73,76 Cystic spaces and calcifications are occasionally
malformed normal splenic tissue; it is uncertain whether they are present.
Splenic lymphangiomas are rare benign tumours composed of
lymph-filled cystic spaces and are most commonly seen in children.
They are usually asymptomatic unless large in size, when they may
present with symptoms due to compression. Rarely they may be
part of a generalised lymphangiomatosis involving multiple sites
in the body. Sonographically the spleen may be normal in size or
enlarged, containing one or more well-defined cystic masses that
may contain fine septa, small calcifications and low level echoes
within the cyst fluid (Fig. 17.34).70,73 Demonstration of intrasplenic
arteries and veins running along the walls of the cysts with colour
Doppler may be a helpful diagnostic feature.77
Other rare benign splenic masses include inflammatory pseudo-
tumours, lipomas, angiomyolipomas and fibromas.
A B
A B
Figure 17.33 Splenic hamartoma. Greyscale (A) and power Doppler (B) images showing a hypervascular hypoechoic solid splenic
mass. (Reproduced from Abbott RM, Levy AD, Aguilera NS, Gorospe L, Thompson WM. Primary vascular neoplasms of the spleen:
Radiologic-pathologic correlation. RadioGraphics 2004;24:1137-1163, provided courtesy of the Armed Forces Institute of Pathology,
Washington, DC.)
direct spread from an adjacent organ or within an area of pre- formation or isolated splenomegaly is also reported (Fig. 17.39).85
existing infarction. Presentation is usually with one or more of Associated features of abdominal tuberculosis such as lymph node
fever, pain and leukocytosis although symptoms may be lacking, enlargement, intestinal wall thickening and ascites may help to
particularly in immunocompromised patients.83 Sonographically suggest the diagnosis; ultrasound-guided fine-needle aspiration
pyogenic abscesses may be single or multiple and have a variety biopsy (FNAB) of the spleen or enlarged lymph nodes is usually
of appearances according to their state of evolution (Fig. 17.37). diagnostic.86,87
Typically they are echo-poor, round or oval but irregular in Fungal infection of the spleen does not usually occur in the
shape, poorly defined with variable posterior acoustic enhance- absence of immune compromise. Candida albicans is the most
ment and absence of internal blood flow on colour Doppler exam- common pathogen and typically produces multiple small (<2cm)
ination (Fig. 17.38). CEUS may demonstrate rim or septal abscesses.70 Four sonographic patterns of hepatosplenic candidiasis
enhancement in the late phase.8 Wedge-shaped abscesses may be are described:88
seen in patients with septic emboli. Occasionally gas locules may 1. wheel within a wheel pattern comprising a peripheral
be demonstrated. This is a diagnostic feature but most abscesses hypoechoic rim encasing an echogenic zone with a central
do not contain gas and the ultrasound appearances must be cor- echo-poor nidus
related with the patients clinical presentation. Ultrasound-guided 2. bulls-eye lesion comprising an echo-poor rim and echogenic
percutaneous aspiration for smaller abscesses (<33.5cm) or central area (Fig. 17.40)
catheter drainage for larger abscesses, combined with antibiotic 3. uniformly hypoechoic nodules
therapy, has replaced splenectomy and is now the treatment of 4. multiple small echogenic foci with variable degrees of
choice for most patients.84 posterior acoustic shadowing representing calcifications late
Involvement of the spleen in Mycobacterium tuberculosis infection in the course of the disease.
(MTB) is rare in non-endemic countries but rising due to the
The type 1 and type 2 patterns appear to be most specific for
increased prevalence of AIDS. The most common ultrasound
candidiasis but are only found in patients who are not
abnormality is multiple hypoechoic nodules, although abscess
neutropenic.
Parasitic splenic abscesses are usually due to hydatid disease and
of these 95% of cases are caused by Echinococcus granulosus. Splenic
A B
Figure 17.36 Presumed pseudocysts; incidental finding of two cystic lesions in asymptomatic patients. A: Cyst containing internal
debris. B: Cyst with wall calcification.
339
CHAPTER 17 Spleen
Splenic cysts
Congenital splenic cysts are rare; most incidentally discovered
cysts are post-traumatic pseudocysts.
Splenic abscess may be sonographically indistinguishable from
other splenic cysts; diagnostic aspiration is indicated where there
is clinical suspicion of infection.
Ultrasound-guided aspiration or catheter drainage is the
treatment of choice for most pyogenic splenic abscesses.
Mycobacterium tuberculosis is the most common cause of
hypoechoic splenic nodules in AIDS patients.
Echinococcal splenic cysts and Candida microabscesses may
show a pathognomonic ultrasound appearance.
A B
Figure 17.41 Hydatid disease. A: Type CE2 hydatid cyst containing multiple daughter cysts completely filling the mother cyst (courtesy
of Professor Okan Akhan, Hacettepe University, Ankara, Turkey). B: Splenic hydatid cyst showing detached floating membranes (water-lily
sign) (courtesy of Professor N. rmeci, Ankara University Medical School, Ankara, Turkey).
A B
Figure 17.42 Examples of focal splenic infarction. A: Cystic appearing infarct (courtesy of Dr P. Sidhu, Kings College Hospital,
London, UK). B: Extensive splenic infarction secondary to hypovolaemic cardiac arrest.
341
CHAPTER 17 Spleen
with CEUS (Fig. 17.43). Infarction may, however, also appear as the latter condition this frequently results in splenic atrophy
round or oval lesions indistinguishable from other focal splenic (autosplenectomy).
masses.97 With time the area of infarction reduces in size and
increases in echogenicity or may disappear completely. Infarction
may be complicated by secondary infection, haemorrhage or Splenic vascular aneurysms
rupture. Chronic (recurring) splenic infarction is particularly seen
The splenic artery is the most common site for visceral arterial
in patients with myeloproliferative and sickle cell disease,98 in
aneurysms. The incidence varies from 0.16% to 10.4% in various
series, and splenic artery aneurysms are more common in women.99
Most are asymptomatic but rarely rupture may occur, which carries
Table 17.3 Aetiology of splenic infarction9395 a high mortality, particularly in pregnant patients. Sonographically
the aneurysm appears as an anechoic mass along the course of the
Haematological Haemoglobinopathies* (esp. sickle cell splenic artery with internal flow on Doppler examination as the
disease) diagnostic feature; wall calcification or thrombus may be present
Lymphoproliferative diseases (Fig. 17.44). Treatment is usually recommended if the aneurysm is
Lymphoma/Leukaemia greater then 2cm in diameter, particularly if increasing in size;
Myelofibrosis catheter embolisation is now preferred to surgery.100 Pseudoaneu-
rysms of the splenic artery may be seen following trauma or pan-
Gauchers disease creatitis. Splenic vein aneurysms are very rare lesions and are
Paroxysmal nocturnal haemoglobinopathy usually an incidental discovery.93
Polycythaemia vera
Embolic Cardiac (endocarditis*, infarction, valvular
disease, atrial fibrillation*, LV aneurysm)
Splenic vein thrombosis and portal
Pancreatic disease (pancreatitis, cancer) hypertension
Vascular Splenic artery aneurysm Isolated thrombosis of the splenic vein (without thrombosis of the
Atherosclerosis* main portal vein) is usually due to pancreatic pathology (pancrea-
titis or carcinoma).101 Patients may present with splenomegaly or
Aortic dissection
gastrointestinal bleeding from isolated gastric varices. Ultrasound
Splenic vein thrombosis may directly demonstrate thrombus within a dilated splenic vein,
Portal hypertension with absent flow or incomplete luminal filling on colour Doppler
Autoimmune Vasculitis (Kawasaki disease, Wegeners examination indicating complete or partial thrombosis (Fig.
granulomatosis, polyarteritis nodosa) 17.45).78,93 When transabdominal ultrasound is non-diagnostic
SLE/Connective tissue disease endoscopic ultrasound is often able to make the diagnosis.102
In patients with portal hypertension ultrasound is frequently able
Infection Meningococcal to demonstrate portosystemic varices (oesophageal, short gastric
Infectious mononucleosis and splenorenal) in the perisplenic area (Fig. 17.46).
Kala-azar
Salmonella
Malaria
Mechanical Splenic torsion Vascular lesions of the spleen
Wandering spleen Splenic infarction is usually due to haematological disorders in
Miscellaneous Amyloidosis younger patients and embolic causes in older patients.
Sarcoidosis Infarction is a common cause of a focal splenic mass.
Splenic infarction typically appears as a low echogenicity
Iatrogenic (liver transplant, catheter wedge-shaped lesion with absent Doppler colour flow.
embolisation, cardiac surgery)
The splenic artery is the most common site for visceral arterial
aneurysms.
*Denotes the most common causes.
A B
Figure 17.44 Splenic artery aneurysm. Greyscale (A) and colour Doppler (B) images of an aneurysm arising from the distal splenic
artery (arrow); note the large areas of low attenuation in the spleen (arrowheads) representing splenic infarction.
342
Differential diagnosis of focal splenic lesions
Splenic calcifications
Many diseases may result in splenic calcification (Table 17.4).
Although accurate diagnosis is not always possible the type of
calcification and presence or absence of an associated mass are
helpful features.
Multiple small echogenic foci, with or without acoustic shadow-
Figure 17.46 Colour Doppler image showing large
ing, are usually the result of calcified granulomatous disease (Fig.
splenorenal varices extending from the splenic hilum towards the
17.49). Linear or curvilinear calcifications may occur in vascular
left kidney.
disease (atheroma or splenic artery aneurysm) or in the walls of
splenic cysts particularly pseudocysts (Fig. 17.36B). Focal dys-
trophic calcification may also arise in old splenic infarction, abscess
and haematoma. Some primary and secondary splenic tumours
Miscellaneous conditions of the spleen may also contain foci of calcification.
A B
Figure 17.48 Spontaneous splenic rupture in a patient with infectious mononucleosis. The spleen is enlarged and there is a large
perisplenic haematoma (arrows). This is almost isoechoic with splenic parenchyma on the greyscale image (A), but easily differentiated
following contrast medium administration (B).
Category Example
Infection Healed granulomas (TB, histoplasmosis,
brucellosis)
Old abscess
Hydatid
Vascular Atherosclerosis
Old haematoma/pseudocyst
Aneurysm
Old infarction
Phlebolith
Neoplastic Haemangioma
Hamartoma
Lymphangioma Figure 17.49 Calcified splenic granulomatous disease. There
Metastasis are multiple small echogenic foci too small to cast an acoustic
Angiosarcoma shadow.
Miscellaneous Sickle cell disease
Haemosiderosis
Sarcoidosis
Amyloid Echo-poor lesions represent the greatest diagnostic challenge.
Congenital cysts However, a number of generalisations can be made:
1. Almost all malignant secondary splenic tumours (lymphoma
and metastasis) are echo-poor.
2. A focal echo-poor mass in a patient with a known diagnosis
of lymphoma can be assumed to represent a lymphomatous
(pseudocyst) and travel to endemic areas (TB, hydatid abscess) deposit.
combined with laboratory data will often allow a presumptive diag- 3. Splenic infarction is relatively common and frequently has a
nosis to be made. characteristic appearance.
Lesions can be broadly divided into those that are cystic, those 4. Increased vascularity within an incidentally discovered
that are echo-poor and those that are echogenic. Simple cystic well-defined hypoechoic lesion on colour Doppler
lesions are likely to be benign and most will be pseudocysts. Diag- examination or in the arterial phase of CEUS tends to indicate
nosis is more difficult when internal echoes are present and cyst a benign process.111
aspiration should be considered in any patient with signs of infec- 5. CEUS may increase diagnostic confidence for certain
tion to exclude abscess formation. Solid, small, well-defined, echo- conditions, particularly splenic infarction and some echo-poor
genic splenic masses are usually benign vascular neoplasms haemangiomas.
(haemangioma or hamartoma); ultrasound surveillance may be When a definitive diagnosis cannot be made further alternative
appropriate in this group. Large, heterogeneous or ill-defined echo- imaging techniques may be diagnostic. When there is remaining
genic masses will require additional imaging or biopsy for uncertainty and the clinical situation requires a definitive diagnosis
diagnosis. ultrasound guided biopsy is both accurate and safe.
344
References
13. Lamb PM, Lund A, Kanagasabay RR, et al. Spleen size: how well do
ULTRASOUND INTERVENTIONS IN linear ultrasound measurements correlate with three-dimensional CT
THE SPLEEN volume assessments? Br J Radiol 2002;75:573577.
14. Sheth SG, Mani S, Tamhankar H, Mehta PJ. Spleen size in health and
disease: a sonographic assessment. J Assoc Phys India 1995;43:
Ultrasound-guided interventional procedures are infrequently per- 182184.
formed in the spleen, probably reflecting the rarity of focal lesions 15. Ishibashi H, Higuchi N, Shimamura R, et al. Sonographic assessment
and anxieties regarding the risk of haemorrhage. Procedures can, and grading of spleen size. J Clin Ultrasound 1991;19:2125.
however, be performed with high levels of accuracy and low rates 16. De Odorico I, Spaulding KA, Pretorius DH, et al. Normal splenic
of complication. volumes estimated using three-dimensional ultrasonography.
Both fine-needle aspiration biopsy (FNAB) and core biopsy of the J Ultrasound Med 1999;18:231236.
spleen are well-established techniques. Prior to biopsy, coagulation 17. Frank K, Linhart P, Kortsik C, Wohlenberg H. Sonographic
determination of spleen size: Standard dimensions in the healthy
is measured and abnormalities corrected if there is significant
adult. Ultraschall 1986;7:134137 [Article in German].
derangement.112 A safe route for biopsy must be identified, particu- 18. Loftus WK, Metreweli C. Normal splenic size in a Chinese
larly avoiding the lung, pleura, kidney and colon. Procedures can population. J Ultrasound Med 1997;16:345347.
usually be performed under local anaesthesia during suspended 19. Hosey RG, Mattacola CG, Kriss V, et al. Ultrasound assessment of
respiration. Following biopsy the patient must be closely observed spleen size in college athletes. Br J Sport Med 2006;40:251254.
to detect evidence of complications particularly bleeding. In a 20. DeLand FH. Normal spleen size. Radiology 1970;97:589592.
large multicentre study of splenic FNAB and core biopsy overall 21. Maymon R, Strauss S, Vaknin Z, et al. Normal sonographic values of
accuracy was 90.9%, the major complication rate was less than 1% maternal spleen size throughout pregnancy. Ultrasound Med Biol
(no deaths or emergency splenectomies) and minor complication 2006;12:18271831.
22. Maymon R, Zimerman AL, Strauss S, Gayer G. Maternal spleen size
rate 5.2%.113 Both FNAB and core biopsy gave similarly high levels
throughout normal pregnancy. Semin Ultrasound CT MRI 2007;28:
of accuracy in this study except for lymphoma, where core biopsy 6466.
performed much better. Core biopsy using an 18-gauge needle does 23. Goodman LR, Aprahamian C. Changes in splenic size after
not appear to carry a higher complication rate than with smaller abdominal trauma. Radiology 1990;176:629632.
needles and has a greater diagnostic accuracy.114 Unlike targeted 24. Sonmez G, Ozturk E, Basekim CC, et al. Effects of altitude on splenic
biopsy of the liver, the route chosen for splenic biopsy should volume: sonographic assessment. J Clin Ultrasound 2007;35:182185.
traverse the minimum amount of normal parenchyma to minimise 25. Grg C, Eichkorn M, Zugmaier G. The small spleen: sonographic
the risk of bleeding; particular care must be taken with lesions close patterns of functional hyposplenia or asplenia. J Clin Ultrasound
to the hilum to avoid injury to the major vessels.115 Despite its rela- 2003;31:152155.
26. Gayer G, Hertz M, Strauss S, Zissin R. Congenital anomalies of the
tive safety, splenic biopsy does carry a higher risk of bleeding than
spleen. Semin Ultrasound CT MRI 2006;27:358369.
biopsy of other abdominal organs and therefore should be limited 27. Mortel KJ, Mortel B, Silverman SG. CT features of the accessory
to cases where no suitable alternative exists.115 spleen. AJR Am J Roentgenol 2004;183:16531657.
Ultrasound-guided aspiration and drainage is now the initial 28. Wadham BM, Adams PB, Johnson MA. Incidence and location of
method of choice for diagnosis and treatment of most patients with accessory spleens. N Engl J Med 1981;304:1111 [Letter].
pyogenic splenic abscesses, with reported success rates of 60100% 29. Subramanyam BR, Balthazar EJ, Horii SC. Sonography of the
and complication rates of 018%.112,115 accessory spleen. AJR Am J Roentgenol 1984;143:4749.
30. Bertolotto M, Gioulis E, Ricci C, et al. Ultrasound and Doppler
features of accessory spleens and splenic grafts. Br J Radiol
1998;71:595600.
31. Katz JF, Kane RA. Sonographic appearance of accessory spleen. J Clin
REFERENCES Ultrasound 1984;12:163165.
1. Grg C. The forgotten organ: contrast enhanced sonography of the 32. Ota T, Ono S. Intrapancreatic accessory spleen: diagnosis using
spleen. Eur J Radiol 2007;64:189201. contrast enhanced ultrasound. Br J Radiol 2004;77:148149.
2. Woolf N. The lymphoreticular system. In: Pathology basic and 33. Barawi M, Bekal P, Gress F. Accessory spleen: a potential cause of
systemic. London: WB Saunders; 1998. p. 941987. misdaignosis at EUS. Gastrointest Endosc 2000;52:769772.
3. Pimpl W, Dapunt O, Kaindl H, Thalhamer J. Incidence of septic and 34. Froehner M, Leike S, Manseck A, et al. Splenunculus mimicking late
thromboembolic-related deaths after splenectomy in adults. Br J Surg local recurrence of renal cell carcinoma. Scand J Urol Nephrol
1989;76:517521. 1998;32:418419.
4. Moore KL, Persaud TVN, editors. The digestive system. In: Before we 35. Zissin R, Gutman M, Evan-Sapir E, Gayer G. Anatomic and
are born. Essentials of embryology and birth defects. 6th ed. pathologic computed tomographic findings following splenectomy.
Philadelphia: WB Saunders; 2003. p. 202227. Semin Ultrasound CT MRI 2007;28:6778.
5. Sherman LS, Potter SS, Scott WJ. Development of the gastrointestinal 36. Mller U, Rthlin M. Splenic neoformation following trauma-
tract. In: Larson WJ, editor. Human embryology. 3rd ed. induced splenectomy diagnosis and function. Swiss Surg
Philadelphia: Churchill Livingstone; 2001. p. 235264. 1995;5:230235 [in German].
6. Vibhakar SD, Bellon EM. The bare area of the spleen: a constant CT 37. Delamarre J, Capron J-P, Drouard F, et al. Splenosis: ultrasound and
feature of the ascitic abdomen. AJR Am J Roentgenol 1984;141: CT findings in a case complicated by an intraperitoneal implant
953955. traumatic haematoma. Gastrointest Radiol 1988;13:275278.
7. Standring S, editor in chief. Spleen. In: Grays anatomy. 39th ed. 38. Sarraf KM, Abdalla M, Al-Omari O, Sarraf MG. Diagnostic
Edinburgh: Elsevier; 2005. p. 12391244. difficulties of pelvic splenosis: case report. Ultrasound Obstet
8. Catalano O, Sandomenico F, Vallone P, et al. Contrast-enhanced Gynecol 2006;27:220221.
sonography of the spleen. Semin Ultrasound CT MRI 2006;27: 39. Tasci Y, Kayikcioglu F, Cavusoglu D, Gokcin H. Splenosis mimicking
426433. pelvic mass. Obstet Gynecol 2005;106:11671169.
9. Catalano O, Lobianco R, Sandomenico F, et al. Real-time contrast- 40. Dawson C, McCormick C, Menai-Williams R, Malone PR.
enhanced ultrasound of the spleen: examination technique and Splenunculus masquerading as an adrenal mass. Br J Urol
preliminary clinical experience. Radiol Med 2003;106:338356. 1995;76:404405.
10. Thorelius L. Contrast-enhanced ultrasound: beyond the liver. 41. Pumberger W, Wiesbauer P, Leitha T. Splenosis mimicking tumor
Eur Radiol 2003;13(S3):N91N108. recurrence in renal cell carcinoma: detection on selective spleen
11. Adamson JW, Longo DL. Anaemia and polycythaemia. In: Kasper scintigraphy. J Pediatr Surg 2001;36:10891091.
DL, Braunwald E, Fauci AS, et al., editors. Harrisons principles of 42. Kinori I, Rifkin MD. A truly wandering spleen. J Ultrasound Med
internal medicine. 16th ed. New York: McGraw-Hill; 2005. 1988;7:101105.
p. 329348. 43. Buehner M, Baker MS. The wandering spleen. Surg Gynecol Obstet
12. Loftus WK, Chow LTC, Metreweli C. Sonographic measurement of 1992;175:373387.
splenic length: correlation with measurement at autopsy. J Clin 44. Erden A, Karaalp G, zcan H, Cumhur T. Wandering accessory
Ultrasound 1999;27:7174. spleen. Surg Radiol Anat 1995;17:8991.
345
CHAPTER 17 Spleen
45. Yilmaz C, Esen OS, Colak A, et al. Torsion of a wandering spleen 74. Willcox TM, Speer RW, Schlinkert RT, Sarr MG. Haemangioma of the
associated with portal vein thrombosis. J Ultrasound Med spleen: presentation, diagnosis and management. J Gastrointest Surg
2005;24:379382. 2000;4:611613.
46. Kessler A, Miller E, Keidar S, et al. Mass at the splenic hilum: a clue 75. Andrews MW. Ultrasound of the spleen. World J Surg 2000;24:
to torsion of a wandering spleen located in a normal left upper 183187.
quadrant position. J Ultrasound Med 2003;22:527530. 76. Tang S, Shimizu T, Kikuchi Y, et al. Color Doppler sonographic
47. Gilman RS, Thomas RL. Wandering spleen presenting as acute findings in splenic hamartoma. J Clin Ultrasound 2000;28:249253.
pancreatitis in pregnancy. Obstet Gynecol 2003;101:11001102. 77. Komatsuda T, Ishida H, Konno K, et al. Splenic lymphangioma:
48. Karmazyn B, Steinberg R, Gayer G, et al. Wandering spleen the US and CT diagnosis and clinical manifestations. Abdom Imaging
challenge of ultrasound diagnosis: report of 7 cases. J Clin 1999;24:414417.
Ultrasound 2005;33:433438. 78. Rolfes RJ, Ros PR. The spleen: an integrated imaging approach.
49. Applegate KE, Goske MJ, Pierce G, Murphy D. Situs revisited: Crit Rev Diagn Imaging 1990;30:4183.
imaging of the heterotaxy syndrome. Radiographics 1999;19: 79. Hansen MB, Moller AC. Splenic cysts. Surg Laparosc Endosc
837852. Percutan Tech 2004;14:316322.
50. Ditchfield MR, Hutson JM. Intestinal rotational abnormalities in 80. Shirkhoda A, Freeman J, Armin AR, et al. Imaging features of splenic
polysplenia and asplenia syndromes. Pediatr Radiol 1998;28:303306. epidermoid cyst with pathological correlation. Abdom Imaging
51. Aster JC. Diseases of white blood cells, lymph nodes, spleen and 1995;20:449451.
thymus. In: Kumar V, Abbas AK, Fausto N, editors. Robbins and 81. Rathaus V, Zissin R, Goldberg E. Spontaneous rupture of an
Cotran pathological basis of disease. 7th ed. Philadelphia: Elsevier epidermoid cyst of spleen: Preoperative ultrasonographic diagnosis. J
Saunders; 2005. p. 661709. Clin Ultrasound 1991;19:235237.
52. Goerg C, Schwerk WB, Goerg K. Sonography of focal lesions of the 82. Dachman AH, Ros PR, Murari PJ, et al. Nonparasitic splenic cysts: a
spleen. AJR Am J Roentgenol 1991;156:949953. report of 52 cases with radiologic-pathologic correlation. AJR Am J
53. Sandrasegaran K, Robinson PJ, Selby P. Staging of lymphoma in Roentgenol 1986;147:537542.
adults. Clin Radiol 1994;49:149161. 83. Ng KK, Lee TY, Wan YL, et al. Splenic abscess: diagnosis and
54. Rademaker J. Hodgkins and non-Hodgkins lymphomas. Radiol Clin management. Hepatogastroenterology 2002;49:567571.
North Am 2007;45:6983. 84. Chou YH, Tiu M, Chiou HJ, et al. Ultrasound-guided interventional
55. Bhatia K, Sahdev A, Reznek RH. Lymphoma of the spleen. Semin procedures in slpenic abscesses. Eur J Radiol 1998;28:167170.
Ultrasound CT MRI 2007;28:1220. 85. Sharma SK, Smith-Rohrberg D, Tahir M, et al. Radiological
56. Spier CM, Kjeldsberg CR, Eyre HJ, Behm FG. Malignant lymphoma manifestations of splenic tuberculosis: a 23-patient case series from
with primary presentation in the spleen. Arch Pathol Lab Med India. Indian J Med Res 2007;125:669678.
1985;109:10761080. 86. Tarantino L, Giorgio A, de Stefano G, et al. Disseminated
57. Siniluoto T, Pivnsalo M, Alavaikko M. Ultrasonography of spleen mycobacterial infection in AIDS patients: abdominal US features and
and liver in staging Hodgkins disease. Eur J Radiol 1991;13:181186. value of fine-needle aspiration biopsy of lymph nodes and spleen.
58. Even-Sapir E, Lievshitz G, Perry C, et al. Fluorine-18 Abdom Imaging 2003;28:602608.
fluorodeoxyglucose PET/CT patterns of extranodal involvement in 87. Suri R, Gupta S, Gupta SK, et al. Ultrasound guided fine needle
patients with non-Hodgkins lymphoma and Hodgkins disease. aspiration cytology in abdominal tuberculosis. Br J Radiol
Radiol Clin North Am 2007;45:697709. 1998;71:723727.
59. Castellino RA. Hodgkin disease: practical concepts for the diagnostic 88. Pastakia B, Shawker TH, Thaler M, et al. Hepatosplenic candidiasis:
radiologist. Radiology 1986;159:305310. wheels within wheels. Radiology 1988;166:417421.
60. Munker R, Stengel A, Stbler A, et al. Diagnostic accuracy of 89. Akhan O, Koroglu M. Hydatid disease of the spleen. Semin
ultrasound and computed tomography in the staging of Hodgkins Ultrasound CT MRI 2007;28:2834.
disease: verification by laparotomy in 100 cases. Cancer 1995;76: 90. WHO Informal Working Group. International classification of
14601466. ultrasound images in cystic echinococcosis for application in clinical
61. Grg C, Weide R, Schwerk WB. Malignant splenic lymphoma: and field epidemiological settings. Acta Tropica 2003;85:253261.
sonographic patterns, diagnosis and follow-up. Clin Radiol 91. Pant CS, Gupta RK. Diagnostic value of ultrasonography in hydatid
1997;52:535540. disease in abdomen and chest. Acta Radiol 1987;28:743745.
62. Goerg C, Schwerk WB, Goerg K, Havemann K. Sonographic patterns 92. rmeci N, Soykan I, Palabiyikoglu M, et al. A new therapeutic
of the affected spleen in malignant lymphoma. J Clin Ultrasound approach for treatment of hydatid cysts of the spleen. Dig Dis Sci
1990;18:569574. 2002;47:20372044.
63. Siniluoto TMJ, Tikkakoski TA, Lhde ST, et al. Ultrasound or CT in 93. Vanhoenacker FM, de Beeck O, De Schepper AM, et al. Vascular
splenic diseases? Acta Radiol 1994;35:597605. disease of the spleen. Semin Ultrasound CT MRI 2007;28:3551.
64. Grg C, Graef C, Bert T. Contrast-enhanced sonography for 94. Gupta S, Kakar A. Splenic infarct of unusual aetiology. J Ind Acad
differential diagnosis of an inhomogeneous spleen of unknown cause Clin Med 2004;5:310314.
in patients with pain in the left upper quadrant. J Ultrasound Med 95. Jaroch MT, Broughan TA, Hermann RE. The natural history of splenic
2006;25:729734. infarction. Surgery 1986;100:743748.
65. Peddu P, Shah M, Sidhu PS. Splenic abnormalities: a comparative 96. Weingarten MJ, Fakhry J, McCarthy J, et al. Sonography after splenic
review of ultrasound, microbubble-enhanced ultrasound and embolization: the wedge-shaped acute infarct. AJR Am J Roentgenol
computed tomography. Clin Radiol 2004;59:777792. 1984;142:957959.
66. Townsend RR, Laing FC, Jeffrey Jr RB, Bottles K. Abdominal 97. Goerg C, Schwerk WB. Splenic infarction: sonographic patterns,
lymphoma in AIDS: evaluation with US. Radiology 1989;171: diagnosis, follow-up and complications. Radiology 1990;174:803807.
719724. 98. Grg C, Zugmaier G. Chronic recurring infarction of the spleen:
67. Lam KY, Tang V. Metastatic tumours to the spleen: a 25-year Sonographic patterns and complications. Ultraschall Med
clinicopathologic study. Arch Pathol Lab Med 2000;124:526530. 2003;24:245249.
68. Schn CA, Grg C, Ramaswamy A, Barth PJ. Splenic metastases in a 99. Trastek VF, Pairolero PC, Bernatz PE. Splenic artery aneurysms.
large unselected autopsy series. Pathol Res Pract 2006;202:351356. World J Surg 1985;9:378383.
69. Goerg C, Schwerk WB, Goerg K. Splenic lesions: sonographic 100. McDermott VG, Shlansky-Goldberg R, Cope C. Endovascular
patterns, follow-up, differential diagnosis. Eur J Radiol 1991;13: management of splenic artery aneurysms and pseudoaneurysms.
5966. Cardiovasc Intervent Radiol 1994;17:179184.
70. Urrutia M, Mergo PJ, Ros LH, et al. Cystic masses of the spleen: 101. Moossa AR, Gadd MA. Isolated splenic vein thrombosis. World J
radiologic-pathologic correlation. RadioGraphics 1996;16:107129. Surg 1985;9:384390.
71. Warshauer DM, Hall HL. Solitary splenic lesions. Semin Ultrasound 102. Wiersema MJ, Chak A, Kopecky KK, Wiersema LM. Duplex Doppler
CT MRI 2006;27:370388. endosonography in the diagnosis of splenic vein, portal vein, and
72. Thompson WM, Levy AD, Aguilera NS, et al. Angiosarcoma of the portosystemic shunt thrombosis. Gastrointest Endosc 1995;42:1926.
spleen: imaging characteristics in 12 patients. Radiology 2005;235: 103. Warshauer DM. Splenic sarcoidosis. Semin Ultrasound CT MRI
106115. 2007;28:2127.
73. Abbott RM, Levy AD, Aguilera NS, et al. Primary vascular 104. Kessler A, Mitchell DG, Israel HL, Goldberg BB. Hepatic and splenic
neoplasms of the spleen: radiologic-pathologic correlation. sarcoidosis: ultrasound and MR imaging. Abdom Imaging 1993;18:
RadioGraphics 2004;24:11371163. 159163.
346
References
105. Sterlacci W, Heiss S, Augustin F, Tzankov A. Splenic rupture, beyond 111. Grg C, Grg K, Bert T, Barth P. Colour Doppler ultrasound patterns
and behind: a histological, morphometric and follow-up study of 254 and clinical follow-up of incidentally found hypoechoic, vascular
cases. Pathobiology 2006;73:280287. tumours of the spleen: evidence for a benign tumour. Br J Radiol
106. Grg C, Clle J, Grg K, et al. Spontaneous rupture of the spleen: 2006;79:319325.
ultrasound patterns, diagnosis and follow-up. Br J Radiol 112. Lieberman S, Libson E, Sella T, et al. Percutaneous image-guided
2003;76:704711. splenic procedures: update on indications, technique, complications
107. Gore RM, Miller FH, Yaghmai V. Acquired immunodeficiency and outcomes. Semin Ultrasound CT MRI 2007;28:5763.
syndrome (AIDS) of the abdominal organs: imaging features. Semin 113. Civardi G, Vallisa D, Bert R, et al. Ultrasound-guided fine needle
Ultrasound CT MRI 1998;19:175189. biopsy of the spleen: high clinical efficacy and low risk in a
108. Yee JM, Raghavendra BN, Horii SC, Ambrosino M. Abdominal multicentre Italian study. Am J Hematol 2001;67:9399.
sonography in AIDS: a review. J Ultrasound Med 1989;8:705714. 114. Liang P, Gao Y, Wang Y, et al. US-guided percutaneous needle biopsy
109. Porcel-Martin A, Rendon-Unceta P, Bascuana-Quirell A, et al. Focal of the spleen using 18-gauge versus 21-gauge needles. J Clin
splenic lesions in patients with AIDS: sonographic findings. Abdom Ultrasound 2007;35:477482.
Imaging 1998;23:196200. 115. Kang M, Kalra N, Gulati M, et al. Image guided percutaneous splenic
110. Kawooya MG, Muyinda Z, Byanyima R, Malwadde EK. Abdominal interventions. Eur J Radiol 2007;64:140146.
ultrasound findings in HIV patients: a pictorial review. Ultrasound
2008;16:6272.
347
CHAPTER
INTRODUCTION 351
Introduction and general principles
EUS EQUIPMENT 351 Endoscopic ultrasound (EUS) refers to the integration of the
modalities of white light video endoscopy and ultrasonography.
ANATOMICAL STRUCTURE OF UPPER GI TRACT 352 Echo-endoscopes are classified by the orientation of the
EUS APPEARANCE OF UPPER GI TRACT 352 transducer; these are radial and curvilinear. The radial echo-
endoscope has a 360 scan plane and is primarily used for
CLINICAL INDICATIONS FOR EUS IN THE UPPER diagnosis, while the curvilinear has a 15 scan plane and is
GI TRACT 353 mostly used as an interventional device.
PRINCIPLES OF EUS CANCER STAGING 353 The ultrasonic appearance of the wall of the upper GI tract
imaged consists of a number (usually five) of bright (hyperechoic)
EUS AND THE OESOPHAGUS 354 and dark (hyoechoic) rings.
Cancer 354
One of the most important uses of EUS is staging of upper GI
Barretts oesophagus 356
malignancies. EUS is also used to investigate submucosal
Submucosal (subepithelial) lesions 358
Benign posterior mediastinal masses 358 abnormalities including vascular structures, as well as for
Oesophageal varices 359 therapeutic applications such as fine-needle aspiration or core
Achalasia and other dysmotility disorders 359 biopsies.
C D
Figure 18.1 Examples of the Olympus and Fujinon echo-endoscopes that are currently available and an example of a mini-probe
transducer.
A: The tip of the Olympus GF-UM series radial echo-endoscope. Diameter of scope series ranges between 12.5 and 13.5mm.
B: The tip of the Olympus MH-908 radial echo-endoscope. Diameter of scope 8.5mm.
C: The tip of the Olympus GF-UE 260 electronic radial echo-endoscope. Diameter of scope 13.8mm.
D: The tip of the Fujinon electronic EG-530UR radial echo-endoscope. Diameter of scope 11.5mm.
E: The tip of the Fujinon 2612MHz mini-probe. Diameter of probe ranges between 2 and 2.6mm.
F: The tip of the Olympus GF-UCT 240 electronic curvilinear echo-endoscope. Diameter of scope 14.6mm.
longitudinally orientated in relation to the endoscope; it is mostly circumferential fibres and outer longitudinal fibres, dependent
used as an interventional device and normally operates at a fre- upon location; the upper third of the oesophagus is mostly com-
quency between 5 and 10MHz.2,68 However, interpretation of the posed of skeletal muscle; the middle third has both skeletal and
ultrasound images can be more difficult compared with those of smooth muscle; and the lowest third is only composed of smooth
radial echo-endoscopes. muscle fibres. The approximate thicknesses of the muscularis
propria circular and longitudinal fibre layers are 500m and
300m, respectively.
The oesophagus is covered by an adventitia until it pierces the
diaphragm, after which it is covered by a serosa, which continues
ANATOMICAL STRUCTURE OF UPPER throughout the outer lining of stomach.
GI TRACT A detailed cross-section of the anatomy of the wall of the oesopha-
gus is shown in Figure 18.2.
The wall of the oesophagus and stomach is made up of a number
of tissue layers of different cellular consistencies. The innermost
layer towards lumen, is the mucosa and is made up of a number of
sublayers, namely epithelium, lamina propria and muscularis EUS APPEARANCE OF UPPER GI TRACT
mucosae. The next layer is the submucosa and is composed of dense
connective tissue. The muscularis propria of the upper GI tract is a As the main operating frequencies of the echo-endoscopes are 5,
muscular layer composed of both skeletal and smooth muscle 7.5, 10, 12 and 20MHz, the tissue detail and number of boundary
fibres. This may be subdivided into sublayers, the inner reflections observed during imaging of the walls of the oesophagus
352
Principles of EUS cancer staging
Epithelium
1st Epithelium
Mucosa
Mucosa
Lamina propria Lamina
propria
2nd
Muscularis mucosae
Muscularis
Submucosa mucosae
3rd Submucosa
a
Muscularis propria
4th b Muscularis
propria
c
Adventitia/serosa
5th Adventitia/
serosa
Figure 18.2 Anatomy of the wall of the oesophagus.
Layer 7: MPL // AD
Hyper
Layer 6: MPL Layer 7: MPL // AD
Hypo Hyper
Mechanical Layer 6: MPL
Layer 5: MPC // MPL Hypo
transducer Hyper Compressed normal
ring artefact oesophageal wall Layer 5: MPC // MPL
Layer 4: MPC Hyper
Hypo Layer 4: MPC
Layer 3: MS // SM // MPC Hypo
Hyper Mechanical Layer 3: MS // SM // MPC
Layer 2: MS transducer Hyper
Hypo ring artefact Layer 2: MS
Layer 1: WB // MS Hypo
Hyper Layer 1: WB // MS
A B Hyper
Figure 18.4 Layers of the oesophageal wall. A: Normal oesophageal wall layers imaged at 20MHz (seven layers were observed).
The image was acquired in the mid oesophagus. The wall layers were most prominent when the wall was perpendicular to the transducer.
The GF-UM2000 echo-endoscope and EU-M2000 processor was used to acquire the image. B: Expanded oesophageal wall layers,
preceding an area of abnormal pathology, acquired at 12MHz (seven layers were observed). The image was acquired in the area of the
mid oesophagus. The GF-UM2000 echo-endoscope and EU-M2000 processor were used to acquire the image. WB, water balloon;
MS, mucosa; SM, submucosa; MPC, muscularis propria circular; MPL, muscularis propria longitudinal; AD, adventitia; Hyper, hyperechoic
layer; Hypo, hypoechoic layer; //, interface.
the TNM staging (primary Tumour, regional Nodes, Metastasis), histological diagnosis is made. Its ability, however, to accurately
with some differences that are organ specific (see Tables 18.1 and determine T stage is limited (sensitivity 4060%) because it cannot
18.2). There is close correlation between TNM staging and group reliably delineate the component layers of the oesophageal wall.23
staging with 5-year survival probability. Furthermore, helical CT scanning cannot define accurately to
T (primary tumour) is the extent of the tumour and is detailed proximal and distal margins of oesophageal tumours and has
from T0 to T4. Figure 18.5 illustrates the corresponding idealised limited accuracy in the detection of lymph nodes measuring <1cm.
EUS images (T1 to T3) to tumour pathology as it invades the With the advent of multi-detector computed tomography (MDCT)
oesophageal wall layers and T4 is the invasion of nearby structures. there has been an increase in the image resolution and a decrease
N (regional node) staging signifies the absence or presence and in the acquisition time compared with helical CT. EUS, however,
number of lymph nodes metastases and is classified as N0 to N3 remains the most accurate modality of oesophageal T staging even
for the oesophagus and N0 to N3 for the stomach according to the compared to MDCT, with accuracies between 71% and 86% for EUS
2009 IUAC TNM classification.12,13 versus accuracies between 42% and 81% for MDCT compared with
To distinguish between malignant and benign nodes, via radial surgical resection.24 The accuracy of locoregional nodal staging
EUS using frequencies above 7MHz, the criteria in Table 18.3 were reported by Sandha et al.24 was 68% for MDCT, 56% for PET and
used.14 A single matching factor signifies a low possible presence of 81% for EUS.
malignancy. However, as the number of matching factors increases, Furthermore, the development of curvilinear scopes which enable
the possibility of the node being malignant also increases, giving aspiration of tissue through a fine needle (EUS FNA) in order to
over 90% certainty if all four criteria are fulfilled (Fig. 18.6). Unfor- obtain tissue samples of the nodes has further increased the accu-
tunately only 25% of malignant nodes will fulfil all four criteria.15 racy of nodal staging (Fig. 18.7). Distal nodal diagnosis around
More recently, the modified EUS malignant lymph node criteria coeliac access and hepatic artery territory is the only area where
have been proposed for the oesophagus that include the four clas- MDCT is superior to EUS with accuracies in the range 8192% while
sical criteria plus three additional: localisation of nodes (coeliac it is 6573% for EUS. Again, the ability of endoscopic ultrasound to
region), number of nodes >5, and presence of T3/4 disease.16 When obtain tissue of the coeliac axis nodes significantly improves accu-
more than three of the seven criteria were present, the accuracy for racy. There is little doubt that EUS is the investigation of choice in
the presence of malignant nodes was over 86%.15 the locoregional staging of oesophageal cancer and selection of
M (metastasis) refers to the presence or absence of metastasis and patients for oesophageal surgery.
is classified as either M0 or M1.12,1721 However, EUS only provides Over the past 5 years there have been several therapeutic devel-
locoregional M classification of the disease (e.g. left lobe of the liver, opments in the management of oesophageal cancer, particularly of
presence coeliac axis lymph nodes). Computed tomography (CT) the early disease. In early tumours without nodal involvement the
or positron emission tomography (PET) are far better placed to treatment possibilities include endoscopic mucosal resection or
provide distant metastasis staging. endoscopic submucosal dissection, while in more advanced disease
with nodal involvement neoadjuvant chemotherapy is used prior
to surgery in order to improve outcome.25 The role of EUS is there-
fore pivotal in guiding the clinician to select the most appropriate
EUS AND THE OESOPHAGUS treatment modality. Illustrative examples of oesophageal cancer
staging are presented in Figure 18.8AE.
There are, however, some limitations to the diagnosis using endo-
Cancer scopic ultrasound. The technique is most accurate in the diagnosis
of T3 and T4 disease (>90%).26 Accuracy is reduced in T1 and T2
Oesophageal cancer is an aggressive malignancy with an overall disease by approximately 10%. There are some caveats in the use
5-year survival of 510%. Two-thirds of patients have inoperable of endoscopic ultrasound. The inflammatory reaction around the
disease at diagnosis.22 Accurate staging of oesophageal cancer is tumour can result in over-staging while it is sometimes impossible
important because survival is closely related to tumour, nodal and to detect microscopic invasion, resulting in underestimation of
presence of metastases (TNM) stage. Usually helical-computed staging. An oblique scanning plane may also give rise to overesti-
tomography (CT) is the first staging investigation once the mation of stage.
354
EUS and the oesophagus
Table 18.1 TNM staging with corresponding grouping for Table 18.2 TNM staging with corresponding grouping for
oesophageal carcinoma and relative survival13 gastric carcinoma and relative survival13
Primary tumour Primary tumour
Stage Tumour involvement Stage Tumour involvement
Tx Cannot be assessed Tx Cannot be assessed
Tis Carcinoma in situ/High-grade dysplasia T1 Lamina propria, submucosa
T1 Lamina propria or submucosa A Lamina propria
A Lamina propria or muscularis mucosae B Submucosa
B Submucosa T2 Muscularis propria
T2 Muscularis propria T3 Subserosa
T3 Adventitia T4 A Perforates serosa
T4 Adjacent structures B Adjacent structures
A Pleura, pericardium, diaphragm, or Regional lymph nodes
adjacent peritoneum
B Other adjacent structures, e.g. aorta, Stage Nodal involvement
vertebral body, trachea
Nx Nodes cannot be assessed
Regional lymph nodes N0 No regional node metastasis
Stage Nodal involvement N1 1 to 2 nodes
N2 3 to 6 nodes
Nx Nodes cannot be assessed N3A 7 to 15 nodes
N0 No regional node metastasis N3B 16 or more nodes
N1 1 to 2 regional lymph nodes
Distant metastases
N2 3 to 6 regional lymph nodes
N3 >6 regional lymph nodes Stage Presence of distant metastases
355
CHAPTER 18 Oesophagus and stomach
Ai Aii
Needle
Calcification
A B
Figure 18.7 Subcarinal nodes. A: EUS-guided FNA from an enlarged subcarinal node. Note the presence of node calcification.
B: Benign subcarinal nodes are often present in smokers and appear flat with a relatively hyperechoic centre.
T3
Aorta T2
Tumour
Spine
Early T3 T3
Lymph
node
A B C
Node Tumour
Extension
Aorta
Node
Large node
Coeliac
axis
D E
Figure 18.8 Examples of locoregional EUS staging of oesophageal cancer. A: T1 disease confined within the first three layers of
the oesophagus (12MHz). B: T2 disease with evidence of infiltration to the muscularis propria. There is a suggestion of early T3 (extension
to the adventitia between 6 and 8 oclock.). C: T3 disease with a large malignant looking node (N1). D: T4 disease with extension to
mediastinum and infiltration of the aorta. Large peritumour nodes are also present. E: Coeliac axis lymph node involvement in a patient
with advanced adenocarcinoma of the lower oesophagus.
357
CHAPTER 18 Oesophagus and stomach
Submucosal (subepithelial) lesions Gastrointestinal stroma tumours (GISTs) are by the far the com-
monest true submucosal lesions. They account for about 65% of all
The ability of EUS to accurately delineate the layers of the gastroin- benign tumours of the oesophagus, although less than 10% of all
testinal tract has made it an ideal modality to investigate these GISTs are localised in the oesophagus. They are characterised by
lesions. Submucosal lesions usually come to clinical attention less growth of the smooth muscle of the muscularis propria, although
frequently than mucosal abnormalities and in many cases they are they occasionally rise from the muscularis mucosa. They can have
found incidentally during routine evaluation of the upper gastroin- varying mitotic activity and those tumours of size less than 2cm
testinal tract, although very occasionally they can ulcerate or bleed. and very low mitotic activity (mitotic count <5/50 high power
fields) are considered of very low risk of malignancy. Under endo-
scopic ultrasound these lesions appear as homogeneous hypoechoic
well-demarcated areas measuring <2cm in size. GISTs with higher
mitotic activity tend to grow larger and the internal echo structure
tends to become more heterogeneous with irregular margins and
appearance of necrotic areas, septa and presence of calcification.28
Satellite lymphadenopathy may be present.
Endoscopic ultrasound is useful in the follow-up of these lesions
to establish whether they grow larger, and if there are worrying
features or size >3cm surgery is recommended (Fig. 18.10A,B). EUS
FNA in most case provides an adequate sample for immunohisto-
chemical staining for c-kit, CD34, CD117 and to determine the
degree of mitotic activity. In recent studies the overall accuracy of
EUS imaging for the diagnosis of malignant GIST was 78% and was
improved to 91% by EUS FNA.29 Other submucosal lesions include
lipomas (Fig. 18.11), cysts, granular cell tumours, fibrovascular
polyps as well as ectopic gastric glandular tissue. Lipomas are the
second commonest lesion after GISTs. They are benign tumours
composed of fat; they are echo bright and appear to arise from the
third layer, which corresponds to the submucosa.
A B
Figure 18.10 GIST in the oesophagus. A: Large multilobular GIST >5cm arising from the fourth layer of the oesophagus. B: GIST in the
oesophagus with benign characteristics homogeneous, hypoechoic with clearly defined borders.
358
EUS and the oesophagus
Varix
Oesophageal varices
Endoscopic ultrasonography is an excellent technique in the diag-
nosis of oesophago-gastric varices.33 In general, intramural vessels
in the oesophagus are imaged as echo-free structures. These are
usually submucosal but also collateral vessels can be visualised.
The ability of endoscopic ultrasound to detect oesophageal varices
is often operator dependent as the endoscope balloon easily com-
presses small varices. The newer electronic radial and linear endo-
scopes equipped with colour flow and Doppler facilities can
delineate in great detail the presence of varices and collateral circu-
lation (Fig. 18.13). Furthermore, enlargement of the azygos vein is
a good indicator of the presence of portal hypertension.
Injection to obliterate oesophageal varices under EUS guidance
has proven to be an effective technique.34 More recently EUS-guided
thrombin injection to control bleeding varices both in the oesopha-
gus and the cardia of the stomach was successfully applied in
complex cases where other treatment options had previously
failed35,36 (Fig. 18.14A, B).
Figure 18.12 EUS of an oesophageal cyst appearing as a Achalasia and other dysmotility disorders
hypoechoic well-demarcated area arising from the submucosal
(second) layer of the oesophagus. Endoscopic ultrasound is occasionally used to differentiate between
true achalasia and extrinsic compression of the lower oesophagus
The two main types are congenital foregut duplication cysts, due to a submucosal lesion or cancerous lesion (pseudo-achalasia).
which are mostly localised but sometimes extend for the whole Typically in achalasia, the fourth layer under EUS appears concen-
length of the oesophagus, and acquired mucous retention cysts, trically thickened in the area corresponding to the lower oesopha-
which are usually small. Occasionally some cysts arise away from geal sphincter. Endoscopic injection of botulinum toxin under EUS
the oesophageal wall and they are more suggestive of bronchogenic guidance has been used to ensure that the botulinum has been
cysts. Cysts are generally asymptomatic, although they can give injected into the lower oesophageal sphincter in the hope of achiev-
symptoms such as chest pain, dysphagia or dyspnoea. Under CT ing a more sustained response.37
they appear as contrast non-enhancing lesions but not uncommonly The development of three-dimensional endoscopic ultra
they are mistaken for malignant tumours, particularly those con- sound may increase the use of this technique in the assessment of
taining thick gelatinous material. specific thickened segments in the oesophagus with a view to a
359
CHAPTER 18 Oesophagus and stomach
Needle
Thrombosed
area
Varices
A B
Figure 18.14 EUS-guided thrombin injection. A: Thrombin injection of bleeding oesophageal varices under EUS guidance using the
therapeutic (linear) echo-endoscope. The needle is seen within the varix. B: Post-thrombin injection: colour power flow EUS shows clot
formation as multiple speckled hyperechoic areas with no blood flow within the injected varix.
Gastric lymphoma
EUS AND THE STOMACH EUS is of important value in the diagnosis of gastric lymphoma
(Fig. 18.17). This, in most cases, is a non-Hodgkins B-cell lym-
phoma that is often difficult to diagnose because of non-specific
Cancer endoscopic findings. Under EUS the abnormal area has poorly
reflective thickened wall characteristics with associated lymph
EUS is a complementary technique in the investigation and staging node enlargement. EUS-assisted FNA of the nearby nodes may
of gastric cancer once a biopsy-based diagnosis is made. It provides provide definitive tissue diagnosis. Endoscopic ultrasonography is
important information on the depth of cancer invasion, nearby very useful in the staging of gastric MALT (mucosa associated
lymph node metastases as well as the presence of ascitic fluid. lymphoid tissue) lymphoma, which is strongly associated with
Although EUS has an important role in the cancer of cardia (junc- Helicobacter pylori infection. This is one of the few lymphomas that
tional), to assess the extension into the oesophagus, it has a rela- can regress completely following eradication therapy as long as it
tively more limited role in the decision-making process for surgical is restricted to the mucosa and submucosa.41 EUS is therefore of
resection of gastric cancer involving the body and antrum. This is particular value in planning treatment for these patients.
because the combination of laparoscopy with peritoneal washings
and abdominal CT scan can in most cases give adequate informa-
tion on which to base the decision for surgical treatment.23 Gastric polyps
In the UK over 80% of cases of gastric cancer have associated
lymphadenopathy due to late diagnosis, which is in striking contrast Polypoid lesions are often encountered in the stomach and in most
with Japan where at least one-third of cancers are diagnosed at an cases they are hyperplastic polyps although on occasions adenoma-
early stage because of screening and, in those cases, <15% have tous polyps are present. The distinction between those polyps can
360
Figure 18.15 Three-dimensional reconstruction of the oesophageal wall of a patient with oesophageal spasm and segmental thickening of the muscularis propria. A targeted
myotomy in that segment resulted in marked clinical improvement.
EUS and the stomach
361
CHAPTER 18 Oesophagus and stomach
only be made histologically; however, endoscopic ultrasound may B). GISTs usually arise from the fourth layer (muscularis propria)
be of value prior to attempted endoscopic removal of polyps to of the stomach. The principles of diagnosis and management
assess vascularity and depth of invasion (Fig. 18.18). already covered under the oesophageal GISTs section equally apply
for the gastric GISTs. In most cases they are asymptomatic and if
Submucosal lesions and they are small (<2cm) no further action is usually necessary,
although some centres prefer a repeat EUS or CT scan a year later
hypertrophic folds to ensure no change in size. It is not uncommon for the larger of
these gastric GISTs to ulcerate and present with acute upper GI
The most common submucosal gastric benign tumour is GIST. The bleeding or pain. The role of endoscopic ultrasound in these cases
stomach is the commonest site of GISTs in the GI tract (Fig. 18.19A, is limited as surgical excision is usually recommended. In general,
surgery for a gastric GIST is technically easier, in contrast to the
oesophageal, where oesophagectomy is often required.
In those cases where the decision for surgery is not immediate,
EUS-guided FNA of the tumour is of value to clarify the histological
diagnosis and determine the degree of mitotic activity. EUS-guided
FNA is also useful in cases of extensive GISTs with high mitotic
activity, when preoperative chemotherapy with imatinib (Gleevec)
is being considered to reduce tumour size, to facilitate surgical
excision.
Other subepithelial lesions include lipomas, which are imaged as
homogeneous hyperechoic submucosal masses arising from the
third layer (Fig. 18.20). Carcinoid tumours present as small rela-
tively hypoechoic tumours arising from the second or third layers
(Fig. 18.21). An aberrant pancreas is presented as a hyperechoic
mass, usually in the antrum of the stomach with occasional ductal
structures present (Fig. 18.22).
Endoscopic ultrasound is often used to differentiate true subepi-
thelial/submucosal lesions from extramural compression (Fig.
18.23). Occasionally, the liver, gallbladder and splenic artery can
imprint on the wall of the stomach (Fig. 18.24). Endoscopic ultra-
sound will visually delineate the anatomy in such cases.
Endoscopic ultrasound is often used to investigate hypertrophic
gastric folds from diffuse pathological conditions, such as gastric
lymphoma or linitis plastica.42
In hypertrophic folds the mucosa and submucosa layers are
thickened but the muscularis and serosal layers are well
preserved. This is in contrast to diffuse malignant processes where
Figure 18.16 Advanced gastric adenocarcinoma with direct there is fusion of layers and extension depending on the disease
invasion of the liver (T4 disease). stage.
Lymph
node
Thickened
mucosa
A B
Figure 18.17 Gastric lymphoma. A: EUS appearances of early gastric MALT lymphoma confined to the superficial layers of the
stomach. The mucosa is thickened with irregular hypoechoic appearance. B: High-grade gastric lymphoma with nearby enlarged
lymph nodes.
362
EUS and the stomach
Gastric varices rounded echo-free structures beneath the mucosa and submucosa
of the fundus with colour flow detection (Fig. 18.25A, B). Further-
more, endoscopic ultrasound can visualise multiple tiny round
EUS performed with the latest generation of electronic scopes with hypoechoic areas within the submucosa of the stomach, which is a
colour flow and Doppler facilities has been particularly useful in pathognomonic finding of portal hypertensive gastropathy. Exami-
the detection of gastric varices; not only in fundal varices but also nation of the deeper structures in these patients usually reveals
in cases of ectopic varices, which are often misdiagnosed as poly- dilation of the mesenteric veins with extensive collateral circulation
poid lesions in the stomach. Gastric varices display as multiple in the perigastric area. With the modern echo-endoscopes with
Polyps
Varices
Figure 18.18 Presence of gastric polyps (hyperechoic Figure 18.20 Gastric lipoma appears as a hyperechoic lesion
protruding into lumen lesions) in a patient with portal hypertension arising from the third layer of the stomach.
and gastric varices (tortuous hypoechoic areas).
A B
Figure 18.19 GIST in the stomach. A: Malignant GIST arising from the fundus of the stomach infiltrating the left lobe of the liver.
The lesion is heterogeneous with necrotic centre in one area and lobular irregular appearance. B: Benign GIST (leiomyoma) that appears
as a round hypoechoic area arising from the fourth layer of the stomach wall.
363
CHAPTER 18 Oesophagus and stomach
Figure 18.21 EUS appearance of a gastric carcinoid. The Figure 18.22 Incidental finding of a pancreatic rest in the
lesion appears relatively hypoechoic arising from the second layer of antrum of the stomach.
the stomach.
Debris
364
EUS and the stomach
Gastric
varices
Ai Aii
Tumour
Ectopic
varices
Figure 18.25 Gastric varices. A: Gastric fundal varices appear as tortuous hypoechoic areas within the gastric wall with (i) standard
B-mode EUS and (ii) under power flow EUS. B: Multiple gastric ectopic varices under colour power flow EUS in a patient with splenic vein
thrombosis due to neuroendocrine tumour of the tail of pancreas.
Doppler facilities, thrombosis of the portal or splenic vein can also and benign disease should always be done histologically.
be identified. The appearances of benign ulcers are those of hypoechoic
More recently, endoscopic ultrasound-guided therapy has been thickening of the area surrounding the ulceration, while
attempted for difficult cases to control gastric variceal bleeding. coexisting fibrosis may present as a linear hyperechoic area at the
Cyanoacrylate (superglue) or thrombin has been used real-time to ulcer base.
obliterate bleeding gastric varices. Alternative techniques used in
our department include the use of a therapeutic endoscope with
injection of thrombin under mini-probe guidance (Fig. 18.26). At
present the role of endoscopic ultrasound in portal hypertension is
still under investigation but this technique appears to be invaluable
for complex cases and can be of assistance in the diagnosis and
treatment.35,36 Stomach
EUS is a complementary technique in the staging of gastric
Duodenum cancer, particularly in cancer of the cardia (junctional), to assess
the extension into the oesophagus, but it has a relatively more
In general the value of endoscopic ultrasound in the duodenum is limited role in the decision-making for surgical resection of gastric
limited because of the rarity of malignancy in this area. However, cancer of the body and antrum.
as in the oesophagus and the stomach, it can be of particular value EUS is of value in the investigation of thickened gastric wall to
in the assessment of duodenal lymphoma, duodenal carcinoma and differentiate gastric linitis plastica from gastric lymphoma or other
benign submucosal tumours (Fig. 18.27). causes of submucosal lesions including gastric varices.
EUS performed with colour flow and Doppler facilities is
particularly useful in the detection of gastric varices, both fundal
Peptic ulcer disease varices and ectopic, which are sometimes misdiagnosed as
polypoid lesions in the stomach. EUS-guided treatment of difficult
The role of endoscopic ultrasound is limited in the investigation of cases of bleeding ectopic varices is gaining wider acceptance.
benign gastroduodenal ulcers. Differentiation between malignancy
365
CHAPTER 18 Oesophagus and stomach
Varices
366
Base of
aortic arch
Tumour
Tumour
Tumour
Figure 18.28 Example of a 3D EUS reconstruction in a patient with oesophageal cancer who was treated with radiotherapy.
EUS in upper GI tract: present and future
367
CHAPTER 18 Oesophagus and stomach
368
19
CHAPTER
Small intestine
Peter M. Rodgers
position and often reduces the amount of soft tissue between probe lymphadenopathy etc. should be sought. The vascularity of the
and target loops. In adult female patients transvaginal scanning abnormal segment should be assessed with colour and power
may give excellent views of pelvis small bowel loops. Doppler.
If a suspicious bowel segment is identified, it should be Diseases in the caecum and appendix are dealt with elsewhere,
specifically examined for bowel thickening and alteration in but it is always valuable to record the finding of a normal appendix,
individual bowel layers (see below). Extraintestinal abnormalities and essential to document whether the appendix has been identified
such as thickened mesenteric fat, interloop fluid, exudates, or not when other pathology is demonstrated in the right iliac fossa.
Ultrasound technique
Focused bowel ultrasound should always be accompanied with a
THE ULTRASOUND APPEARANCE OF
general examination of the abdomen and pelvis. NORMAL SMALL BOWEL WALL
Lower-frequency probes are essential for examining bowel loops
in deeper recesses. At diagnostic transabdominal US frequencies, under favourable
Higher-frequency probes are essential for detailed analysis of conditions, five distinct bowel wall layers can be discerned. Viewed
bowel wall changes. transversely these are appreciated as concentric circles of alternat-
Graded compression brings bowel loops within reach of the ing hyper- and hypoechogenicity. These layers approximate to the
high-frequency probe and displaces bowel gas. histological structures (Fig. 19.2):
Specific bowel settings should be defined or optimised (with the 1. superficial mucosa (fine bright line)
application specialist if necessary). 2. deep mucosa including the lamina propria (grey)
3. submucosa (bright)
4. muscularis propria (dark)
5. serosa (fine bright line)
Comparison of histological measurements with in-vivo and
in-vitro ultrasound measurements indicate that strong interface
echoes tend to exaggerate the thickness of the submucosa at the
expense of the adjacent hypoechoic layers.2 The visibility of the fine
bright interface reflections of the serosa/adventitia and the super-
ficial mucosa is highly dependent on the echogenicity of adjacent
structures and is most easily seen where there is fluid in the bowel
lumen or ascites between bowel loops.
At lower diagnostic frequencies and less favourable conditions at
least the two most prominent layers are evident: the bright submu-
cosa (third layer) and the dark muscularis propria (fourth layer),
Lumen
Figure 19.2 Normal small bowel ultrasound. A: Graphic representation of a transverse US view of distal small bowel demonstrating
the five-layer structure. B, C: Transverse US images of normal distal small bowel in contracted and distended states. Only the bright
submucosa and dark muscularis propria are easily discernible.
370
Crohns disease
due to their relative thickness and high contrast. The deep mucosa exaggerated, distorted, diminished or obliterated. The high resolu-
is of similar thickness but being of intermediate echogenicity is tion of US provides a unique opportunity to identify the specific
more easily lost against the luminal contents. bowel layers affected, to characterise the lesions and diagnose the
The normal small bowel wall is up to 23mm thick,3,4 varying underlying process.
with the state of contraction/relaxation (Fig. 19.2). Small bowel
folds consisting of mucosa and submucosa, but not muscularis Bowel lumen
propria, extend into the lumen. In the jejunum these folds are taller,
slightly thicker and more numerous than in the ileum where folds
Commonly when the bowel wall is thickened, the bowel lumen is
are absent or sparse; in the collapsed state at fasting US examina-
compromised, becoming narrowed or strictured. An uncommon
tion, jejunal folds fill the lumen and may be perceived as a herring
exception to this is aneurysmal dilatation, where the lumen in the
bone pattern.
diseased segment enlarges; this is a particular feature of intestinal
Peristaltic waves pass along small bowel segments at a frequency
lymphoma and thought to be due to destruction of the autonomic
determined by multiple factors, such as gastric distension. As elec-
nerve plexus in the bowel wall by infiltrating tumour.6
tive US examinations are usually performed after a period of
Dilatation of the bowel lumen is seen proximal to the obstructing
fasting, the intestines are generally observed in a quiescent state but
lesion, where it may initially be accompanied by increased peristal-
some peristalsis should be seen in healthy bowel segments.
sis. Dilatation with no peristalsis may be due to late stage obstruc-
Slung in the peritoneal cavity on a long mesentery, the small
tion or paralytic ileus (most commonly seen after abdominal
bowel is mobile and adjacent loops are easily displaced by compres-
surgery).
sion. Healthy small bowel is easily compressed (note: excessive
compression may give false measurements).
The intestinal blood supply runs in the mesentery to the Bowel plasticity/mobility/peristalsis
mesenteric border of the bowel and branches (vasa recta) extend
around to the antimesenteric border, perforating at intervals to Most disease processes result in stiffening of the affected bowel
access the bowel wall. In health these bowel wall vessels are barely, segment(s), which is observed at US as more rigid, less compress-
if at, all visible on colour or power Doppler.5 ible, less easily displaced and with reduced or absent peristalsis.
In optimal conditions, small oval mesenteric lymph nodes may
be demonstrated, but if easily seen, numerous or enlarged, these Altered blood flow
should be considered significant and an intestinal cause sought.
Mesenteric fat within the visceral peritoneum is commonly Where an abnormal bowel segment or mass is identified, examina-
observed as alternating hypo- and hyperechoic bands, which may tion with colour or power Doppler may usefully demonstrate an
cause confusion, mimicking longitudinal sections of bowel loops. associated alteration in blood flow (e.g. hyperaemia in actively
This is easily solved by altering the plane of interrogation when the inflamed segments).
bands persist and are confirmed not to be tubular structures.
Extramural changes
THE ULTRASOUND APPEARANCES OF Bowel wall disease may extend out to involve adjacent loops or
ABNORMAL SMALL BOWEL solid organs, or be the result of external disease involving the bowel
loop. Direct or secondary involvement of mesenteric structures may
Before considering specific diseases of the small bowel it is worth also be seen.
noting the general characteristics altered by pathology that may be
observed at US, which form a useful checklist during examinations. Mesenteric lymphadenopathy
These are as follows:
n bowel wall thickness Lymph node size, shape (oval/round), echotexture (hyper/
n bowel wall layers hypoechoic, heterogeneous), smooth or irregular surface,
n bowel lumen conglomeration/matting, should be documented as these may aid
n bowel plasticity/mobility/peristalsis in narrowing the diagnosis.
n altered blood flow
n mesenteric/interloop changes.
The most common US feature of small intestinal pathology is thick- Crohns disease (CD) is a lifelong inflammatory gastrointestinal
ening of the bowel wall, which may be focal or diffuse, circumfer- condition of uncertain aetiology characterised by episodes of remis-
ential or segmental. Thickening may be due to the presence of sion and relapse and the development of serious complications. The
oedema, haemorrhage, inflammation, tumour growth or infiltra- disease course may be modified by medical therapy but 90% will
tion. Any of these may result in the classic US feature of a hypoe- require surgery within 10 years of diagnosis.7 US has a useful role
choic circumferential thickening around a strong echogenic centre
(lumen),variously referred to as the target sign, ring sign or pseudo-
kidney sign. Abnormal small bowel US features
Tumours may produce focal expansion towards/into the bowel
Small bowel wall thickness >3mm is probably abnormal; > 4mm
lumen (endoeccentric) to produce a polyp or polypoid mass, or
is definitely so.
away from the lumen (exoeccentric) into the peritoneal cavity dis-
Bowel wall thickening may be due to oedema, haemorrhage,
placing adjacent bowel loops.
inflammation/infection or tumour.
Thickened bowel wall segments should be interrogated for
Bowel wall layers changes in bowel wall layers, altered vascularity, perienteric fluid
or fat proliferation.
Where bowel wall thickening is observed with high-frequency If bowel wall is thickened, check lymph nodes and liver.
transducers, the normal bowel layer pattern may be preserved,
371
CHAPTER 19 Small intestine
in diagnosing CD,8,9 assessing and monitoring disease activity and Bowel wall thickening diagnostic threshold
identifying complications.10
CD may involve any part of the gastrointestinal tract and may The earliest changes of mucosal interface interruption and thicken-
involve multiple segments at the same or different times. Large ing limited to the mucosal layer may be subtle, insensitive and open
bowel disease, ileocolic and terminal ileal disease are the most to inter-observer error. Reliance therefore tends to be placed on
common patterns with the terminal ileum being involved in up to absolute measurements of bowel wall thickening. The normal small
75% of cases at presentation. Proximal small bowel CD without bowel wall thickness is taken to be up to 3mm (this varies consider-
terminal ileal involvement is seen in only 3% of cases.11 ably with peristaltic distension and contraction). The sensitivity and
The inflammatory process may extend through all the bowel specificity for the diagnosis of CD by wall thickening is determined
layers and beyond, resulting in intraperitoneal disease and involve- by the threshold set for defining abnormal thickness. A meta-
ment of adjacent bowel loops and/or organs. analysis of studies using US measurements of wall thickening to
Inflammatory episodes commence in the mucosa with an immune diagnose CD reported an 88% sensitivity and 93% specificity with
response to the trigger event(s). Through leaky vessels, an initially a diagnostic threshold of >3mm, changing to 75% and 97% respec-
humoral and subsequently cellular immune response results in tively when the threshold is raised to >4mm.14
thickening of the mucosal layer and damage to the mucosal surface.
The submucosa generally thickens in response to the hypervascu-
larity or inflammatory cellular infiltration. But CD is characterised Bowel wall layers (mural stratification)
by transmural inflammation that extends out to involve the muscu- Careful examination of the involved segment may show one of the
laris propria and serosa, interrupting sonographic layers and blur- following patterns:
ring or completely obliterating stratification in either a segmental
1. Isolated thickening of the mucosa (Figs 19.3, 19.4) which
or circumferential fashion.
may be accompanied by interruption of the lumen-interface
As the inflammation becomes more chronic, fibrosis may make
echo (layer 1) due to sloughing of the mucosal surface, and/
this exaggeration or loss of stratification permanent. The inflamed
or tiny bright echoes due to gas in mucosal ulcers.
segment becomes more rigid and less compressible, with the loss
2. Thickening of the mucosa and submucosa with clear
of normal peristaltic activity. Where there is circumferential involve-
preservation of the bowel layers (Fig. 19.5) producing a
ment of the bowel wall, the lumen becomes narrowed and there
target sign.
may be dilatation of the proximal healthy bowel. Asymmetrical
3. Segmental or circumferential hypoechoic thickening of the
involvement of the bowel wall with disease predominantly affect-
full thickness of the bowel wall with the layers being
ing the mesenteric border may result in ballooning of the anti-
indistinct or completely absent (Figs 19.6, 19.7). Irregular
mesenteric wall (pseudo-sacculation).
Clinical features of CD
Muscularis
Patients with CD may present at any age, but most commonly in (long thin arrow)
Submucosa
late teens and early adulthood.
Diarrhoea of more than 6 weeks duration, abdominal pain and
weight loss are the most common presenting symptoms. The young
patient with right iliac fossa pain and a mass may easily be misdi-
agnosed as having acute appendicitis. Blood and/or mucus in the
stool generally indicate colonic involvement. Perianal fistulas are
present in 10% of patients at presentation.12 Extraintestinal involve-
ment is also common, particularly an associated inflammatory
arthropathy.
Crohns disease
Patients are often children or young adults and most commonly
have a history of diarrhoea and abdominal pain. B C
US is very good at identifying terminal ileal and ileocolic CD.
Bowel layers may be separately thickened, or bowel layers may Figure 19.3 Crohns disease: acute terminal ileitis with
be indistinct/blurred or obliterated by hypoechoic transmural mucosal thickening only. A young adult female presented with
inflammation. diarrhoea and weight loss. A: Longitudinal US of distal ileum with
Actively inflamed segments show increased vascularity on power nodular thickening of mucosa with normal submucosa and muscle
Doppler and associated lymphadenopathy. layers. B: Adjacent mesenteric lymphadenopathy. C: Spot image
Look for CD complications; stricture, abscess and fistula. from a concurrent barium study showing aphthous and shallow
terminal ileum ulcers (white arrows).
372
Crohns disease
Muscularis Submucosa
Lumen Mucosa
i ii
A B
Figure 19.5 Crohns disease: acute ileitis (preserved layers). Longitudinal (A) and transverse (B) images of ileum showing thickened
mucosa (interrupted long white arrow), thickening submucosa (long solid white arrow) but normal muscle layer (short white arrow) and no
peri-intestinal fat wrapping or fluid.
Figure 19.6 Crohns disease: acute ileitis with segmental transmural inflammation.
Transverse scan of distal ileum demonstrating thickening of mucosa and submucosa (pattern 2) with
a small segment of transmural inflammation breaching the submucosa (white arrow).
Figure 19.7 Crohns disease: circumferential transmural inflammation. A: Transverse scan of a diseased segment of distal ileum. The
inflamed wall is thickened and hypoechoic with loss of layers (long white arrow). The lumen is narrowed. The segment is surrounded by
subserosal creeping fat (short white arrows). B: Longitudinal scan of the same bowel segment. Transmural hypoechoic thickening with
deep ulcers and inflammatory exudate on the serosal surface.
A
B
Fistula
In up to one-third of patients, penetrating fissures can extend to
create an abnormal communication between the lumen of the
disease bowel segment and adjacent bowel loops (enteroenteric or
enterocolic fistula), the skin (enterocutaneous fistula) or any adja-
cent hollow organ (uterus, bladder etc.).
The communication between adherent bowel loops may be dif-
ficult to identify and underestimated by all imaging modalities. At
US fistulas are identified as irregular tubular hypoechoic tracks20
(Fig. 19.11) and occasionally may demonstrate small hyper-reflective
air bubbles within (Fig. 19.13),21 but the presence of adjacent
indrawn, angulated bowel loops connected by mixed hypoechoic
inflammatory exudate is highly suspicious of fistula formation
(Fig. 19.12).
Disease activity
Figure 19.10 Crohns disease: abscess. A well-circumscribed
Management decisions in CD require reliable assessments of anterior abdominal wall abscess (long white arrow). Deep to the
disease activity. Clinical assessment and laboratory results are abscess is a bowel loop showing transmural inflammation (short
central and scoring systems such as the Crohns Disease Activity white arrow).
375
CHAPTER 19 Small intestine
A B
Figure 19.11 Crohns disease: enterocutaneous fistula. A and B: Irregular hypoechoic fistula (long white arrows) track through the
anterior abdominal wall and subcutaneous tissues.
Figure 19.12 Crohns disease: enteroenteric fistula. A: Interloop inflammatory exudate is seen between the thickened hypoechoic
bowel loop (white arrow) and adjacent normal bowel loops. B: Power Doppler scan demonstrates hyperaemia in the inflammatory exudate.
for imaging investigations. Exceptions to this are a group of infec- The absence of transmural inflammatory changes/complications
tions that mimic acute appendicitis, and chronic infections, particu- and the relatively short course of symptoms help to distinguish
larly intestinal tuberculosis, that may mimic inflammatory bowel acute infectious ileocaecitis from Crohns disease. Most importantly,
disease. this condition is distinguished from acute appendicitis and an
unnecessary operation avoided.
Infectious ileocaecitis
Intestinal tuberculosis
Yersinia, Campylobacter and Salmonella bacteria are well-known
causes of acute diarrhoeal illnesses, usually self-limiting, diagnosed In Western countries, where tuberculosis is no longer endemic, this
symptomatically and not intentionally referred for imaging disease has re-emerged particularly in migrant populations and
investigations. those immunocompromised by HIV/AIDS.
Uncommonly, however, these organisms may produce an enteric Non-specific symptoms such as abdominal pain, weight loss,
infection confined to the ileocaecal region, patients presenting anaemia and fever predominate but patients may present with
with right iliac fossa symptoms of pain and tenderness; diarrhoea symptoms of intestinal obstruction or palpable abdominal mass.
may be minimal or absent. The severity of symptoms varies but in Though any part of the gastrointestinal tract can be affected, ile-
more acute cases may result in unnecessary appendectomy, and in ocaecal involvement is most common but isolated ileal or jejunal
more protracted cases may be mistaken for Crohns disease or disease does occur and is a particular feature of atypical tuberculo-
appendix mass. sis (e.g. Mycobacterium avium intracellulare).
Ultrasound examination reveals a symmetrical thickening of the Ultrasound features25,26 include bowel thickening with luminal
wall of the terminal ileum and caecum confined to the mucosal and narrowing and superficial or deep ulcers. Typically the bowel thick-
submucosal layers with no extension to the muscularis, serosa or ening involves the terminal ileum, ileocaecal valve and caecum
beyond into the mesentery. It has been reported that the extent of (Figs 19.15, 19.16). Lymphadenopathy is common and may form
caecal/colonic involvement may vary with the specific pathogen.24 conglomerate (matted) lymph node masses. Bowel loops may be
Local mesenteric lymph nodes are usually enlarged. The visualised matted together by interloop exudates or abscesses. Extraintestinal
appendix is normal (Fig. 19.14). disease may produce ascites or peritoneal thickening.
A B
A B
377
CHAPTER 19 Small intestine
Figure 19.16 Ileocaecal tuberculosis. This 47-year-old Asian woman with previous pulmonary TB presented with weight loss and
abdominal pain. A: Sonogram showing an irregular, hypoechoic contracted caecum, the ileocaecal valve (arrowhead) and thickened
terminal ileum with distorted but preserved stratification. B: Doppler US showed no hyperaemia. C: An earlier CT scan of the same patient
showing the thickened contracted caecum (white arrow), fixed, open ileocaecal valve (arrowhead), a dilated terminal ileum, and multiple
enlarged mesenteric lymph nodes (interrupted white arrows).
378
Small bowel vasculitis
Target organs/bowel
Type of vasculitis Affected vessel type/size segments Bowel lesions/complications
Polyarteritis nodosa Medium to smaller arteries Kidneys, liver, intestines Penetrating ulcers/haemorrhagic infarcts
Rheumatoid vasculitis Medium sized vessels Joints/intestines Segmental infarction/intestinal strictures
Systemic lupus Small vessels Small intestine Segmental necrosis/perforation
erythematosus
HenochSchnlein Post-capillary venulitis Small intestine (distal ileum) Gastrointestinal bleeding, mucosal/
purpura submucosal haemorrhage/ulcers/
intussusception
Behets syndrome Small vessels Skin/joints/CNS intestines Shallow/deep ulcers/perforation
(ileocaecal)
ChurgStrauss Large vessels Lung/skin/intestines (small Ulcers/necrosis/perforation
syndrome and large)
Data from Herlinger H, Maglinte DT, Birnbaum BA. Clinical Imaging of the Small Intestine, 2nd Edition, Springer, 2001.
379
CHAPTER 19 Small intestine
A B
seen. Studies differ on distinguishing between inflammation and to full-blown obstruction), bleeding (usually non-visual but
ischaemia on wall thickening alone30,31 but US colour/power occasionally as frank haemorrhage), and uncommonly with a pal-
Doppler may show normal, reduced or absent blood flow in the pable mass.
ischaemic bowel wall in contrast to the hyperaemia of acute inflam-
matory conditions32 (Fig. 19.17). Malignant small bowel tumours
About two-thirds of symptomatic small bowel tumours are malig-
SMALL BOWEL TUMOURS nant and over 95% of these are adenocarcinomas, carcinoids, lym-
phomas or sarcomas (malignant gastrointestinal stromal tumours
Primary small bowel tumours are rare. Although the small bowel or leiomyosarcomas).30
constitutes 75% of the length and 90% of the surface area of the
gastrointestinal tract, it is the site of only 25% of benign and less Adenocarcinoma
than 5% of malignant gastrointestinal tract tumours. Large bowel
Adenocarcinomas are the most common primary small bowel
cancer is 60 times more common. Protective factors may include,
malignancy and usually develop in the duodenum or proximal
among others, rapid cell turnover, fast transit times, alkaline intes-
jejunum. There is an increased risk of adenocarcinoma in long-
tinal contents and the scarcity of bacteria.33
standing Crohns disease and these lesions may occur in the ileum.
Sonographically these tumours may be intraluminal or intramu-
Clinical presentation ral, annular, polypoid or infiltrative, echogenic masses or target
lesions (Fig. 19.18).34,35 The lesions spread to lymph nodes, liver and
Symptomatic lesions, whether benign or malignant, most com- peritoneum. Lymphadenopathy is usually less marked than with
monly present with abdominal pain (intermittent or progressing lymphomas.
380
Small bowel tumours
A B
Figure 19.18 Primary intestinal adenocarcinoma. A 53-year-old man presented with abdominal pain and vomiting. A: US Long view of
an hypoechoic annular tumour (white arrow) with an irregular surface occluding the third part of the duodenum deep to the superior
mesenteric artery (arrowhead). B: US transverse scan of the tumour beneath the SMA.
A B C
382
Small bowel tumours
A B
Figure 19.21 Ileal lymphoma. Middle-aged HIV-positive man. A: Transverse US scan showing a small bowel lesion with hypoechoic
circumferential wall thickening. B: Barium study confirming the small circumferential lesion in the ileum (white arrow). Non-Hodgkins
lymphoma was confirmed on US-guided percutaneous needle biopsy.
A B
Figure 19.22 Exophytic GIST tumour. A 62-year-old man presented with acute intestinal haemorrhage. RIF US scan shows a large,
mixed echogenicity, dumbbell-shaped tumour (A) which demonstrates central anechoic necrotic cavities and hypervascularity on Doppler
scan (B), and (C) a gas-filled ulcer (white arrow) on the surface of the tumour (arrowhead) in the bowel lumen. US-guided needle biopsy
confirmed the diagnosis prior to therapy.
383
CHAPTER 19 Small intestine
A B
Figure 19.23 Serosal/peritoneal metastatic tumour deposits. A 57-year-old woman had intra-abdominal secondary tumours at
the time of presentation with a primary caecal adenocarcinoma. US-guided needle biopsy allowed histological confirmation prior to
chemotherapy, avoiding colonoscopy. A: Right iliac fossa US scan showed a 2cm diameter echogenic peritoneal/serosal secondary.
B: Concurrent CT scan image showing the metastatic deposit (thick white arrow) and the caecal primary tumour beneath (long white
arrow).
Intussuscipiens Intussusceptum
Indrawn
mesentery
B
A Sandwich
Lymph nodes in a
crescent of mesenteric fat
i ii
D
C
Figure 19.24 Intussusception. A: Graphic illustration of an intussusception showing the relationships of indrawn inner bowel segment
(intussusceptum) and associated mesentery including vessels and nodes within the outer bowel sleeve (intussuscipiens). B: Doughnut sign.
Transverse sonogram showing the thick ring of two outer bowel walls (short white arrow) and the bright centre of mesentery and nodes
(long white arrow). C: Crescent in doughnut sign. Transverse sonogram and accompanying graphic showing the crescent of mesenteric fat
and nodes around the collapsed indrawn bowel segment the intussusceptum. D: Sandwich sign. Longitudinal sonogram showing the
outer layers (white arrow), the intussuscipiens (interrupted arrow) and mesenteric lymph nodes (white arrowhead).
REFERENCES
1. Puylaert JB. Ultrasound of acute GI tract conditions. Eur Radiol
2001;11:18671877.
2. Kimmey MB, Martin RW, Maggitt RC, et al. Histologic correlates of
gastrointestinal ultrasound images. Gastroenterology 1989;96:
433441.
3. Fleicher AC, Muhletaler CA, James AR Jr. Sonographic assessment of
the bowel wall. AJR Am J Roentgenol 1981;136:887891.
4. Hata J, Haruma K, Yamanaka H, et al. Ultrasonographic evaluation of
the bowel wall in inflammatory bowel disease: comparison of in vivo
and in vitro studies. Abdom Imaging 1994;19:395399.
5. Esteban JM, Maldonaldo L, Sanchiz V, et al. Activity of Crohns
disease assessed by colour Doppler ultrasound analysis of the affected
loops. Eur J Radiol 2001;11(8):14231428.
6. OMalley ME, Wilson SR. US of Gastrointestinal tract abnormalities
with CT correlation. Radiographics 2003;23(1):5972.
7. Gardiner KR, Dasari BV. Operative management of small bowel
Crohns disease. Surg Clin North Am 2007;87:587610.
8. Sheridan MB, Nicholson DA, Martin DF. Transabdominal sonography
as the primary investigation in patients with suspected Crohns
disease or recurrence; a prospective study. Clin Radiol
1993;48:402404.
9. Parente F, Greco S, Molteni M, et al. Role of early ultrasound in
detecting inflammatory intestinal disorders and identifying their
anatomical location within the bowel. Aliment Pharmacol Ther
2003;18:10091016.
10. Maconi G, Bollani S, Bianchi Porro G. Ultrasonographic detection of
intestinal complications in Crohns disease. Dig Dis Sci
1996;41:16431648.
Figure 19.25 Small bowel obstruction. A subsequent sonogram 11. Thoreson R, Cullen JJ. Pathophysiology of inflammatory bowel
of the patient with metastatic peritoneal tumours, as bowel disease. Surg Clin North Am 2007;87:575585.
obstruction developed (Fig. 19.23). demonstrating dilated, fluid-filled 12. Stange EF, Travis SP, Vermeire S, et al. European evidence based
jejunal loops, characterised by the fold length and frequency. Cine consensus on the diagnosis and management of Crohns disease:
loops capture the typical increased peristalsis with to and fro definitions and diagnosis. CCO Gut 2006;55;i1i15.
movement of liquid and more solid contents. 13. Fraquelli M, Colli A, Casazza G, et al. Role of US in detection of
Crohns disease: meta-analysis. Radiology 2005;236:95101.
14. Fraquelli M, Colli A, Casazza G, et al. Role of US in detection of Crohn
disease: meta-analysis. Radiology 2005;236:95101.
15. Hata J, Haruma K, Suenaga K, et al. Ultrasonographic assessment of
inflammatory bowel disease. Am J Gastroenterol 1992;87:443447.
16. Sheehan AL, Warren BF, Gear MW, et al. Fat-wrapping in Crohns
disease: pathological basis and relevance to surgical practice. Inflamm
Bowel Dis 2008;14(11):15551561.
17. Kratzer W, Schmidt SA, Mittrach C, et al. Contrast-enhanced
wideband harmonic imaging ultrasound (SonoVue): a new technique
for quantifying bowel vascularity in Crohns disease. Scand J
Gastroenterol 2005;40(8):985991.
18. Maconi G, Bollani S, Bianchi Porro G. Ultrasonographic detection of
intestinal complications in Crohns disease. Dig Dis Sci
1996;41:16431648.
19. van Oostayen J, Wasser M, van Hogezand R, et al. Doppler
sonography evaluation of superior mesenteric artery flow to assess
Crohns disease activity. AJR Am J Roentgenol 1997;168:429433.
20. Gasche C, Moser G, Turetschek K, et al. Transabdominal bowel
sonography for the detection of intestinal complications in Crohns
disease. Gut 1999;44:112117.
21. Sarrazin J, Wilson S. Manifestations of Crohns disease at US.
Radiographics 1996;16(3):499520.
22. Ruess L, Nussbaum Blask AR, Bulas DI, et al. Inflammatory bowel
disease in children and young adults: correlation of sonographic and
clinical parameters during treatment. AJR Am J Roentgenol
2000;175:7984.
23. Drews BH, Barth TF, Hnle MM, et al. Comparison of sonographically
measured bowel wall vascularity, histology and disease activity in
Crohns disease. Eur Radiol 2009;19:13791386.
24. Puylaert JB, Van der Zant FM, Mutsaers JA. Infectious ileocaecitis
caused by Yersinia, Campylobacter, and Salmonella: clinical,
radiological and US findings. Eur Radiol 1997;7:39.
Figure 19.26 US-guided needle biopsy. The linear echogenic 25. Kedar RP, Shah PP, Shivde RS, et al. Sonographic findings in
cutting needle (white arrow) is shown within the circumferential gastrointestinal and peritoneal tuberculosis. Clin Radiol 1994;49:
2429.
hypoechoic small bowel lesion.
26. Sharma MP, Bhatia V. Abdominal tuberculosis. Indian J Med Res
2004;120:305315.
27. Shirahama M, Takafumi K, Ishibashi H, et al. Intestinal anisakiasis: US
in diagnosis. Radiology 1992;185:789793.
28. Frisoli JK, Desser TS, Jeffrey RB. Thickened submucosal layer: a
sonographic sign of acute gastrointestinal abnormality representing
386
References
submucosal edema or hemorrhage. AJR Am J Roentgenol 40. Nylund K, degaard S, Hausken T, et al. Sonography of the small
2000;175:15961599. intestine. World J Gastroenterol 2009;15(11):13191330.
29. Teefey SA, Roarke MC, Brink JA, et al. Bowel wall thickening: 41. Burkill GJ, Badran M, Al-Muderis, et al. Malignant gastrointestinal
differentiation of inflammation from ischaemia with color Doppler stromal tumour: distribution, imaging features, and pattern of
and duplex US. Radiology 1996;198:547551. metastatic spread. Radiology 2003;226:527532.
30. Seigel MJ, Friedland JA, Hildebolt CF. Bowel wall thickening in 42. Byrne AT, Goeghegan T, Govender P, et al. The imaging of
children: differentiation with US. Radiology 1997;203:631635. intussusception. Clin Radiol 2005;60:3946.
31. Teefey SA, Roarke MC, Brink JA, et al. Bowel wall thickening: 43. del-Pozo G, Intussusception: US findings with pathologic correlation
differentiation of inflammation from ischaemia with color Doppler the crescent in doughnut sign. Radiology 1996;199:688692.
and duplex US. Radiology 1996;198:547551. 44. Chaubal N, Dighe M, Shah M, et al. Sonography of the gastrointestinal
32. Shirahama M, Umeno Y, Tomimasu R, et al. The value of colour tract. J Ultrasound Med 25:8797.
Doppler ultrasonography for small bowel involvement of adult 45. Hardy SM. The sandwich sign. Radiology 2003;226:651652.
Henoch-Schnlein purpura. Br J Radiol 1998;71:788791. 46. Montali G, Croce F, De Pra L, et al. Intussusception of the bowel: a
33. Neugut AI, Jacobson JS, Suh S, et al. The epidemiology of cancer of new sonographic pattern. Br J Radiol 1983;56:621623.
the small bowel. Cancer Epidemiol Biomarkers Prev 1998;7:243251. 47. Mateen MA, Saleem S, Chandrasekhar Rao P, et al. Transient small
34. Bin W, Jianguo L, Baowei D. Sonographic appearances of small bowel bowel intussusceptions: ultrasound findings and clinical significance.
tumours. Clin Radiol 1992;46:3033. Abdom Imaging 2006;31(4):410416.
35. Maglinte DT, Herlinger H. Small bowel neoplasms. In: Herlinger H, 48. Ko YT, Lim JH, Lee DH, et al. Small bowel obstruction: sonographic
Maglinte DD, Birnbaum BA, editors. Clinical imaging of the small evaluation. Radiology 1993;188(3):649653.
intestine. New York: Springer-Verlag; 2001. p. 377438. 49. Castiglione F, Rispo A, Cozzolino A, et al. Bowel sonography in adult
36. Rioux M, Langis P, Naud F. Sonographic appearance of primary small celiac disease: diagnostic accuracy and ultrasonographic features.
bowel carcinoid tumour. Abdom Imaging 1995;20(1):3743. Abdom Imaging 2007;32:7377.
37. Chua SC, Rozalli FI, OConnor SR. Imaging features of primary 50. Tudor GR, Rodgers PM, West KP. Bowel lesions: percutaneous
extranodal lymphomas. Clin Radiol 2009;64:574588. US-guided 18-gauge core biopsy preliminary experience. Radiology
38. Goerg C, Schwerk WB, Goerg K. Gastrointestinal lymphoma: 1999;212:594597.
sonographic findings in 54 patients. AJR Am J Roentgenol 51. Ledermann HP, Binkert C, Frhlich E, et al. Diagnosis of symptomatic
1990;155:795798. intestinal metastases using transabdominal sonography and
39. Katz SC, DeMatteo RP. Gastrointestinal stromal tumours and sonographically guided puncture. AJR Am J Roentgenol
leiomyosarcomas. J Surg Oncol 2008;97:350359. 2001;176:155158.
387
CHAPTER
When the appendix has a deep orientation in the pelvis, patients Acute appendicitis
can present with diarrhoea as the inflamed appendix irritates the
rectum. In such cases graded compression with a forced upward Acute appendicitis is one of the commonest acute abdominal condi-
sweeping motion of the transducer can be useful. The upward tions presenting to the emergency department. The highest inci-
sweep of the transducer helps to move the caecum superiorly on to dence of appendicitis is in teenagers and young adults and there is
the psoas muscle and thereby increases the visibility of the entire a familial tendency to develop appendicitis. The clinical diagnosis
distal appendix (Fig. 20.3). of appendicitis may be overlooked and misinterpreted, leading to
Transverse and longitudinal scans of the abdomen should also delay in treatment or unnecessary surgery. Diagnosis of acute
be performed in order to detect atypical locations of the appendix. appendicitis in children can be particularly difficult as a significant
In obese individuals, 35MHz probes may be needed. Accurate proportion of patients present with atypical symptoms. Diagnosis
localisation of the appendix is useful as an atypical location may of appendicitis may also be delayed in infants as they are unable
alter the surgical approach. Once visualised, the appendix needs to to provide clinical information or localise pain.
be evaluated in its entirety as inflammation may only be located in Acute appendicitis occurs when the lumen of the appendix is
a small segment such as the appendiceal tip. Visualisation of a obstructed by a faecalith, mucous plug or fibrosis. Rarely the
normal-sized, compressible appendix has high negative predictive appendiceal orifice may be obstructed by tumours, infections or
value for acute appendicitis.4 foreign bodies. Perforation of the appendiceal wall may occur if
there is advanced inflammation and transmural necrosis. In older
children and adults the perforation is sealed off by the adjacent
omentum and therefore localised abscesses are formed. In younger
children, due to the smaller size of the omentum, perforation may
Postileal lead to widespread peritonitis. Conversely in obese patients, the
0.5% abundant mesenteric and omentum fat may mask symptoms of
appendicitis or perforation.
Caecum
Preileal In children appendicitis is invariably associated with vomiting
1% and aversion to food. Elderly patients have the highest mortality
rates as the usual signs and symptoms of appendicitis may be
Retrocaecal diminished or absent, which leads to a higher rate of perforation
74% and resultant greater morbidity and mortality. Acute appendicitis
is also the commonest non-gynaecological acute abdominal condi-
Terminal tion complicating pregnancy.
ileum Ultrasound plays a valuable role in the diagnosis of acute appen-
dicitis.1,57 Using ultrasound the appendix can be directly visual-
Subcaecal ised, thereby confirming or excluding appendiceal pathology.
1.5% Furthermore, complications related to appendicitis and alternative
diagnoses mimicking appendicitis may also be demonstrated using
Pelvic this modality. Ultrasonography has been shown to have similar
21% accuracy for detection of acute appendicitis as compared to CT
examinations.8
On ultrasonography the inflamed appendix is seen as a thick-
Figure 20.1 Schematic diagram showing locations of the ened, non-compressible, tubular structure at the site of tenderness
vermiform appendix. (Fig. 20.4). A layered appearance corresponding to the mural
A B
Figure 20.2 Normal appendix. A: Transverse view of the normal appendix (arrow) showing a layered mural pattern. Asterisk = caecum.
B: Longitudinal view of the normal appendix (arrow) showing a layered mural pattern.
389
CHAPTER 20 Appendix, colon and rectum
A B
A B
Figure 20.4 Acute appendicitis. A: Inflamed appendix seen as a tubular, non-compressible structure (arrow). The layered mural structure
is evident. B: Inflamed appendix containing an echogenic appendicolith (arrow) with posterior acoustic shadowing. Note inflamed, non-
compressible fat overlying the appendix (arrowheads).
structure can also be seen with high-frequency probes. Up to 30% heterogeneous with specular artefacts. A non-compressible appen-
of cases with appendicitis may have an intraluminal appendicolith.5 dix with an external diameter of greater than 6mm is the most
Appendicoliths are characteristically seen as highly reflective accurate predictor of acute appendicitis.6 The finding of a normal
lesions within the appendiceal lumen with posterior acoustic shad- appendix measuring less than 6mm has high negative predictive
owing (Fig. 20.4). Appendicoliths should be distinguished from air value (98%) for acute appendicitis.6
or inspissated faecal matter, which can produce similar acoustic Inflamed mesentery and omentum surrounding the appendix
shadowing, although the shadowing seen due to air tends to be appear non-compressible and of increased reflectivity. Most patients
390
Appendix
A B
A B
with acute appendicitis may also have enlarged mesenteric nodes is termed an appendiceal phlegmon. Usually these are treated con-
(Fig. 20.5). Inflammation also leads to hyperaemia and hyperper- servatively as surgery can be difficult in such cases. On ultrasonog-
fusion of the appendix, which manifests as increased colour Doppler raphy an appendiceal phlegmon is seen as a non-compressible,
signal in the appendix, mesentery and reactive lymph nodes poorly-defined mass. The mass is predominantly poorly reflective
(Fig. 20.5). but may have bright areas due to contained inflamed fat. Poorly
An irregular contour or disruption of the layered appearance of defined, linear, low reflective streaks may be seen that correspond
the appendix is suggestive of perforation or impending rupture to liponecrotic tracks and inflammatory adhesions (Fig. 20.7).
(Fig. 20.6). Other findings that are associated with perforation If a circumscribed pus collection is present, the mass is termed
include asymmetrical wall thickening, fluid collections, ileus and an appendiceal abscess. Abscesses are seen as fluid collections
increased pericaecal echogenicity (Fig. 20.6). Two of these findings with contained air pockets or fluid levels (Fig. 20.7). Most appendi-
loss of the submucosal layer and pericaecal fluid have been ceal abscesses resolve spontaneously; however, if pain and fever
reported to have a significant correlation with appendiceal persists percutaneous drainage under CT or US guidance may
performation.9 be necessary.
Once perforation occurs, there may be generalised peritonitis.
However, in the majority of cases, the peritoneal spillage is con-
tained in the right iliac fossa as the mesenteric fat and omentum Pitfalls and differential diagnosis
seal the perforation.
Patients with delayed presentation or with appendiceal perfora- A false positive diagnosis of acute appendicitis may be made in
tion may present with a right iliac fossa mass. Such a mass typically patients with intra-abdominal inflammation. The appendix may be
consists of the inflamed appendix with adherent omental and falsely thickened in patients with sigmoid diverticulitis, perforated
mesenteric fat, lymphadenopathy and inflammatory adhesions and peptic ulceration or inflammatory bowel disease.10 Caecal tumours
391
CHAPTER 20 Appendix, colon and rectum
A B
Figure 20.7 Appendiceal phlegmon and abscess. A: Phlegmon is seen as a large poorly reflective mass with internal bright areas
(arrow) inferior to the caecum (arrowheads). B: Appendiceal abscess with multiple fluid levels and air pockets (arrows).
Ultrasound in acute appendicitis older age group with the exception of carcinoid tumours. Many
primary appendiceal tumours present with symptoms similar to
Non-compressible, tender appendix with external diameter acute appendicitis and most tumours except for adenocarcinomas
>6mm. and carcinoids larger than 2cm are managed by appendicec-
Appendicoliths are present in up to a third of cases. tomy.14,15 All appendiceal tumours are associated with a high inci-
Lymphadenopathy is present in up to 50% of cases. dence of a synchronous and metachronous colonic tumours.15
Free fluid, asymmetric appendiceal thickening, mesenteric
inflammation and ileus are strongly suggestive of appendiceal
perforation. Mucocele
Retrocaecal and pelvic regions should be routinely assessed in A primary appendiceal mucocele is relatively rare, with reported
the patients with suspected appendicitis. incidence of 0.20.3%, and is more common in females than males.16
Most mucoceles are asymptomatic and found incidentally at surgery.
Mucoceles are usually benign and are formed due to obstruction of
may obstruct the appendiceal orifice with resultant dilatation the appendiceal orifice secondary to fibrosis, faecaliths or scarring.
leading to an incorrect diagnosis of appendicitis or an appendiceal The obstruction causes sterile accumulation of mucus within the
mass. A distended, non-tender appendix has been reported in appendiceal lumen leading to mucocele formation.
amoebic colitis. Malignant mucoceles occur secondary to mucin-secreting adeno-
The commonest cause of a false negative examination is the ina- carcinomas. If there is appendiceal perforation due to such a
bility to visualise the appendix on ultrasonography. Inability to mucocele, there is peritoneal seeding of the malignant cells leading
locate the appendix may be due to an atypical location; lack of an to pseudomyxoma peritonei.
adequate ultrasonographic window due to ileus; or generalised Mucoceles are usually incidental findings on ultrasonography
peritonitis that limits graded compression. Occasionally the normal and present as tubular, well-defined structures in the right lower
proximal appendix is demonstrated whereas the inflamed tip is abdomen (Fig. 20.8). A pear-shaped appearance has been described
overlooked, leading to a false negative examination. Furthermore, on ultrasonography. The contents may be of variable echogenicity;
inflammation and thickening of the terminal ileum secondary to however, low or intermediate reflectivity is typical and there may
appendicitis may be erroneously labelled as Crohns disease or be contained septations. Bright, reflective foci within the mass
infectious ileocolitis. or its wall may also be seen corresponding to dystrophic calcif
Many other clinical conditions may mimic appendicitis, and it is ication. Curvilinear mural calcification is a highly suggestive
important to distinguish between these conditions. These include feature on ultrasonography, although this is seen in only 50% of
caecal diverticulitis, infectious ileitis, mesenteric lymphadenitis, cases (Fig. 20.8).
ovarian cysts, tubo-ovarian abscesses, urological conditions, epip- It may be difficult to differentiate between benign and malignant
loic appendagitis, infective ileitis, inflammatory bowel disease and mucoceles. However, mucoceles resulting from benign obstruction
Meckels diverticulitis.11,12 The normal appendix may have a diam- rarely exceed 2cm in size, and larger mucoceles should be consid-
eter of greater than 6mm in patients who have undergone radio- ered to be malignant. Malignant mucoceles may demonstrate irreg-
therapy or those with cystic fibrosis.13 ular thickening of the wall and infiltration of the surrounding
Ultrasonography can be useful in distinguishing between these mesentery. Rarely, mucoceles may become infected and present
differential diagnoses. In patients with equivocal ultrasound find- with symptoms and ultrasonographic features indistinguishable
ings and especially in obese patients, CT examinations can be from acute appendicitis. Fluid levels and air pockets within a
useful. mucocele are indicative of a superadded infection. The differential
diagnosis of a mucocele includes a tubo-ovarian abscess, hydros-
alpinx, enteric duplication cysts and peri-appendiceal abscesses.
Appendiceal tumours
Primary tumours of the appendix are rare and are found in only
Carcinoid tumour
0.51.0% of appendicectomy specimens at pathological examina- The commonest primary appendiceal neoplasm is a carcinoid
tion. Most primary tumours affect individuals in the middle to tumour and they constitute up to 80% of primary appendiceal
392
Appendix
A B
Figure 20.8 Appendiceal mucoceles. A: Incidentally discovered cystic lesion of the appendix with low reflectivity, bright margins
and debris (arrow). B: Dense, curvilinear calcification with shadowing (arrow) in the right iliac fossa consistent with a calcified mucocele.
Asterisk = caecum.
A B
Figure 20.9 Appendiceal tumours. A: Longitudinal image of the right iliac fossa in a patient with suspected appendicitis shows a small
appendiceal mass at the tip of the appendix (arrow). Note infiltration of the adjacent mesentery (arrowhead). Carcinoid tumour was found
on surgery. B: 3D image of the right iliac fossa shows a large mass arising from the appendix (arrow). Adenocarcinoma was identified on
histopathology. Asterisk = caecum.
tumours.16 Most appendiceal carcinoid tumours are only detecta- cification may be present within the mass and there may be hyper-
ble at microscopic level and are incidentally discovered during vascularity on Doppler studies.
histological examination of an appendicectomy specimen. Most of
these incidentally discovered tumours are less than 1cm in size.17
Unlike carcinoids occurring at other gastrointestinal sites, appen-
Other tumours
diceal carcinoids are seen in younger adults and typically follow Primary adenocarcinomas of the appendix are very rare. Ultrasono-
an indolent course. Appendicectomy appears to be adequate graphic features of these tumours are that of a diffuse or focal
treatment for such incidentally detected tumours, although for enlargement of the appendix with adjacent lymphadenopathy (Fig.
tumours larger than 2cm a right hemicolectomy may need to be 20.9). Tumours may appear as solid, poorly reflective lesions or
performed. solid lesions with internal cystic changes.
Carcinoids may present with acute appendicitis. Larger tumours Lymphoma of the appendix may manifest as homogeneous thick-
are seen as poorly reflective masses and may show infiltrative and ening of the entire appendiceal wall. Aneurysmal dilatation of the
desmoplastic reaction in the surrounding mesentery (Fig. 20.9). Cal- appendix may be present.18
393
CHAPTER 20 Appendix, colon and rectum
Figure 20.10 Appendiceal Crohns disease. Transverse image Figure 20.11 Stump appendicitis. Patient with history of
of the right iliac fossa in a patient with known Crohns disease appendicectomy. A: Transverse image of the right iliac fossa shows
shows diffuse thickening of the appendix (arrow) with preserved a tubular structure with hyperaemia (arrow) at the caecal pole.
stratification and surrounding fibrofatty proliferation. A fistula is also Presumptive diagnosis of stump appendicitis was made. B: Axial
seen as a linear track (arrowheads). CT image confirms inflamed appendiceal stump (arrow).
394
Colon
be identified in the right iliac fossa by tracing down the colon from Some investigators have advocated using ultrasonography after
the hepatic flexure. Gentle compression on the abdomen using the instillation of a water or saline enema (hydrocolonic ultrasonography)
transducer helps to provide better views of the colon. The transverse for optimal assessment of the colon.2224 In this technique patients
and sigmoid colon may be variable in position as they are suspended need to ingest a large amount of oral electrolyte solution prior to
by their respective mesenteries within the peritoneal cavity. The the examination followed by warm water or saline enema. Com-
transverse colon can be scanned by following its contour in a trans- parison of hydrocolonic ultrasonography with optical colonoscopy
verse direction between the hepatic and splenic flexures. Similarly has not been promising.25 This has been mainly due to problems
the sigmoid colon is traced between the distal descending colon and with adequate bowel preparation, artefacts from faecal matter and
the rectum. In thin individuals and children, high-frequency linear the inability to obtain diagnostic images of all segments of the colon
transducers can be used that provide detailed colonic images. in large or obese patients. Furthermore, in view of other more sensi-
On transabdominal ultrasonography, the colon typically demon- tive tests (e.g. CT colonography) being available for evaluation of
strates a stratified mural pattern. Usually three layers can be identi- the colon, the use of this technique has fallen out of favour.
fied corresponding to the submucosa, mucularis propria and the
mucosa. Haustrations can be identified as indentations in the
contour of the bowel (Fig. 20.12). If there is sufficient intraluminal Congenital abnormalities
fluid in the colon or ascites, the entire mural structure may be visu-
alised. However, more often than not, there is air within the lumen Most anorectal and colonic congenital anomalies manifest in the
that obscures the colonic wall distal from the transducer. The paediatric population. In adult patients the congenital anomaly
normal thickness of the colonic wall is less than 3mm. If a lesion most commonly encountered is a colonic duplication cyst. Usually
associated with the colon is found, its true relation or attachment duplication cysts are asymptomatic, but occasionally they may per-
to the colon should be confirmed by observation during deep inspi- forate and cause intussusception or bowel obstruction. Malignancy
ration and expiration and abdominal compression. Lesions intrinsic has also been reported in duplication cysts.26 Most cases demon-
to or attached to the colon will move with the bowel during respira- strate a bright, reflective inner mucosal layer and a darker, poorly
tion or compression. reflective outer muscular layer on ultrasonography.27 These layers
A B
Figure 20.14 Diverticular disease. A: Longitudinal scan of the descending colon showing multiple diverticula as outpouching from the
colonic wall. B: Transvaginal scan of the distal sigmoid colon shows diverticulum with highly reflective inspissated material causing acoustic
shadowing (arrow).
395
CHAPTER 20 Appendix, colon and rectum
A B
are often non-uniform in thickness and the cyst may contain inter- or eccentric mural thickening secondary to hypertrophy of the mus-
nal septa and echogenic debris (Fig. 20.13). cular layer (Fig. 20.14). Inspissated faecal matter or air within the
diverticulum may produce acoustic shadowing (Fig. 20.14).
Diverticulitis An inflamed diverticulum is usually seen as a poorly reflective
structure adjacent to the colonic wall. There is tenderness on direct
Colonic diverticula are formed by herniation of the colonic mucosa compression over the lesion and the inflamed diverticulum may be
through the muscular layer. These herniations occur at weak points surrounded by echogenic, non-compressible fat.2933 The diverticu-
in the colonic wall, such as between the longitudinal taenia coli or lum often contains a faecalith or inspissated material which is seen
at the entry point of blood vessels.28 The sigmoid colon is the area as an highly reflective, bright lesion. The colonic segment involved
most commonly affected by diverticular disease. Sigmoid diver- may demonstrate circumferential or eccentric mural thickening and
ticula are commonly multiple. hyperaemia (Fig. 20.15).
On ultrasonography, diverticula are seen as rounded outpouchings Diverticulitis may progress to a pericolic abscess or perforation.
adjacent to the colonic wall. There may be associated circumferential Abscesses manifest as anechoic collections adjacent to the colon and
396
Colon
may contain pockets of air or debris (Fig. 20.15).5 Scanning in a the stratification or layering of the bowel wall is preserved, whereas
decubitus position may help to establish localised perforation by this pattern is lost in advanced, transmural inflammation (Fig.
allowing air to collect under the peritoneum (Fig. 20.15). Complica- 20.17). Therefore in early disease, ultrasound shows colonic wall
tions secondary to diverticulitis such as a fistula can also be dem- thickening with preserved stratification. More advanced inflamma-
onstrated on ultrasonography. Fistulae are seen as linear, low-echo tion results in transmural ulcers, which can be detected using high-
tracks and a typical colo-vesical fistula may demonstrate air within frequency probes and are seen as low-echo linear streaks in the
the bladder. bowel wall. Distended perforating vessels may be visualised along
The accuracy rate of ultrasonography in detecting diverticulitis these deep ulcers. Transmural ulcers eventually penetrate the
has been reported to be 8095%.33 Ultrasonography can be used to serosa and cause inflammation in the adjacent mesenteric tissue,
monitor resolution of diverticulitis or a diverticular abscess. Percu- leading to formation of small para-intestinal abscesses and sinus
taneous ultrasound-guided drainage of diverticular abscesses is an tracts (Fig. 20.17). These tiny abscesses start as small inflammatory
established procedure with excellent follow-up results. masses that are seen as ill-defined, low-reflectivity areas adjacent to
the inflamed bowel segment. Larger abscesses may contain fluid
levels and brightly reflective signals due to contained air bubbles.
Right-sided diverticulitis Sinuses may track through the wall of an adjacent organ and form
Right-sided diverticulitis occurs more commonly in younger a fistula. Fistulae typically manifest as linear, poorly reflective
patients, women and persons of Asian ethnicity. Isolated right- tracks on ultrasonography. Larger sinus tracks and fistulae may
sided diverticular disease is uncommon and may be due to a single contain high signal echoes due to contained air or purulent mate-
congenital diverticulum. Congenital right-sided diverticula are true rial. Hyperaemia within fistulae on Doppler studies has been shown
diverticula as they contain all the colonic wall layers. Inflammation to correlate with inflammatory activity.38
of a right-sided diverticulum may mimic appendicitis and it is In the inflammatory phase of Crohns colitis there is associated
important to distinguish between these conditions as right-sided oedema and fibrofatty proliferation of the surrounding omental and
diverticulitis is treated conservatively and abscess formation is mesenteric fat. This inflamed and oedematous fat around inflamed
rare.34 Ultrasonographic appearances of right-sided diverticulitis colon has increased reflectivity and non-compressible appearance.
are similar to left-sided diverticulitis except for location along the Other ultrasonographic hallmarks of Crohns disease include
caecum or ascending colon and a normal appendix (Fig. 20.16). involvement of the small bowel and skip lesions. Studies have
shown high volume flow in the mesenteric arteries on Doppler
sonography in patients with actively inflamed bowel segments. In
Inflammatory colitis the chronic phase of the disease there is marked fibrosis and fatty
infiltration of the submucosal layer. These pathological changes
The two major forms of inflammatory colitis are Crohns disease lead to marked echogenic thickening of the submucosal layer. Stric-
(also called Crohns colitis) and ulcerative colitis. Ultrasonography tures may form, which are most commonly seen as low-reflectivity,
can be used to assess the extent of colitis and has been shown to stenotic lesions with proximal obstruction.
have good correlation with disease activity. Typical ultrasono-
graphic features in the inflammatory colitides include mural thick-
ening, loss of haustral pattern, reduced compressibility and lack of Ulcerative colitis
peristalsis.35,36
Ulcerative colitis is mainly a mucosal or superficial ulcerating
disease, and therefore the inflammation is limited to the mucosa
Crohns colitis and submucosa (Fig. 20.18). As a result the colonic thickening is less
marked than that in Crohns disease. The stratified appearance of
Crohns colitis has a transmural inflammatory progression similar the bowel is maintained and there is no evidence of fistulae or
to the disease seen in small bowel. As a result it causes marked sinuses. The involvement of the colon is contiguous and there are
colonic wall thickening.37 In early or superficial ulcerating disease no skip lesions.
Occasionally it may be difficult to differentiate between ulcera-
tive colitis and Crohns colitis on ultrasonography; however, the
presence of transmural changes, mesenteric abnormalities, skip
lesions, small intestinal involvement and marked mural thickening
should prompt the diagnosis of Crohns disease (Table 20.1). On
ultrasonography, a thickened colonic wall of greater than 7mm
with loss of stratification has been considered to be typical of
Crohns disease, whereas a thickness of 47mm with preservation
of the stratification is more typical in ulcerative colitis.
A D
Figure 20.17 Crohns colitis. A: Longitudinal image of the descending colon (arrow) shows marked mural thickening. There is loss of
stratification in one segment (arrowhead) suggestive of transmural inflammation. B: Doppler study of the descending colon shows
hyperaemia. Corkscrew, transmural vessels are seen indicative of fissuring ulcers (arrow). C: Transverse image shows contiguous, diffuse
thickening of the caecum (arrowhead) and terminal ileum (arrow). D: Entero-colic fistula is seen as a linear, reduced reflectivity track
between the ascending colon (arrowhead) and adjacent ileum. A small amount of air (arrow) is present in the fistula indicative of fistula
patency.
398
Colon
Infective colitis
Tuberculous colitis
Intestinal tuberculosis typically affects the ileocaecal region. Iso-
lated tuberculous colitis is extremely rare and only affects less than
3% of patients with documented intestinal tuberculosis. The most
commonly observed pattern is concentric thickening of the ileum
and caecum (Fig. 20.19). There may be associated ascites and
mesenteric lymphadenopathy in the majority of patients.39,40
Although the lymphadenopathy may be discrete, matted and cavi-
tating lymph nodes are more frequent. Cavitating nodes have an
anechoic central area. The ascites may be clear or may contain septa- Figure 20.19 Tuberculous ileocolitis. Transverse ultrasound
tions and debris.41,42 Mesenteric and omental thickening is also image of the right iliac fossa shows concentric thickening of the
present in tuberculous ileocolitis. Chronic tuberculous ileocolitis terminal ileum (arrow), necrotic, anechoic lymph nodes (asterisk),
may lead to a cicatrisation and fibrosis of the bowel and patients ascites (curved arrow). Note marked omental thickening
may present with ileocolic strictures, mesenteric retraction and (arrowhead). (Figure courtesy of Dr S. Rawat.)
399
CHAPTER 20 Appendix, colon and rectum
A B
Figure 20.20 Amoebic colitis. A: Longitudinal image shows diffuse thickening of the ascending colon (arrowhead) and mass-like
thickening of the caecum (arrow) (image courtesy of Dr S.B. Vijayraghavan). B: Thickened, fluid-filled caecum, terminal ileum (arrowheads)
and distended non-tender appendix (arrow).
A B
Figure 20.21 Pseudomembranous colitis. A: Longitudinal scan of the descending colon shows marked polypoid thickening of
the colonic wall and narrowing of the lumen. B: Transvaginal scan shows diffusely thickened colon (arrow) with preserved stratification.
Note deep ulcer (arrowhead) causing mucosal disruption and small linear pseudomembranes (thin arrow).
bowel obstruction. An echogenic peritoneum has also been reported Pseudomembranous colitis
in tuberculous infections of the gastrointestinal tract.
There has been a significant rise in the incidence of pseudomem-
branous colitis, mainly due to the increased use of prophylactic and
broad-spectrum antibiotics. Antibiotic treatment leads to alteration
Amoebic colitis in the colonic bacterial flora leading to proliferation of Clostridium
Amoebic intestinal infection is caused by the protozoal organism difficile. Toxins produced by Clostridium difficile lead to pseudomem-
Entamoeba histolytica. The trophozoite invades the intestinal mucosa branous colitis that commonly presents with diarrhoea, abdominal
causing colitis and disseminates through the portal bloodstream pain, distension and systemic symptoms. Patients may occasionally
to cause abscesses, typically in the liver. Patients with intestinal present with an acute abdomen.
infection may present with diarrhoea, abscesses and systemic The most common ultrasonographic feature of pseudomembra-
symptoms. Pathological findings include discrete colonic ulcers, nous colitis is diffuse thickening of the colonic wall (Fig. 20.21).43
segmental colonic involvement or diffuse colitis. The ascending The thickening varies with the severity of the disease but is gener-
colon is frequently involved and the terminal ileum is invariably ally much more marked than in other colitides. Typically the haus-
spared. tral pattern is preserved although the haustral thickening may have
Ultrasonographically amoebic colitis manifests as diffuse, poorly a polypoid appearance with marked narrowing of the lumen. Strati-
reflective thickening of the colon (Fig. 20.20). Short segmental fication of bowel layers may be preserved in mild cases. Scanning
involvement may present as a mass lesion (termed amoeboma), with high-frequency transducers may reveal mucosal defects
which is difficult to differentiate from a tumour. Amoebomas are caused by ulcers (Fig. 20.21). Pseudomembranes, which are the
typically seen in the caecum. The presence of a liver abscess with hallmark of this disease, are seen as linear, bright structures and
right colonic abnormality should alert the ultrasonologist to the they are best visualised on a real-time examination. Ascites may be
presence of amoebic colitis. The normal terminal ileum helps to detected in the majority of patients. In severe cases there is almost
distinguish amoebic colitis from Crohns colitis. A dilated, non- complete effacement of the lumen due to the mural oedema. The
tender appendix has been reported in cases of amoebic colitis. rectosigmoid region is most commonly affected, with contiguous
400
Colon
Typhlitis Tuberculous colitis involves the ileocaecal region and there may
be associated cavitating lymphadenopathy, ascites and omental
Typhlitis or neutropenic enterocolitis is encountered in patients thickening.
with immunosuppressive disorders (e.g. acquired immune defi- Amoebic colitis may present as a caecal mass (amoeboma).
ciency syndrome or leukaemia), transplant recipients or after chem- Campylobactor and Salmonella cause modest thickening of the
otherapy. The underlying pathological mechanism is considered to colonic mucosa.
be secondary to mucosal damage of the bowel with subsequent Yersinia enterocolitis causes modest thickening of the colonic and
bacterial or fungal invasion. The most commonly involved site is ileal mucosa with associated lymphadenopathy.
the caecum and ascending colon, although any bowel segment Typhlitis commonly involves the caecum and ascending colon.
including the small intestine may be involved. The characteristic Pseudomembranous colitis caused marked mural thickening,
pathological findings of neutropenic enterocolitis are oedema, prominent haustral folds and ascites.
ulceration and inflammation of the bowel wall. Advanced cases
may also have haemorrhagic necrosis of the bowel wall.44
The ultrasound features of neutropenic enterocolitis include
diffuse bowel wall thickening and oedema of the right colon and
distal ileum (Fig. 20.22). The affected segment may appear mass-
like as there is loss of the typical layered and haustral pattern. Peri- clinically mimic acute appendicitis and it is important to visualise
caecal stranding, ascites and pneumatosis may also be present.45 the normal appendix, to exclude acute appendicitis.
The differential diagnosis in the appropriate clinical setting of
known neutropenia includes infective colitis (e.g. pseudomembra- Ischaemia
nous colitis) and graft-versus-host reaction. The combined involve-
ment of small and large bowel favours neutropenic enterocolitis The majority of cases of ischaemic colitis are due to non-occlusive
over pseudomembranous colitis. Isolated right-sided pseudomem- vascular disease. The most common cause is vascular hypoper-
branous colitis is uncommon and patients typically have greater fusion due to arteriosclerosis, vasogenic shock and cardiac condi-
bowel wall thickening. Patients with graft-versus-host reaction tions. Ischaemia due to vascular occlusion by thrombus, emboli or
have generalised involvement of the small and large bowel. Identi- other causes is less frequent. The most commonly affected site is
fication of neutropenic enterocolitis is important in order to initiate the splenic flexure, followed by descending and sigmoid colon.
appropriate medical treatment. Ischaemic colitis is the commonest vascular disorder of the gas-
trointestinal tract in patients over 65 years of age.
Other infections Ultrasonography has a high degree of sensitivity for detecting
colonic abnormalities in ischaemic colitis. Ultrasonographic find-
Other less common organisms that cause colitis include Yersinia, ings in ischaemic colitis include segmental or circumferential
Campylobacter and Salmonella infections. In all these infections the colonic wall thickening, pericolic changes, reduced or absent peri-
terminal ileum and/or the caecum are involved. Ultrasonographi- stalsis and diminished blood flow on Doppler studies (Fig. 20.24).
cally the bowel thickening is moderate and limited to mucosa and Typically the wall stratification is preserved and loss of stratifica-
submucosa.5 Usually there is no mesenteric fat involvement, fistula- tion is indicative of advanced transmural ischaemia and a worse
tion or abscesses formation. Prominent haustrations of the right prognosis.46 Absence of Doppler flow in the abnormal segment is
colon have been reported in these infections. Yersinia enterocolitis also considered to be a sign of worse clinical outcome. High resis-
is usually associated with enlarged mesenteric lymph nodes and tive index blood flow (>0.60) on Doppler studies has also been
there is ileal and colonic thickening (Fig. 20.23). Campylobacter and reported. Ascites may also be present in cases with established
Salmonella infections mainly cause colonic thickening and minimal ischaemic changes and infarcted bowel segments demonstrate
small bowel involvement. Yersinia enterocolitis in particular can mural pneumatosis.
401
CHAPTER 20 Appendix, colon and rectum
A B
Figure 20.24 Ischaemic colitis. A: Longitudinal view shows thickened descending colon with absence of blood flow. The mural
stratification is maintained. B: Transverse view shows diffuse, poorly reflective thickening (arrow), loss of the mural stratification and
absence of blood flow. Focal area of pneumatosis is seen (arrow) with oedema of the paracolic fat and ascites (arrowhead).
Tumours presence of endometrial tissue outside the uterine cavity and the
myometrium. The most frequent locations are in the pouch of
Although ultrasound is not the primary modality for diagnosis of Douglas, with other sites having a lesser frequency. The rectovagi-
colonic cancer, the widespread use of ultrasonography in abdomi- nal septum may also be frequently involved. When there is bowel
nal conditions may result in the incidental detection of these involvement, patients may complain of symptoms similar to irrita-
tumours. Tumours of the colon typically manifest as localised, ble bowel syndrome. Deeper invasion of the bowel wall may cause
poorly reflective masses related to the bowel. Thickening of the scarring and stricture formation that can lead to obstruction.50 The
bowel can produce the pseudo-kidney appearance (Fig. 20.25).47 reported incidence of intestinal involvement ranges from 3% to 34%
Ultrasonographic features commonly associated with colonic and in up to 70% of cases the rectum or sigmoid is involved.51 Other
cancer include localised, eccentric mural thickening, an irregular less common sites include the appendix, caecum and ileum.
contour, abnormal or lack of peristalsis and loss of the layered Transabdominal ultrasonography should be combined with
appearance of the bowel wall.48 Colonic tumours can also manifest endo-cavitary scanning (endorectal or transvaginal) for a compre-
as circumferential thickening of the bowel or as a polypoid mass, hensive assessment of colonic endometriosis. Endometriomas can
and the thickening is usually more marked than that seen in infec- present as nodular, plaque-like, cystic or complex lesions. Small
tive or inflammatory colitides (Fig. 20.25). Mucinous adenocarcino- nodules or plaque-like lesions are the most difficult to demonstrate
mas may contain calcifications that are seen as echogenic foci with ultrasonographically. These lesions are typically of reduced reflec-
shadowing on ultrasonography. Abrupt loss of mural stratification tivity on ultrasonography (Fig. 20.28) and may be only seen on
is also typical of colon cancer. Locally advanced tumours show transrectal examinations. Larger nodules are more easily demon-
infiltration of the adjacent fat planes, other abdominal viscera and strated on transabdominal scanning and appear as low-reflectivity
liver metastases (Fig. 20.25). Serosal or omental metastases that lesions and can cause puckering and kinking of the bowel wall.
involve the colon typically appear as poorly reflective infiltrative or Attachment of these lesions to the colon is confirmed on dynamic
mass lesions. scans during respiration. Larger nodules can demonstrate blood
Small polypoid lesions may not be reliably detected on transab- flow on Doppler studies. Accurate assessment of the depth of rectal
dominal ultrasonography; however, hydrocolonic ultrasonography wall involvement can be made on transrectal ultrasonography,
has been reported to have a high degree of accuracy in the detection which is useful in surgical planning.
of such lesions.24 Transabdominal scanning has been shown to have
a high detection rate of right-sided and rectal cancers.49
Colonic lymphomas are rare and typically seen in immunocom- Intussusception
promised patients, or those who have undergone organ transplan- Colonic intussusception is rare in adults and is most commonly
tation. The commonest type of large bowel lymphoma is the B-cell associated with a malignant tumour.52 The commonest reported
type and they manifest with marked bowel wall thickening. The type is an ileocolic intussusception. Lipomas are the most common
mural thickening may be circumferential, eccentric or nodular. benign cause of colonic intussusception. Ultrasonographically the
Aneurysmal dilatation of the lumen may be seen, which is thought findings are that of a bowel mass with concentric layers of hyper-
to be secondary to autonomic neural plexus destruction by tumour and hypoechogenicity. On longitudinal views the alternating layers
infiltration (Fig. 20.26). produce a trident or pitchfork appearance.53 The intussusception
The colon is the commonest site involved by gastrointestinal may contain mesenteric fat and the bowel may appear thickened
lipomas. Colonic lipomas are generally asymptomatic unless they due to oedema (Fig. 20.29). Contained mesenteric vessels may show
cause bleeding or intussusception. They are typically seen as poly- normal Doppler signal. The finding of an intussusception in an
poid intraluminal lesions with high reflectivity (Fig. 20.27). adult should raise the suspicion of an underlying tumour.
Miscellaneous conditions
Epiploic appendagitis
Endometriosis Appendices epiploicae are fatty tags attached to the serosal surface
of the colon. They usually measure 12cm in thickness and 25cm
Endometriosis affects women of childbearing age and typically in length. Venous infarction or torsion of these appendages
manifests with pain or infertility. Endometriosis is defined as the may result in localised inflammation, which is termed epiploic
402
Colon
A D
B E
C F
Figure 20.25 Colonic tumours. A: Diffuse, eccentric thickening of the colon (arrow) producing the pseudo-kidney sign. B: Polypoid
intraluminal mass with a dilated feeding vessel (arrow). C: Mucinous colonic tumour shows extensive calcification in the hepatic flexure
tumour (arrowhead) and calcified liver metastases (arrow). D: Locally advanced colonic tumour shows extensive infiltration of the paracolic
fat and peritoneum (arrow). Arrowhead = colon. E: Polypoid colonic mass with loss of stratification, marked mural thickening and extension
into pericolonic fat (arrow). F: Recurrent tumour (arrow) seen as diffuse, low-reflectivity lesion involving the colon (curved arrow) and ileum
(arrowhead).
403
CHAPTER 20 Appendix, colon and rectum
Figure 20.26 Colonic lymphoma. Circumferential thickening of a long segment of the sigmoid colon (arrow) is seen with distended,
air-filled lumen (aneurysmal dilatation).
A B
Figure 20.27 Lipoma. A: Transverse image of the transverse colon shows a bright, reflective mass (arrow) filling the colonic lumen.
B: Axial CT image confirms the colonic lipoma as a fatty intraluminal lesion (arrow).
A B
Figure 20.28 Endometriosis. A: Nodular, poorly reflective lesion (arrow) seen attached to the sigmoid colon (asterisks). B: Axial CT
image shows enhancing lesion (arrow) attached to the sigmoid.
404
Rectum and anal canal
A B
Figure 20.29 Intussusception. A: Ileocolic intussusception seen as a target lesion with an alternating high and low reflective pattern
(arrow). B: Longitudinal view shows ileal segment and mesenteric fat (arrowhead) inside the colonic lumen (arrow). A trilaminar or trident
appearance is evident.
A B
Figure 20.30 Epiploic appendagitis. A: Lenticular lesion with a dark rim (arrow) adjacent to the colon. B: Epiploic appendagitis seen as
a lenticular echogenic lesion (arrow) arising from the colon.
mechanical rotating single-crystal transducer. More recently fixed the normal adult and it gradually thickens with advancing age.
crystals with 360 field of view have been developed for endoanal A thickness of greater than 3.5mm is abnormal in any age. The
ultrasonography. Biplane capabilities on a single transducer that length of the sphincters may be determined on volume or three-
allows axial and perpendicular views and Doppler capability have dimensional scans. Ascertaining the length of the sphincter is
also been developed.57,58 Alternative techniques such as transvagi- important in order to assess the level of disruption.
nal and transperineal scanning have also been advocated for evalu-
ation of the anal sphincters. However, there are limitations to these
approaches; firstly transvaginal scanning can only be used in Indications for endoanal sonography
women, and secondly, the anatomical configuration of the vagina
and anal canal with the perineal body in between does not allow Assessment of sphincter abnormalities.
true axial imaging of the sphincters. Therefore only an oblique view Diagnostic work-up of faecal incontinence and evaluation of anal
of the anal canal can be obtained via the transvaginal approach, pain.
which is suboptimal for assessing the circular sphincter complex. Assessment of anal sepsis.
Use of transvaginal and transperineal scanning should be reserved Staging of anorectal tumours, particularly prior to local treatment.
as an adjunct to standard endosonography and may be particularly
useful in stenotic anal lesions or tumours where the standard endo-
anal approach may not be possible. Normal anatomy
For an endosonographic examination, the probe is inserted into
the rectum and withdrawn gently through the anal canal to obtain
a view of the sphincter complex. Endoanal ultrasonography should Anal canal
be performed with the patient in the prone position as this provides
a symmetrical view of the sphincter complex and also allows accu- On endoanal ultrasonography four distinct layers in the anal canal
rate views of the anterior aspect of the external sphincter.59 Although can be determined (Fig. 20.31).60 These are:
scanning in the lateral decubitus position may be easier and more 1. The subepithelium, which is seen as a moderately echogenic
comfortable for the patient, it produces distortion of the sphincter layer that is adjacent to the probe surface. The subepithelium
complex. is of uniform echogenicity and may contain venous channels.
Degassed water can be instilled to provide a good ultrasono- 2. The internal sphincter is seen as a clearly defined layer with
graphic window for examination of the rectum. This method is low reflectivity. It is circular in shape and measures 23mm
useful in assessing the rectal tumours as it reduces overstaging by in the normal adult. There is some asymmetry of the internal
decreasing artefacts produced by faecal matter, rectal air or the sphincter high in the anal canal. This asymmetry is more
tumour itself. prominent in females where the anterior aspect is ill-defined
The scan should be oriented as a clock-face in such a way that 3 as the sphincter merges with the perineal body. The internal
oclock corresponds to the left side of the patient. Images are sphincter terminates at the dentate line.
obtained at high, mid and low anal canal levels. Measurements of 3. The longitudinal muscle is seen as a moderately reflective
the sphincter thickness should be obtained at the 3 and 9 oclock layer in between the internal and external sphincters and is a
positions. The internal sphincter measures approximately 2mm in continuation of the longitudinal muscles of the rectum.
A B
Figure 20.31 Normal anal anatomy. A: Image at high level shows the four layers. Arrow = internal sphincter; Arrowhead = external
sphincter. Bright subepithelial layer is seen adjacent to the endoanal probe. Moderately reflective longitudinal muscle layer is between the
external and internal sphincters. Amorphous appearing perineal body is seen anteriorly. B: Image at low level shows brightly reflective fibres
of the subcutaneous external sphincter (arrowhead). The poorly reflective internal sphincter is seen ending at this level.
406
Rectum and anal canal
4. The external sphincter is composed of striated muscle and is submucosal and serosal layers appear bright; whereas the muscu-
of moderate and varied reflectivity. With ageing there is laris mucosae and muscularis propria are of reduced reflectivity.
increased thickening of the internal sphincter and increased
reflectivity. Anorectal tumours
Endoanal images should be obtained at high, mid and low levels
in the anal canal. The high level corresponds to the level of the Endoanal and transrectal ultrasonography can be used to stage anal
puborectalis and deep external sphincter. In males the external tumours based on depth of invasion. Typically anal cancers are
sphincter is roughly symmetrical whereas in females the anterior poorly reflective and clearly demarcated from adjacent structures.
portion of the external sphincter is deficient and replaced by the Tumour confined to the subepithelium is classed as T1; limited to
perineal body. The internal sphincter and longitudinal muscle is sphincter muscles is classed as T2; extending through the external
clearly visualised at this level. sphincter is classed as T3; involving adjacent pelvic structures is
The mid level corresponds to the superficial part of the external classed as T4.
sphincter. The internal sphincter terminates at the lower end of this Transrectal ultrasonography has high accuracy in the staging of
level. At this level the sphincters are symmetrical and the pubococ- rectal cancer.61 A meta-analysis has indicated that ultrasonography
cygeal ligaments are seen posteriorly. has significantly higher specificity for predicting muscularis propria
The low level starts caudal to the termination of the internal and perirectal tumour extension compared to MRI or CT.62 Perirec-
sphincter. The longitudinal muscle may appear slightly wider at tal invasions are seen as poorly reflective extensions traversing the
this level. The predominant structure at this level is the subcutane- rectal wall and extending into the adjacent serosa and mesorectum
ous part of the external sphincter. (Fig. 20.32). In routine practice, overstaging is more of a problem
than understaging. This is because most tumours are surrounded
Rectum by inflammatory and desmoplastic reaction around their margins.63
It is difficult to distinguish between desmoplastic and inflammatory
Typically the rectum demonstrates a five-layer pattern on transrec- reaction from tumour infiltration on ultrasonography, which leads
tal ultrasonography. These layers are seen as alternating bands of to overstaging. Another disadvantage of endoanal ultrasonography
increased and reduced reflectivity. The balloonmucosa interface, is the inability to evaluate stenotic tumours.
A B
Endoanal ultrasonography can also be used in the follow-up of External sphincter injuries most commonly relate to obstetric
rectal cancers. Tumour recurrence typically manifests as an amor- injuries. Episiotomies are typically seen as well-defined scars in the
phous, poorly reflective mass. Endoanal ultrasound can be used to right lateral quadrant. Penetrating and traumatic anal sphincter
perform targeted biopsies of the bowel or extramural lesions. injuries are seen as well-defined tracks and may be seen in any
quadrant.
Anal sepsis
Endoanal ultrasonography is useful in the detection of anal sepsis
and in particular the identification of internal opening of fistula-in-
ano.64 It must be borne in mind that the track leading up to the
mucosal surface is rarely seen; rather the site is identified as a
poorly reflective area in the intersphincteric space adjacent to the
internal sphincter (Fig. 20.33). Trans-sphincteric fistulae are seen as
tracts that extend across the external sphincter into the ischioanal
fossa. An inherent disadvantage of using high-resolution probes in
endoanal ultrasonography is the inability to resolve ischioanal and
supralevator infections. Trans-sphincteric tracks and ischioanal or
ischiorectal extensions are better seen on cross-sectional examina-
tions such as MR imaging. Endoanal ultrasonography cannot reli-
ably distinguish between infection and fibrosis as both appear as
linear tracks of low reflectivity. Hydrogen peroxide injection and
3D imaging can be used to demonstrate opening and anatomy of
the track.65
Anal trauma
Loss of continuity of any sphincter is abnormal. Marked thinning
or breaks in the internal or external sphincters are a sign of trauma.
These defects may be acquired as a result of injury sustained during
labour or after anal stretch procedures. Obstetric tears are typically
situated anteriorly and if the internal sphincter is involved, the
defect is seen is the same segment.66 Isolated tears of the internal
sphincter are not seen in obstetric injuries (Fig. 20.34). Well-defined Figure 20.33 Anal sepsis. Fistula-in-ano at 12 oclock position
defects may be seen in the internal sphincters after lateral sphinc- seen as a poorly reflective area (arrow) associated with a posterior
terotomy procedures. horse-shoe abscess in the intersphincteric plane.
A B
Figure 20.34 Anal trauma. A: Obstetric injury during labour. There is break of the internal and external sphincters at the 10 oclock
position (arrow). B: Multiple disruptions of the sphincters (arrowheads) after penetrating anal injury (image courtesy Dr I Ramachandran).
408
References
14. Pickhardt PJ, Levy AD, Rohrmann CA, Kende AI. Primary neoplasms
Anal sphincter abnormalities of the appendix manifesting as acute appendicitis: CT findings with
Obstetric injuries are commonly situated anteriorly and involve pathologic comparison. Radiology 2002;224(3):775781.
15. Connor SJ, Hanna GB, Frizelle FA. Appendiceal tumors: retrospective
internal and external sphincters.
clinicopathologic analysis of appendiceal tumors from 7,970
Isolated internal sphincter injuries are not seen in obstetric
appendectomies. Dis Colon Rectum 1998;41(1):7580.
injuries. 16. Pickhardt PJ, Levy AD, Rohrmann CA, Kende AI. Primary neoplasms
Traumatic injuries may occur in any quadrant. of the appendix: radiologic spectrum of disease with pathologic
Solitary rectal ulcer syndrome is the most common cause of correlation. Radiographics 2003;23(3):645662.
internal sphincter thickening. 17. Moertel C, Weiland L, Nagorney D, Dockerty M. Carcinoid tumor of
the appendix: treatment and prognosis. N Engl J Med 1987;317(27):
16991701.
18. Pickhardt PJ, Levy AD, Rohrmann CA, et al. Non-Hodgkins
lymphoma of the appendix: clinical and CT findings with pathologic
Miscellaneous conditions correlation. AJR Am J Roentgenol 2002;178(5):11231127.
19. Ripolls T, Martnez MJ, Morote V, Errando J. Appendiceal
involvement in Crohns disease: gray-scale sonography and color
Doppler flow features. AJR Am J Roentgenol 2006;186(4):
Solitary rectal ulcer syndrome 10711078.
Solitary rectal ulcer syndrome is the commonest cause of internal 20. Baldisserotto M, Cavazzola S, Cavazzola LT, et al. Acute edematous
sphincter thickening.67 The thickening is most commonly in the stump appendicitis diagnosed preoperatively on sonography. AJR Am
J Roentgenol 2000;175(2):503504.
range of 3.54.5mm. There is also associated thickening of the
21. Shin L, Halpern D, Weston S, et al. Prospective CT diagnosis of stump
subepithelium which is thought to be secondary to intra-anal appendicitis. AJR Am J Roentgenol 2005;184:S6264.
intussusception.68 22. Bru C, Sans M, Defelitto MM, et al. Hydrocolonic sonography for
evaluating inflammatory bowel disease. AJR Am J Roentgenol
2001;177(1):99105.
Other sphincter abnormalities 23. Limberg B. Diagnosis of acute ulcerative colitis and colonic
Crohns disease by colonic sonography. J Clin Ultrasound
Marked thickening of the internal sphincter over 5mm suggests
1989;17(1):2531.
internal sphincter myopathy, a genetic disorder affecting women. 24. Limberg B. Diagnosis and staging of colonic tumors by conventional
Internal sphincter less than 2mm in thickness suggests age-related abdominal sonography as compared with hydrocolonic sonography.
degeneration. Manual dilatation or anal stretch procedures can N Engl J Med 1992;327(2):6569.
cause multiple tears or fragmentation of the external sphincter (Fig. 25. Chui DW, Gooding G, McQuaid KR, et al. Hydrocolonic
20.34). Fibrosis and granulation in the sphincters are seen as areas Ultrasonography in the detection of colonic polyps and tumors.
of heterogeneous signal. N Engl J Med 1994;331(25):16851688.
26. Tong SC, Pitman M, Anupindi SA. Best cases from the AFIP: ileocecal
enteric duplication cyst: radiologic-pathologic correlation.
REFERENCES Radiographics 2002;22(5):12171222.
27. Barr LL, Hayden CK, Stansberry SD, Swischuk LE. Enteric duplication
1. Puylaert JB. Acute appendicitis: US evaluation using graded cysts in children: are their ultrasonographic wall characteristics
compression. Radiology 1986;158(2):355360. diagnostic? Pediatr Radiol 1990;20(5):326328.
2. Yabunaka K, Katsuda T, Sanada S, Fukutomi T. Sonographic 28. Sinha R. Jejunal diverticulosis: sonographic diagnosis. J Clin
appearance of the normal appendix in adults. J Ultrasound Med Ultrasound 2006;34(2):8487.
2007;26(1):3743. 29. Pradel J, Adell J, Taourel P, et al. Acute colonic diverticulitis:
3. Lee J, Jeong YK, Hwang JC, et al. Graded compression sonography prospective comparative evaluation with US and CT. Radiology
with adjuvant use of a posterior manual compression technique in the 1997;205(2):503512.
sonographic diagnosis of acute appendicitis. AJR Am J Roentgenol 30. OMalley ME, Wilson SR. US of gastrointestinal tract abnormalities
2002;178(4):863868. with CT correlation. Radiographics 2003;23(1):5972.
4. Puylaert JB, Rutgers PH, Lalisang RI, et al. A prospective study of 31. Vijayaraghavan SB. High-resolution sonographic spectrum of
ultrasonography in the diagnosis of appendicitis. N Engl J Med diverticulosis, diverticulitis, and their complications. J Ultrasound
1987;317(11):666669. Med 2006;25(1):7585.
5. Puylaert JB. Ultrasound of acute GI tract conditions. Eur Radiol 32. Wilson S, Toi A. The value of sonography in the diagnosis of acute
2001;11(10):18671877. diverticulitis of the colon. AJR Am J Roentgenol 1990;154(6):1199
6. Kessler N, Cyteval C, Gallix B, et al. Appendicitis: evaluation of 1202.
sensitivity, specificity, and predictive values of US, Doppler US, and 33. Ledermann HP, Borner N, Strunk H, et al. Bowel wall thickening on
laboratory findings. Radiology 2004;230(2):472478. transabdominal sonography. AJR Am J Roentgenol
7. Chan I, Bicknell SG, Graham M. Utility and diagnostic accuracy of 2000;174(1):107115.
sonography in detecting appendicitis in a community hospital. AJR 34. Oudenhoven LF, Koumans RK, Puylaert JB. Right colonic
Am J Roentgenol 2005;184(6):18091812. diverticulitis: US and CT findings new insights about frequency and
8. Keyzer C, Zalcman M, De Maertelaer V, et al. Comparison of US and natural history. Radiology 1998;208(3):611618.
unenhanced multi-detector row CT in patients suspected of having 35. Fraquelli M, Colli A, Casazza G, et al. Role of US in detection of Crohn
acute appendicitis. Radiology 2005;236(2):527534. disease: meta-analysis. Radiology 2005;236(1):95101.
9. Quillin SP, Siegel MJ, Coffin CM. Acute appendicitis in children: value 36. Horsthuis K, Bipat S, Bennink RJ, Stoker J. Inflammatory bowel
of sonography in detecting perforation. AJR Am J Roentgenol disease diagnosed with US, MR, scintigraphy, and CT: meta-analysis
1992;159(6):12651268. of prospective studies. Radiology 2008;247(1):6479.
10. van Breda Vriesman AC, Puylaert JBCM. Mimics of appendicitis: 37. Sarrazin J, Wilson S. Manifestations of Crohn disease at US.
alternative nonsurgical diagnoses with sonography and CT. AJR Am J Radiographics 1996;16(3):499520.
Roentgenol 2006;186(4):11031112. 38. Maconi G, Sampietro GM, Russo A, et al. The vascularity of internal
11. Puylaert JB, van der Zant FM. Mesenteric lymphadenitis or fistulae in Crohns disease: an in vivo power Doppler ultrasonography
appendicitis? AJR Am J Roentgenol 1995;165(2):490. assessment. Gut 2002;50(4):496500.
12. Puylaert JB, Oudenhoven LF, Koumans RK. Right-sided diverticulitis 39. Gritzmann N, Hollerweger A, Macheiner P, Rettenbacher T.
masquerading as acute appendicitis. Ned Tijdschr Geneeskd Transabdominal sonography of the gastrointestinal tract. Eur Radiol
1998;142(23):1350. 2002;12(7):17481761.
13. Menten R, Lebecque P, Saint-Martin C, Clapuyt P. Outer diameter of 40. Chaubal N, Dighe M, Shah M, Chaubal J. Sonography of the
the vermiform appendix: not a valid sonographic criterion for acute gastrointestinal tract. J Ultrasound Med 2006;25(1):8797.
appendicitis in patients with cystic fibrosis. AJR Am J Roentgenol 41. Lee DH, Ko YT, Yoon Y, Lim JH. Sonographic findings of intestinal
2005;184(6):19011903. tuberculosis. J Ultrasound Med 1993;12(9):537540.
409
CHAPTER 20 Appendix, colon and rectum
42. Lee DH, Lim JH, Ko YT, Yoon Y. Sonographic findings in tuberculous 57. Berton F, Gola G, Wilson SR. Perspective on the role of transrectal and
peritonitis of wet-ascitic type. Clin Radiol 1991;44(5):306310. transvaginal sonography of tumors of the rectum and anal canal. AJR
43. Ramachandran I, Sinha R, Rodgers P. Pseudomembranous colitis Am J Roentgenol 2008;190(6):14951504.
revisited: spectrum of imaging findings. Clin Radiol 2006;61(7): 58. Sudakoff GS, Quiroz F, Foley WD. Sonography of anorectal, rectal, and
535544. perirectal abnormalities. AJR Am J Roentgenol 2002;179(1):
44. Kirkpatrick IDC, Greenberg HM. Gastrointestinal complications in the 131136.
neutropenic patient: characterization and differentiation with 59. Law PJ, Bartram CI. Anal endosonography: technique and normal
abdominal CT. Radiology 2003;226(3):668674. anatomy. Gastrointest Radiol 1989;14(4):349353.
45. Teefey S, Montana M, Goldfogel G, Shuman W. Sonographic diagnosis 60. Frudinger A, Bartram CI, Halligan S, Kamm M. Examination
of neutropenic typhlitis. AJR Am J Roentgenol 1987;149(4):731733. techniques for endosonography of the anal canal. Abdom Imaging
46. Ripolls T, Sim L, Martnez-Prez MJ, et al. Sonographic findings in 1998;23(3):301303.
ischemic colitis in 58 patients. AJR Am J Roentgenol 2005;184(3): 61. Heneghan JP, Salem RR, Lange RC, et al. Transrectal sonography in
777785. staging rectal carcinoma: the role of gray-scale, color-flow, and
47. Anderson DR. The pseudokidney sign. Radiology 1999;211(2):395397. Doppler imaging analysis. AJR Am J Roentgenol 1997;169(5):
48. Shirahama M, Koga T, Ishibashi H, et al. Sonographic features of 12471252.
colon carcinoma seen with high-frequency transabdominal ultrasound. 62. Bipat S, Glas AS, Slors FJM, et al. Rectal cancer: local staging and
J Clin Ultrasound 1994;22(6):359365. assessment of lymph node involvement with endoluminal US,
49. Lee DH, Ko YT, Shin GH, et al. Sonographic detection of rectal CT, and MR imaging a meta-analysis. Radiology 2004;232(3):
carcinoma. Clin Imaging 2002;26(1):3034. 773783.
50. Doniec JM, Kahlke V, Peetz F, et al. Rectal endometriosis: high 63. Maier AG, Barton PP, Neuhold NR, et al. Peritumoral tissue reaction at
sensitivity and specificity of endorectal ultrasound with an impact for transrectal US as a possible cause of overstaging in rectal cancer:
the operative management. Dis Colon Rectum 2003;46(12):16671673. histopathologic correlation. Radiology 1997;203(3):785789.
51. Carbognin G, Guarise A, Minelli L, et al. Pelvic endometriosis: US and 64. Halligan S, Stoker J. Imaging of fistula in ano. Radiology
MRI features. Abdom Imaging 2004;29(5):609618. 2006;239(1):1833.
52. Kim YH, Blake MA, Harisinghani MG, et al. Adult intestinal 65. Buchanan GN, Bartram CI, Williams AB, et al. Value of hydrogen
intussusception: CT appearances and identification of a causative lead peroxide enhancement of three-dimensional endoanal ultrasound in
point. Radiographics 2006;26(3):733744. fistula-in-ano. Dis Colon Rectum 2005;48(1):141147.
53. Huang BY, Warshauer DM. Adult intussusception: diagnosis and 66. Frudinger A, Ballon M, Taylor SA, Halligan S. The natural history of
clinical relevance. Radiol Clin North Am 2003;41(6):11371151. clinically unrecognized anal sphincter tears over 10 years after first
54. van Breda Vriesman AC, Lohle PN, Coerkamp EG, Puylaert JB. vaginal delivery. Obstet Gynecol 2008;111(5):10581064.
Infarction of omentum and epiploic appendage: diagnosis, 67. Halligan S, Sultan A, Rottenberg G, Bartram CI. Endosonography of
epidemiology and natural history. Eur Radiol 1999;9(9):18861892. the anal sphincters in solitary rectal ulcer syndrome. Int J Colorectal
55. Rioux M, Langis P. Primary epiploic appendagitis: clinical, US, and CT Dis 1995;10(2):7982.
findings in 14 cases. Radiology 1994;191(2):523526. 68. Marshall M, Halligan S, Fotheringham T, et al. Predictive value of
56. Bartram CI, Frudinger A. Handbook of anal endosonography. internal anal sphincter thickness for diagnosis of rectal intussusception
Petersfield: Wrightson Biomedical; 1997. in patients with solitary rectal ulcer syndrome. Br J Surg
2002;89(10):12811285.
410
CHAPTER
Superior
mesenteric artery Coeliac axis
Adrenal Adrenal
Pyramid
Cortex
Spleen Papilla
Liver
Pancreas
Renal artery
Interlobar
IVC Aorta
artery
Colon
Colon Small
bowel Arcuate Pelvis of
artery kidney
Striate arteries
P
D
IVC Ao
DC
AC
V
K
K
Anterior
perirenal
fascia
Figure 21.6 Renal length measurement. A: Line diagram to show the renal length measurement and possible sources of error in
obtaining maximum lengths by failing to get the best scanning plane. B and C: A normal kidney with true maximum length of 11cm
shown to have an apparent length of 8.6cm due to inaccurate orientation.
A B
Figure 21.8 Renal arteries. A: The right renal artery (RRA, arrow) is seen passing behind the inferior vena cava (IVC). B: Decubitus/
Coronal view from the right flank showing the origins of the renal arteries. Ao, aorta; LRA, left renal artery.
Perirenal structures
The movement of the kidney during respiration may be impeded
by a variety of intra- and extrarenal abnormalities, thus providing
useful diagnostic clues. In addition, in patients with small fibrotic
kidneys, the movement of the kidney in the perirenal tissues may
allow their identification and definition in difficult cases.
The perirenal fat, pararenal areas and adrenal areas should all be
assessed briefly. If renal abnormalities are present, other more
remote sites such as the liver, para-aortic areas, IVC, line of the
ureters, pelvis and the bladder may need to be examined.
Renal vessels
Assessment of the renal vessels by imaging and Doppler may be
required. In slim patients the renal arteries can often be identified
on colour Doppler from an anterior approach as they leave the Figure 21.9 Transverse view showing the left renal vein
aorta, the right renal artery being located as it passes behind the passing between the superior mesenteric artery (SMA) and the
IVC (Fig. 21.8A); the left renal artery is more difficult to demon- aorta and the origins of the renal arteries. Ao, aorta; IVC, inferior
strate24 and accessory arteries are usually not visualised.25 In some vena cava; LRA, left renal artery; LRV, left renal vein; RRA, right
patients use of both decubitus positions with the upper arm raised venal vein.
may allow visualisation of the renal arteries (Fig. 21.8B). Using a
flexible approach, the origins and proximal segments of one or both
arteries can be detected in a significant number of patients, although visualisation of both the main renal arteries and their intrarenal
this may take some time. The intrarenal arteries are easier to dem- branches, together with a reduction in the time necessary to perform
onstrate within the renal sinus, or the interlobar segments. They are the examination.27
identified using colour Doppler with the patient breathing quietly, Similarly the renal veins can be visualised both from an anterior
rather than holding their breath, as this induces dyspnoea and or anterolateral approach; the left renal vein may be seen as it passes
increases respiratory movement of the kidney when the patient behind the superior mesenteric artery and in front of the aorta (Fig.
breathes. Spectral Doppler waveforms can be recorded as necessary 21.9). It often appears to be narrowed at this point with some
during short periods of suspended respiration; it is good practice peripheral dilatation but this is a normal appearance and not a sign
to obtain spectral traces from the upper, middle and lower seg- of obstruction.28 The right renal vein is shorter and is seen passing
ments of the kidney so that any significant differences due to acces- medially from the hilum of the kidney to the IVC. In fatter or more
sory arteries are detected and resistive indices for each side can be difficult patients it may be necessary to try to locate the vessel at or
averaged.26 The use of echo-enhancing agents can improve near the hilum of the kidney from a lateral approach and trace it
417
CHAPTER 21 Kidneys: anatomy and technique
A B
Figure 21.10 A and B: Two views of an ectopic left kidney (K) lying adjacent to the iliac vessels and bladder (B) in a patient with
ascites (A).
proximally as far as possible towards the IVC or aorta, but it may particularly on the right (Fig. 21.11). The significance of moderate or
be impossible to demonstrate the entire length in many obese even marked degrees of vertical movement is controversial; medial
patients. movement may be of greater clinical importance. Patients should
therefore be examined in both decubitus positions as well as supine
Ectopic kidneys, technique and upright if symptoms are attributed to nephroptosis.29,30
If a normal kidney is not seen in the renal fossa, the possibility that
the kidney is atrophic or hypoplastic must be considered. The con-
tralateral kidney should be reassessed for evidence of compensa- NORMAL APPEARANCES ON
tory hypertrophy. If it is unusually large, this implies that the ULTRASOUND
other kidney is non-functional or absent, while a normal-sized
contralateral kidney implies that there may well be another
kidney present somewhere with a reasonable amount of function- Renal parenchyma
ing tissue.
The patient should then be carefully examined beginning with
the renal fossa on the side of the missing kidney, passing down the Cortex and medulla
flank and psoas muscle into the pelvis (Fig. 21.10). If this does not
The normal kidneys can usually be identified without difficulty
reveal the missing kidney, the pelvis should be searched carefully
because of the difference in reflectivity between the parenchyma
and also the opposite flank to detect crossed renal ectopia. The
and surrounding fat. The outer margin of the cortex is well defined
ectopic kidney may look like a kidney but it may also be somewhat
due to the renal capsule, but the inner margin of the parenchyma,
indeterminate in nature. In these cases, colour Doppler may show
adjacent to the echoes from the sinus fat, is less well defined (Fig.
a regular, renal pattern of vascularity.
21.12). The renal cortical reflectivity can be assessed subjectively by
comparison with that of the adjacent liver or spleen, assuming that
Nephroptosis these organs are normal.31
Normal cortex has a reflectivity less than that of the adjacent liver
Examination for ptosis of a kidney is not usually very rewarding on and spleen but the degree of difference is, to some extent, equip-
ultrasound as it is difficult to find stable landmarks to compare the ment dependent and this distinction may be less obvious with some
renal position when the patient moves from horizontal to vertical, makes of scanner, or with particular settings for pre- and post-
or supine to decubitus positions. Assessing the position of the processing (see Chapter 1).32 However, if the renal cortex is brighter
kidney in relation to the twelfth rib in the prone and erect position than the normal liver, this strongly suggests the presence of paren-
may give some assessment of vertical movement. Alternatively, chymal disease.
lumbar transverse processes can be identified in slim patients and The medullary pyramids are less reflective than the cortex and
used as fixed reference points. Examination in the lateral decubitus can be identified with modern equipment as echo-poor oval struc-
positions may reveal significant medial mobility of the kidney, tures, evenly distributed around the inner margin of the cortical
418
Normal appearances on ultrasound
A B
Figure 21.11 Nephroptosis. A: The right kidney is seen in a normal position on a transverse scan. B: With the patient lying on the left
side, the kidney is seen to have crossed the midline and now lies across the spine (Sp) with much of it lying to the left of the aorta (Ao).
This was asymptomatic and an incidental finding. IVC, inferior vena cava.
A B
Figure 21.12 Normal kidney. A: Normal kidney showing cortex and pyramids with bright central sinus echoes. B: Transverse view of a
normal kidney at the level of the renal hilum. The renal vein can be seen passing out of the plane of image towards the IVC.
parenchyma adjacent to the sinus echoes.33,34 Small, highly reflective Assessment of parenchymal thickness around the margin of a
foci may be seen at the margins between the medullary pyramids kidney helps to detect and assess scarring secondary to childhood
and the adjacent cortex representing the interlobar and arcuate pyelonephritis, reflux or infarction. The parenchyma normally thins
arteries (Fig. 21.13); their nature can be confirmed by Doppler. The with age5,35 but part of this impression of thinning is due to the
margin between the pyramids and the adjacent cortex is usually development of sinus lipomatosis where the amount of fat in the
well defined but in the presence of generalised parenchymal inflam- renal sinus is increased.29 This results in thinning of the parenchyma
mation or oedema, this corticomedullary differentiation may be lost but there is a less marked decrease in renal length because the
or, in some circumstances, enhanced.31 This feature is more readily parenchymal atrophy is compensated, to some extent, by the
detected in transplants where visualisation is better because their increase in fat.4 Normal values for parenchymal thickness have not
superficial position allows high-frequency transducers, e.g. been published but some authors suggest that a thickness less than
57.5MHz, to be used (see Chapter 28). 1.5cm is indicative of thinned parenchyma.22
419
CHAPTER 21 Kidneys: anatomy and technique
A B
Figure 21.14 Renal splenic hump. A: Longitudinal view of a left kidney with a splenic hump. B: The bright echoes in the hump
represent sinus fat, confirmed on this transverse view.
420
Normal appearances on ultrasound
These normal cortical variants can often be distinguished on The renal sinus, collecting system
ultrasound, but if doubts persist echo-enhancing agents are of value
in confirming normal parenchyma, as their use shows enhancement
and vessels
identical to normal parenchyma and a normal pattern of vessels.
CT and MR scanning may also be helpful and if doubt persists, an The renal sinus is normally seen as an area of high reflectivity (the
isotope scan will show normal parenchymal uptake. central echo complex) due to the fat that surrounds the blood
vessels and collecting system. The outline of the renal sinus can
vary from smooth to moderately irregular with small components
extending around the papillae and septa of Bertin. In some patients
the elderly, patients on steroid treatment and the obese the fat
of the renal sinus can increase in amount, a change known as sinus
lipomatosis.4,38 This may be apparent on ultrasound but if any doubt
persists, a CT scan can be of help in assessment. Conversely, the
amount of fat in the renal sinus is reduced in cachectic patients and
neonates and the renal sinus is then less well visualised. Tumour
infiltration or oedema should be considered if the sinus echoes are
indistinct or absent in patients who are not cachectic.
The components of the collecting system and major branches of
the arteries and veins may be distinguished within the renal sinus
in some patients (Fig. 21.16). In patients who are dehydrated to any
extent (including an overnight fast) the peripheral collecting system
is not usually visible, but in those undergoing a diuresis, or in
patients with a full bladder, the renal pelvis and its major tributaries
can be distinguished as splitting of the renal sinus echoes.39 If this
is suspected, or if there is a question of possible obstruction, a repeat
scan when the diuresis is completed and the bladder has been
emptied should demonstrate emptying of the upper collecting
system (Fig. 21.17).
Some prominence of the collecting system is often seen in preg-
nancy.40 Slight distension of the pelvis and its main branches is
apparent as early as 12 weeks gestation and by 20 weeks this is
detected in up to three-quarters of patients on the right side; slightly
fewer show similar changes on the left. By 36 weeks gestation more
obvious dilatation may be shown in about two-thirds of patients
(Fig. 21.18). These changes usually disappear quickly after delivery
(within 48 hours) although minor distension of the collecting system
may persist.40,41 The cause of this dilatation is a matter of some
debate but mechanical factors from the enlarging uterus, hormonal
factors, increased blood flow and parenchymal hypertrophy have
all been implicated.41
The renal pelvis usually lies predominantly within the renal sinus
Figure 21.15 Septum of Bertin (arrows) at the upper pole but it may lie partly or completely outside the kidney. In this situ-
extending into the renal sinus echoes. ation the extrarenal component may act as a sump for urine,
A B
Figure 21.16 Intrarenal vessels. A: The normal renal sinus showing several small echo-free spaces which correspond to the main
branches of the arteries and veins together with central components of the collecting system. B: Colour Doppler confirms the vascular
nature of these spaces. These do not extend to the peripheral parts of the sinus, unlike dilated calyces which can be followed outwards.
421
CHAPTER 21 Kidneys: anatomy and technique
A B
Figure 21.17 Physiological hydronephrosis. A: Pre- and B: post-micturition images (on different machines) of the right kidney showing
resolution of dilatation of the collecting system following emptying of the bladder.
Figure 21.18 Physiological hydronephrosis of pregnancy. Figure 21.19 Prominent extrarenal pelvis. Transverse view of a
Moderate distension of the collecting system in a non-obstructed kidney with a prominent extrarenal pelvis which might be mistaken
kidney during the third trimester of pregnancy. for a parapelvic cyst or collection.
showing as a collection of fluid close to the medial aspect of the also tends to be higher in older patients (over the age of 60 years).44
kidney on ultrasound (Fig. 21.19). The distinction from obstruction, Care must therefore be taken when interpreting Doppler findings
parapelvic cyst or other collections may be difficult but careful in these patients as a high RI may be due to physiological factors,
examination, particularly in the transverse plane, usually defines rather than pathology. In the majority of the adult population,
the true nature of the appearances, especially if calyces are seen however, an RI of 0.7 is considered to be the upper limit of normal.45
connecting to the collection. Duplex systems may also be identi- The shape of the renal artery waveform is discussed in the section
fied as the sinus echoes of the two moieties are separated by paren- on renal artery stenosis in Chapter 23.
chymal tissue. The veins are fairly wide and the blood within them is normally
The renal vessels can often be visualised and examined with echo-free except for the inconstant demonstration of moving echoes
Doppler. In some patients the normal veins may be sufficiently from red cell rouleaux. The left renal vein may show some dilata-
prominent to simulate early obstruction, although their true nature tion distal to the point where it passes between the aorta and the
is apparent on colour Doppler. The normal renal vascular bed has superior mesenteric artery; this is a normal variant and does not
a low resistance so the arterial signals show high diastolic flow (Fig. represent significant obstruction.28
21.20). This feature is seen in the main renal arteries, the interlobar The kidneys normally move down with inspiration. The degree
arteries and the arcuate arteries.42 The resistance index (RI) in the of travel is similar to that of adjacent liver on the right and of the
renal arteries is consequently relatively low with typical normal spleen on the left. Real-time ultrasound allows for slight differences
values of 0.580.64 being reported.43 It should be noted that the RI in the movement of the kidneys in relation to adjacent structures to
shows greater variability in children: one study reported a range be detected. Loss of respiratory movement may be due to diaphrag-
from 0.34 to 0.94 in a group of children aged 115 years, with no matic paralysis but if this is not the case then it may be a sign of
significant relationship between age, renal size or gender.43 The RI intra- or perirenal pathology producing some fixation of the kidney.
422
Congenital variants of renal structure and position
A B
Figure 21.20 A: Doppler signal from the right renal artery, as it passes behind the IVC showing the normal high diastolic flow. B: The
normal intrarenal waveform showing the characteristic early systolic peak (ESP) (arrow).
Ectopic kidneys
The kidneys may develop anywhere along the urogenital ridge of
the fetus and so, if they are not in a normal position, they should Figure 21.21 Duplex collecting system. Image of the left kidney
be searched for along the psoas muscles and down into the pelvis showing a column or bar of cortex separating the renal sinus
(see Fig. 21.10). Ectopic kidneys are more common on the left side, echoes into two parts in a patient with duplication of the collecting
some 80% of them being found at, or below, the level of the iliac system and upper ureters.
crest on the ipsilateral side.46 An ectopic kidney can be recognised
by its overall similarity in shape, size and structure to normal
kidneys, although like horseshoe kidneys (see below) ectopic
kidneys are associated with malrotation and a predisposition to unwary; colour Doppler is of value as it usually shows the vascular
dilatation of the collecting system.47 However, pelvic kidneys may architecture compatible with renal vessels (Fig. 21.22B). Conversely
develop with unusual shapes and degrees of rotation and also may the colon may lie in the vacant renal fossa and this may give a false
show some dilatation of the collecting system.48 These unusual fea- impression of a normally situated kidney.49
tures may make an ectopic kidney difficult to recognise as a kidney, The ectopic kidney usually lies on the correct side of the abdomen
especially if it is an unexpected finding and presents as a mass or pelvis; much more rarely, approximately 1 in 1000 births, it lies
during an examination (Fig. 21.22A). The overall appearance may on the opposite side under a normally positioned kidney (crossed
lead to confusion with a bowel tumour or lymph node mass, by the renal ectopia). The crossed, ectopic kidney is almost always fused
423
CHAPTER 21 Kidneys: anatomy and technique
A B
Figure 21.22 Ectopic kidney. A: Ectopic kidney in the right iliac fossa. B: Colour Doppler shows regular renal arrangement of vessels.
A B
Figure 21.23 Crossed fused renal ectopia. A: A large (13.2cm) reniform mass lies on the right psoas muscle. No kidney could be
seen in the left abdomen. B: Another crossed fused ectopia in which the two components are easily distinguished.
with the other kidney (crossed fused renal ectopia) to produce a Horseshoe kidneys
long, kidney-shaped flank mass, usually with two sinus echo com-
plexes (Fig. 21.23).48 In crossed renal ectopia the ureter from the
ectopic kidney crosses the midline to enter the bladder on the Horseshoe kidneys are a congenital variant, occurring in about 1 in
normal side.12 400 of the population, where the kidneys are linked by tissue
Pancake kidneys are fused ectopic kidneys, usually lying cen- between their lower poles.47,50 The size of this bridge or isthmus
trally in a low abdominal or pelvic position. The normal renal varies from a thin connective tissue band to a full thickness of renal
outlines are not clearly seen and distortions of the renal sinus may parenchyma (Fig. 21.25): usually there is some functioning paren-
add to the difficulties in recognition, although the absence of normal chyma across the midline. Visualisation of the isthmus depends on
kidneys in the renal fossae should alert the examiner to the possibil- its size and the build of the patient; it lies in front of the aorta and
ity (Fig. 21.24).48 Again, colour Doppler is of value in demonstrating IVC and it may be confused with a lymph node mass, pancreatic
a renal pattern of vessels. If there is doubt over the nature of a pos- tumour, aortic aneurysm, retroperitoneal fibrosis or dilated bowel.51
sible ectopic kidney a DMSA isotope scan will confirm the presence Even if the isthmus cannot be identified, the presence of a horseshoe
of renal tissue but CT or arteriography may be required in a few kidney may be suspected from the abnormal shape and orientation
cases for full assessment. of the renal components.52 The long axis of a kidney making up part
424
Congenital variants of renal structure and position
A B
Figure 21.24 Pancake kidney. A: Part of a pancake kidney lying centrally in the pelvis above the bladder. A second component is seen
lying anteriorly. B: CT scan confirms the ectopic kidney.
A B
Figure 21.25 Horseshoe kidney. A: Transverse scan showing a horseshoe kidney with the isthmus crossing in front of the aorta (Ao);
the renal sinus echoes can be seen in the right and left renal components. B: Longitudinal scan showing the isthmus of the horseshoe
kidney anterior to the aorta.
of a horseshoe anomaly is more vertical than normal and is posi- are thought to result from intra-uterine insults which have affected
tioned with the lower pole more medial than the upper pole. In renal development and it may not be possible to make an accurate
addition, there is a degree of malrotation so that the collecting distinction between true congenital hypoplasia and acquired
systems are directed more anteriorly than normal. change.53 Ultrasound provides information on the size of the con-
tralateral kidney but estimates of relative function are best carried
Hypoplasia and atrophy out with isotope renography.
The distinction between these two abnormalities can be difficult on Congenital solitary kidney
ultrasound alone unless there are signs of pre-existing renal disease
such as cortical scarring or a dilated collecting system. A relatively A congenital solitary kidney is more common than ectopia with an
large renal artery or vein is an indication of atrophy since hypoplas- incidence of approximately 1 in 1300 neonates,54 it is more common
tic kidneys have small vessels that are difficult to visualise (Figs on the left side.46 The unilateral absence of a kidney may be due
21.26 and 21.27). However, many cases of congenital hypoplasia to aplasia or agenesis, with aplasia being more common; the
425
CHAPTER 21 Kidneys: anatomy and technique
development of the fetal kidney starts but then fails and the renal
tissue subsequently atrophies.55 Neonatal scanning shows the failed
kidney, which subsequently shrinks and involutes. Agenesis is
rarer; here, the renal tissue fails to develop and so there is no visible
renal tissue.54 In distinction from renal ectopia, the contralateral
kidney shows compensatory hypertrophy. A loop of bowel, usually
colon, may lie in the vacant renal fossa and this can be mistaken for
a kidney.49 The diagnosis may be suggested by ultrasound but it
may require confirmation by isotope studies, CT or angiography in
order to exclude an atrophic or ectopic kidney.
REFERENCES
1. Harrison RG. The urogenital system. In: Romanes GJ, editor.
Cunninghams textbook of anatomy. 12th edn. Oxford: Oxford
University Press; 1981. p. 531.
2. Myers MA. The extraperitoneal spaces: normal and pathologic
anatomy. In: Myers MA, Dynamic radiology of the abdomen. New
York: Springer-Verlag; 1976. p. 116.
3. Brandt TD, Neimann HL, Dragowski MJ, et al. Ultrasound
determination of normal renal dimensions. J Ultrasound Med
Figure 21.26 Hypoplastic kidney. A small but otherwise
1982;1:4952.
normal-appearing kidney suggestive of hypoplasia. Renal length 4. Cronan JJ, Rosenfield AT. Normal size of the adult kidney by real-time
6.08cm. ultrasound (abstract). AJR Am J Roentgenol 1990;154:195.
5. Emamian SA, Nielsen MB, Pedersen JF, Ytte L. Kidney dimensions at
sonography: correlation with age, sex and habitus in 665 adult
volunteers. AJR Am J Roentgenol 1993;160:8386.
6. Wolpert SM. Variation in kidney length during the intravenous
pyelogram. Br J Radiol 1965;38:100103.
7. Cietak KA, Newton JR. Serial quantitative maternal nephro-
sonography in pregnancy. Br J Radiol 1985;58:405413.
8. Farrant P, Meire HB. Ultrasonic measurement of renal inclination; its
importance in measurement of renal length. Br J Radiol
1978;51:628630.
9. Kang KY, Lee YJ, Park SC, et al. A comparative study of methods of
estimating kidney length in kidney transplantation donors. Nephrol
Dial Transplant 2007;22(8):23222327.
10. Hodson J. The lobar structure of the kidney. Br J Urol 1972;44:246261.
11. Pick JW, Anson BJ. The renal vascular pedicle. Analysis of 430
body-halves. J Urol 1940;44:411434.
12. Williams H. Renal revision: from lobulation to duplication what is
normal? Arch Dis Child Online 2007;92:ep152ep158.
13. Dalla Palma L, Rossi M. Advances in radiological anatomy of the
kidney. Br J Radiol 1982;55:404412.
14. Carter AR, Horgam JG, Jennings TA, Rosenfield AT. The junctional
parenchymal defect. A sonographic variant of renal anatomy.
Radiology 1985;154:499502.
15. Kenney IJ, Wild SR. The renal parenchymal junctional line in children:
ultrasonic frequency and appearances. Br J Radiol 1987;60:865868.
16. Dalla Palma L, Bazzichi M, Cressa C, Tommasini G. Radiological
anatomy of the kidney revisited. Br J Radiol 1990;63:680690.
Figure 21.27 Atrophic kidney. A small atrophic kidney measuring 17. Hederstrom E, Forsberg L. Accuracy of repeated kidney size
5.8cm. There are no specific features to suggest the aetiology. estimation by ultrasonography and urography in children. Acta Radiol
1985;26:603607.
18. Ablett MJ, Coulthard A, Lee REJ, et al. How reliable are ultrasound
measurements of renal length in adults? Br J Radiol 1995;68:10871089.
19. Rasmussen SN, Haase L, Kjeldsen H, Hancke S. Determination of
Congenital variants renal volume by ultrasound scanning. J Clin Ultrasound
1978;6:160164.
Ectopic kidney: a kidney which is sited in an abnormal location.
20. Hricak H, Lieto R P. Sonographic determination of renal volume.
Crossed renal ectopia: an ectopic kidney which is sited on the Radiology 1983;148:311312.
contralateral side of the abdomen. 21. Christiansen JS, Gamelgaard J, Frandsen M, Parving HH. Increased
Crossed, fused renal ectopia: the ectopic kidney is on the kidney size, glomerular filtration rate and renal plasma flow in
contralateral side of the abdomen and fused to the normotopic short-term insulin dependent diabetics. Diabetologia 1981;20:451456.
kidney on this side. 22. Feldt-Rasmussen B, Hegedus L, Mathiesen ER, Deckert T. Kidney
Congenital solitary kidney: One of the kidneys fails to develop volume in type 1 (insulin dependent) diabetic patients with normal or
(agenesis), or starts to develop but subsequently fails and increased urinary albumen excretion: effect of long-term improved
metabolic control. Scand J Clin Lab Invest 1991;51:3136.
atrophies (aplasia).
23. Roger SD, Beale AM, Cattell WR, Webb JAW. What is the value of
Horseshoe kidney: the two kidneys are linked by a bridge of tissue
measuring renal parenchymal thickness before renal biopsy? Clin
between their lower poles, this may be a simple fibrous band, or Radiol 1994;49:4549.
functioning renal tissue. 24. Robertson R, Murphy A, Dubbins PA. Renal artery stenosis: the use of
Duplex kidney: the renal collecting system is divided into two duplex ultrasound as screening technique. Br J Radiol 1988;61:
moieties and the ureters from these may join between the kidney 196201.
and the bladder, or have separate insertions into the bladder. 25. Desberg AL, Paushter DM, Lammert GK, et al. Renal artery stenosis:
evaluation with color flow imaging. Radiology 1990;177:749753.
426
References
26. Keoghan MT, Kliewer MA, Hertzberg BS, et al. Renal resistive indices: hydronephrosis of pregnancy. Radiology 1983;146:167170.
variability in Doppler US measurement in a healthy population. 42. Taylor KJW, Burns PN, Woodcock JP, Wells PNT. Blood flow in deep
Radiology 1996;199:165169. abdominal vessels: ultrasonic pulsed Doppler analysis. Radiology
27. Karasch T, Rubin J. Diagnosis of renal artery stenosis and renovascular 1985;154:487493.
hypertension. Eur J Ultrasound 1998;7(Suppl. 3):S27S39. 43. Platt JF, Ellis JH, Rubin JM. Examination of the native kidneys with
28. Buschi AJ, Harrison RB, Brenbridge AN, et al. Distended left renal duplex Doppler ultrasound. Semin Ultrasound CT MR
vein: CT/sonographic normal variant. AJR Am J Roentgenol 1991;12:308318.
1980;135:339342. 44. Gill B, Palmer LS, Koenigsberg M, Laor E. Distribution and variability
29. Atlas SW, Rochester D, Panella JJ, Larson R. The utility of ultrasound of resistive index values in undilated kidneys in children. Urology
in the diagnosis of wandering abdominal viscera. J Clin Ultrasound 1994;44:897901.
1985;13:275277. 45. Terry JD, Rysavy JA, Frick MP. Intrarenal Doppler: characteristics of
30. Patel AS, Barber-Riley WP. Symptomatic medial nephroptosis. Br J ageing kidneys. J Ultrasound Med 1992;11:647651.
Radiol 1982;55:244246. 46. Meyers MA, Whalen JP, Evans JA, Viamonte M. Malposition and
31. Rosenfield AT, Siegel NJ. Renal parenchymal disease. Histopathologic displacement of bowel in renal agenesis and ectopia: new
sonographic correlation. AJR Am J Roentgenol 1981;137:793798. observations. AJR Am J Roentgenol 1973;117:323333.
32. Platt JF, Rubin JM, Bowerman RA, Maru CS. The inability to detect 47. Singer A, Simmons MZ, Maldjian PD. Spectrum of congenital
kidney disease on the basis of echogenicity. AJR Am J Roentgenol renal anomalies presenting in adulthood. Clin Imaging 2008;32:
1988;151:317319. 183191.
33. Rosenfield AT, Taylor KJW, Grade M, DeGraaf CS. Anatomy and 48. Sanders RC. Normal ultrasonic anatomy of the genitourinary system.
pathology of the kidney by grey-scale ultrasound. Radiology In: Resnick MI, Sanders RC, editors. Ultrasound in urology. 2nd edn.
1978;128:737744. Baltimore: Williams & Wilkins; 1984. p. 76.
34. Marchal G, Verbeken E, Ogen R, et al. Ultrasound of the normal 49. Mascatello V, Lebowitz RL. Malposition of the colon in left renal
kidney: a sonographic, anatomic and histologic correlation. agenesis and ectopia. Radiology 1976;120:371376.
Ultrasound Med Biol 1986;12:9991009. 50. Whitehouse GH. Some urographic aspects of the horseshoe kidney
35. MacLachlan M, Wasserman P. Changes in size and distensibility of the anomaly a review of 59 cases. Clin Radiol 1975;25:107114.
ageing kidney. Br J Radiol 1981;54:488491. 51. Mindell HJ, Kupic EA. Horseshoe kidney: ultrasonic demonstration.
36. Hardwick D, Hendry GMA. The ultrasonic appearances of the septa of AJR Am J Roentgenol 1977;129:526527.
Bertin in children. Clin Radiol 1984;35:107112. 52. Bannerjee B, Brett I. Ultrasound diagnosis of horseshoe kidney. Br J
37. Mahoney BS, Brooke-Jeffrey R, Laing FC. Septa of Bertin: a Radiol 1991;64:898900.
sonographic pseudotumour. J Clin Ultrasound 1983;11:317319. 53. Friedland GW. Congenital anomalies of the urinary tract. In: Friedland
38. Yeh H, Milty HA, Wolf BS. Ultrasound of renal sinus lipomatosis. GW, Filly R, Goris ML, et al, editors. Uroradiology: an integrated
Radiology 1977;124:799801. approach. New York: Churchill Livingstone; 1983. p. 1483.
39. Morin ME, Baker DA. The influence of hydration and bladder 54. Hiraoka M, Tsukahara H, Ohshima Y, et al. Renal aplasia is the
distension on the sonographic diagnosis of hydronephrosis. J Clin predominant cause of congenital solitary kidneys. Kidney Int
Ultrasound 1979;7:192194. 2002;61:18401844.
40. Cietak KA, Newton JR. Serial qualitative maternal nephrosonography 55. Hitchcock R, Burge DM. Renal agenesis: an acquired condition?
in pregnancy. Br J Radiol 1985;58:399404. J Paediatr Surg 1994;29:454455.
41. Peake SC, Roxburgh HB, Langlois SL. Ultrasonic assessment of the
427
22
CHAPTER
Pelvi-ureteric dilatation
Tze M. Wah
expertise.15,16 In late pregnancy when the pregnant woman presents intravenous urography is now obsolete in the assessment of preg-
with physiological painful hydronephrosis, the ureter is dilated to nant women with symptoms of acute renal colic.17
the middle third, which usually tapers off and has a smooth outline
on the MR urogram (Fig. 22.1). In contrast, those with pathological Pathological
painful hydronephrosis in pregnancy, renal oedema and a dilated
ureter can be traced to the source of obstruction on the T2-weighted
It is important to diagnose obstructive uropathy promptly in order
sequences on MR urogram (Fig. 22.2A and B). The role of
to salvage the renal tissues and prevent irreversible renal failure as
a result of late diagnosis. Ultrasound plays an important role in the
early assessment of patients with suspected voiding difficulty and
renal colic or loin pain when unenhanced CT is not available or
contraindicated.
A B
Figure 22.2 A: Coronal oblique thin slice MR urography shows an oedematous right kidney with high signal fluid around the kidney and a
dilated ureter that can be traced past the gravid uterus to the right ureteric orifice. B: Axial thin slice T2-weighted MR urography of the
bladder shows the swollen right ureteric orifice and a small passed stone in the bladder that is seen as a round signal void area in the
dependent part (arrow). (A and B courtesy of Dr John Spencer).
429
CHAPTER 22 Pelvi-ureteric dilatation
Ureteral stones
Ultrasound can be used to detect stones in the upper ureter, the
distal ureter or around the vesico-ureteric junction portion of the
ureter behind a filled bladder29 (Fig. 22.7A and B). Many other
approaches have been advocated to visualise the distal ureteral
stone using the transvaginal, rectal or perineal route.3234 Obstruct-
ing calculi causing dilatation in the mid-ureter may also be seen
adjacent to the common iliac vessels but these are often not visu-
alised. The most difficult scenario is when the stone is not causing
any ureteric dilatation and ultrasound is unhelpful in delineating
the cause or the level of obstruction (Fig. 22.8A and B). However,
currently this group of patients presenting acutely with loin
Figure 22.3 Axial US shows a small stone around the midpolar pain are investigated primarily with unenhanced CT KUB810
region which displays intense distal acoustic shadowing (arrow). (Fig. 22.9).
430
Causes of pelvi-ureteric dilatation
A B
Figure 22.4 Staghorn calculus. A: Longitudinal US shows that there is echogenic material in the pelvicalyceal system but this does not
cast posterior acoustic shadowing; this should raise suspicion of a staghorn calculus. B: Unenhanced CT (CT KUB) in the coronal plane
shows the staghorn calculi in the right kidney.
A B
Figure 22.5 Staghorn calculus. A: Longitudinal US here can be misleading as the appearances suggest two fragments of stones within
the calyces; ultrasound underestimates the extent of the staghorn calculi in the left kidney, which is better seen on the unenhanced axial
CT KUB (B).
A B
Figure 22.7 Longitudinal US shows a dilated right pelvicalyceal system (A) and hydroureter that can be traced to the vesico-
ureteric junction (B). The obstruction is caused by an echogenic obstructing stone seen on the axial bladder US examination (C).
432
Causes of pelvi-ureteric dilatation
A B
Figure 22.8 Unenhanced axial CT KUB shows (A) no hydronephrosis or secondary signs of obstructive uropathy in a patient presenting
with acute right renal colic. A small stone is seen at the vesico-ureteric junction causing the obstruction (B).
Blood clot
Blood clot within the dilated pelvicalyceal system is also known as
haemo-hydronephrosis. This can be due to trauma, an infective
Figure 22.11 Longitudinal US shows soft tissue filling the mid process or malignancy. Often it is impossible to delineate whether
and lower pole calyces consistent with transitional cell carcinoma. the blood clot is causing the obstruction or is the result of an
This is causing obstructive dilatation of the upper pole calyces. obstructing lesion causing the bleeding. Any patient presenting
with acute renal colic from a blood clot should be investigated fully
in order to establish the diagnosis. Ultrasound usually shows low
level echoes in the urine within a dilated collecting system, very
similar to those of pyonephrosis, and clinical correlation is usually
the only way to differentiate the two clinical settings (Fig. 22.14A
and B). Occasionally an echogenic blood clot can be seen within the
renal sinus48 or impacted at the pelvi-ureteric junction.
Papillary necrosis
The renal papillae are situated in the renal medulla adjacent to the
calyces. The renal medulla and papillae are vulnerable to ischaemic
necrosis partly because of the special blood supply arrangement
and partly due to the hypertonic environment. They are particularly
susceptible to ischaemia as a result of hypoxia at the medullary
junction in individuals with diabetes or on long-term anti-
inflammatory medication or due to analgesia overuse/abuse. Other
causes include sickle cell disease, pyelonephritis, renal vein throm-
bosis, tuberculosis and obstructive uropathy. Those renal papillae
that necrose, slough off and blunt the calyces. The sloughed
papillae may be impacted in the infundibulum of the calyces and
cause calyceal obstruction.
It is difficult to detect papillary necrosis on ultrasound unless it
is at an advanced stage.49,50 Features may include a prominent pel-
Figure 22.12 Longitudinal US shows absent vascular flow vicalyceal system with increased cortico-medullary differentiation.
within the transitional cell carcinoma filling the mid and lower pole The investigation of choice is with conventional intravenous urog-
calyces. raphy (Fig. 22.15);49,50 however, CT urography is used increasingly
to assess some patients in selected indications. Contrast-enhanced
CT urography is often better at depicting a full range of classical
features including contrast material-filled clefts in the renal medulla,
does not display a Doppler signal (Fig. 22.12). Sometimes TCC non-enhanced lesions surrounded by rings of excreted contrast
obstructs the pelvicalyceal system and can be visualised as an intra- material, and hyperattenuated medullary calcification.51
luminal mass within a dilated collecting system or within the
bladder (Fig. 22.13AC). In the advanced stages, TCC may invade
the renal parenchyma and this is indistinguishable from renal cell
Infections
carcinoma. In the late stage it can also invade the renal vein and Infections within the pelvicalyceal system and ureter can present
inferior vena cava, very similar to renal cell carcinoma.43 with localised infundibular, PUJ or ureteric strictures. The common
It is important to be aware that there are many other causes of causes are tuberculosis52 and fungal infections.
masses within the collecting system. Blood clot can typically be An infundibular stricture usually results in a localised
confused with TCC but normally resolves with time. Fungus balls proximal calyceal dilatation and appears as a rounded fluid-filled
can mimic TCC but this is usually seen as a very echogenic mass.44,45 space. This can be seen adjacent to the margin of the renal sinus,
Other causes include prominent renal papillae that have projected but sometimes within the sinus. The ultrasound appearances of
into a dilated pelvicalyceal system46 or a sloughed papilla can be the obstructive calyceal dilatation are indistinguishable from
seen as a mobile intra-luminal mass; lymphoma and extramedul- non-obstructive calyceal dilatation and frequently urographic
lary haemopoiesis that infiltrate the renal sinus may also simulate techniques such as CT urogram are required for a more
TCC on ultrasound.47 definitive diagnosis.
434
Causes of pelvi-ureteric dilatation
Figure 22.13 Longitudinal and axial US shows a dilated pelvicalyceal system (A and B) caused by a small transitional cell
carcinoma at the right vesico-ureteric junction (C).
A B
Figure 22.14 Axial US shows low level echoes within a mildly dilated pelvicalyceal system consistent with blood clot (A). There is
no colour Doppler signal within it (B). The patient presented with haematuria.
437
CHAPTER 22 Pelvi-ureteric dilatation
A C
will usually resolve when draining the bladder after an interval on ultrasound, perirenal fluid may be detected but the PUJ disrup-
of either urethral or suprapubic catheterisation. Therefore a repeat tion is not normally seen. Contrast-enhanced CT with excretory
scan following catheterisation, usually after 57 days, is important phase is the imaging technique to detect this high-grade renal
to ensure resolution of the upper tract dilatation. injury.
A B
Figure 22.20 Longitudinal (A) and axial (B) ultrasound shows the Mickey Mouse sign.
B
A
C D
Figures 22.21 Longitudinal ultrasound shows the grading of hydronephrosis. A: Non-dilated pelvicalyceal system. B: Mild
hydronephrosis. C: Moderate hydronephrosis. D: Marked hydronephrosis.
As for the dilated distal ureter, this may be shown behind the urine-
filled bladder. FUNCTIONAL EVIDENCE USING
Whenever there is evidence of pelvi-ureteric dilatation, the cause DOPPLER TECHNIQUE
of obstruction should be obtained if possible. Often complementary
imaging such as CT (with or without contrast), retrograde studies
and MR urography may be required to delineate the cause. The Renal blood flow changes
choice of the test will be dependent on patient factors such as
the renal function and the clinical suspicion for the cause of Complete acute obstructive uropathy is normally accompanied by
obstruction. altered renal blood flow and raised renal pelvic pressure. In the
440
Management of obstructive uropathy
A B
Figures 22.22 Reflective index (RI). Doppler ultrasound shows a normal RI in the right kidney (A) and abnormal RI (= 0.77) in the
obstructed left kidney (B) in a patient who presented acutely with left loin pain. (Courtesy of Jane Smith.)
early stage (within the first few hours post obstruction), there is However, an increase in RI is a non-specific indicator for obstruc-
increased renal blood flow which is likely to be related to the dilata- tion. This is because RI tends to increase in a wide range of renal
tion of the afferent arterioles in the acute setting.67 pathologies such as chronic renal disease, acute tubular necrosis,
At the intermediate stage (35 hours post obstruction), the renal haemolytic uraemic syndrome, acute renal vein thrombosis,
blood flow decreases, probably as a result of prostaglandins and pyelonephritis, renal transplant rejection and subcapsular renal
other vasoactive substances due to induced vasoconstriction of the collection.7679
afferent arterioles.68 This usually persists for 24 hours, and at the In acute obstructive uropathy caused by a ureteric stone, the RI
same time, the pressure within the collecting system normalises elevation occurs around 68 hours post obstruction.71,75,80 The most
towards the baseline. useful indicator is the inter-renal RI difference for locating the site
The renal blood flow can be evaluated with the ultrasound of obstruction71,75 (Fig. 22.22A and B). This may be demonstrated in
Doppler technique using the resistance index (RI).6971 The time lines up to 20% of subjects without pelvicalyceal system dilatation.75,80
for the RI changes are as expected from the pathophysiology of However, many studies have a lower sensitivity (4244%)81,82 when
obstructive uropathy, increasing 6 hours post acute obstructive compared with Platts group (87%).80 This could be due to the wide
uropathy and remaining at a peak from 6 to 48 hours. Thereafter range of RIs in normal subjects, time-related response of the RI to the
the RI remains elevated but less markedly so than in the obstruction, possibility of partial or intermittent obstruction, hydra-
earlier stage.71 tion status and probably the use of analgesics that are vasodilators.83
In chronic obstructive uropathy, taking serial RI measurements
30 minutes after intravenous furosemide administration has been
advocated, as this has been shown to be more sensitive than without
DOPPLER TECHNIQUE furosemide.84 Sensitivity was 95% in detecting renal obstruction
when an RI threshold of greater than 0.75 was used to diagnose
urinary tract obstruction.84
Normal RI
Ureteric jets
Measurement of the RI should be obtained from the interlobar or
arcuate arteries. This is sampled using a sample volume of 25mm Ureteric jets may be visualised when scanning a full bladder as
and with a low frequency range (low pulse repetition frequency) and highly echogenic streams on greyscale ultrasound or as areas of
a low wall filter.7 At least three measurements need to be sampled colour on Doppler examination.85,86 The ureteric jets are usually
from three different sites and with three to five waveforms recorded symmetrical on both sides.86
from each site in order to allow calculation of an average RI.72 For optimal assessment, the patient should be hydrated with
The normal RI is less than 0.7,73 though it is higher in neonates 600mL to 1L of fluid. About 1530 minutes following hydration,
and infants. In the first year, the RI is usually greater than 0.7 the bladder should be examined for a period of at least 5 minutes
and it may persist at this level for up to 4 years.74 In the adult, to look for the jet of urine. In high-grade obstruction, most patients
there is a wide variability in the RI even amongst normal individu- demonstrate no ureteric jet; conversely, in low-grade obstruction,
als. In addition, this measurement also varies depending on the very few patients have abnormal flow86 (Fig. 22.23A and B).
site of sampling; hence it is important to obtain an average
measurement.
A B
Figure 22.23 A: Axial ultrasoundshows a left vesico-ureteric junction stone. B: Doppler ultrasound shows that there is flow past the stone
suggesting that the stone is causing only an incomplete obstruction.
A
B
(with excretory phase) are the investigations of choice depending event of crushing renal failure or when there is evidence of
on the clinical scenario. pyonephrosis.
MAG-3 renogram is very useful in assessing the relative function
of the obstructed and non-obstructed kidneys. This information will
allow the clinician to determine whether there is any mileage in Pyonephrosis
saving the chronically obstructed kidney.
The treatment of obstructive uropathy is essentially dependent Pyonephrosis is a urological emergency and performing percutane-
on the cause and radiologists are frequently involved in the acute ous nephrostomy in this situation is very rewarding as it is a life-
setting when there is a need to relieve an obstructed system in the saving procedure.
442
References
The patient normally presents with loin pain and fever. Ultra- ultrasound and isotope renography in evaluation of symptomatic
sound will reveal an obstructed pelvicalyceal system which hydronephrosis in pregnancy. Clin Radiol 2000;55(6):446453.
contains internal echoes consistent with an infected system (Figs 16. Spencer JA, Chahal R, Kelly A, et al. Evaluation of painful
hydronephrosis in pregnancy: magnetic resonance urographic patterns
22.20B and 22.21B).
in physiological dilatation versus calculous obstruction. J Urol
2004;171(1):256260.
Percutaneous nephrostomy 17. Royal College of Radiologists. Making the best use of clinical
radiology services (MBUR) 6th edn, Uroradiology Section 2007.
Ultrasound is the modality of choice to guide the puncture of the Available at: http://mbur.nhs.uk.
18. Sommer FG, Taylor KJW. Differentiation of acoustic shadows due to
dilated pelvicalyceal system. Both free hand and guide attachments
calculi and gas collections. Radiology 1980;135:399403.
fixed to the ultrasound transducer techniques are safe and widely 19. Rubin JH, Adler RS, Bude RO, et al. Clean and dirty shadowing at US:
practised.87 Assessing the dilated system is usually achieved with a a reappraisal. Radiology 1991;181:231236.
19G or 20G sheathed needle through the perinephric tissue along 20. Haddad MC, Sharif HS, Shahed MS, et al. Renal colic: diagnosis and
the line of the ultrasound beam. Local anaesthetic is infiltrated outcome. Radiology 1992;184:8388.
under ultrasound guidance and the procedure is performed under 21. King W, Kimme-Smith C, Winter J. Renal stone shadowing: an
breath holds during suspended inspiration in the cooperative investigation of contributing factors. Radiology 1985;154:191196.
patient or during gentle respiration in confused patients. When the 22. Pollack HM, Arger PH, Goldberg BB, Mulholland SG. Ultrasonic
dilated system is successfully accessed, a small amount of the detection of non-opaque renal calculi. Radiology 1978;127:233237.
23. Weill FS, Bihr E, Rohmer P, Zeltner F. Renal sonography. Berlin:
infected urine should be sent for microbiology assessment. All
Springer-Verlag; 1987. p. 54.
patients with suspected pyonephrosis should be given prophylactic 24. Zwirewich CV, Buckley AR, Kidney MR, et al. Renal matrix calculus:
antibiotics before the collecting system is punctured because punc- sonographic appearance. J Ultrsound Med 1990;9:6164.
turing of the system can lead to septicaemia. 25. Kimme-Smith C, Perella RR, Kaveggia LP, et al. Detection of renal
Depending of the configuration and degree of the dilatation, stones with real time sonography: effect of transducers and scanning
Seldinger and one-stab techniques may be used to site the nephros- parameters. AJR Am J Roentgenol 1991;157:975980.
tomy. In moderate to marked hydronephrosis, both the Seldinger 26. Scanlan KD. Sonographic artifacts and their origins. AJR Am J
technique (Fig. 22.24AC) and the one-stab technique using the Roentgenol 1991;156:12671272.
trocar assembly can be easily performed using ultrasound guidance 27. Choyke PL, Pahira JH, Davros WJ, et al. Renal calculi after shock-wave
lithotripsy: US evaluation with an in-vitro phantom. Radiology
alone. When the system is minimally dilated, the Seldinger tech-
1989;170:139144.
nique is usually performed using both ultrasound and fluoroscopic 28. Middleton WD, Dodds WJ, Lawson TL, Foley WD. Renal calculi:
guidance in the interventional suite. sensitivity for detection with ultrasound. Radiology 1988;167:239244.
29. Baumgartner BR, Steinberg HV, Ambrose SS, et al. Sonographic
REFERENCES evaluation of renal stones treated by extracorporeal shock-wave
lithotripsy. AJR Am J Roentgenol 1987;149:131135.
1. Talner LB. Urinary obstruction. In: Grainger RG, Allison DJ, editors. 30. Kane RA, Manco LG. Renal arterial calcification simulating
Diagnostic radiology. Edinburgh: Churchill Livingstone; 1997. p. 1419. nephrolithiasis on sonography. AJR Am J Roentgenol 1983;140:101104.
2. Amis ES, Cronan JJ, Pfister RC, Yoder IC. Ultrasonic inaccuracies in 31. Amis ES, Hartman DS. Renal ultrasonography 1984: a practical
diagnosing renal obstruction. Urology 1982;19:101105. overview. Radiol Clin North Am 1984;22:315332.
3. Curry NS, Gobien RP, Schabel SI. Minimal dilatation obstructive 32. Laing FC, Benson CB, DiSalvo DN, et al. Distal ureteral calculi:
nephropathy. Radiology 1982;143:531534. detection with vaginal US. Radiology 1994;192:545548.
4. Ellenbogen PH, Scheible FW, Talner BL, Leopold GR. Sensitivity of 33. Lerner RM, Rubens D. Distal ureteral calculi: diagnosis by transrectal
grey scale ultrasound in detecting urinary tract obstruction. AJR Am sonography. AJR Am J Roentgenol 1986;147:11891191.
J Roentgenol 1978;130:731733. 34. Hertzberg BS, Kliewer MA, Paulson EK, Carroll BA. Distal ureteral
5. Talner LB, Scheible W, Ellenbogen PH, et al. How accurate is calculi: detection with transperineal sonography. AJR Am J Roentgenol
ultrasonogaphy in detecting hydronephrosis in azotaemic patients? 1994;163:11511153.
Urol Radiol 1981;3:16. 35. Leder RA, Dunnick NR. Transitional cell carcinoma of the pelvicalices
6. Webb JAW, Reznek RH, White FE, et al. Can ultrasound and and ureter. AJR Am J Roentgenol 1990;155:713722.
computed tomography replace high dose urography in patients with 36. Korobkin M. CT urography. Eur Radiol 2005;15(Suppl 4):D82D84.
impaired renal function? Q J Med 1984;53:411425. 37. Caoili EM, Cohan RH, Inampudi P, et al. MDCT urography of upper
7. Platt JF. Duplex Doppler evaluation of native kidney dysfunction: tract urothelial neoplasms. AJR Am J Roentgenol 2005;184(6):
obstructive and non-obstructive disease. AJR Am J Roentgenol 18731881.
1992;158:10351042. 38. Noroozian M, Cohan RH, Caoili EM, et al. Multislice CT urography:
8. Chowdhury FU, Kotwal S, Raghunathan G, et al. Unenhanced state of the art. Br J Radiol 2004;77 Spec No 1:S74S86.
multidetector CT (CT KUB) in the initial imaging of suspected acute 39. Van Der Molen AJ, Cowan NC, Mueller-Lisse UG, et al. CT
renal colic: evaluating a new service. Clin Radiol 2007;62(10):970977. Urography Working Group of the European Society of Urogenital
9. Pfister SA, Deckart A, Laschke S, et al. Unenhanced helical computed Radiology (ESUR). CT urography: definition, indications and
tomography vs intravenous urography in patients with acute flank techniques. A guideline for clinical practice. Eur Radiol
pain: accuracy and economic impact in a randomized prospective trial. 2008;18(1):417.
Eur Radiol 2003;13:25132520. 40. Subramanyam BR, Raghavendra BN, Madamba MR. Renal transitional
10. Sandhu C, Anson KM, Patel U. Urinary tract stones Part 1: Role of cell carcinoma: sonographic and pathologic correlation. J Clin
radiological imaging in diagnosis and treatment planning. Clin Radiol Ultrasound 1982;10:203210.
2003;58:415421. 41. Grant DC, Dee GJ, Yoder IC, Newhouse JH. Sonography in
11. Heidenreich A, Desgrandchamps F, Terrier F. Modern approach of transitional cell carcinoma of the renal pelvis. Urol Radiol 1986;8:15.
diagnosis and management of acute flank pain: review of all imaging 42. Janetschek G, Putz A, Feichtinger H. Renal transitional cell carcinoma
modalities. Eur Urol 2002;41:351362. mimicking stone echoes. J Ultrasound Med 1988;7:8386.
12. Dhar M, Denstedt JD. Imaging in diagnosis, treatment, and follow-up 43. Hartman DS, Pyatt RS, Dailey E. Transitional cell carcinoma of the
of stone patients. Adv Chronic Kidney Dis 2009;16(1):3947. kidney with invasion into the renal vein. Urol Radiol 1983; 5:8387.
13. Cietak KA, Newton JR. Serial qualitative maternal nephrosonography 44. Stuck K, Silver TM, Jaffe MH, Bowerman RA. Sonographic
in pregnancy. Br J Radiol 1985;58:399404. demonstration of renal fungus balls. Radiology 1981;142:473474.
14. Hertzberg BS, Carroll BA, Bowie JD, et al. Doppler US assessment of 45. Kintanar C, Cramer BC, Reid WD, Andrews WL. Neonatal renal
maternal kidneys: analysis of intrarenal resistivity indexes in normal candidiasis: sonographic diagnosis. AJR Am J Roentgenol 1986;
pregnancy and physiologic pelvicaliectasis. Radiology 147:801805.
1993;186:689692. 46. Dillard JP, Talner LB, Pinckney L. Normal renal papillae simulating
15. Spencer JA, Tomlinson AJ, Weston MJ, Lloyd SN. Early report: calyceal defects on sonography. AJR Am J Roentgenol 1987;
comparison of breath-hold MR excretory urography, Doppler 148:895896.
443
CHAPTER 22 Pelvi-ureteric dilatation
47. Tuite MJ, Weiss SL. Ultrasound and computed tomographic 69. Dodd GD, Kaufman PN, Bracken RB. Renal artery duplex Doppler
appearance of extramedullary haemopoiesis encasing the renal pelvis. ultrasound in dogs with urinary obstruction. J Urol 1991;145:644646.
J Clin Ultrasound 1991;19:238240. 70. Ulrich JC, York JP, Koff SA. The renal vascular response to acutely
48. Rosenfield AT, Taylor KJ, Dembner AG, Jacobson P. Ultrasound of elevated intrapelvic pressure: resistance index measurements in
renal sinus: new observations. AJR Am J Roentgenol 1979; experimental obstruction. J Urol 1995;154:12021204.
133(3):441448. 71. Opdenakker L, Oyen R, Vervlossen I, et al. Acute obstruction of the
49. Ulreich S. Ultrasound in the evaluation of renal papillary necrosis. renal collecting system: the intrarenal resistive index is a useful yet
Radiology 1983;148(3):864. time dependent parameter for diagnosis. Eur Radiol 1998;8:14291432.
50. Hoffman JC, Schnur MJ, Koenigsberg M. Demonstration of renal 72. Keogan MT, Kliewer MA, Hertzberg BS, et al. Renal resistive indexes:
papillary necrosis by sonography. Radiology 1982;145:785787. variability in Doppler US measurement in a healthy population.
51. Jung DC, Kim SH, Jung SI, et al. Renal papillary necrosis: review and Radiology 1996;199:165169.
comparison of findings at multi-detector row CT and intravenous 73. Platt JF, Rubin JM, Ellis JH. Distinction between obstructive and
urography. Radiographics 2006;26(6):18271836. non-obstructive pyelocaliectasis with duplex Doppler sonography. AJR
52. Premkumar A, Lattimer J, Newhouse JH. CT and sonography of Am J Roentgenol 1989;153:9971000.
advanced urinary tract tuberculosis. AJR Am J Roentgenol 1987; 74. Bude RO, DiPietro MA, Platt JF, et al. Age dependency of the renal
148:6569. resistive index in healthy children. Radiology 1992;184:469473.
53. Privett JT, Jeans WD, Roylance J. The incidence and importance of 75. Rodgers PM, Bates JA, Irving HC. Intrarenal Doppler ultrasound
renal duplication. Clin Radiol 1976;27:521530. studies in normal and acutely obstructed kidneys. Br J Radiol
54. Hartman GW, Hodson CJ. The duplex kidney and related 1992;65:207212.
abnormalities. Clin Radiol 1969;20:387400. 76. Platt JF, Ellis JH, Rubin JM, et al. Intrarenal arterial Doppler
55. Nusbacher N, Bryk D. Hydronephrosis of the lower pole of the duplex sonography in patients with non-obstructive renal disease: correlation
kidney: another renal pseudotumour. Am J Roentgenol of resistive index with biopsy findings. AJR Am J Roentgenol
1978;130:967969. 1990;154:12231227.
56. Fernbach SK, Zawin JK, Lebowitz RL. Complete duplication of the 77. Mostbeck GH, Kain R, Mallek R, et al. Duplex Doppler sonography in
ureter with ureteropelvic junction obstruction of the lower pole of the renal parenchymal disease. Histopathologic correlation. J Ultrasound
kidney: imaging findings. Am J Roentgenol 1995;164:701704. Med 1991;10:189194.
57. Snyder HM 3rd, Lebowitz RL, Colodny AH, et al. Ureteropelvic 78. Platt JF, Rubin JM, Ellis JH. Acute renal failure: possible role of duplex
junction obstruction in children. Urol Clin North Am 1980;7:273290. Doppler US in distinction between acute prerenal failure and acute
58. Wah TM, Weston MJ, Irving HC. Lower moiety pelvic-ureteric junction tubular necrosis. Radiology 1991;179:419423.
obstruction (PUJO) of the duplex kidney presenting with pyonephrosis 79. Patriquin HB, ORegan S, Robitaille P, Paltiel H. Hemolytic-uremic
in adults. Br J Radiol 2003;76(912):909912. Erratum in: Br J Radiol syndrome: intrarenal arterial Doppler patterns as a useful guide to
2004;77(915):269. therapy. Radiology 1989;172:625628.
59. Campbell JE. Ureteral peristalsis in duplex renal collecting systems. 80. Platt JF, Rubin JM, Ellis JH. Acute renal obstruction: evaluation with
AJR Am J Roentgenol 1967;99:557584. intrarenal duplex Doppler and conventional US. Radiology 1993;
60. Whitaker RH, Flower CD. Ureters that show both reflux and 186:685688.
obstruction. Br J Urol 1979;51:471474. 81. Tublin ME, Dodd GD, Verdile VP. Acute renal colic: diagnosis with
61. Mascatello VJ, Smith EH, Carrera GF, et al. Ultrasonic evaluation of duplex Doppler US. Radiology 1994;193:697701.
the obstructed duplex kidney. AJR Am J Roentgenol 1977;129:113120. 82. Older RA, Stoll HL, Omary RA, Watson LR. Clinical value of
62. Nussbaum AR, Dorst JP, Jeffs RD, et al. Ectopic ureter and ureterocele: renovascular resistive index measurement in the diagnosis of acute
their varied sonographic manifestations. Radiology 1986;159:227235. obstructive uropathy. J Urol 1997;157:20532055.
63. Gosling JA, Dixon JS. The structure of the normal and hydronephrotic 83. Cronan JJ, Tublin ME. Role of the resistive index in the evaluation of
upper urinary tract. In: OReilly PH, Gosling JA, editors. Idiopathic acute renal obstruction. AJR Am J Roentgenol 1995;164: 377378.
hydronephrosis. Berlin: Springer; 1982. 84. Mallek R, Bankier AA, Etele-Hainz A, et al. Distinction between
64. Notley RG. The structural basis for normal and abnormal ureteric obstructive and nonobstructive hydronephrosis: value of diuresis
motility. Ann R Coll Surg Engl 1971;49:248. duplex Doppler sonography. AJR Am J Roentgenol 1996;166:113117.
65. Kamholtz RG, Cronan JJ, Dorfman GS. Obstruction and the minimally 85. Burge HJ, Middleton WD, McClennan BL, Hildebolt CF. Ureteral jets
dilated renal collecting system: US evaluation. Radiology in healthy subjects and in patients with unilateral ureteral calculi:
1989;170:5153. comparison with colour Doppler US. Radiology 1991;180:437442.
66. Morin ME, Baker DA. The influence of hydration and bladder 86. Dubbins PA, Kurtz AB, Darby J, Goldberg BB. Ureteric jet effect: the
distension on the sonographic diagnosis of hydronephrosis. J Clin echographic appearance of urine entering the bladder. Radiology
Ultrasound 1979;7:192194. 1981;140:513515.
67. Vaughan ED, Shenasky JH, Gillenwater JY. Mechanism of acute 87. Wah TM, Weston MJ, Irving HC. Percutaneous nephrostomy insertion:
haemodynamic response to ureteral occlusion. Invest Urol outcome data from a prospective multi-operator study at a UK
1971;9:109118. training centre. Clin Radiol 2004;59:255261.
68. Curhan GC, Zeidl ML. Urinary tract obstruction. In: Brenner BM,
editor. The kidney. Philadelphia: WB Saunders; 1996. p. 1944.
444
CHAPTER
Renal size
INTRODUCTION
In acute disorders when there is oedema or inflammatory infiltrate,
A wide range of disorders can affect the parenchyma of the kidney, there is usually swelling of the parenchyma and an increase in
producing varying degrees of acute or chronic impairment of func- overall size (Fig. 23.1). However, in the majority of cases of acute or
tion. Patients may be referred for ultrasound with one of several subacute medical renal disease the size of the kidneys remain within
different clinical pictures. They may have suffered a sudden dete- normal limits. In chronic renal disease the kidneys tend to contract
rioration in function with no previous history of renal disease, or as fibrotic changes develop, but the degree to which this occurs is
may have known renal impairment but have deteriorated suddenly very variable and correlation with renal function as well as with the
or more quickly than was expected from their clinical history. type of pathology is poor.24 In some types of chronic renal disease,
Ultrasound is a valuable investigation in the assessment of such as amyloid, the kidneys may enlarge in the initial stages but
patients with impaired renal function from any cause as it does not later contract. Enlargement may also occur if severe acquired cystic
rely on function or require the administration of intravascular con- disease of renal failure develops. In addition, the kidneys are often
trast. Contrast medium may be deleterious to already impaired large in diabetic patients until nephrosclerosis supervenes, when
kidneys which may not have sufficient residual function for they may shrink to normal or below normal size (see below).
445
CHAPTER 23 Medical diseases of the kidney
Cortical changes
In acute nephropathies the cortex may swell and increase in thick- Figure 23.3 Glomerulonephritis and nephrotic syndrome.
ness. The cortical reflectivity may be either reduced (Fig. 23.2), as Increased prominence of the pyramids in a patient with
in acute renal vein thrombosis, or markedly increased, as in some glomerulonephritis and nephrotic syndrome.
cases of acute glomerulonephritis and acute interstitial nephritis
(Fig. 23.3). Assessment of cortical reflectivity can be difficult. In the
past it was compared to that of the adjacent liver or spleen assum- Scarring can be distinguished from fetal lobation by assessing the
ing that these were normal and an estimate made of whether the relationship of the defect to the underlying pyramid and calyx.
reflectivity was less than, equal to or greater than the liver or spleen. With fetal lobation the cortical indentation overlies the interval
In extreme cases of disease the reflectivity of the cortex can be between pyramids rather than overlying a pyramid itself, which is
similar to the renal sinus.2 Normal cortex is generally less reflective the case with cortical scarring.
than the liver or spleen. However, some modern ultrasound Calcification in the cortex may be apparent following acute
machines may not demonstrate much difference between the cortical necrosis and rarely in some cases of chronic
kidney and the adjacent liver in normal patients.5,7 This is a feature glomerulonephritis.
of the equipment pre- and post-processing characteristics and these
should be optimised to enhance display of subtle contrasts between
low-amplitude echoes. Medullary changes and
In chronic disease the reflectivity of the cortex is also variable. corticomedullary differentiation
While the cortex may show no apparent change in appearance in
some patients with severely impaired function, there is a tendency The medullary pyramids may be more prominent in many cases of
for cortical thinning to occur. This is usually proportional to the parenchymal disease as the increased cortical reflectivity increases
overall decrease in renal length but there is no consistent correlation contrast with the echo-poor medullary tissue. In other cases there
with the underlying renal disease.8 Some conditions, such as vesico- may be a decrease in the degree of corticomedullary differentiation
ureteric reflux or segmental infarction, result in cortical scarring. so that the pyramids are poorly defined or even indistinguishable
446
Medical renal diseases
Figure 23.4 Acute glomerulonephritis. Loss of corticomedullary Figure 23.6 Tumour thrombus in the right renal vein extending
differentiation in a patient with acute glomerulonephritis. into the IVC in a patient with renal cell carcinoma.
Vascular disorders
Glomerulonephritis
true velocities may be a problem as adequate visualisation of
the renal artery for angle correction can be difficult.12,23 This term covers a variety of conditions which primarily affect the
n Acceleration time greater than 0.07s: this is measured in the glomerulus. Clinically they are defined by any precipitating factors,
intrarenal arteries and is the time taken from the start of the the clinical presentation and the findings on biopsy. The appear-
systolic acceleration to the systolic peak (Fig. 23.8).27,29 ances on ultrasound are completely non-specific in terms of the
n Loss of the early systolic peak and tardus parvus waveform: pathological type, the degree of renal impairment and the progno-
the normal intrarenal renal artery waveform shows a small sis.2,3 There is some correlation between the degree of reflectivity
peak at peak systole; loss of this and progressive flattening of and interstitial infiltrative changes or fibrosis but this is not of any
the waveform due to slower acceleration (tardus) and slower value in determining the cause of renal impairment or predicting
peak velocities (parvus) correlates with a proximal stenosis the outcome.5,6,44,45
>60% (Fig. 23.8).30 In the acute stages the kidneys can be normal in appearance or
they may show increased cortical reflectivity; they may be normal
The value of Doppler in the assessment of renal artery stenosis is
in size or enlarged. If chronic renal disease develops there is a ten-
that a positive diagnosis indicates a significant lesion but if the
dency for the kidneys to shrink but the degree to which this occurs
study is technically inadequate or has an indeterminate or negative
is variable, as is the amount of increased cortical reflectivity which
result, it does not rule out a lesion and further imaging with iso-
develops or persists. Changes in corticomedullary differentiation
topes or magnetic resonance angiography will be required. The use
also occur, with loss of definition being broadly related to the
of echo-enhancing agents improves the visualisation of both the
degree of inflammation and cellular infiltrate within the paren-
main and peripheral arteries, together with the diagnostic yield, but
chyma (Fig. 23.4). In post-streptococcal glomerulonephritis there
their role has yet to be fully defined.35,36
have been reports of multiple intrarenal echo-poor masses sepa-
rated by highly reflective bands of tissue, although this is not an
Hypertensive renal disease invariable feature.46
causes but a variety of vasculitic and other conditions have been are involved but occasionally the abnormalities may be limited to
described in association with this disorder.47 just two or three pyramids. If calculi form these may be detected in
The renal pyramids are more vulnerable to ischaemic change the region of the pyramids or calyces (Fig. 23.10) and if ureteric
because of the specific arrangement of their blood supply and their obstruction results then this too can be detected on ultrasound.
hypertonic environment so that conditions which further reduce
blood flow or oxygenation produce ischaemic change.48 The initial
changes of central or peripheral papillary necrosis are not visual-
ised on ultrasound but are well seen on intravenous urography and
CT. If total papillary necrosis develops, these changes can be
detected on ultrasound (Fig. 23.9). Calcification of affected papillae
may occur, causing highly reflective regions in the papillae.49 The
affected papillae may slough off, producing small round or trian-
gular cystic areas in the medullary region that can be demonstrated
on ultrasound.50 These sloughed papillae may cause ureteric
obstruction and, if they are calcified, may be mistaken for calculi.51
In the initial stages the renal size and outline are normal but some
loss of renal volume does occur in chronic stages and the renal
outline may become a little irregular due to areas of atrophy
and compensatory hypertrophy, especially if analgesic intake
has ceased.47
A B
Figure 23.10 Medullary sponge kidney. A and B: Two examples of medullary sponge kidneys with calcifications in the medullary
pyramids in two different patients.
450
Miscellaneous disorders
A B
Figure 23.11 Nephrocalcinosis. A: Moderate changes of nephrocalcinosis in a patient with renal tubular acidosis. B: More marked
changes in another patient with hypercalcaemia.
Patients with sickle cell disease may develop papillary necrosis (see Many diseases progress slowly to complete renal failure as neph-
above) but in addition other changes have been reported on ultra- rons are destroyed and the kidney becomes unable to maintain
sound in the kidneys of patients with both homozygous (SS) sickle adequate function. The kidneys are usually contracted (Fig. 23.16)
cell disease, or sickle cell trait (SC). Increased reflectivity can be seen but the appearances do not correlate with the underlying pathol-
in up to a quarter of teenagers without symptoms of renal disease.74 ogy, except in cases of adult polycystic disease.
This may be distributed focally in the renal medulla or diffusely Small, contracted kidneys can be difficult to recognise on ultra-
throughout the parenchyma. The explanation for these changes sound, particularly on the left side, as their reflectivity may be very
have not been clarified but it has been suggested74 that the focal similar to that of adjacent perirenal fat. Larger kidneys are less dif-
medullary changes may be due to mild nephrocalcinosis or possibly ficult to locate. Sometimes the outline of a small kidney is only
iron deposition and the diffuse changes to interstitial and glomeru- apparent from its pattern of movement during respiration.
lar changes that are found in sickle cell disease; however, further
work is required. In another report from the same cohort of sub- Acquired cystic disease of the kidney
jects,75 the same group reported that the mean and height-adjusted
renal length was greater in patients with the homozygous than with The native kidneys of patients with end-stage renal disease are not
the heterozygous form of the disease, which in turn were greater simply small, contracted, fibrotic lumps. In a significant proportion
than the measurements for normal controls. The changes in the of patients (60%) proliferative changes lead to the development of
renal microcirculation result in an increase in the vascular resist- small cysts and adenomas,81,82 a condition called acquired cystic
ance, which is reflected in an increase in the resistance and pulsatil- disease of the kidney (ACDK). These changes are usually seen in
ity indices, especially in patients with severe disease.76 An increase dialysis patients but they may be encountered occasionally in
in the resistive index has been reported as an early predictor of patients with severe renal impairment who have not yet reached
renovascular changes in sickle cell disease and can alert clinicians dialysis.82 Rarely malignant changes can occur and this should be
to the early stages of these changes.77.Sickle cell disease is a rare suspected in any dialysis patient who develops loin pain or
cause of renal cortical calcification. haematuria.81
453
CHAPTER 23 Medical diseases of the kidney
A B
Figure 23.16 End-stage renal disease. A and B: Two examples of small contracted kidneys (6cm) in patients with end-stage renal
disease.
A B
Figure 23.17 Acquired cystic disease of the kidneys. A: Marked changes of acquired cystic disease of the kidney showing multiple
echo-poor areas throughout. B: A different case with a solid lesion towards the lower pole anteriorly (arrow).
The ultrasound appearances vary from a few echo-poor cyst-like changes tend to persist after transplantation85 but a functioning
areas to multiple, usually small, cysts. In severe cases the kidneys transplant appears to protect against the development of these
may be enlarged. Differentiation of small cysts from small adeno- changes in patients without ACDK before operation and there is
mas may be difficult on ultrasound (Fig. 23.17) but this is probably some evidence to suggest that they may even reverse in some cases
not clinically significant in most cases as postmortem studies show following a successful transplant.86,87
a mixture of cystic and solid proliferative changes throughout the
kidneys.83 It is, however, important to identify larger or enlarging,
solid lesions which may represent malignant neoplasms. Dialysis patients
The severity of the changes of ACDK is related to the duration
of time on dialysis, either haemodialysis or continuous ambulatory Patients in end-stage renal failure require dialysis to maintain meta-
peritoneal dialysis (CAPD). Associations with age, sex, type of bolic stability. Two forms have been developed: haemodialysis
disease and haematocrit have also been suggested but the evidence (HD) and continuous ambulatory peritoneal dialysis (CAPD).
for these is still inconclusive. Long-term follow-up shows that the Ultrasound can play a part in the assessment of complications
changes progress slowly and are more pronounced in men.84 The arising in both groups of patients.
454
Renal biopsy
A B
Figure 23.21 Visualisation of biopsy needle. A: The end of the needle is seen adjacent to the renal parenchyma at the lower pole.
B: Following activation of the needle, this is now seen within the cortex of the lower pole.
with platelets between 40000 and 80000/mL. Below 40000/mL a Biopsy is undertaken using a spring-loaded cutting needle. In our
platelet transfusion should be instituted to cover the biopsy. The experience an 18-gauge needle retrieves adequate samples for diag-
PTR should be <1.2 but urgent biopsy with a PTR <1.4 may be justi- nosis in the majority of cases95 but a 16-gauge needle may also be
fied. A PTR >1.4 should be treated with appropriate blood products used without increasing significantly the risk of post-procedural
prior to or during biopsy. haemorrhage. The needle is inserted under direct ultrasound
After appropriate informed consent has been obtained, the control to just above the lower pole of the kidney. The patient can
kidneys are scanned with the patient supine to assess overall shape be asked to vary the depth of respiration to place the kidney in the
and size, as well as to exclude obstruction as a potential cause of appropriate location and then asked to hold their breath. The needle
the impaired renal function. If the kidneys are significantly reduced is then advanced until the tip is seen to impinge on the capsule and
in length (<9cm) with thinned parenchyma (<15mm) it is generally the kidney to move slightly in response to gentle pressure from the
considered that there is irreversible disease and the amount of needle (Fig. 23.21). The biopsy device is then activated and the
useful tissue retrieved at biopsy may not be adequate for accurate needle withdrawn. Care must be taken when the needle tip is close
diagnosis. However, this is not always the case and some patients to the capsule to ensure that it does not lacerate the kidney as the
with parenchymal thickness <15mm may still have potential for kidney moves with respiration.
improvement with appropriate treatment.4 A further potential In normal circumstances, two satisfactory cores of tissue are suf-
problem with thinned parenchyma is that the biopsy needle is more ficient, although more may sometimes be required for specific his-
likely to impinge on the larger blood vessels in the renal sinus, tological techniques. Our practice is to put the first core into
which will increase the risk of post-biopsy haemorrhage. formaldehyde for standard fixing and staining procedures. For the
second core, 23mm of tissue from the cortical (outer) end of the
Technique sample are removed and put into glutaraldehyde for electron
microscopy and the remainder is put onto filter paper in a container
with a small amount of isotonic solution to be kept fresh for immun-
For biopsy of the native kidneys, the patient is best positioned
ofluorescence studies, or frozen section.
prone with a pillow under the stomach to compress the kidneys
Following the procedure the patient is returned to the ward and
posteriorly. If the patient is unable to lie prone, then a semi-
asked to lie quietly in bed for 46 hours with half-hourly pulse and
decubitus position can be used. In patients with haematuria loin
blood pressure checks. If all is satisfactory, then the patient can
pain syndrome it has been suggested that biopsy of the more symp-
resume normal activity, or go home, if the biopsy is being per-
tomatic side may be of value; patients with a focal lesion will also
formed as a day case procedure.
have the side for biopsy predetermined. Otherwise, the kidney to
be identified is chosen as the one that is easier to biopsy safely, as
whatever process is present will affect both kidneys. Usually, the Complications
left kidney is preferred, as it is more easily seen below the twelfth
rib and is normally the one nearer the operator. The aim of the Complications following renal biopsy are usually mild and self-
exercise is to target the lower pole of the kidney, so that the larger limiting. Pain or discomfort at the site of biopsy may occur when
vessels in the renal sinus are less likely to be punctured. the anaesthetic wears off but can usually be treated with oral anal-
After appropriate skin cleansing, local anaesthetic is instilled into gesia. More severe pain may be associated with bleeding and hae-
the skin and subcutaneous tissues. The amount required will vary matoma formation.
from patient to patient; in sensitive patients use of a spinal needle Post-biopsy haemorrhage may result in mild haematuria, or a
under direct ultrasound control to infiltrate anaesthetic down to the small perirenal haematoma; these bleeds are usually self-limiting
renal capsule may be required; in other patients, anaesthetising the but, rarely, more severe haemorrhage may require angiography
skin and subcutaneous tissues may be all that is required. and embolisation. Haemorrhage can also occur if an intercostal
456
Renal biopsy
A B
Figure 23.22 Post-biopsy haematomas. A: A small haematoma at the lower pole following renal biopsy (arrows). B: A larger
haematoma, which was associated with significant haematuria and clot retention (arrows).
selected for biopsy is usually the more accessible pole of the kidney. 18. Hricak H. Sonographic manifestation of renal vein thrombosis:
This will depend to some extent on the location and orientation of experimental study. Invest Radiol 1981; 16:3035.
the transplant. If possible, it is better not to traverse the peritoneal 19. Rosenfield AT, Zeman RK, Cronan JJ, Taylor KWT. Ultrasound in
experimental and clinical renal vein thrombosis. Radiology
cavity, which may come down over part of the kidney. Suitable
1980;137:735741.
access may be achieved with an approach below the incision in a 20. Parvey HR, Eisenberg RL. Image directed Doppler sonography of the
fairly horizontal plane, rather than a vertical approach through the intrarenal arteries in acute renal vein thrombosis. J Clin Ultrasound
lower abdominal wall. Depending on the position chosen it is worth 1990;18: 512516.
using colour Doppler to identify the inferior epigastric artery, if 21. Spies JB, Hricak H, Slemmer T. Sonographic evaluation of
there is a possibility that this may lie in the region of the needle track. experimental acute renal arterial occlusion in dogs. AJR Am J
Either 18-gauge or 16-gauge needles can be used and two cores Roentgenol 1984;142:341346.
should be obtained. In cases of recent transplantation, where the 22. Labropoulos N, Ayuste B, Leon LR. Renovascular disease among
main diagnostic dilemma is distinction between rejection and acute patients referred for renal duplex ultrasonography. J Vasc Surg
tubular necrosis, it is not necessary to provide a specimen for elec- 2007;46:731737.
23. Guzman RP, Zierler RE, Isaacson JA, et al. Renal atrophy and arterial
tron microscopy. However, in cases of renal transplant dysfunction
stenosis: a prospective study with duplex ultrasound. Hypertension
occurring months or years after transplantation, it is useful to 1994;23:346350.
include a specimen for electron microscopy, as one of the causes for 24. Greene ER, Avasthi PS, Hedges JW. Non-invasive Doppler assessment
the deterioration of function in the transplant may be return of the of renal artery stenosis and haemodynamics. J Clin Ultrasound
original disease process that caused renal failure in the first place. 1987;15:653659.
Transplants that have been in place for several years may develop 25. Pick JW, Anson BJ. The renal vascular pedicle, anatomical study of 430
a chronic graft versus host reaction around them. This is not usually body halves. J Urol 1940;44:411434.
of clinical significance but the dense fibrotic shell that may form 26. Desberg AL, Paushter DM, Lammert GK, et al. Renal artery stenosis:
around the kidney in these circumstances can be difficult to pierce evaluation with color Doppler flow imaging. Radiology
1990;177:749775.
with the biopsy needle unless firm pressure is applied to ensure
27. Berland LL, Koslin DB, Routh WD, Keller FS. Renal artery stenosis:
that the needle goes forward into the kidney when activated and prospective evaluation with color duplex US compared with
that it does not simply bounce back and recoil from the kidney. angiography. Radiology 1990;174:421442.
28. Li J, Jiang Y, Zhang S, et al. Evaluation of renal artery stenosis with
hemodynamic parameters of Doppler sonography. J Vasc Surg
REFERENCES 2008;48:323328.
29. Handa N, Fukanaga R, Etani H, et al. Efficacy of echo-Doppler
1. Ritchie WW, Whitely Vick C, et al. Evaluation of azotaemic patients: examination for the evaluation of renovascular disease. Ultrasound
diagnostic yield of initial ultrasound examination. Radiology Med Biol 1988;14:15.
1988;167:245247. 30. Stavros AT, Parker SH, Yakes WF, et al. Segmental stenosis of the renal
2. Hricak H, Cruz C, Romanski R, et al. Renal parenchymal disease: artery: pattern recognition of tardus and parvus abnormalities with
sonographichistologic correlation. Radiology 1982;144:141147. duplex sonography. Radiology 1992;184:487492.
3. Quaia E, Bertolotto M. Renal parenchymal diseases: is characterization 31. Schwerk WB, Restrepo IK, Stellwaag M, et al. Renal artery stenosis:
feasible with ultrasound? Eur Radiol 2002;12:20062020. grading with image-directed Doppler US evaluation of renal resistive
4. Burkhardt H, Hahn T, Gladisch R. Is kidney size a useful predictor of index. Radiology 1994;190:785790.
renal function in the elderly? Clin Nephrol 2003;59:415422. 32. Bude RO, Rubin JM. Detection of renal artery stenosis: it is more
5. Webb JAW. The role of ultrasonography in the diagnosis of intrinsic complicated than originally thought. Radiology 1995;196:612613.
renal disease. Clin Radiol 1994;49:589591. 33. Williams GJ, Macaskill P, Chan SF, et al. Comparative accuracy of
6. Moghazi S, Jones E, Schroepple J, et al. Correlation of renal renal duplex sonographic parameters in the diagnosis of renal artery
histopathology with sonographic findings. Kidney Int stenosis: Paired and unpaired analysis. AJR Am J Roentgenol
2005;67:15151520. 2007;188:798811.
7. Platt JF, Rubin JM, Bowerman RA, Marn CS. The inability to detect 34. Kohler TR, Zierler RE, Martin RL, et al. Noninvasive diagnosis of
kidney disease on the basis of echogenicity. AJR Am J Roentgenol renal artery stenosis by ultrasonic duplex scanning. J Vasc Surg 1986;
1988;151:317319. 4:450456.
8. Roger SD, Beale AM, Catell WR, Webb JAW. What is the value of 35. Karasch T, Rubin J. Diagnosis of renal artery stenosis and renovascular
measuring renal parenchymal thickness before renal biopsy? Clin hypertension. Eur J Ultrasound 1998;7(suppl 3):S27S39.
Radiol 1994;49:4549. 36. Correas JM, Claudon M, Tranquart F, Hlnon AO. The kidney: imaging
9. Taylor KJW, Burns PN, Woodcock JP, Wells PNT. Blood flow in deep with microbubble contrast agents. Ultrasound Q 2006;22:5366.
abdominal vessels: ultrasonic pulsed Doppler analysis. Radiology 37. Luke RG. Nephrosclerosis. In: Schreier RW, Gottschalk CW, eds.
1985;154:487493. Diseases of the kidney. 4th edn. Boston: Little Brown; 1988. p.
10. Rifkin MD, Pasto ME, Goldberg BB. Duplex Doppler examination in 15731595.
renal disease: evaluation of vascular involvement. Ultrasound Med 38. Rasmussen HH, Ibel LS. Acute renal failure. Multivariate analysis of
Biol 1985;11:341346. causes and risk factors. Am J Med 1982;73:211218.
11. Avasthi PS, Greene ER, Scholler C, Fowler CR. Non-invasive diagnosis 39. Rosenfield A. Experimental acute tubular necrosis: ultrasound
of renal vein thrombosis by ultrasonic echo-Doppler flowmetry. appearance. Radiology 1985;157:771774.
Kidney Int 1983;23:882887. 40. Nomura G, Kinoshita E, Yamagata Y, Koga N. Usefulness of renal
12. Robertson R, Murphy A, Dubbins PA. Renal artery stenosis: the use of ultrasonography for assessment of severity and course of acute
duplex ultrasound as a screening technique. Br J Radiol tubular necrosis. J Clin Ultrasound 1984;12:135139.
1988;61:196201. 41. Rosenfield AT, Zeman RK, Cicchetti DV, Siegel NJ. Experimental acute
13. Platt JF, Ellis JH, Rubin JM. Examination of the native kidneys with tubular necrosis: US appearance. Radiology 1985;157:771774.
duplex Doppler ultrasound. Semin Ultrasound CT MR 42. Platt JF, Rubin JM, Ellis JH. Acute renal failure: possible role of duplex
1991;12:308318. Doppler US in distinction between acute prerenal failure and acute
14. Platt J F, Ellis J F, Rubin J M, et al. Intrarenal arterial Doppler tubular necrosis. Radiology 1991;179:419423.
sonography in patients with nonobstructive renal disease: correlation 43. Cosgrove DO, Chan KE. Renal transplants: what ultrasound can and
of resistive index with biopsy findings. AJR Am J Roentgenol cannot do. Ultrasound Q 2008;24:7787.
1990;154:12231227. 44. Paivansalo M, Huttunen K, Suramo I. Ultrasonographic findings in
15. Zubarev AV. Ultrasound of renal vessels. Eur Radiol renal parenchymal disease. Scand J Urol Nephrol 1985;19:119123.
2001;11:19021915. 45. Page JE, Morgan SH, Eastwood JB, et al. Ultrasound findings in renal
16. Clark RA, Wyatt GM, Colley DP. Renal vein thrombosis: an parenchymal disease: comparison with histological appearances. Clin
underdiagnosed complication of multiple renal abnormalities. Radiol 1994;49:867870.
Radiology 1979; 132:4350. 46. Rochester D, Aronsen AJ, Bowie JD, Kunzman A. Ultrasonic
17. Schwerk WB, Schwerk WN, Rodeck G. Venous renal tumour appearance of acute poststreptococcal glomerulonephritis. J Clin
extension: a prospective US evaluation. Radiology 1985; 156:491495. Ultrasound 1978;6:4950.
458
References
47. Nanra RS. Analgesic induced renal disease. In: Schrier RW, Gottschalk 74. Walker TM, Serjeant GR. Increased renal reflectivity in sickle cell
CW, eds. Diseases of the kidney. 4th edn. Boston: Little Brown; 1988. disease: prevalence and characteristics. Clin Radiol 1995;50:
p. 12021207. 566569.
48. Jung DC, Kim SH, Jung SI, et al. Renal papillary necrosis: review and 75. Walker TM, Beardsall K, Thomas PW, Serjeant GR. Renal length in
comparison of findings at multi-detector row CT and intravenous sickle cell disease: observations from a cohort study. Clin Nephrol
urography. Radiographics 2006;26:18271836. 1996;46:384388.
49. Weber M, Braun B, Kohler H. Ultrasonic findings in analgesic 76. Aikimbaev KS, Oguz M, Guvenc B, et al. Spectral pulsed Doppler of
nephropathy. Nephron 1985;39:216222. renal vascular resistance in sickle cell disease: clinical implications. Br
50. Hoffman JC, Schnerr MJ, Koenigsberg M. Demonstration of renal J Radiol 1996;69:11251129.
papillary necrosis by sonography. Radiology 1982;45:785787. 77. Taori KB, Chaudhary RS, Attarde V, et al. Renal Doppler indices in
51. Cheung H, Chan PSF, Metreweli C. Case report: echogenic necrotic sickle cell disease: early radiological predictors of renovascular
renal papillae simulating calculi. Clin Radiol 1992;46:6162. changes. AJR Am J Roentgenol 2008;191:239242.
52. Yendt ER. Medullary sponge kidney. In: Schrier RW, Gottschalk CW, 78. Mukerjee S. Hepatorenal syndrome. eMedicine, 2008: http://www.
eds. Diseases of the kidney. 4th edn. Boston: Little Brown; 1988. p. emedicine.com/med/topic1001.htm.
573582. 79. Platt JF, Ellis JH, Rubin JM, et al. Renal duplex Doppler
53. Palubinskas AJ. Renal pyramidal structure opacification in excretory ultrasonography: a noninvasive predictor of kidney dysfunction and
urography and its relation to medullary sponge kidney. Radiology hepatorenal failure in liver disease. Hepatology 1994;20:362369.
1963;81:963970. 80. Platt JF, Marn CS, Baliga PK, et al. Renal dysfunction in hepatic
54. Sage MR, Lawson AD, Marshall VR, Ryall RL. Medullary sponge disease: early identification with renal duplex Doppler US in patients
kidney and urolithiasis. Clin Radiol 1982;33:435438. who undergo liver transplantation. Radiology 1992;183:801806.
55. Toyoda K, Miyamoto Y, Ida M, et al. Hyperechoic medulla of the 81. Thompson BJ, Jenkins DAS, Allan PL, et al. Acquired cystic disease of
kidneys. Radiology 1989;173:431434. the kidney: an indication for renal transplantation? BMJ
56. Kim Y-G, Kim B, Kim M-K, et al. Medullary nephrocalcinosis 1986;293:12091210.
associated with long-term furosemide abuse in adults. Nephrol Dial 82. Mickisch O, Bommer J, Bachman S, et al. Multicystic transformation of
Transplant 2001;16:23032309. kidneys in chronic renal failure. Nephron 1984;38:9399.
57. Glazer GM, Callen PW, Filly RA. Medullary nephrocalcinosis: 83. Hughson MD, Hennigar GR, McManus JFA. Atypical cysts, acquired
sonographic evaluation. AJR Am J Roentgenol 1982;138:5557. renal cystic disease, and renal cell tumours in end stage dialysis
58. Sefczek RJ, Beckman I, Lupetin AR, Dash N. Sonography of acute kidneys. Lab Invest 1980;42:475480.
cortical necrosis. AJR Am J Roentgenol 1984;142:553554. 84. Ishikawa I, Saito Y, Asaka M, et al. Twenty year follow-up of acquired
59. Gross HH, Hricak H, Filly RA. Ultrasonography in patients with acute renal cystic disease. Clin Nephrol 2003;59:153159.
renal failure. In: Resnick MI, Sanders RC, eds. Ultrasound in urology. 85. Heinz-Peer G, Schoder M, Rand T, et al. Prevalence of acquired cystic
2nd edn. Baltimore: Williams & Wilkins; 1984. p. 147168. kidney disease and tumors in native kidneys of transplant recipients: a
60. Kodner CM, Kudrimoti A. Diagnosis and management of acute prospective US study. Radiology 1995;195:667671.
interstitial nephritis. Am Fam Physician 2003;67:25272534. 86. Vaziri ND, Darwish R, Martin DC, Hosteller J. Acquired renal cystic
61. Scott PP, Scott WW, Siegelman SS. Amyloidosis: an overview. Semin disease in renal transplant recipients. Nephron 1984;37:203205.
Roentgenol 1986;21:103112. 87. Ishikawa I, Yuri T, Kitada H, Shinoda A. Regression of acquired cystic
62. Kim SH, Han JK, Lee KH, et al. Abdominal amyloidosis: spectrum of disease of the kidney after successful renal transplantation. Am J
radiological findings. Clin Radiol 2003;58:610620. Nephrol 1983;3:310314.
63. Ekelund L. Radiographic findings in renal amyloidosis. AJR Am J 88. Moran MR, Rodriguez JMR, Boyero MR, et al. Flow of dialysis fistulas.
Roentgenol 1977;129:851853. Non-invasive study performed with standard Doppler equipment.
64. Subramanyam BR. Renal amyloidosis in juvenile and rheumatoid Nephron 1985;40:6366.
arthritis: sonographic features. AJR Am J Roentgenol 1981;136:411412. 89. Weber M, Kuhn FP, Quintes W, et al. Sonography of arterio-venous
65. Christiansen JS, Gamelgaard J, Frandsen M, Parving HH. Increased fistulae in dialysis patients. Clin Nephrol 1984;22:258261.
kidney size, glomerular filtration rate and renal plasma flow in short 90. Middleton WD, Picus DD, Marx MV, Melsen GL. Color Doppler
term insulin dependent diabetics. Diabetologia 1981;20:451456. sonography of haemodialysis vascular access: comparison with
66. Segel MC, Lecky JW, Slasky BS. Diabetes mellitus: the predominant angiography. AJR Am J Roentgenol 1989;152:633639.
cause of bilateral renal enlargement. Radiology 1984;153:341342. 91. Holland P. Sclerosing encapsulated peritonitis in chronic ambulatory
67. Feldt-Rasmussen B, Hegedus L, Mathiesen ER, Deckert T. Kidney peritoneal dialysis. Clin Radiol 1990;41:1923.
volume in type 1 (insulin dependent) diabetic patients with normal or 92. Hollman A, McMillan M, Briggs JD, et al. Ultrasound changes in
increased urinary albumen excretion: effect of long-term improved sclerosing peritonitis. following continuous ambulatory peritoneal
metabolic control. Scand J Clin Lab Invest 1991;51:3136. dialysis. Clin Radiol 1991;43:176179.
68. Derchi LE, Martinoli C, Saffioti S, et al. Ultrasonic imaging and 93. Cronan JJ. Percutaneous biopsy. Radiol Clin North Am
Doppler analysis of renal changes in non-insulin dependent diabetes 1996;34:12071223.
mellitus. Acad Radiol 1994;1:100105. 94. Murchison J, Cozens N, Allan PL, Winney RJ. Comparison of 18G
69. Banholzer P, Haslbeck M, Edelman E, et al. Sonographic changes in renal biopsy with conventional 14G technique. Br J Radiol
the size of the kidneys in type I diabetes as a method of early 1992;65:594597.
detection of diabetic nephropathy. Ultraschall Med 1988;9:255259. 95. Cozens NJ, Murchison JT, Allan PL, Winney RJ. Conventional
70. Platt JF, Rubin JM, Ellis JH. Diabetic nephropathy: evaluation with 15G needle technique for renal biopsy compared with ultrasound-
renal duplex Doppler US. Radiology 1994;190:343346. guided spring-loaded 18G needle biopsy. Br J Radiol 1992;65:
71. Stanley JH, Cornella R, Loevinger E, et al. Sonography of systemic 594597.
lupus nephritis. AJR Am J Roentgenol 1984;142:11651168. 96. Hergesell O, Felten H, Andrassy K, et al. Safety of ultrasound guided
72. Longmaid HE, Rider E, Tymkin J. Lupus nephritis. New sonographic percutaneous renal biopsy: retrospective analysis of 1090 consecutive
findings. J Ultrasound Med 1987;6:7579. cases. Nephrol Dial Transplant 1998;13: 975977.
73. Platt JF, Rubin JM, Ellis JH. Lupus nephritis: predictive value of 97. Werner M, Oshadchy A, Plotkin E, et al. Increased detection of early
conventional and Doppler US and comparison with serologic and vascular abnormalities after renal biopsies by color Doppler
biopsy parameters. Radiology 1997;203:8286. sonography. J Ultrasound Med, 2007;26:12211226.
459
CHAPTER
A B
A B
Figure 24.4 Pyonephrosis. A: An obstructed kidney with superimposed pyonephrosis. Low-level echoes from debris are visible in
the dilated collecting system. B: A chronically obstructed pyonephrosis with marked parenchymal loss and significant debris within
the collecting system.
A B
A B
Figure 24.6 Xanthogranulomatous pyelonephritis. A: An enlarged kidney (thin arrows) with loss of normal architecture and multiple
cystic areas around a dilated collecting system. B: A different patient with loss of architecture, thickening of the collecting system walls
(arrows) with a calculus (*) and debris in the collecting system.
466
CHAPTER
of Doppler studies in transplant rejection is not discussed in this The right renal artery passes behind the inferior vena cava, then
chapter. roughly posterior to the renal vein to the renal hilum. The left renal
artery runs more directly behind the left renal vein (though not
always directly behind) to the left renal hilum (Fig. 25.1).
Accessory renal arteries are common. It has been estimated that
RELEVANT VASCULAR ANATOMY 22% of patients have more than one artery on one or both sides,
and 2% have three or more accessory arteries (most accessory arter-
The renal arteries normally arise from the aorta about 1.5cm below ies are missed on ultrasound Doppler studies). Accessory renal
the origin of the superior mesenteric artery. The renal artery origins arteries usually arise from the aorta separately from the main trunk
may leave the aorta at a near right angle, or may have a shallower (Fig. 25.2). They occasionally arise from the common iliac artery,
angle. They usually run in a lateral direction although the right the superior mesenteric, inferior mesenteric, adrenal or right hepatic
renal artery origin often leaves the aorta anterolaterally and then arteries. They enter the kidney towards the poles rather than at the
curves downwards and backwards. hila. Most enter the lower pole.
Coeliac axis
Superior mesenteric
artery
Figure 25.1 The main renal arteries. A: An anatomical diagram. B, C: axial plane scans. B: The right renal artery is seen passing
posterior to the vena cava. The right-hand image shows a lateral origin and in the case shown on the left, the right renal artery leaves the
aorta in an anterolateral direction. C: The left renal artery runs posterior to the renal vein.
468
Renal Doppler studies the normal pattern
Arcuate arteries
The renal arteries divide into a variable number of branches Interlobar arteries
usually at or just before the renal hila, although 15% of renal arteries
divide early. The branches form two groups that supply the anterior Segmental arteries
and posterior parts of the kidney respectively. These enter the kidney,
where they are termed segmental arteries. The segmental arteries Renal trunk
divide into the interlobar arteries which run between the pyramids
into the cortex, where they branch into arcuate arteries which form Renal vein
arcades around the corticomedullary junction. The arcuate arteries
then give off many cortical arteries that run radially into the cortex.
These give off the afferent glomerular arteries (Fig. 25.3).
About 90% of the renal blood flow supplies the renal cortex; only
10% the medullary pyramids. This fact is relatively unimportant in
Doppler studies, but is important in the understanding of contrast-
enhanced studies (Fig. 25.4).
The right renal vein runs anterior to the artery to enter the vena
cava. The left renal vein also runs anterior to the artery. It usually
runs more truly parallel to the artery than the right (Fig. 25.1),
although it often wanders slightly. It usually runs between the
aorta and the superior mesenteric artery. Occasionally it runs posterior B
to the aorta (retro-aortic), and occasionally it divides into two branches
that run anterior and posterior to the aorta (circumaortic). Figure 25.3 The renal arteries are seen dividing into the
smaller intrarenal branches. A: Colour Doppler. B: Line diagram.
2. In the main renal trunk and its major branches, the systolic
peak may be rounded or pointed. The peak velocity is about
1.5 metres per second, varying between 1.0 and 2.0 metres per
second. As the intrarenal arteries branch into ever smaller
arteries, the systolic peak becomes more rounded and the
peak velocity becomes lower.
3. From the systolic peak there is a gentle curve to the end of
diastole, and then the next systolic rise. The velocity at the
end of diastole is between 0.4 and 0.3 of the peak systolic
velocity. This may be quantified by several ratios, the most
common being the resistance index (RI). The difference
between the systolic and diastolic velocities decreases a little
(the RI increases) in the smaller arteries towards the periphery
of the kidney.
As the arteries branch towards the periphery of the kidney, their
velocities decrease and the Doppler trace becomes lower. In per-
fectly healthy kidneys, the shape of the waveform is maintained. In
Figure 25.4 Contrast-enhanced ultrasound study (CEUS) of many older patients and in patients with small vessel disease the
a normal kidney. Right: At 15 seconds following intravenous waveform becomes progressively damped. This phenomenon is
injection of contrast the cortex is well perfused (white). As the renal present in many older patients, including those with apparently
pyramids receive only 10% of the renal blood flow, at this stage normal renal function. It may well, however, be due to subclinical
there is less contrast in them and they appear relatively dark. Left: vascular disease.
At 25 seconds sufficient contrast has accumulated in the renal The flow pattern in the renal veins is unremarkable. It varies from
pyramids to make them an equal contrast density to the cortex. continuous to weakly pulsatile flow.
471
CHAPTER 25 Vascular disorders of the kidney
Figure 25.8 Renal artery stenosis. The stenosis is seen on the Figure 25.9 Renal artery stenosis. The spectral waveform is
colour map image as a narrow segment of artery. Often the pale. This is because the power is spread over a larger range of
narrowing is not as clearly seen. Even when it is well seen, spectral velocities. The waveform is nevertheless sufficiently clear to
Doppler is necessary to confirm the stenosis and to assess its establish high velocity and diagnose renal artery stenosis.
severity.
A B
beam and the line of the artery (the Doppler angle) is very impor- present in a short length of the artery. The turbulence is only
tant in order to avoid error. An angle of less than 60 is ideal, present for about 1cm, the increased velocity for less. While the
though it is not always possible, particularly from the anterior majority of stenoses due to atheroma occur at or near the renal
approach. Spectral studies are best obtained in a breath hold; artery origin, some occur along the artery, and occasionally even in
however, this is not always possible. Diagnostic traces may be segmental arteries. Stenoses due to fibromuscular hyperplasia
obtained with the patient breathing; usually at the end of expira- typically occur distal to the origin and are often multiple. It is
tion. A long series of traces, as may be produced in a breath hold, therefore necessary to study the renal artery at more than one site,
will not be obtained, but one full systolic/diastolic waveform is the minimum being three points, origin, mid and hilar. It is some-
all that is needed for interpretation. times possible to run the pulsed wave Doppler along the frozen
It must be understood that in the detection of renal artery steno- colour image of the artery and to study, in real-time, the whole
sis, the changes in waveform that are being sought may only be length. This is ideal.
472
Renovascular hypertension renal artery stenosis
A B
Figure 25.11 Renal artery stenosis. Flow disturbance. A: There is a very irregular spiky maximal velocity envelope, with bright, high
power signal at all velocities, including reversed velocities displayed below the baseline (turbulence). B: In this case the envelope is
smoother, but there is bright, high power signal at all velocities (spectral broadening). Compare the normal renal artery waveform shown in
Figure 25.5 where the high signal is concentrated near the maximum velocity envelope.
Table 25.1 Renal causes of hypertension Table 25.2 Indications for renovascular screening in
hypertension
Renovascular causes
1. Severe hypertension
1. Renal artery stenosis due to atheroma or fibromuscular 2. Difficult to control brittle hypertension
hyperplasia 3. Severe rapid onset flash pulmonary oedema
2. Renal arteriovenous fistula or malformation 4. Onset at a young age (less than 30 years old) or in children
3. Renal artery aneurysm 5. A renal bruit on clinical examination
6. A previous ultrasound study showing a significant
Renal non-vascular causes discrepancy in renal size
7. Deterioration of renal function after onset of treatment with
1. Polycystic kidneys ACE inhibitors
2. Scars
3. Almost any chronic renal disease
4. Renal trauma (Page kidney) Relative indications
8. Late age of onset (more than 60 years)
9. Severe coexisting atheromatous disease
Table 25.4 Tests for renal artery stenosis3 Table 25.5 Criteria for small kidneys
Test Area under the curve Right >2.5cm smaller than left
Left >1.5cm smaller than right
Contrast-enhanced CT 0.99
Contrast-enhanced MRI 0.99
Non-contrasted MRI 0.97
Patients with a high or moderately high suspicion of renal artery
Doppler ultrasound 0.93 stenosis on clinical grounds (Table 25.2) have renal Doppler studies.
Captopril isotope study 0.89 Those that have a positive diagnosis or a high probability on the
Captopril test 0.72 Doppler study proceed to catheter angiography and are consented
for angioplasty at the same procedure provided the angiogram
confirms the diagnosis.
Those that have equivocal renal Doppler studies, those in whom
MR angiography the Doppler study is a technical failure and those in whom the
Doppler study is negative, but there is a very high or increasingly
Magnetic resonance angiograms may be obtained without the use high clinical suspicion of renal artery stenosis, have contrast CT (or
of gadolinium contrast, using flow-specific sequences. The quality sometimes contrast MRI) studies.
of these is, however, generally considered too low for use in the Patients with hypertension but an intermediate or low suspicion
detection of renal artery stenosis. MR angiograms with gadolinium of renal artery stenosis have ultrasound studies, without Doppler,
are of higher quality, comparable to multislice CT, with similar and careful measurement of renal length.
accuracy (Table 25.4). They were considered as an alternative to CT
angiography in patients with renal impairment, but the possible
link between gadolinium use in patients with renal impairment and
Abnormalities on greyscale ultrasound
nephrogenic sclerosing dermopathy is a contraindication to use of studies in hypertension
the technique in patients with poor renal function.
Ultrasound is widely used in patients with hypertension. The
conditions that may cause renal hypertension are listed in
Captopril isotope renography Table 25.1.
Captopril isotope renography relies on changes in the shape of the There are a number of pathologies other than renal artery stenosis
uptake curve of an isotope renogram after administration of capto- that cause small kidneys, and these may all be found in patients
pril if a renal artery stenosis is present. The technique is non- with hypertension. However, whilst the combination of a small
invasive and radiation dose in low. Sensitivity and specificity are, kidney and hypertension may be coincidental, the combination
however, also low. increases the probability of renal artery stenosis sufficiently to
warrant a renal Doppler study.
Renal size may be measured in absolute terms, usually pole to
The captopril test pole length. Tables are available that relate renal size to patient size,
and in children to age (see Chapter 21). It is more common, however,
This is the least accurate test and is not now used. to make a more general judgement on renal size less than 9cm
being regarded as small in adults, with subjective allowance being
Doppler ultrasound made for patient height and age. Comparison of the length on both
sides is usually made. As the left kidney is commonly longer than
The main disadvantage of Doppler ultrasound is that it is extremely the right, a different figure is used for each side (Table 25.5).
operator dependent with a long learning curve. It is more difficult It is important to know, however, that measurement of renal
to perform and sometimes technically not possible in large patients length on an ultrasound study is imprecise. It is very important
and in patients who cannot hold their breath. The percentage of to ensure that a scan plane is obtained that includes the whole
cases that end as technical failures depends on the skill of the opera- length of the kidney. Even with careful technique there is some lack
tor, the quality of the equipment and also on the criteria of a techni- of reproducibility. Nevertheless, the technique is sufficiently accu-
cally successful test. Some studies have reported technical failure rate for clinical use.
rates of 40%, others less than 10%. These apparently daunting facts
have led some to regard Doppler studies as inappropriate in the Abnormalities in renal Doppler studies
investigation of renal artery stenosis. In the view of the author this
is not true.
in hypertension
In children, slim young women with suspected fibromuscular
dysplasia and in transplant kidneys, Doppler ultrasound has a high An arterial stenosis causes changes in the blood flow pattern. These
technical success rate and high sensitivity and specificity. Overall may be detected on a Doppler study. Proximal to the stenosis the
accuracy in all patients with suspected renovascular hypertension flow pattern is usually normal. The exception to this is a very severe
has been a subject of much debate. A comprehensive meta-analysis3 stenosis causing near or total occlusion. In this case there is absent
quoted on the Cochrane database using catheter angiography as the or sometimes reversed diastolic flow. At the stenosis there is
gold standard has shown that Doppler ultrasound has a high sen- increased peak systolic velocity. Immediately distal to the stenosis
sitivity and specificity. This indicates that it is a highly appropriate there is flow disturbance (spectral broadening, turbulence) and in
test (Table 25.4). the distal arteries there is a damped waveform.4 Each of these fea-
While any analysis is open to debate, it is clear that, next to cath- tures will be discussed in turn.
eter angiography, contrast-enhanced CT or contrast-enhanced MRI
are the most accurate tests. Doppler ultrasound is, however, not far Increased velocity
behind. This would seem to support those who advocate Doppler
ultrasound as the primary screening test for patients at high risk on Increased velocity at a stenosis is due to the Venturi effect caused
clinical grounds of having renal artery stenosis. As opinions and by the narrowing. This may be compared with squeezing the end
practices vary so greatly, I will outline current practice in my of a garden hosepipe to increase the velocity and length of the water
department. That is not to say that it is necessarily best practice. jet. The increase in velocity only occurs at a certain degree of
475
CHAPTER 25 Vascular disorders of the kidney
Table 25.6 Criteria for increased peak systolic velocity Table 25.7 Definition of common parameters
High specificity
Systolic rise time Time between the beginning and
1. 2.2 metres per second end of the systolic rise curve
2. >3.5 velocity in the renal artery proximal to the stenosis or Systolic upstroke Systolic frequency/second
the opposite renal artery
Acceleration index Systolic upstroke/carrier frequency
3. >3.5 the velocity in the aorta or the iliac artery (renal-aortic
ratio and reno-ileal ratio) Resistance index, RI (S D)/S where S = systolic
velocity and D = diastolic velocity
Good compromise of sensitivity and specificity
Parameters of a damped waveform:
1. >2 metres per second
2. >2 velocity in the renal artery proximal to the stenosis or 1. Systolic rise time >100 milliseconds
the opposite renal artery 2. Systolic acceleration index <3.75kHz/s
3. >2 the velocity in the aorta or the iliac artery (renal aorto- 3. Resistance index >0.7 (>0.8 indicates a poor result if
renal and reno-ileal ratios) angioplasty is performed)
High sensitivity
Flow disturbance (turbulence)
1. >1.8 metres per second
2. >1.5 the velocity in the renal artery proximal to the stenosis Flow disturbance (loosely termed turbulence) occurs distal to steno-
or the opposite renal artery sis for a length of about 1cm and may be detected in stenoses of
3. >1.5 the velocity in the aorta or the iliac artery (aorto-renal over 40%. Flow disturbance is characterised by a chaotic pattern of
and ileo-renal ratios) colour on the colour flow map. This is, however, unreliable as other
factors such as aliasing may occur if the pulse repetition frequency
(PRF) is too high, and may mimic turbulence. The pattern on spec-
severity of stenosis, which is generally accepted to be about 6070% tral Doppler is more reliable. The waveform has an irregular outline
stenosis. There are several ways of defining the level of peak systo- to the maximal velocity envelope. There is high power flow at
lic velocity that indicates a significant stenosis. Table 25.6 gives a all velocities, including reversed flow. This is termed spectral
set of typical values. The levels chosen depend on whether priority broadening. This causes a very white spectral pattern from the
is given to high sensitivity or high specificity. In our department baseline to the irregular maximal velocity envelope and below the
we use the compromise criteria. baseline (Fig. 25.11). Flow disturbance also has a characteristic
The elevated velocity is only present in a small length of artery sound on audio Doppler.
at and immediately distal to the stenosis. It is important therefore
to study the whole artery with a minimum of three points being
studied. Careful angle correction is also necessary, with an angle of Damping the parvus tardus waveform
insonation of less than 60 being highly advantageous.
The colour map may show the high velocity as aliasing. This A damped waveform is found in all the arteries distal to a severe
produces a confused area of mixed colour (Fig. 25.7). The appear- stenosis. To cause this there must be a significant pressure drop
ances on colour are, however, highly dependent on settings and across the stenosis. As with other parameters, the degree of stenosis
angles. They cannot be relied on in isolation, though they often that causes damping is debated, but it probably occurs somewhere
indicate a part of the artery that warrants further investigation by between a 60% and an 80% or more stenosis. The waveform is flat-
spectral Doppler. The actual stenosis may sometimes be seen as a tened, hence the term damped. More accurately there is a slow rise
narrowed area of artery, but often this feature is not easily appreci- to the systolic peak. There is decreased maximal systolic and diasto-
ated (Fig. 25.8). lic velocity, but the systolic velocity is decreased to a greater extent
The spectral Doppler waveform shows a high systolic peak indi- than the diastolic. Hence the difference between systolic and diasto-
cating high velocity (Fig. 25.7). At the point of high velocity the lic velocities is reduced (Fig. 25.12). The waveform has been termed
spectral waveform often appears pale. This is because the power is the parvus tardus (low and slow) waveform. Parvus refers to the
spread over a larger velocity range (Fig. 25.9). Although the high- decreased velocities, tardus to the slow rise to the systolic peak.
velocity jet occurs at the stenosis and flow disturbance occurs The two features of the waveform may be quantified. The slow
immediately distal to the stenosis, there is an area where there is rise to the systolic peak may be measured by placing a cursor on
both high velocity and flow disturbance (Fig. 25.10). the baseline at the beginning of systole. This may be extrapolated
As well as these changes being shown on the spectral waveform, from the spectral curve. Another cursor is placed at the first systolic
they also have a characteristic sound on audio Doppler. The pitch peak. This is a small peak followed by a notch and is caused by
increases and the volume decreases. It is easy to recognise once closure of the aortic valve (Fig. 25.13). From the position of these
heard. two points the time between them (the systolic rise time) and the
slope of the systolic rise (the systolic upstroke) or the systolic accel-
Renal artery stenosis eration may be calculated. There is software on most ultrasound
machines that will do this. The decreased difference between systo-
In atheromatous renal artery stenosis, the long-term results of lic and diastolic velocities may be measured by obtaining any ratio
angioplasty and stenting are poor. The need for diagnosis is between them. The ratio most commonly used is the resistance
therefore debatable. index (RI) (Fig. 25.13). Normal values are also available for this.
In cases of fibromuscular hyperplasia and in transplanted kidneys, Normal values and those that indicate renal artery stenosis are
the results of angioplasty and stenting are reasonably good, so a available (Table 25.7).
diagnostic test is required.
Doppler ultrasound, in experienced hands, though inferior to CT
angiography or MR angiography, is a good test.
The technique of Doppler studies for
Combining two or more criteria, i.e. elevated peak systolic renal artery stenosis
velocity, turbulence, damping of the distal waveforms, improves
accuracy. The general technique of renal Doppler studies is described earlier
in this chapter. A complete study should ideally include a colour
476
Renal artery occlusion and renal infarction
Doppler study of the whole volume of the kidney with pulsed wave Hypertension in patients with
Doppler (spectral analysis) of at least three segmental or interlobar
arteries and a colour Doppler study of the main renal arteries. A
renal transplants
search should be made for accessory renal arteries (though they are The principles of Doppler detection of renal artery stenosis are
often missed). This is obviously a theoretical limitation of renal similar in transplanted kidneys. There are, however, some differ-
Doppler as it is recognised that stenoses in accessory renal arteries ences, which are discussed here, though reference should also be
may cause hypertension. In practice, however, this is so uncommon made to Chapter 28. Hypertension is common in renal transplant
that it does not invalidate the use of Doppler ultrasound in the recipients. Most cases have no identifiable cause. Renal artery ste-
investigation of hypertension. nosis is, however, relatively common in renal transplants.
Some centres study the intrarenal vessels only. This is undoubt- As stated, many renal transplant patients are hypertensive.
edly a quicker and more practical method of screening, but has Factors that raise the possibility of a stenosis are severe hyperten-
limitations.5,6 These are discussed below. sion, sudden onset or worsening of the hypertension and difficulty
in controlling the hypertension. These factors are indications for a
renal Doppler study.
Doppler study of the intrarenal vessels The transplanted kidney is far easier to study by Doppler than
the native kidney. It is near the body surface and moves little
Study of the intrarenal arteries is far easier than study of the main with respiration (Fig. 25.14). If there is more than one renal artery,
trunk (see the section on the technique of renal Doppler studies) then this will be known from the operation report. Technical fail-
and may be achieved in almost 100% of patients (some extremely ures in Doppler studies of the transplanted kidney are therefore
large patients may be technical failures). The limitations of this are unusual.
discussed below. It is common practice, however, to start the The Doppler features of renal artery stenosis, whatever the aetiol-
Doppler study with the intrarenal arteries. ogy, are the same in the transplanted kidney as in the native kidney.
There is usually mild to moderate turbulence at the transplant
Limitations of the damped artery origin. This is due to the surgical anastomosis and should
not be interpreted as a sign of stenosis unless severe or accompa-
(parvus tardus) waveform nied by high velocity or distal damping. The transplanted renal
Some care should be taken when interpreting the presence or artery often has one or two bends. At a bend in an artery there is
absence of a damped waveform in isolation. Only severe stenoses increased velocity. If the bend is tight, the peak systolic velocity
cause distal damping. There must be a significant pressure drop may even exceed 2 metres per second. There will, however, be no
across the stenosis. turbulence or distal damping.
Also it may be demonstrated that to produce a damped wave-
form, the arteries distal to a stenosis must be compliant (elastic).
This may not be the case if there is extensive atheroma or, in a
transplanted kidney on immunosuppressants, which may cause the RENAL ARTERY OCCLUSION AND
renal artery to be encased in fibrous tissue. RENAL INFARCTION
There are conditions other than arterial stenosis that may produce
a damped waveform. These include chronic renal failure from Renal artery occlusion may be chronic (of gradual onset) or acute.
almost any cause, small vessel disease, old age (probably also due The aetiology, presentation, symptoms, signs and imaging appear-
to subclinical small vessel disease), severe aortic valve stenosis and ances are different in the two forms of the disease. Renal infarction
coarctation of the aorta. In the transplanted kidney, iliac artery is a result of real artery occlusion.
stenosis and chronic rejection may cause damping. It follows that a Chronic renal artery occlusion occurs when renal arteries that are
damped waveform should not be relied on in isolation, particularly stenosed, usually due to atheroma, slowly progress to complete
if renal function is poor. Peripheral renal arteries have low veloci- occlusion. Symptoms and signs are similar to those of severe steno-
ties. This may mimic damping, particularly if the Doppler angle is sis with hypertension and renal impairment, particularly if the
poor. This is discussed in the section on the technique of renal disease is bilateral or superimposed on other chronic renal diseases
Doppler studies. such as hypertensive nephropathy. As there is slow progression
there are no acute symptoms.
Acute renal artery occlusion occurs when thrombus or choles-
Doppler study of the renal trunk terol plaque breaks off from a proximal source and occludes the
Because of the limitations of a study of the intrarenal arteries alone, vessel. Occlusion of the main trunk affects the whole kidney; occlu-
most centres will include a study of the main renal artery.7 For more sion of a branch artery causes a segmental infarct. The source of
details see the section on the technique of renal Doppler studies. thrombus is usually aortic or proximal renal artery atheroma, mural
This is technically more difficult, particularly in large patients and thrombus in an aortic aneurysm or from the left heart in cases of
those who cannot hold their breath. Technical failure rates of up to ventricular infarct with mural thrombus, atrial fibrillation or suba-
40% have been reported. In most centres the figure is probably cute bacterial endocarditis. Aortic dissection or dissection of the
lower than this, but a technical failure rate of 1020% is common. renal artery, often caused by angiography catheter studies, are
Accessory renal arteries, present in about 22% of people, are usually other causes. Symptoms of acute renal artery occlusion are sudden
not detected. onset of flank or lower back pain, nausea and vomiting. There is
usually haematuria, proteinuria and hypertension. Bilateral occlu-
sion results in acute renal failure with anuria.
Children with hypertension Segmental infarcts may also occur in renal transplants when there
is a small polar accessory artery. These small arteries often throm-
Renal Doppler studies on children are often technically easier than
bose in the immediate postoperative period.
in adults. While young children may find it difficult to stay still, the
relative closeness of the renal arteries to the transducer and the
ability to displace overlying bowel gas with light transducer pres- Greyscale ultrasound appearances
sure outweigh the disadvantages. Technical failures are less
common than in adults. This makes Doppler ultrasound an appro- There is little published material on this subject. In cases of chronic
priate diagnostic test in children with hypertension. The Doppler occlusion the kidney slowly shrinks to a small end-stage kidney.
signs and velocity values are the same as in adults. Acute occlusion causes initial swelling of the kidney, which rapidly
477
CHAPTER 25 Vascular disorders of the kidney
A B
Figure 25.15 Renal infarct. A: Two days after the onset of pain there is a well-defined hyperechoic wedge shape area indicating the
infarct. B: A larger infarct showing a hyperechoic area. Typically larger infarcts are less wedge shaped than smaller ones.
A B
Figure 25.17 Renal infarcts. A: A colour flow image of the same case as shown in Figure 25.15A.There are vessels with Doppler flow
either side of, but not in, the infarct. B: Another case with multiple infarcts. A few vessels are seen, but the vasculature is clearly abnormal.
Figure 25.21 Renal cell cancer extending into the IVC. The
moderately echodense tumour is seen with its upper border below
the hepatic veins (right-hand image). The distance between the
cranial extent of the tumour and the hepatic veinIVC junction has
been measured (left-hand image). This is very useful in planning the
surgery.
ARTERIOVENOUS FISTULA
An arteriovenous fistula is a communication between an artery and
vein, either direct or via a pseudoaneurysm. Most are caused by
diagnostic renal biopsy. Other causes are radio-frequency (RF) abla-
tion of renal tumours, stab wounds and blunt trauma.
Arteriovenous fistulae and pseudoaneurysms are common fol-
lowing renal biopsy. Some studies where all post-biopsy patients
were imaged have shown that 1550% develop a fistula. The vast
majority are asymptomatic or have only transient symptoms (hae- Figure 25.25 Arteriovenous fistula. Left: There are high systolic
maturia and flank pain). The majority presumably thrombose or velocities through the fistula. The systolic peak is broadened. Right:
remain small with low flow. A very small minority, less than 1%, The venous waveform. There is a weakly pulsatile (arterialised)
are either sufficiently large de novo, or enlarge over time to present waveform. There is turbulence.
with symptoms or signs such as haematuria, loin pain, hyperten-
sion or deteriorating renal function.
Doppler appearances11,12
Descriptions of Doppler appearances are sparse; however, the
appearances are similar to those of acquired AV fistulae. Circoid
and cavernous AVMs may be distinguished by their vascular pat-
terns (Figs 25.2625.29).
Figure 25.27 Cavernous arteriovenous malformation.
The large single feeding artery and draining vein are shown.
Prognosis
A renal artery aneurysm is said to be at high risk of rupture if it is
greater than 2cm and at intermediate risk if it is between 1.5cm
and 2cm. Intraparenchymal aneurysms are usually very small
(microaneurysm) and not at risk of rupture.
Ultrasound appearances
Figure 25.29 Arteriovenous malformation. There is high There are few descriptions of the ultrasonic appearances of renal
velocity, turbulent and slightly pulsatile arterialised flow in the artery aneurysms. The ultrasound appearances of aneurysms per
draining vein. se are well described, and those originating from the renal artery
have typical features. It is possible that renal artery aneurysms may
be misinterpreted as cortical or parahilar cysts if Doppler is not
used. This is particularly true of small intraparenchymal
aneurysms. The main renal trunk is notoriously difficult to study
and unless a dedicated Doppler study is performed, on a cursory
Table 25.9 Aetiology of renal artery aneurysms
look, with colour Doppler, renal artery aneurysms will often be
Extraparenchymal (85%) missed.
Saccular or fusiform Fibromuscular, dysplasia
Kawasaki disease
False or dissecting Blunt trauma, surgery, Renal artery aneurysm
angiographic catheter injury
These are rare.
Intraparenchymal (15%) They are visible on the colour flow image.
A tortuous artery may simulate the appearance.
Polyarteritis nodosa
Neurofibromatosis
Tuberculosis
Mycotic VASCULAR ASPECTS OF RENAL
EhlersDanlos syndrome
PARENCHYMAL DISEASE AND
DOPPLER STUDIES
Doppler studies are widely used, in conjunction with diagnostic
biopsy, in the investigation of renal transplant dysfunction. This is
not discussed further here but is covered in Chapter 28. Doppler
Table 25.10 Types of renal artery aneurysms studies are less widely used in the investigation of parenchymal
disease, as opposed to primarily vascular disease, in the native
Extraparenchymal Saccular (70%) kidney. Doppler studies do have a role, however, and contrast-
Fusiform (20%) enhanced ultrasound, while not in routine clinical use in the kidney,
Dissecting (10%) may play a part in the future.1315
Intraparenchymal Saccular
485
CHAPTER
Figure 26.1 Simple renal cyst (between cursors) on the upper Figure 26.3 Beak sign. The margins of the kidney extend around
pole of the kidney. Note the increased through transmission of the cyst to form a small beak of renal tissue this confirms the cyst
sound and the clearly defined margins. is renal in origin.
487
CHAPTER 26 Renal cystic disorders
Multiple simple cysts Some syndromes produce multiple renal cysts, but once established
these syndromes usually have innumerable cysts affecting both
The likelihood of finding more than one cyst in a kidney increases kidneys equally. Multiple simple cysts associated with the normal
with age. Each cyst should retain the characteristics of a simple cyst. ageing process may affect the two kidneys in an asymmetric way
and they will always remain countable. The cysts are often of dis-
parate size (Fig. 26.4).
Simple renal cysts
Commonest renal mass lesion.
Increase in prevalence with age. COMPLICATED RENAL CYSTS
Increase in size with age.
Usually asymptomatic. Complicated renal cyst refers to any cyst that does not display
Symptoms due to local pressure effects, infection and entirely simple features. The aim is to identify those features that
haemorrhage. raise the likelihood of underlying haemorrhage, infection, ischae-
Malignant transformation virtually never occurs. mia or malignancy and also to identify those cysts that even though
complicated need no further action.
Septations
A few fine septations of less than 1mm thickness do not stop a cyst
from being regarded as simple. An arbitrary distinction exists that
when a cyst contains more than three or four septations, it is termed
multiloculated. The concern arises when septations are thicker than
a millimetre or show nodularity. It has been suggested that finding
cysts within septa is a marker of malignancy in paediatric cysts.14
Alternatively, finding blood flow in a septum with colour
Doppler, particularly high-velocity pulsatile flow, is a marker of
malignancy.15 More recently, work has concentrated on the role of
contrast-enhanced ultrasound in detecting malignancy. There is a
tendency for the contrast-enhanced ultrasound to upgrade the level
of concern over a cyst compared with multislice CT scans16 and there
is some evidence that the diagnosis of cystic malignancy is more
accurate with contrast-enhanced ultrasound.17 All of this work is
based on the Bosniak grading system derived from his seminal paper
Figure 26.4 Multiple simple renal cysts. The kidney is normal on CT grading published in 1986.18 There have been numerous
size and has several large simple cysts distorting its outline. The papers proving the worth of the system and updating its relevance
fine septations seen in one of the cysts do not stop it being to modern scanners and contrast-enhanced ultrasound (Table 26.1).
regarded as simple.
C
B
F
E
Figure 26.5 A sequence of cysts to illustrate the Bosniak categories. A: A single fine septum is seen, placing this cyst in category
II. B: The septa show minimal thickening, category IIF. C: There is nodular calcification on the septa, category IIF. D: There is a more
complex area adjacent to the septa that showed enhancement on CT, category III. E and F: Frankly malignant lesion with an obvious solid
component, category IV, shown on US (E) and CT (F).
A B
Figure 26.6 Clot retraction in a haemorrhagic renal cyst. The overview (A) and a more magnified view (B) of the organised echoes in
one of the cysts. These represent clot within the cyst.
489
CHAPTER 26 Renal cystic disorders
Haemorrhage debris (Fig. 26.8) and the walls may thicken up due to inflammatory
change. Contained gas may be present. At this point, an infected
Cysts should have anechoic contents; when this is not the case, the cyst is to all intents and purposes no different to an abscess. Such
echoes may be due to haemorrhage, infection, proteinaceous mate- an abscess may spontaneously rupture.26 It is best to aspirate and
rial or colloid. The rate of haemorrhage into simple cysts is based drain infected cysts or abscesses as they are relatively resistant to
on studies predating the advent of sophisticated ultrasound, but is antibiotic treatment.
usually quoted as about 6%. There is a greater rate of haemorrhage Patients with polycystic kidney disease may present with symp-
in patients with polycystic kidney disease, which is, in part, due to toms of an infected cyst. It may be impossible to tell with ultrasound
the great number of cysts present and their greater vulnerability to alone which of the many cysts is the infected one. Positron emission
trauma because of the large size of the kidneys. A fresh haemor- tomography combined with CT can allow accurate identification of
rhage is anechoic, gaining echoes over time. These echoes may settle the culprit.27
out to form layers. Eventually, clot retraction (Fig. 26.6), calcifica- Hydatid (echinococcosis) cysts of the kidney represent a rare
tion and thickening of the cyst wall or formation of septa may occur. form of renal infection. Even though hydatid disease is endemic in
Haemorrhagic cysts are associated with malignancy. Haemorrhage
is hyperdense on CT and is included in Bosniaks classification.
Follow-up of haemorrhagic cysts is prudent either with US or CT
to ensure they are benign. Conversely, benign haemorrhagic cysts
may mimic malignancy and lead to unnecessary surgery.21 Careful
evaluation with contrast-enhanced US or CT should avoid this
mishap.
Perirenal haemorrhage (Fig. 26.7) is also associated with renal
cystic disease, with large retroperitoneal bleeds22 or haemoperito-
neum23 being reported in association with acquired cystic kidney
disease in those on dialysis. Other renal mass lesions, such as angi-
omyolipomas or renal cell carcinomas, may also produce perirenal
haemorrhage.24 The bleed may be large enough to obliterate the
underlying lesion and mimic the features of a complex cystic mass.
If initial imaging does not reveal the underlying cause it is impera-
tive that follow-up imaging is performed once the haematoma has
resolved to look for the underlying cause. It may take up to a year
for a tumour to manifest itself.25
Infection
A pre-existing cyst may become infected or an infection may mani-
fest as an abscess or other complex cystic lesion. Infection of a pre-
existing cyst is either via haematogenous spread or by direct
inoculation during trauma or iatrogenic cyst puncture.
A pre-existing cyst that has become infected may remain indis-
tinguishable from a simple cyst or it may attain quite complex
appearances. It is the clinical picture of fever, flank pain and a
raised white cell count that points towards infection. Infected cysts Figure 26.7 CT scan showing a subcapsular haematoma
may contain echogenic fluid, which may layer out with dependent compressing the renal substance.
A B
Figure 26.8 Debris. A: Layering of debris in the dependent portion of the cyst is seen secondary to infection. B: Similar layering out of
debris is seen in this kidney with pyonephrosis.
490
Complicated renal cysts
Calcification
Calcification is reported in 13% of renal cysts.29 CT is usually better
at detecting calcification than ultrasound. Bright foci in cyst walls
or septa that show ring-down artefact are often seen on ultrasound
but do not correlate with calcification on CT images. Most calcifica- Figure 26.10 A polycystic kidney showing a dense focus of
tions have occurred as a result of a previous cyst complication, such calcification (arrow) with acoustic shadowing.
A B
Figure 26.9 Calcification. A: A small bright focus is seen on an otherwise thin septum in the cyst. This is a small benign calcification.
B: Shows another example in a larger cyst. The calcification shows acoustic shadowing. Care needs to be taken to distinguish this from
an erroneous diagnosis of a dilated renal pelvis containing a stone.
491
CHAPTER 26 Renal cystic disorders
calcifications is merely a reflection of the greater propensity to cyst central necrosis (50%). The cystic component usually shows low-
haemorrhage or infection seen in polycystic kidney disease. level echoes. Next most commonly (30%), a cystic mass might have
Milk of calcium cysts contain a colloidal suspension of calcium several cystic spaces with thick nodular intervening masses con-
crystals (viscous collection of calcium carbonate, calcium phosphate taining adenocarcinoma. Asymmetric necrosis of a carcinoma pro-
or calcium oxalate); these gravitate to form a layer of dependent duces a cystic mass with a solid mass eccentrically placed in its wall
high-reflectivity, which is enough to form shadowing. These cysts (Fig. 26.12).36 These three patterns with their substantial solid com-
are usually asymptomatic. They represent a calyceal diverticulum ponents are quite different to the lesions described in the previous
that has lost its communication with the collecting system. A pitfall paragraph and will all fall into the Bosniak IV category requiring
is to mistake a milk of calcium cyst for a calculus,32 though in some surgery.
cases of stasis, milk of calcium may form in calyces. Demonstrating
the characteristic layering is diagnostic, but often better seen on CT.
Cystic malignancy
The initial premise of the Bosniak classification was to identify cysts
that did not require surgery. Grades I and II do not need surgery,
whereas grades III and IV should be offered surgery, with an
increased likelihood of malignancy being found in the higher grade.
An absence of change in grade IIF lesions helps support the conten-
tion that they are benign. Some authors advocate biopsy of grade
III lesions in an attempt to avoid unnecessary surgery,33 though
there is always the problem of sampling error leading to a false
negative diagnosis, as well as the risk of tumour seeding down the
needle track. The best chance of cure for renal cell carcinoma is
excision of the primary mass before it has metastasised, hence a
high index of suspicion needs to be maintained for cystic masses.
Approximately 1 in 10 renal cell carcinomas will manifest primarily
as a cystic mass. The presence of enhancement with intravenous
contrast agents (on ultrasound, CT or MR) dramatically increases
the likelihood that a lesion is malignant.
Extensively cystic renal neoplasms such as might be classified as
Bosniak II or III lesions fall into one of three diagnoses: multilocular
cystic renal cell carcinoma, cystic nephroma and mixed epithelial
and stromal tumour (MEST) of the kidney.34 These conditions are
indistinguishable preoperatively and biopsy is often misleading.
Multilocular cystic renal cell carcinoma probably only forms 4% of
all renal cell carcinomas (Fig. 26.11).35 Whatever the diagnosis,
prognosis is generally good and nephron-sparing surgery should
be considered. Figure 26.11 Renal cell carcinoma. A coronal reformatted image
Most renal cell carcinomas showing central cystic change are from a CT scan showing a multilocular cystic renal cell carcinoma
unilocular with thick irregular walls because they have undergone at the upper pole of the right kidney.
A B
Figure 26.12 Asymmetric necrosis. Ultrasound (A) and CT (B) of a renal cell cancer that has shown asymmetric necrosis to produce a
cystic mass with an eccentrically placed solid mass in its wall.
492
Differential diagnosis of a renal cyst
A B
Figure 26.15 Two views of a paracalyceal cyst containing milk of calcium. This casts an acoustic shadow.
A B
494 Figure 26.17 A fetal example of an obstructed upper moiety in a duplex kidney resembling a cyst (A) and associated with a
ureterocele (B).
Differential diagnosis of a renal cyst
are elongated and run alongside the adjacent pelvicalyceal system a cystic neoplasm preoperatively turns out to be a lymphangioma
(Fig. 26.19). on postoperative histology.
Renal lymphangiectasia and lymphangiomas are part of the same
spectrum of lymphatic ectasia and may occur in the peripelvic Haematoma
space or perirenal space.39 The usual diagnostic error is to confuse
them with hydronephrosis rather than cysts.40 Very rarely, the lym-
A recent haematoma may be indistinguishable from a cyst. The
phangioma is shown to communicate with the excretory system.41
diagnosis should be suspected if there is a history of trauma.
Peripelvic lymphangiectasia is associated with perivascular cysts
Sequential ultrasound scans will show development of echoes
(probably dilated lymph vessels), most easily seen in the peri-aortic
within the lesion as it matures and eventually clot retraction (a
space. Perirenal cysts seen in lymphangiectasia appear to arise in a
pattern analogous to the maturation of a haemorrhagic ovarian
capsular location rather than from the renal cortex.42
cyst). Doppler ultrasound is useful to show that the kidney is still
Lymphangiectasia and lymphangiomas are benign lesions. Inter-
perfused after renal trauma. Iatrogenic trauma, usually following
vention is only needed if they are causing pain by local space-
biopsy, may show a focal haematoma and be associated with aneu-
occupying effects. Occasionally, resection of a lesion thought to be
rysm or arteriovenous fistula formation. Despite this, most iatro-
genic haematomas or arteriovenous fistulae are not associated with
long-term sequelae and usually resolve spontaneously.43 Contrast-
enhanced CT is the preferred imaging modality in the assessment
of blunt renal trauma. It not only shows the renal trauma but is
sensitive for associated trauma to other abdominal viscera.
Some haematomas occur spontaneously as a result of an unsus-
pected underlying lesion such as an angiomyolipoma.44 Other
tumours are also implicated, e.g. metastatic trophoblastic tumour.45
These spontaneous bleeds usually adopt a subcapsular location and
compress the underlying parenchyma (Fig. 26.20). Rarely, over the
long term, osmotic forces may cause the subcapsular haematoma
to swell and compress the kidney enough to compromise its func-
tion the so-called page kidney. The compressed kidney may be
hard to discern around the margin of the cyst on ultrasound.
A B
Figure 26.19 Peripelvic cysts. Ultrasound (A) shows elongated cysts paralleling the course of the pelvicalyceal system. They are easy to
mistake for hydronephrosis but CT urography (B) shows the contrast-filled pelvicalyceal system running between the cysts.
495
CHAPTER 26 Renal cystic disorders
entities, however, show no diagnostic difficulty once they are inter- of the lower urinary tract.48 Renal abscesses from haematogenous
rogated with colour Doppler ultrasound, although some care spread usually arise in the renal cortex and those from ascending
needs to be taken with lesions showing very low, slow flow with infection in the medulla. Perirenal abscesses arise from rupture of
compensatory adjustment of the Doppler parameters to allow a renal abscess or direct haematogenous spread. Common underly-
detection. Occasionally CT will misinterpret a venous varix as an ing conditions include diabetes mellitus, cirrhosis, urinary obstruc-
enhancing mass.46 These vascular anomalies may have no symp- tion and stones.
toms and can be picked up incidentally on investigations done for Ultrasound signs may be non-specific initially, showing global
other purposes.47 enlargement of the kidney and a focal mass (Fig. 26.22). If progres-
sion to true abscess occurs then typical appearances are of a thick-
Renal abscess walled mass with a liquefied centre containing turbid echoes (Fig.
26.23). CT outperforms ultrasound in identifying abscess forma-
tion49 and is indicated if ultrasound is inconclusive. Ultrasound
Before antibiotics, haematogenous spread of Staphylococcus aureus
alone has a risk of incorrect diagnosis about 14 times higher than
was the common cause of renal and perirenal abscess formation. In
when combined with CT scan. Ultrasound tends to miss perine-
recent times, it is more common for infection to be caused by
phric abscesses associated with pyonephrosis, and gas-forming
Escherichia coli and Klebsiella pneumoniae from ascending infections
abscesses. Emphysematous infections carry a risk of misdiagnosis
19 times greater with ultrasound alone than with CT. CT is also
better at identifying underlying stones than ultrasound. Ultrasound
is particularly insensitive to mid-ureteric calculi.
A B
Figure 26.21 Aneurysm. The sonolucent structure by the hilum of this transplant kidney could be mistaken for a cyst on greyscale
ultrasound (A) but power Doppler (B) clearly shows it is an aneurysm containing blood flow.
496
Differential diagnosis of a renal cyst
A B
Figure 26.24 Infected cysts may look identical to a thick-walled abscess and have uniform internal echoes (A). Layering of debris may
also occur (B).
A B
Figure 26.25 Cystic nephroma. A and B: Two examples of a focal collection of cysts surrounded by a capsule as seen in cystic
nephromas. Differentiation from a multilocular cystic carcinoma can be impossible preoperatively.
497
CHAPTER 26 Renal cystic disorders
Recently described is a new entity, the mixed epithelial and may be obstructed by oxalate crystals, interstitial fibrosis or hyper-
stromal tumour. It is likely that this forms part of the same spectrum plasia. Cysts continue to form in end-stage failure and development
as a multilocular cystic nephroma.50 Morphologically they are the of ACKD is associated with being on dialysis, whether haemodialy-
same, with multiple non-communicating cysts, though there are sis or peritoneal. Men are much more commonly affected. The rate
histological differences. of increase in size is greatest in young men and this may mimic the
The difficulty with these lesions, be they cystic nephroma (CN) onset of polycystic disease. The longer someone has been on dialy-
or MEST, is to distinguish them from multilocular cystic malig- sis the more likely they are to have ACKD. Transplantation of a
nancy. Other potential diagnostic confusions can exist with multi- functioning kidney gives protection against the development of
cystic dysplastic kidney or abscesses. Both CN and MEST are likely ACKD and may even cause some changes to regress. There is a
to be graded as Bosniak III lesions on imaging, with MEST more well-known association with cystic renal cell carcinoma, occurring
likely to show enhancing nodules. Both CN and MEST are benign in 19% of those with ACKD.53 Failure of a cyst to regress following
entities that are usually treated with excision, the true diagnosis transplantation when all the other cysts are regressing is suspicious
being made following resection. One series, however, reports two for the development of renal cell carcinoma. The Bosniak classifica-
patients with CN having concomitant renal cell carcinomas and one tion is useful to assess the risk of malignancy in each cyst, but since
patient with MEST having a sarcomatous component.51 the likelihood of renal carcinoma in complicated cysts of ACKD is
high (about 50%), it is prudent to offer resection even in Bosniak
Localised cystic disease IIF lesions.
Most patients with ACKD are asymptomatic but flank pain, hae-
maturia and colic may develop if the cysts rupture or bleed.
Simple renal cysts may occur in an asymmetric fashion and occa-
Typical ultrasound features are of a small, bright kidney contain-
sionally the only cysts present will be clustered together in one part
ing a number of small (0.53.0cm) cysts, either cortical or medul-
of one kidney. It should be possible to identify each cyst as a sepa-
lary (Fig. 26.26). Cysts are commoner at areas of scarring. If enough
rate entity, although if cysts are abutting each other their walls may
cysts develop the kidney may become enlarged. Small cysts may be
be mistaken for a dividing septum in a single cyst. Other differential
indistinguishable from solid lesions. Haemorrhagic complications
possibilities to be kept in mind are multicystic dysplastic change in
have the same imaging appearances as in other cysts. One series
one moiety of a duplex kidney or focal dilation of one part of the
showed that over a 7-year period, 17% of ACKD patients suffered
collecting system.
large haemorrhagic cysts and 13% large perinephric haematomas.54
If patients are also being treated with anticoagulants, then episodes
of haemorrhage are more likely to occur and they may be large
Differential diagnosis of a renal cyst enough to be life-threatening.
Interestingly, the transplant kidney, even if left in place after it
Medullary pyramids evenly spaced, triangular shape. has failed, almost never develops ACKD.
Papillary necrosis typical position of a pyramid and may contain
an echogenic focus.
Hydronephrosis dilated calyces show communication with each
other. Acquired cystic kidney disease
Lymphatic cysts may be impossible to distinguish from the
pelvicalyceal system without using CT urography. Associated with dialysis, prevalence increasing with increasing
Haematoma recent history of trauma is helpful. Look for an length of dialysis.
underlying lesion. Cysts of 0.53.0cm form in failing kidneys that are not otherwise
Aneurysms colour Doppler helps avoid misdiagnosis. cystic.
Abscesses clinical features of fever and raised white cell count. Usually asymptomatic.
Hydatid be aware of this in people from endemic areas. Commoner in men.
Cystic nephroma multiloculated benign tumours; diagnosis may Renal transplantation provides protection against developing
not be possible without histology. cysts.
Increases the likelihood of spontaneous renal haemorrhage.
Strong association with cystic renal cell carcinoma.
normal contralateral kidney to have reduced growth.55 Most cases Polycystic kidney disease
of multicystic dysplastic kidney are sporadic but there has been the
occasional reported instance of familial recurrence.56 Autosomal recessive polycystic kidney disease (ARPKD) may
Ultrasound features are of numerous discrete cysts of varying present in utero or in childhood and has been categorised into
sizes replacing all or nearly all of the renal substance (Fig. 26.27). perinatal, neonatal, infantile and juvenile forms. All forms are
The cysts show no inter-communication, distinguishing them from caused by the same genetic defect related to chromosome 6p21.57
a hydronephrosis. The outline of the kidney is uneven due to the Pathologically the features are of bilateral kidney involvement
presence of the cysts. with multiple microcysts and liver involvement with portal and
A similar process of post-obstructive cystic dysplasia (Fig. 26.28) interlobular fibrosis. The ultrasound features are of bilateral, sym-
of the kidney may occur as a response to urinary tract obstruction metrically enlarged, smooth-outlined kidneys (Fig. 26.29). They are
at other times in utero. In these instances, the kidney may show a of generally increased reflectivity due to the numerous interfaces
hydronephrotic renal pelvis surrounded by a cortex replaced by provided by the microcysts (each being too small to individually
innumerable cysts of different sizes. Otherwise, distinction from a resolve). Occasionally a discrete cyst may develop and the bright-
true multicystic dysplastic kidney may be impossible on imaging. ness of the kidney may reduce around its periphery as the size of
Ureteroceles are occasionally seen on the ipsilateral side to a mul- the microcyst expands. The kidneys may appear normal initially.
ticystic dysplastic kidney. A not uncommon scenario is for the kidneys to look normal at the
A B
Figure 26.27 Multicystic dysplastic kidney. A: Transverse view of the fetal abdomen shows a unilateral right multicystic dysplastic
kidney between the cursors and a normal left kidney; prognosis is good. B: Bilateral multicystic dysplastic kidneys in a fetus; prognosis is
poor as there is no urine production and hence no liquor.
499
CHAPTER 26 Renal cystic disorders
A B
Figure 26.29 Autosomal recessive polycystic kidney disease. A: Longitudinal view of a fetus with ARPKD. The kidneys are
symmetrically smooth, bright and large. There is no liquor, indicating these kidneys have ceased to function. B: Pathological specimen of
an autosomal recessive polycystic kidney showing numerous tiny elongated cysts peripherally.
time of the 20-week in-utero anatomy scan but to have become with ADPKD and increase in size and number with age. Women
enlarged and non-functioning by term pregnancy. If the condition suffer more severe liver disease than men. Cysts may occur in other
is diagnosed in utero, then the prognosis is generally poor and the organs too, being reported in seminal vesicles, pancreas, spleen and
baby may succumb at birth due to underdeveloped lungs caused ovary.
by a lack of liquor. Those that have a lesser degree of renal involve- Patients with ADPKD suffer from infective or haemorrhagic com-
ment are usually diagnosed at a later age; they may have better plications of their renal cysts. The symptoms and signs are the same
renal function but will suffer from portal hypertension secondary as the same complication in someone with an isolated cyst but
to the hepatic cysts and periportal fibrosis. Children who survive because there are so many cysts the frequency with which an
the perinatal period have a better prognosis than is generally per- ADPKD individual is affected is greater. It can be difficult to tell
ceived.58 The parents have a 1 in 4 chance of having another which cyst of the many present is responsible for the patients
affected child. symptoms. Positron emission tomography helps to identify the
Autosomal dominant polycystic kidney disease (ADPKD) usually culprit.27 Polycystic kidneys are more likely to suffer from trauma
presents in the fourth or fifth decade of life with renal impairment, because they are enlarged. Calculi are seen in up to 20% of ADPKD
hypertension, haematuria and abdominal pain. The commonest patients. Smaller calculi usually pass spontaneously even if renal
mode of presentation is with hypertension.59 The condition may function is impaired. The management of larger calculi is compli-
also be detected serendipitously during ultrasound imaging for cated by the presence of the cysts, percutaneous techniques and
other reasons. ADPKD is caused by a mutation in PKD1 (chromo- lithotripsy being relatively contraindicated.
some 16p13.3) or PKD2 (chromosome 4q2123).60 Those with the
PKD2 mutation show a lesser severity of disease. Screening of off-
spring of affected adults is normally by ultrasound. The essence of Von HippelLindau disease
the test is that renal cysts in normal people are rare below the age
of 30 so detection of cysts forms the basis of diagnosis. The criteria Von HippelLindau disease is inherited in an autosomal dominant
have been modified recently so that if the genotype of the family is fashion with variable expression and penetrance of the gene and is
unknown, those with the less severe PKD2 form will not be missed.61 characterised by the development of a variety of benign and
The presence of three or more renal cysts (unilateral or bilateral) in malignant tumours.63 The spectrum of clinical manifestation is
those aged 15 to 39 years, two or more cysts in each kidney at ages wide. It usually presents after the second decade of life and will
40 to 59 years, and four or more cysts in each kidney for those over feature one or more of the following: renal cysts 75%; cerebellar
60 years of age is enough in the presence of an established family haemangioblastoma 3560%; retinal angiomatosis 50%; renal aden-
history to confirm the diagnosis. Conversely, an at-risk individual ocarcinoma 2545% (Fig. 26.31); phaeochromocytoma 10%;
older than 40 years who has fewer than two renal cysts does not endolymphatic sac tumours; epididymal cystadenomas; and
have the disease. pancreatic cysts and tumours. The commonest causes of death
Once the condition of ADPKD becomes established, innumerable are renal cell carcinomas and complications from cerebellar
renal cysts of varying sizes disrupt the normal architecture of the haemangioblastomas.
kidney and the kidneys become considerably enlarged (Fig. 26.30). Genetic testing is available, but, because the syndrome may man-
The size of the kidneys is related to renal function and hyperten- ifest in many different ways, imaging is essential in identifying
sion; an increase in cyst volume correlates with decline in renal tumours. Screening is advocated as the tumours in von Hippel
function. Magnetic resonance can be used to obtain volumes of the Lindau disease are treatable and early detection allows more con-
entire kidney in a reproducible fashion and show changes over as servative procedures, in turn improving the patients length and
short a period as 6 months.62 Liver cysts occur in up to 67% of those quality of life.
500
Cystic diseases of the kidney
A B
Figure 26.30 Autosomal dominant polycystic kidney disease on ultrasound (A) and coronal reformatted CT (B). Note the differing
sizes of the cysts and that there are cysts in the liver. This is an advanced example with the kidneys greatly enlarged by innumerable cysts.
Earlier in the onset of the disease the cysts may be much less numerous.
A B C
Figure 26.31 Von HippelLindau disease. Screening is used to detect the onset of renal disease with either cysts or solid tumours.
A: A complex cyst developing next to a more simple cyst. Magnetic resonance (B, C) is a better tool to assess the kidneys once the
initial lesions are detected by ultrasound screening.
501
CHAPTER 26 Renal cystic disorders
502
References
A
B
503
CHAPTER 26 Renal cystic disorders
complex cystic renal masses using the Bosniak classification system. 42. Surabhi VR, Menias C, Prasad SR, et al. Neoplastic and non-neoplastic
Clin Hemorrheol Microcirc 2008;39:171178. disorders of the perirenal space: cross-sectional imaging findings.
17. Quaia E, Bertolotto M, Cioffi V, et al. Comparison of contrast- Radiographics 2008;28:10051017.
enhanced sonography with unenhanced sonography and contrast- 43. Chichakli R, Krause R, Voelzke B, Turk T. Incidence of perinephric
enhanced CT in the diagnosis of malignancy in complex cystic renal hematoma after percutaneous nephrolithotomy. J Endourol
masses. AJR Am J Roentgenol 2008;191:12391249. 2008;22:12271232.
18. Bosniak MA. The current approach to renal cysts. Radiology 44. Lenton J, Kessel D, Watkinson AF. Embolisation of renal
1986;158:110. angiomyolipomas: immediate complications and long-term outcomes.
19. Ascenti G, Mazziotti S, Zimbaro G, et al. Complex cystic renal masses: Clin Radiol 2008;63:864870.
characterization with contrast-enhanced US. Radiology 2007;243: 45. Vijay RK, Kaduthodil MJ, Bottomley JR, Abdi S. Metastatic gestational
158165. trophoblastic tumour presenting as spontaneous subcapsular renal
20. Israel GM, Bosniak MA. How I do it: evaluating renal masses. haematoma. Br J Radiol 2008;81:e234e237.
Radiology 2005;236:441450. 46. Deibler AR, Nadig SN, Curry N, et al. Intrarenal varix presenting as
21. Fujii Y, Higashi Y, Owada F, et al. Benign haemorrhagic renal cysts an enhancing renal mass with calcifications. J Urol 2001;166:997998.
mimicking cystic renal cell carcinoma. Hinyokika Kiyo 47. Asakuma J, Miyajima A, Sawazaki H, et al. Incidentally discovered
1993;39:11131117. giant renal arteriovenous malformation. Int J Urol 2001;8:322325.
22. Moore AE, Kujubu DA. Spontaneous retroperitoneal hemorrhage due 48. Lee BE, Seol HY, Kim TK, et al. Recent clinical overview of renal and
to acquired cystic kidney disease. Hemodial Int 2007;11(Suppl 3): perirenal abscesses in 56 consecutive cases. Korean J Intern Med
S38S40. 2008;23:140148.
23. Borras M, Valdivielso JM, Egido R, et al. Haemoperitoneum caused by 49. Stojadinovic M, Micic S, Milovanovic D. Ultrasonographic and
bilateral renal cyst rupture in an ACKD peritoneal dialysis patient. computed tomography findings in renal suppurations: performance
Nephrol Dial Transplant 2006;21:789791. indicators and risks for diagnostic failure. Urol Int 2008;80:389397.
24. Zhang JQ, Fielding JR, Zou KH. Etiology of spontaneous perirenal 50. Jevremovic D, Lager DJ, Lewin M. Cystic nephroma (multilocular cyst)
hemorrhage: a meta-analysis. J Urol 2002;167:15931596. and mixed epithelial and stromal tumour of the kidney: a spectrum of
25. Prando A, Prando D, Prando P. Renal cell carcinoma: unusual imaging the same entity? Ann Diagn Pathol 2006;10:7782.
manifestations. Radiographics 2006;26:233244. 51. Lane BR, Campbell SC, Remer EM, et al. Adult cystic nephroma and
26. Vaidyanathan S, Hughes PL, Oo T, Soni BM. Spontaneous rupture of mixed epithelial and stromal tumor of the kidney: clinical,
an infected renal cyst and external drainage through a lumbar surgical radiographic, and pathologic characteristics. Urology 2008;71:
scar in a male patient with cervical cord injury: a case report. J Med 11421148.
Case Reports 2008;2:154. 52. Bisceglia M, Galliani CA, Senger C, et al. Renal cystic diseases: a
27. Soussan M, Sberro R, Wartski M, et al. Diagnosis and localisation of review. Adv Anat Pathol 2006;13:2656.
renal cyst infection by 18F-fluorodeoxyglucose PET/CT in polycystic 53. Schwarz A, Vatandaslar S, Merkel S, Haller H. Renal cell carcinoma in
kidney disease. Ann Nucl Med 2008;22:529531. transplant recipients with acquired cystic kidney disease. Clin J Am
28. Hosch W, Stojkovic M, Janisch T, et al. The role of calcification for Soc Nephrol 2007;2:750756.
staging cystic echinococcosis. Eur Radiol 2007;17:25382545. 54. Levine E, Slusher SL, Grantham JJ, Wetzel LH. Natural history of
29. Hartman DS, Choyke PL, Hartmann MS. A practical approach to the acquired renal cystic disease in dialysis patients: a prospective
cystic renal mass. Radiographics 2004;24:S101S115. longitudinal CT study. AJR Am J Roentgenol 1991;156:501506.
30. Israel GM, Bosniak MA. Calcification in cystic renal masses: is it 55. Fanos V, Sinaguglia G, Vino L, et al. Multicystic dysplastic kidney and
important in diagnosis? Radiology 2003;226:4752. contralateral vesicoureteral reflux. Renal growth. Minerva Pediatr
31. Levine E, Grantham JJ. Calcified renal stones and cyst calcifications in 2001;53:9598.
autosomal dominant polycystic kidney disease: clinical and CT study 56. Belk RA, Thomas DF, Mueller RF, et al. A family study and the natural
in 84 patients. AJR Am J Roentgenol 1992;159:7781. history of prenatally detected unilateral multicystic dysplastic kidney.
32. Vaidyanathan S, Hughes PL, Soni BM. Bilateral renal milk of calcium J Urol 2002;167:666669.
masquerading as nephrolithiasis in patients with spinal cord injury. 57. Sessa A, Righetti M, Battini G. Autosomal recessive and dominant
Adv Ther 2007;24:533544. polycystic kidney diseases. Minerva Urol Nefrol 2004;56:329338.
33. Harisinghani MG, Maher MM, Gervais DA, et al. Incidence of 58. Guay-Woodford LM, Desmond RA. Autosomal recessive polycystic
malignancy in complex renal masses (Bosniak category III): should kidney disease: the clinical experience in North America. Pediatrics
imaging-guided biopsy precede surgery? AJR Am J Roentgenol 2003;111:10721080.
2003;181:755758. 59. Rabbani MA, Ali SS, Murtaza G, et al. Clinical presentation and
34. Hora M, Hes O, Michal M, et al. Extensively cystic neoplasms in outcome of autosomal dominant polycystic kidney disease in Pakistan:
adults (Bosniak classification II or III) possible common histological a single centre experience. J Pak Med Assoc 2008;58:305309.
diagnoses: multilocular cystic renal cell carcinoma, cystic nephroma, 60. Harris PC, Torres VE. Polycystic kidney disease. Annu Rev Med 2008
and mixed epithelial and stromal tumour of the kidney. Int Urol Oct 23: epub ahead of print.
Nephrol 2005;37:743750. 61. Pei Y, Obaji J, Dupuis A, et al. Unified criteria for ultrasonographic
35. Gong K, Zhang N, He Z, et al. Multilocular cystic renal cell carcinoma: diagnosis of ADPKD. J Am Soc Nephrol 2008 Oct 22: epub ahead of
an experience of clinical management for 31 cases. J Cancer Res Clin print.
Oncol 2008;134:433437. 62. Kistler AD, Poster D, Krauer F, et al. Increases in kidney volume in
36. Cai S, Li J, Jiang Y, et al. Sonographic patterns and differential autosomal dominant polycystic kidney disease can be detected within
diagnoses of cystic renal carcinomas. Chin Med Sci J 2002;17: 6 months. Kidney Int 2008 Oct 29: epub ahead of print.
164167. 63. Leung RS, Biswas SV, Duncan M, Rankin S. Imaging features of von
37. Nicolau C, Vilana R, Del Amo M, et al. Accuracy of sonography with a HippelLindau disease. Radiographics 2008;28:6579.
hydration test in differentiating between excretory renal obstruction 64. Fatihi el M, Khanfri N, Niang A, et al. Renal manifestations of
and renal sinus cysts. J Clin Ultrasound 2002;30:532536. tuberous sclerosis complex. Ann Med Interne (Paris) 2003;154:255258.
38. Amis ES, Cronan JJ. The renal sinus: an imaging review and proposed 65. Rakowski SK, Winterkorn EB, Paul E, et al. Renal manifestations of
nomenclature for sinus cysts. J Urol 1988;139:11511159. tuberous sclerosis complex: incidence, prognosis, and predictive
39. Wadhwa P, Kumar A, Sharma S, et al. Renal lymphangiomatosis: factors. Kidney Int 2006;70:17771782.
imaging and management of a rare renal anomaly. Int Urol Nephrol 66. Scolari F, Ghiggeri GM. Nephronophthisis-medullary cystic kidney
2007;39:365368. disease: from bedside to bench and back again. Saudi J Kidney Dis
40. Sarikaya B, Akturk Y, Bekar U, Topaloglu S. Bilateral renal Transpl 2003;14:316327.
lymphangiomatosis mimicking hydronephrosis: multidetector CT 67. Rohatgi R. Clinical manifestations of hereditary cystic kidney disease.
urographic findings. Abdom Imaging 2006;31:732734. Front Biosci 2008;13:41754197.
41. Pancione L, Giacomelli G, Moroni M, et al. Lymphangioma 68. Chuang YF, Tsai TC. Sonographic findings in familial juvenile
communicating with the excretory system. Minerva Urol Nefrol nephronophthisis-medullary cystic disease complex. J Clin Ultrasound
2008;60:6567. 1998;26:203206.
504
CHAPTER
practice in the past to assume all solid renal masses are renal cell
INTRODUCTION 505 carcinoma, especially if they showed enhancement with contrast
PSEUDO-TUMOURS 505 medium, proof being obtained only after radical nephrectomy.
Column of Bertin 505 Nowadays, it is possible to recognise benign solid renal masses
Dromedary hump 505 with imaging, so that surgery can be avoided. There are also a
Persistent fetal lobulation versus renal scarring 505 variety of pseudo-tumours that can mimic the presence of a true
Splenorenal fusion 505 mass and provide a pitfall for the unwary.
Focal pyelonephritis 507
Xanthogranulomatous pyelonephritis 507
Granulomatous renal pseudo-tumours 507
Extramedullary haematopoiesis 507 PSEUDO-TUMOURS
Arteriovenous malformations 507
BENIGN SOLID MASSES 508 Renal pseudo-tumours can be categorised as developmental, infec-
Adenoma 508 tious, granulomatous or vascular in nature.1 Ultrasound can iden-
Papillary adenoma 508 tify most of these lesions if care is taken, but on occasion recourse
Metanephric adenoma 508 to CT or MRI will be needed to confirm their nature.
Management 508
Oncocytoma 508
Appearances 508 Column of Bertin
Angiomyolipoma 509
Appearances 510 This is a normal part of the kidney, comprising normal cortical
Differential diagnosis 511 tissue extending between the renal pyramids and projecting into
Treatment 512 the renal sinus fat. This cortex can be hypertrophied and can resem-
Other benign solid renal masses 512 ble a mass (Fig. 27.1), often of slightly greater echogenicity than the
MALIGNANT RENAL MASSES 512 cortex because of anisotrophy. It is most commonly seen in the
Renal cell carcinoma 512 middle third of the kidney and more frequently on the left than
Presentation 513 the right. If contrast medium is given, either ultrasonic microbub-
Screening 513 bles or CT, the column of Bertin will show the same enhancement
Appearances 513 as normal cortex.
Rare presentations 513
Staging 513
Treatment 517 Dromedary hump
Collecting duct and medullary carcinoma 517
Transitional cell carcinoma 517 This is a focal bulge on the lateral margin of the left kidney, formed
Aetiology 517 as an adaptation to the available space next to the spleen (Fig. 27.2).
Symptoms 518
Enhancement with contrast agents is the same as normal cortex.
Ultrasound findings 518
Other tests 519
Patterns of spread 520 Persistent fetal lobulation versus
Treatment 520 renal scarring
Lymphoma 521
Leukaemia 521
Metastases 521 The fetal kidneys have prominent lobes that may be separated by
Sarcoma and other rare renal tumours 521 indentations on the cortical surface. These contours have usually
Hereditary tumours and syndromes 522 diminished by birth but occasionally persist into adulthood. The
indentations are positioned in between the renal pyramids, which
MINIMALLY INVASIVE TREATMENT OF RENAL CELL
is in contrast to true renal scarring from reflux nephropathy where
CARCINOMA 522
Radio-frequency ablation of renal cell carcinoma 523
the scar overlies the pyramid (Fig. 27.3). Cortical infarcts do produce
scars between the pyramids, but they are usually isolated. The
abnormality of the cortical contour produced by any of these mech-
anisms may mimic the presence of a focal renal lesion. Likewise,
preserved normal cortex within a very scarred kidney may mimic
INTRODUCTION the appearance of a mass.
Cystic renal masses are the commonest renal mass lesions. They are Splenorenal fusion
discussed in Chapter 26. Solid renal masses, although less common
than cysts, are still often detected serendipitously during cross- Heterotopic splenic tissue very rarely occurs within the kidney,
sectional imaging performed for other reasons. It has been the either congenitally or secondarily due to splenosis following
505
CHAPTER 27 Solid renal masses
A B
Figure 27.1 Column of Bertin. This is a normal projection of cortical tissue into the renal sinus fat. It can appear slightly more echogenic
than normal cortex and can appear mass-like due to hypertrophy as in A. Colour Doppler (B) shows the normal vascularity around the
column.
A B
Figure 27.2 Dromedary hump. This is a normal variant seen on the left kidney only; a focal bulge on the lateral margin of the kidney that
can simulate a mass, as in A. Colour Doppler (B) shows it to have normal vascularity.
Infectious:
Abscess
Focal pyelonephritis
Scarring
Granulomatous:
Xanthogranulomatous pyelonephritis
Sarcoidosis
Malacoplakia
Tuberculosis
Figure 27.3 Dense calcification is seen in the renal cortex at the
Vascular:
site of a scar identified as such by its relationship to the
Extramedullary haematopoiesis
underlying renal pyramid.
Arteriovenous malformation
Renal pelvic haematomas
Subcapsular haemorrhage
506
Pseudo-tumours
splenectomy or splenic trauma. The heterotopic splenic tissue forms be of increased, decreased or similar reflectivity to normal cortex.2
a mass within the kidney, which is either asymptomatic or found The absence of a cortical bulge helps to distinguish the condition
as a result of a search for causes of anaemia (hypersplenism). The from a tumour, though, since the clinical presentation is one of
diagnosis should be considered in those who have had splenectomy infection with fever, flank pain and pyuria, the diagnosis is not
or splenic trauma in the past. Cross-sectional imaging simply dem- normally in doubt. Harmonic imaging improves detection of focal
onstrates an enhancing mass, but a radioisotope 99mTc sulphur pyelonephritis and it can be used to monitor resolution with treat-
colloid scan will show uptake, confirming the splenic nature of the ment. Microbubble contrast agents can perform a similar role.
lesion.
Xanthogranulomatous pyelonephritis
Focal pyelonephritis
This is a rare inflammatory condition, usually secondary to chronic
Lobar nephronia, acute focal pyelonephritis and focal bacterial renal tract obstruction due to stones (70% will have a staghorn
nephritis are synonyms for the same condition. In essence, the calculus). The infection results in destruction of the normal renal
condition is a focal area of pyelonephritis within a lobar distribu- cortex. A characteristic feature pathologically is the presence of
tion. It is commoner in diabetics and immunocompromised people. xanthoma cells, which are lipid-laden macrophages. These produce
It represents an inflammatory mass that does not contain any pus, areas in the resulting mass that contain enough fat for it to be detect-
although progression to an abscess will occur if treatment is inad- able at CT scan. Diabetic patients are particularly prone to develop-
equate. Ultrasound shows a mass or wedge-shaped area that ing xanthogranulomatous pyelonephritis. Presentation is with
extends from the medulla to the cortical margin (Fig. 27.4). It can chronic ill-health rather than any features of acute infection.
Ultrasound will show single or multiple low-echo masses in the
parenchyma of an enlarged kidney and a central echogenic focus
due to the obstructing calculus. No recognisable kidney structure
may remain. There is no sign on ultrasound that confirms the diag-
nosis, but CT may be helpful by showing the presence of fat and
calculi. If the mass has arisen in the absence of calculi it is more
likely that a misdiagnosis of renal cell carcinoma will be made.
Xanthogranulomatous pyelonephritis
A mimic of malignancy.
Associated with calculi and diabetes.
A chronic infective complication of renal obstruction.
No characteristic features on US.
CT may identify the fat present in the lipid laden macrophages.
Extramedullary haematopoiesis
Failure of haematopoiesis in the bone marrow prompts other sites
to transform to undergo haematopoiesis. The common sites are
spleen, liver and lymph nodes but many other areas may uncom-
monly transform too, including the kidney. Myelofibrosis, chronic
myeloproliferative disorder and polycythaemia vera are common
causes. A renal mass in association with these diseases should give
pause for thought. There are no specific imaging features and
biopsy will be needed to make the distinction from lymphoma or
other tumours.
Arteriovenous malformations
Colour-flow Doppler should make this diagnosis straightforward
B at ultrasound. Care needs to be taken though, as although most
arteriovenous malformations will be secondary to trauma or con-
Figure 27.4 Focal pyelonephritis. Longitudinal (A) and transverse genital, they are occasionally associated with underlying renal cell
(B) views of the right kidney showing focal increased echogenicity carcinomas. In this instance the shunt may be so large and the
in the upper pole of the kidney. The history of fever, flank pain and cancer so small that the tumour is relatively hard to discern. Mag-
urinary tract infection made the diagnosis of focal pyelonephritis. netic resonance can be useful in this context.
507
CHAPTER 27 Solid renal masses
Adenoma Management
Small solid renal lesions present a management problem as there is
There used to be an arbitrary distinction made in the past that solid no way with imaging to tell if they are benign or not (Fig. 27.5).
lesions less than 3cm in size were benign and they were often called However, it is known that small tumours usually grow slowly,
adenomas. It is now apparent that the diagnosis of a renal adenoma usually less than 0.5cm per year, and that these tumours are most
is no longer tenable on imaging. unlikely to metastasise whilst they are smaller than 3cm. It is also
It is considered that all clear cell containing tumours are carcino- known that the majority of benign tumours are less than 4cm in
mas and that there is no such thing as a clear cell adenoma.3 Even size.7 Options for management include watchful waiting or sur-
very small clear cell tumours may show metastasis so it is better to veillance, particularly in elderly patients or those too unfit to
consider these lesions as having greater or lesser aggressiveness survive intervention. New techniques are being tried: laparoscopic
depending on their presentation. partial nephrectomy, enucleation, ablation and high-intensity
focused ultrasound.8 These have to be weighed against traditional
Papillary adenoma open surgical techniques. Clearly, there is a need for histological
proof in these non-traditional approaches such as ablation to ensure
Papillary adenomas do exist and may be found in about 40% of that like is being compared with like in terms of outcome. Ultra-
autopsies of those aged over 70 years.4 They are also found in scle- sound-guided biopsy is advocated in the diagnosis of small renal
rosed end-stage kidneys and in acquired cystic disease kidneys. masses, particularly those that are homogeneous and non-cystic,9
There is a continuum of development to transformation to carci- as it is these that are most likely to be benign. Another series10
noma. It is important to realise that by definition (WHO 2004 clas- showed that renal biopsy of focal masses altered the clinical
sification) papillary adenomas are all less than 5mm in size. decision-making in 60% of cases. There was no evidence of any
Histological features are identical to papillary carcinomas, although tumour seeding in their series of 152 biopsies.
the carcinomas may exhibit greater amounts of chromosomal aber-
ration. There is no imaging test or feature to allow distinction from
any other small tumour. Oncocytoma
Oncocytomas are commoner in men, usually asymptomatic and
Metanephric adenoma most often found by chance in the sixth or seventh decade. The
tumour contains oncocytes, large cells with mitochondria-rich, eosi-
Metanephric adenoma is considered a rare benign renal neoplasm
nophilic cytoplasm. They represent up to 6% of all renal epithelial
with a peak incidence in the fifth decade of life (range from 5 to 83
neoplasms and generally follow a benign course without metasta-
years) and is commoner in women.4 They represent 1% of renal
sis. Most are not correctly diagnosed before operation, only 20% in
tumours less than 7cm in size.3 Half are found incidentally and 10%
one series,11 being usually mistaken for renal cell carcinoma. There
are associated with polycythaemia. The polycythaemia promptly
is also the problem that oncocytomas may be associated with renal
resolves once the tumour is removed or ablated. Histogenetically
cell carcinoma either as hybrid tumours or as two adjacent lesions
they are considered to be at the most hyper-differentiated, benign
that have grown into each other (collision tumours).
end of the nephroblastoma spectrum. This may account for the
report of metastasis in two recent cases.5 Metanephric adenoma
typically appears as a well-defined, unencapsulated, solid mass.
Ultrasound shows a hyper-echogenic lesion that also has increased
Appearances
through transmission of sound.6 CT shows them to be of increased Ultrasound appearances may vary, with oncocytomas displaying all
attenuation compared to normal kidney on unenhanced scans. types of echogenicity from reduced to increased reflectivity. The
Larger lesions may be expansile and may show cystic degeneration characteristic feature associated with oncocytomas is the presence
and calcification. There are no distinguishing features on imaging of a central scar and a spoke-wheel pattern of enhancement. This is
A B
Figure 27.5 Small renal tumours may be uncharacterised on imaging. This is an 11mm echogenic lesion that looked like normal cortex
on CT but is clearly different on US (A) and shows deviation of adjacent vessels (B).
508
Benign solid masses
A
B
findings at imaging but they can present with flank pain and bleed- Appearances
ing. They are commoner in women by a factor of four and usually
found after the age of 40 years. AML may occur as single or multiple lesions in one or both kidneys.
AML may exist as an isolated entity (about 80% of the total) or The sporadic lesions are usually in middle-aged women and uni-
in about 20% be associated with tuberous sclerosis or pulmonary lateral whereas in tuberous sclerosis, lesions are more likely to be
lymphangiomyomatosis. Tuberous sclerosis is an autosomal domi- small and multiple. The appearance of an AML depends on the
nant neurocutaneous syndrome that has benign congenital tumours proportion of each of the different tissues. Typically, on ultrasound,
in multiple organs.19 The classic triad of epilepsy, mental disability the fat in the AML produces a highly reflective mass, with bright-
and adenoma sebaceum is relatively uncommon, so radiology plays ness similar to renal sinus fat (Fig. 27.7). Up to a third of AMLs may
a part in finding the tumours: cardiac rhabdomyomas, renal AMLs show acoustic shadowing. Larger lesions may show intralesional
and subependymal tubers, though many different organs may be aneurysms as well as hypervascular components. It is these that
affected. Eighty per cent of tuberous sclerosis patients will have predispose to spontaneous haemorrhage (Fig. 27.8). The likelihood
renal AMLs (Fig. 27.6). of spontaneous bleeding increases once an AML is larger than 4cm
C D
Figure 27.7 A small angiomyolipoma seen on US (A) and CT (B, C). Ultrasound shows a small brightly echogenic focus in the renal
cortex. The CT scans, both unenhanced and enhanced, show a small focus of cortical fat to correspond to the AML. D: A slightly larger
AML in the renal cortex in another patient.
510
Benign solid masses
A B
Figure 27.8 A large AML on ultrasound (A) associated with a perinephric haematoma on CT (B). The CT shows the AML contains
predominantly fat.
A B
Figure 27.9 Milk of calcium cyst. Transverse (A) and longitudinal (B) views showing how these cysts can mimic the appearance of a
small cortical AML.
511
CHAPTER 27 Solid renal masses
to confirm the presence of fat and make the diagnosis of AML Other benign solid renal masses
though even this has pitfalls. Fat may be present in a few renal cell
carcinomas20 and is commoner in the papillary cell variant,21 Other benign solid tumours do occur but they are generally very
although these tumours often have calcification too which is not rare or not often detected on imaging.4
seen in AML. Up to 5% of AMLs will contain minimal or no fat4
and be potentially indistinguishable from carcinoma, although n Haemangioma. These are rare lesions that are typically solitary
ultrasound shows a very uniform isoechoic appearance and CT will and arise from the renal pyramids. They characteristically
show increased attenuation on unenhanced images.22 A perirenal show early intense enhancement with ultrasonic contrast
liposarcoma can mimic the appearances of a large exophytic AML. agents that persist on delayed imaging. They are associated
In this instance, an AML is likely to show a marginal defect in the with syndromes such as SturgeWeber and Klippel
kidney and enlarged tumoral vessels, whereas a liposarcoma is Trnaunay and may cause haematuria and renal colic.
n Leiomyoma. These are rare lesions that typically arise from the
more likely to show smooth compression of the kidney and exten-
sion outside of the perirenal space. Biopsy is not often needed in renal capsule. They may be quite large and show cystic
the diagnosis of typical fat-rich AML but it may be helpful in fat- degeneration or haemorrhage.
n Reninoma. An extremely rare tumour that produces a triad of
poor lesions or in suspected liposarcoma.23 A meta-analysis of the
published literature has concluded that all non-calcified, echogenic findings: poorly controlled hypertension; hypokalaemia; and
lesions found on ultrasound in the kidney require a CT scan to rule high plasma rennin levels. Usually found in young adults and
out a renal cell carcinoma.24 smaller than 3cm in size, there are no specific imaging
findings.
n Medullary fibromas. Autopsy series describe these lesions
Treatment commonly but as they are usually less than 5mm in size they
are not often found on imaging. Their typical location is in the
Small AMLs (less than 4cm) do not need to be treated. Asympto-
renal pyramid.
matic lesions need no more than conservative treatment and follow-
up. Lesions larger than 4cm should be removed using
nephron-sparing techniques in order to prevent the occurrence of
complications, primarily those of spontaneous haemorrhage. Those
patients that present with spontaneous bleeding should be consid-
MALIGNANT RENAL MASSES
ered for coil embolisation at catheter angiography if the bleeding is
active and ongoing. Surgery is reserved for when the patient has
recovered from the acute episode of bleeding.
Renal cell carcinoma
Renal cell carcinoma (RCC) accounts for about 2% of adult malig-
nancies and represents about 90% of adult primary renal tumours.
Most of these tumours occur sporadically, but there is an associa-
Angiomyolipoma
tion with von HippelLindau disease (Fig. 27.10) and tuberous scle-
Benign mesenchymal neoplasm. rosis. There is a male to female preponderance of two to one. The
Commoner in women. peak age of incidence is 50 to 70 years. Predisposing risk factors
20% of AML are associated with tuberous sclerosis. include smoking, long-term dialysis and exposure to lead, cadmium
May be single or multiple. or diethylstilbestrol.
Typically appear as a bright cortical mass. Renal cell carcinoma is thought to arise from the convoluted
AMLs bigger than 4cm have an increased chance of bleeding. tubules of the renal cortex; 7080% are of the clear cell type, 1015%
Potential problem distinguishing AML from small bright RCC. are papillary cell and about 5% are chromophobe-type. The features
CT or MR can be used to confirm fat in an AML. seen on ultrasound do not bear any useful relationship to the cell
type of the renal cell carcinoma, although papillary tumours are
A B
Figure 27.10 Von HippelLindau disease. A and B: There are at least three renal lesions seen in this patient with von HippelLindau
disease. They have subsequently grown and proved themselves to be renal cell carcinomas.
512
Malignant renal masses
more likely to show poor enhancement with contrast agents on CT increased, decreased or similar when compared to the normal renal
scan and chromophobe tumours may have a homogeneous bright cortex. The larger tumours are more likely to be of similar reflectiv-
ultrasound texture without necrosis. ity but may also have central necrosis or haemorrhage (Fig. 27.12).
Tumours less than 3cm in size are more likely to be of increased
echogenicity: hence the need for care when differentiating them
Presentation from angiomyolipoma, which will also appear bright (Fig. 27.13).
Common symptoms at presentation are painless haematuria, flank Calcification is found in 30% of RCCs but not in angiomyolipoma.
pain and a palpable mass together with anorexia and weight loss. This calcification may be rim-like but is more commonly central. CT
However, with the increasing use of cross-sectional imaging for and MR can be used to look for fat, which indicates an angiomyol-
other reasons, the proportion of tumours that are detected at less ipoma rather than an RCC.
than 3cm in size is increasing; these are chance findings prior to The differential diagnosis of a solid or partly solid renal mass
any symptoms. on ultrasound includes tumours, haematomas, infections and
There is a belief that finding a varicocele in a man should prompt the pseudo-tumours described earlier in this chapter. Ultrasound
a search of the kidneys for an underlying cancer, but this is an contrast agents can enable distinction of these lesions. Hyper-
association based on very old papers from before the days of cross- enhancement in the late phase (3090 seconds after agent injection)
sectional imaging. The cancers described in those papers were huge is the most useful feature indicating a renal cell carcinoma (Fig.
and clinically palpable. Current evidence suggests that both condi- 27.14).30 Heterogeneity of enhancement is also an indicator of malig-
tions are relatively common and can be expected to coexist in a few nancy, as most angiomyolipomas show a smooth enhancement
people. Young men presenting with a varicocele do not have an pattern which washes out in the late phase. One pitfall is that some
increased rate of renal cancer. In older men, late presentation of papillary cancers may not show much enhancement.
varicocele may, rarely, be due to tumour thrombus spread along Colour and spectral Doppler features of high velocity and turbu-
the left renal vein obstructing the gonadal vein but there is no true lence are non-specific and do not help in the diagnosis of tumour
association between a varicocele and renal cancer. In contrast, there but will help distinguish cystic from solid lesions (Fig. 27.15). The
is an association between non-Hodgkins lymphoma and renal cell pattern of vessels on colour Doppler may help indicate a pseudo-
carcinoma, particularly in those patients with bulky abdominal tumour such as a prominent column of Bertin.
disease.25 Imaging does not allow differentiation between the two Multiple tumours may develop in an asynchronous or synchro-
diagnoses so biopsy is required. nous fashion. A patient who has one kidney removed for a sporadi-
Some patients present with spontaneous renal or perirenal haem- cally occurring tumour has a 2% chance of another tumour
orrhage. This blood may be enough to obliterate the underlying developing in the remaining kidney. There is also a 2% chance that
tumour on initial imaging. Consequently, follow-up imaging will a tumour in the contralateral kidney may exist at the time of initial
be needed once the acute bleed has resolved to look for an underly- diagnosis. Synchronous occurrence of more than one tumour in the
ing tumour. same kidney is quoted as 5% but some histological studies of
nephrectomy specimens quote a higher rate, up to 25%, but the
tumours are usually less than 5mm in size. Finding more than one
tumour should prompt a search for associated syndromes such as
Screening von HippelLindau disease.
Since between 25% and 40% of tumours are found incidentally,
interest has been raised in providing a screening service. An initial
ultrasound study of 9959 volunteers yielded only 9 cancers (0.1%); Rare presentations
sensitivity at 1-year follow-up was 82% but the positive predictive Occasionally, the metastases from renal cell cancer may become
value was only 50%.26 A further ultrasound study looking at a more apparent before the primary tumour in the kidney can be detected.25
focused elderly population of 6678 volunteers found an incidence An example is the development of para-aortic adenopathy with no
of solid renal tumours of 0.32%.27 Screening with ultrasound is well detectable primary tumour. Arteriovenous malformations (AVMs)
tolerated and those treated show good survival rates. One group in are associated with renal cell cancer. These AVMs can be large
whom screening is worthwhile is those with acquired cystic disease enough to obscure visualisation of the tumour. We know of two
of the kidney secondary to renal failure.28 They have a prevalence patients in whom the initial diagnosis was thought to be pancreatic
of cancer of 19%, 50% due to clear cell and 50% due to papillary neuroendocrine tumours with an incidental renal AVM but which
carcinoma. turned out to be renal cell cancer metastases to the pancreas from
a tumour hidden by the AVM. Occasionally, RCC can present as a
single large cyst (Fig. 27.16). This is not a cyst that has turned
Appearances malignant but an RCC that has always been cystic.
Ultrasound features are of a solid tumour mass, distorting the
normal renal architecture often with a ball pattern of growth
rather than an infiltrative pattern (Fig. 27.11).29 Reflectivity may be Staging
Renal cell carcinoma spreads either locally into adjacent structures
or by haematogenous spread. Survival worsens as the stage of the
513
CHAPTER 27 Solid renal masses
A B
514 Figure 27.12 Renal cell carcinoma. A: Ultrasound shows an exophytic tumour with some central low-echo areas that could be
necrosis. B: CT of the same lesion.
Malignant renal masses
A B
Figure 27.13 Renal cell carcinoma. A: Ultrasound shows a uniformly echogenic mass that could be mistaken for an AML. B: CT scan
shows there is no fat in the lesion, confirming it is an RCC and not an AML.
A B
A B
Figure 27.16 A rare example of a large, purely cystic RCC on US (A) and CT (B). Other than size, there are no features to suggest
malignancy.
good local staging and may demonstrate the extent of tumour show a central infiltrative pattern. This is an important distinction
thrombus better than other tests but it is insensitive for lung to make as TCC is treated by nephroureterectomy rather than just
metastases. nephrectomy alone. Histology is required.
Renal medullary carcinoma is sometimes confused with collect-
ing duct tumours but the lesions are distinct clinical entities. Renal
Treatment medullary carcinoma occurs almost exclusively in people with
Surgery with radical nephrectomy is the standard treatment. It may sickle cell trait and affects a young age group, 15 to 27 years old.
be useful in large tumours to angiographically embolise the tumour The commonest presentation is with gross painless haematuria. The
preoperatively to ease dissection and reduce blood loss. Surgery tumours have a predilection for the right kidney. They are centrally
can still be useful, even in people with known metastases. It has a located and infiltrative. Most have central necrosis. Metastases are
cytoreductive effect that can improve the effect of adjuvant usually present at initial diagnosis. The literature suggests that
treatments. these tumours are not readily visible at sonography34 and hence
Partial nephrectomy can be offered as a nephron-sparing tech- people with sickle cell trait and gross haematuria should be inves-
nique in those whose tumours do not transgress the renal hilum. tigated with CT.
Surgery may be done as a traditional open procedure or
laparoscopically.
Ablative techniques such as radio-frequency ablation are a good
alternative in smaller tumours and are discussed separately at the Transitional cell carcinoma
end of this chapter.
Chemotherapy, immunotherapy and radiotherapy all have Tumours of the renal pelvis represent 10% of solid renal tumours,
appropriate uses for the management of disseminated disease. with the majority of these being transitional cell carcinomas (TCCs).
The great majority of TCCs arise in the bladder, with only 5% of
TCCs arising in the upper tracts. This is because the bladder has a
Collecting duct and medullary carcinoma much greater surface area of urothelium and because urine remains
in contact with it for greater periods of time. The majority of upper
Collecting duct carcinoma differs from renal cell carcinoma in two tract TCCs occur in the extrarenal pelvis, some in the infundibular
main ways. Firstly, instead of arising from the convoluted tubules regions and only a quarter in the ureter.35 The left and right kidneys
of the renal cortex as RCC cell types do, it arises from the renal are affected equally and 2 4% of renal TCCs will occur bilaterally.
medulla, possibly the distal collecting ducts of Bellini.32 Secondly, Any patient with TCC of the bladder has a 4% risk of developing
it has an infiltrative pattern of growth rather than a ball-like mass upper tract TCC. This same risk persists even after cystectomy.36 If
lesion. There is a 2:1 preponderance of men affected and the mean the upper tract tumour is the presenting lesion, there is a 30% risk
age at presentation is 55 years. It has a central and medullary of developing a bladder tumour. Because multicentric TCC and
pattern of infiltration, although these tumours tend to be large at synchronous or metachronous presentations are common, urologi-
presentation (around 8cm), which can hide their central origin. It cal follow-up needs to be systematic and accurate.
is an aggressive tumour with a relatively poor prognosis.33 It tends
to be isoechoic to normal parenchyma but some of the tumours are
bright and since they are large lesions, this is another potential
distinguishing feature from RCC as most bright RCCs are smaller
Aetiology
than 3cm. Overall, though the diagnosis may be suspected because Men are affected three times more often than women. The peak age
of a central infiltrative pattern, the imaging features are not suffi- at presentation is between 50 and 70. Smoking is an important risk
cient to make the diagnosis (Fig. 27.17). Furthermore, transitional factor, increasing the relative risk two to three times. Carcinogenic
cell carcinoma (TCC) arising in the pelvicalyceal system may also substances excreted in the urine act locally on the urothelium: these
517
CHAPTER 27 Solid renal masses
A
B
include; aniline, benzidine, aromatic amine, azo dyes, cyclophos- a hydronephrosis or not. Generally, tumours by the time they
phamide and heavy caffeine consumption.37 Analgesic abuse par- become visible on ultrasound look like a central soft tissue mass
ticularly of phenacetin predisposes to a highly invasive type of surrounded by the echogenic fat of the renal sinus (Fig. 27.18).
TCC. Structural anomalies, such as horseshoe kidney, that lead to Squamous metaplasia leads to formation of keratin pearls that look
stasis of urine and prolong the contact time of any carcinogen are like highly echogenic foci within the mass or on its surface. There
also associated with an increased prevalence of this disease. may be dilated calyces around the mass. TCC has an infiltrative
pattern of growth so the reniform shape of the kidney is not lost
Symptoms until late in the disease. Sometimes the dilation of the surrounding
calyces is the only ultrasonic sign of the disease (Fig. 27.19).
The most common presenting symptom is haematuria. The stand- Fat within the normal renal sinus can appear as relatively low-
ard work-up for haematuria has been urine cytology, cystoscopy echo and mimic a tumour. This pitfall in diagnosis can be avoided
and intravenous urography (IVU) in the past. IVU was superseded by assessing if there is posterior acoustic shadowing, an ill-defined
by ultrasound as the initial screening tool because of its better posterior margin and traversing hilar vessels. These three signs
ability to pick up solid parenchymal renal masses and because most indicate it is just low-echo fat. Tumour will displace vessels and
upper tract urothelial tumours cause some degree of pelvicalyceal have a defined posterior margin.
dilation.38 However, the advent of multidetector CT scans has Dilation of the pelvicalyceal system with urine can provide a
meant that CT urography has become the most sensitive screening negative contrast that allows the presence of small filling defects or
tool and is rapidly replacing ultrasound in the initial work-up.39 sessile thickening of the urothelium to be appreciated (Fig. 27.20).
Blood clots or infective debris can mimic soft tissue masses. Finding
blood flow within a mass confirms it is tumour, although con-
Ultrasound findings versely the absence of blood flow does not mean it is not tumour
The ultrasound appearances of TCC are variable depending on (Fig. 27.21). Doppler studies are otherwise unhelpful as tumour
whether the tumour is sessile or papillary and whether it produces grade, stage and size are not related to vascularity.40
518
Malignant renal masses
Other tests
The best radiological investigation is a CT urogram (Fig. 27.22). This
will accurately depict stones and has a high sensitivity for TCC in
Figure 27.19 Transitional cell carcinoma. Ultrasound (A) shows the upper pole calyx is dilated but it is hard to identify anything else in
the kidney. Axial CT (B) shows the left kidney is diffusely replaced by tumour (TCC) compare it to the normal right kidney. CT in the
coronal urographic phase (C) shows the right kidney excretes normally but the left does not. The dilated upper pole calyx is shown
as well.
519
CHAPTER 27 Solid renal masses
A B
Figure 27.20 A: The urine in the dilated renal pelvis acts to outline a small mural nodule of tissue (arrow). B: The renal pelvis and proximal
ureter are filled with material. Ultrasound cannot tell if this is tumour or blood clot.
A B
Figure 27.21 Transitional cell carcinoma. A: A soft tissue mass fills the lower pole calyces. B: Colour Doppler does not show any
blood flow in the lesion but this does not mean that it is not tumour. It was subsequently proven to be TCC.
A B
Figure 27.22 Transitional cell carcinoma. A: Ultrasound of the kidney failed to identify a tumour. B: CT urogram shown in the coronal
plane revealed a TCC filling the upper pole calyces on the left. It is for this reason that CT urography is replacing ultrasound in many
centres in the investigation of unexplained haematuria.
Figure 27.23 Lymphoma. Ultrasound (A) shows a mass in the lower pole of the left kidney. CT (B) confirms the renal abnormality but
also shows a huge left para-aortic node. Ultrasound guided biopsy (C) of the renal mass confirmed it was a lymphoma.
A B
Figure 27.25 Retroperitoneal liposarcoma. A: Ultrasound shows the right kidney is displaced and surrounded by increased fat.
B: CT confirms the extensive retroperitoneal fat which on resection was confirmed to be due to a liposarcoma.
currently available are image-guided energy ablative therapy and the hydro-dissection technique. In addition, CT is particularly
laparoscopic partial nephrectomy. useful when treating posteriorly located renal cell carcinomas or if
Nowadays, there are many new developments in energy ablative the tumour predominantly has a parenchymal or central location,
technologies to treat renal cell carcinoma. These are either with as this allows easier targeting of the tumour. Monitoring of the
heat-based ablative energy, such as radio-frequency ablation (RFA) treatment response during and after the energy ablation can be
or microwaves, or with cold-based ablative energy such as cryoab- performed with a contrast-enhanced examination using CT in
lation.4753 Preliminary results show that treatment is safe and effec- patients without contrast allergy or impaired renal function. There
tive, with good medium-term outcome data, for both RFA and are a small number of operators who prefer to use ultrasound guid-
cryoablation therapy of small renal cell carcinomas.4752 ance to insert the initial needle electrode and then use CT to assess
RFA had initially enjoyed greater popularity in interventional the needle electrodes position in relation to the adjacent intra-
radiology because of the smaller RFA needle electrode size, which abdominal structures.
allowed radiologists to perform image-guided treatment with ease.
Recently, cryoablation is also gaining momentum as there is a new
comparable-sized needle electrode (around 17G) available for the
radiologist to use with image guidance. Microwave therapy is a Radio-frequency ablation of renal
new technology and many operators believe that there is great cell carcinoma
potential for this technology in the future. Currently this treatment
is only available in selected research institutions around the world. Radio-frequency ablation destroys tumour by using the frictional
Minimally invasive therapy of renal cell carcinomas is evolving heat generated by radio-frequency waves. When the temperature
rapidly. Only time will tell which type of energy-based ablative rises above 60C, this leads to cell death by destruction of the cel-
therapy will be the optimum treatment option. However, regardless lular membrane and denaturing of proteins. The technologies that
of the type of energy we might use for treatment in the future, most are available in commercial markets currently are either impedance
published series agree that image-guided treatment of small RCCs or temperature controlled systems.
has great promise and long-term outcome data are currently All treatments should ideally be performed in the CT interven-
awaited to validate the treatment. tional suite with both CT and US available to guide the therapy. All
The energy ablative therapy may be delivered via open established centres worldwide primarily use CT to guide treatment
surgery, a laparoscopic approach or via image guidance under and peri-procedural monitoring of treatment. Many operators who
ultrasound (US), computed tomography (CT) or magnetic reso- started with US guidance alone have since realised that it is inad-
nance imaging (MRI). equate for needle placement and it limits targeting for more awk-
The majority of interventional radiologists involved in this wardly positioned tumours such as those located close to the bowel
therapy utilise CT as the main imaging guidance technique to treat or ureter.
renal cell carcinomas. This is because CT is more widely available For US-guided treatment, the RFA needle electrode can be
and cost effective than open MRI for guidance. CT allows good inserted directly under US guidance (Fig. 27.26). During the thermal
visualisation of all the electrode tips, especially with multi-tined ablation, an echogenic cloud becomes visible (Fig. 27.27), and this
expandable electrodes; this is important for accurate needle elec- tends to obscure the needle electrode. This makes subsequent
trode positioning. Precise visualisation of the tips of the tines is needle readjustment difficult if only US guidance is used for treat-
crucial in order to avoid thermal injury to surrounding intra- ment. Therefore, all established centres treating complex renal
abdominal viscera such as colon or retroperitoneal structures tumours use CT to check the needle electrodes position during
during the ablative treatment. It also allows operators to perform treatment and subsequent repositioning of the needle electrode.
523
CHAPTER 27 Solid renal masses
A B
Figure 27.28 A: The contrast-enhanced CT shows a small renal cell carcinoma at the upper pole of the left kidney B: The RFA needle is
inserted into the tumour under CT guidance.
For CT-guided treatment, this may involve using US or CT for minimise the risk of thermal injury to the collecting system. If such
the initial needle electrode placement (Fig. 27.28). CT is then used an injury occurs, it causes a subsequent ureteric stricture.55,56
to check the position of the needle electrode, especially with the Patient selection is crucial. The referral should come from the
multi-tined probe where some of the tines could be in close relation cancer network, according to the NICE recommendations. As the
to colon or ureter. If the tumour is too close to any intra-abdominal treatment evolves, indications have expanded from curative to
structure such as the colon, a hydrodissection technique may be palliative intent. The indications include non-surgical candidates,
required to move the colon away from the tumour in order to avoid patients with a solitary kidney, and von HippelLindau disease
thermal injury.54 patients with RCC. Patients with metastatic disease undergoing
For centrally located renal tumours or a tumour closely related immunotherapy may also be considered for this therapy to debulk
to the ureter, a cold pyeloperfusion technique can be used to the primary tumour.
524
Minimally invasive treatment of renal cell carcinoma
Evaluation prior to treatment includes attending the tumour Pre RFA imaging often consists of a combination of US, CT and
ablation clinic for staging and counselling, laboratory investigations MRI. They are used for staging, planning of therapy and as a base-
such as clotting and baseline renal function, and biopsy of the line for post RFA changes. After RFA, imaging follow-up is variable
tumour either before/just prior to therapy. depending on the operators experience. Most institutions have
Factors that influence the outcome of the therapy are size and patient follow-up at 1, 3, 6 and 12 months post treatment and annu-
location. For tumours smaller than 3cm in diameter, complete abla- ally thereafter. Contrast-enhanced US may be useful for those who
tion can be achieved in 90% of the cases treated with a single treat- still use US guidance alone to guide re-treatment (Fig. 27.29). It is
ment session. For tumours between 3 and 5.5cm, 100% successful well recognised that cross-sectional imaging with CT (Fig. 27.30)
ablation is achievable with exophytic tumours and 70% of the cases and/or MRI (Fig. 27.31), depending on the availability of resources,
are treated in a single session.57 The tumour locations can be divided are the best imaging techniques for follow-up.
into: exophytic, parenchymal, central/mixed location. The exo- After the procedure, the patient is monitored for gross haematu-
phytic tumours have the best treatment outcome from the oven heat ria. They must be able to pass urine before discharge. If there is
effect. This is due to the surrounding pararenal fat acting as a heat concern regarding complications then early imaging is advised.
insulator to maximise the ablation effect. Minor complications are more common. These are microscopic
A B
Figure 27.29 A: The contrast-enhanced US shows a small renal cell carcinoma at the lower pole of the right kidney B: Post RFA, the
zone of ablation is seen as an echo-poor area, following US contrast administration.
A B
Figure 27.30 A: The contrast-enhanced CT shows a small renal cell carcinoma at the upper pole of the left kidney, B: Post RFA, the CT
shows lack of enhancement within the zone of ablation.
525
CHAPTER 27 Solid renal masses
A B
Figure 27.31 A: The contrast-enhanced MRI shows a small renal cell carcinoma at the lower pole of the left kidney B: Post RFA, the MRI
shows a clear margin of the ablated zone that displays a lack of enhancement.
4. Prasad SR, Surabhi VR, Menias CO, et al. Benign renal neoplasms in
Ablation treatment of renal cell carcinoma adults: Cross-sectional imaging findings. AJR Am J Roentgenol
2008;190:158164.
Radio-frequency ablation, microwave ablation and cryoablation
5. Bastos Netto JM, Esteves TC, Mattos RD, et al. Metanephric adenoma:
are all possible. a rare differential diagnosis of tumor in children. J Pediatr Urol
Image-guided approaches favour CT over US. 2007;3:340341.
Tumours less than 5.5cm are suitable for treatment. 6. Fielding JR, Visweswaran A, Silverman SG, et al. CT and ultrasound
Exophytic tumours give the best results. features of metanephric adenoma in adults with pathologic
Risk of damage to adjacent structures can be minimised with correlation. J Comput Assist Tomogr 1999;23:441444.
hydrodissection or pyeloperfusion. 7. Li G, Cuilleron M, Gentil-Perret A, Tostain J. Characteristics of
Best performed within a multidisciplinary cancer network image-detected solid renal masses: implication for optimal treatment.
environment. Int J Urol 2004;11:6367.
8. Ramirez ML, Evans CP. Current management of small renal masses.
Can J Urol 2007;14(Suppl 1):3947.
9. Reichelt O, Gajda M, Chyhrai A, et al. Ultrasound-guided biopsy of
homogenous solid renal masses. Eur Radiol 2007;52:14211426.
haematuria in up to two-thirds of cases, perirenal haematoma and 10. Maturen KE, Nghiem HV, Caoili EM, et al. Renal mass core biopsy:
post RFA syndrome.58 Major complications are rare and include accuracy and impact on clinical management. AJR Am J Roentgenol
haemorrhage that requires blood transfusion, renal failure from 2007;188:563570.
acute tubular necrosis, urinoma/calyceal-cutaneous fistula and ure- 11. Fan YH, Chang YH, Huang WJ, et al. Renal oncocytoma: clinical
teric injury.49,59,60 experience of Taipei Veterans General Hospital. J Chin Med Assoc
In order to set up a programme, good core interventional radiol- 2008;71:254258.
ogy skills are required for those performing the procedure, as the 12. de la Cruz Burgos R, Martel Villagran J. Renal oncocytoma.
technical success and complication rate is directly related to the Fundamental radiologic manifestations and enhancement patterns in
tri-phase helical CT. Radiologica 2007;49:109114.
operators experience.61 Service development also requires coopera-
13. Kondo T, Nakazawa H, Sakai F, et al. Spoke-wheel-like enhancement
tive work within a cancer network, adequate resources and a multi- as an important imaging finding of chromophobe cell renal carcinoma:
disciplinary team approach. To date, renal RFA is a safe and a retrospective analysis on computed tomography and magnetic
minimally invasive technique with good medium-term outcome resonance imaging studies. Int J Urol 2004;11:817824.
data (within 5 years). Currently, long-term outcome data are 14. Siu W, Hafez KS, Johnston WK 3rd, Wolf JS Jr. Growth rates of renal
awaited, though it is hoped and expected that these will be compa- cell carcinoma and oncocytoma under surveillance are similar. Urol
rable to surgery. Oncol 2007;25:115119.
15. Hes O, Michal M, Sima R, et al. Renal oncocytoma with and without
intravascular extension into branches of renal vein have the same
REFERENCES morphological, immunohistochemical, and genetic features. Virchows
Arch 2008;452:193200.
1. Bhatt S, MacLennan G, Dogra V. Renal pseudotumors. AJR Am J 16. Mogorovich A, Giannarini G, De Maria M, et al. Multifocal and
Roentgenol 2007;188:13801387. bilateral renal oncocytoma: a case report and review of the literature.
2. Dubbins P. Ultrasound in acute urinary tract infection. BMUS Bull Arch Ital Urol Androl 2007;79:130134.
2003;11:2529. 17. Ameri C, Contreras P, Villasante N, et al. Solid renal masses up to
3. Algaba F. Renal adenomas: Pathological differential diagnosis with 4cm. Analysis of the diagnostic procedures, TNM staging and
malignant tumors. Adv Urol 2008; epub. surgical treatment. Actas Urol Esp 2006;30:772783.
526
References
18. Kozlowska J, Okon K. Renal tumours in post-mortem material. Pol J 42. Sheth S, Ali S, Fishman E. Imaging of renal lymphoma: patterns of
Pathol 2008;59:2125. disease with pathologic correlation. Radiographics 2006;26:11511168.
19. Umeoka S, Koyama T, Miki Y, et al. Pictorial review of tuberous 43. Pradeep R, Madhumathi DS, Lakshmidevi V, et al. Bilateral
sclerosis in various organs. Radiographics 2008;28:e32. nephromegaly simulating Wilms tumour: a rare initial manifestation
20. Strotzer M, Lehner KB, Becker K. Detection of fat in a renal cell of acute lymphoblastic leukaemia. J Pediatr Hematol Oncol
carcinoma mimicking angiomyolipoma. Radiology 1993;188:427428. 2008;30:471473.
21. Garin JM, Marco I, Salva A, et al. CT and MRI in fat-containing 44. Office for National Statistics. Registrations of cancer diagnosed in
papillary renal cell carcinoma. Br J Radiol 2007;80:e193e195. 2003, England. ONS; 2006.
22. Jinzaki M, Tanimoto A, Narimatsu Y, et al. Angiomyolipoma: imaging 45. Landis SH, Murray T, Bolden S, Wingo PA. Cancer statistics, 1999.
findings in lesions with minimal fat. Radiology 1997;205:497502. CA Cancer J Clin 1999;49(1):831.
23. Nelson CP, Sanda MG. Contemporary diagnosis and management of 46. Lee CT, Katz J, Shi W, et al. Surgical management of renal tumors
renal angiomyolipoma. J Urol 2002;168:13151325. 4cm or less in a contemporary cohort. J Urol 2000;163(3):730736.
24. Farrelly C, Delaney H, McDermott R, Malone D. Do all non-calcified 47. McDougal WS, Gervais DA, McGovern FJ, Mueller PR. Long-term
echogenic renal lesions found on ultrasound need further evaluation follow up of patients with renal cell carcinoma treated with radio
with CT? Abdom Imaging 2008;33:4447. frequency ablation with curative intent. J Urol 2005;174(1):6163.
25. Prando A, Prando D, Prando P. Renal cell carcinoma: unusual imaging 48. Gervais DA, McGovern FJ, Arellano RS, et al. Radiofrequency ablation
manifestations. Radiographics 2006;26:233244. of renal cell carcinoma: part 1, Indications, results, and role in patient
26. Filipas D, Spix C, Schulz-Lampel D, et al. Screening for renal cell management over a 6-year period and ablation of 100 tumors. AJR
carcinoma using ultrasonography: a feasibility study. BJU Int Am J Roentgenol 2005;185(1):6471.
2003;91:595599. 49. Gervais DA, Arellano RS, McGovern FJ, et al. Radiofrequency ablation
27. Malaeb BS, Martin DJ, Littooy FN, et al. The utility of screening renal of renal cell carcinoma: part 2, Lessons learned with ablation of 100
ultrasonography: identifying renal cell carcinoma in an elderly tumors. AJR Am J Roentgenol 2005;185(1):7280.
asymptomatic population. BJU Int 2005;95:977981. 50. Levinson AW, Su LM, Agarwal D, et al. Long-term oncological and
28. Schwarz A, Vatandaslar S, Merkel S, Haller H. Renal carcinoma in overall outcomes of percutaneous radio frequency ablation in high
transplant recipients with acquired cystic kidney disease. Clin J Am risk surgical patients with a solitary small renal mass. J Urol
Soc Nephrol 2007;2:750756. 2008;180(2):499504; discussion 504. Epub 2008 Jun 11.
29. Dyer R, DiSantis DJ, McClennan BL. Simplified imaging approach for 51. Permpongkosol S, Link RE, Kavoussi LR, Solomon SB. Percutaneous
evaluation of the solid renal mass in adults. Radiology 2008;247: computerized tomography guided cryoablation for localized renal cell
331343. carcinoma: factors influencing success. J Urol 2006;176(5):19631968;
30. Fan L, Lianfang D, Jinfang X, et al. Diagnostic efficiency of contrast- discussion 1968.
enhanced ultrasonography in solid renal parenchymal lesions with 52. Hinshaw JL, Shadid AM, Nakada SY, et al. Comparison of
maximum diameters of 5cm. J Ultrasound Med 2008;27:875885. percutaneous and laparoscopic cryoablation for the treatment of solid
31. Ho SSY. Renal cell carcinoma. In: Ahuja AT, editor. Diagnostic renal masses. AJR Am J Roentgenol 2008;191(4):11591168.
imaging, ultrasound. Salt Lake City: Amirsys; 2007. 53. Trembley BS, Ryan TP, Strohbehn JW. Interstitial hyperthermia:
32. Pickhardt PJ, Siegel CL, McLarney JK. Collecting duct carcinoma of physics, biology and clinical aspects. In: Urano M, Douple E, editors.
the kidney: are imaging findings suggestive of the diagnosis? AJR Am Physics of microwave hyperthermia in hyperthermia and oncology,
J Roentgenol 2001;176:627633. vol 3. Utrecht, the Netherlands: Verlag Springer; 1992. p. 1198.
33. Prasad SR, Humphrey PA, Catena JR, et al. Common and uncommon 54. Farrell MA, Charboneau JW, Callstrom MR, et al. Paranephric water
histologic subtypes of renal cell carcinoma: imaging spectrum with instillation: a technique to prevent bowel injury during percutaneous
pathologic correlation. Radiographics 2006;26:17951806. renal radiofrequency ablation. AJR Am J Roentgenol 2003;181(5):
34. Blitman NM, Berkenblit RG, Rozenblit AM, Levin TL. Renal medullary 13151317.
carcinoma: CT and MRI features. AJR Am J Roentgenol 2005;185: 55. Wah TM, Koenig P, Irving HC, et al. Radiofrequency ablation of a
268272. central renal tumor: protection of the collecting system with a
35. Browne RFJ, Meehan CP, Colville J, et al. Transitional cell carcinoma of retrograde cold dextrose pyeloperfusion technique. J Vasc Interv
the upper urinary tract: spectrum of imaging findings. Radiographics Radiol 2005;16(11):15511555.
2005;25:16091627. 56. Cantwell CP, Wah TM, Gervais DA, et al. Protecting the ureter during
36. Tran W, Serio AM, Raj GV, et al. Longitudinal risk of upper tract radiofrequency ablation of renal cell cancer: a pilot study of retrograde
recurrence following radical cystectomy for urothelial cancer and the pyeloperfusion with cooled dextrose 5% in water. J Vasc Interv Radiol
potential implications for long-term surveillance. J Urol 2008;179: 2008;19(7):10341040.
96100. 57. Gervais DA, McGovern FJ, Wood BJ, et al. Radio-frequency ablation of
37. Gupta R, Paner GP, Amin MB. Neoplasms of the upper urinary tract: a renal cell carcinoma: early clinical experience. Radiology
review with focus on urothelial carcinoma of the pelvi-calyceal system 2000;217(3):665672.
and aspects related to its diagnosis and reporting. Adv Anal Pathol 58. Wah TM, Arellano RS, Gervais DA, et al. Image-guided percutaneous
2008;15:127139. radiofrequency ablation and incidence of post-radiofrequency ablation
38. Datta SN, Allen GM, Evans R, et al. Urinary tract ultrasonography in syndrome: prospective survey. Radiology 2005;237(3):10971102.
the evaluation of haematuria a report of over 1,000 cases. Ann R Coll 59. Wah TM, Irving HC. Acute tubular necrosis following radiofrequency
Surg Engl 2002;84:203205. ablation of a renal cell carcinoma. Cardiovasc Intervent Radiol 2007
39. Anderson EM, Murphy R, Rennie AT, Cowan NC. Multidetector Nov 6 (epub ahead of print).
computed tomography urography (MDCTU) for diagnosing urothelial 60. Wah TM, Irving HC. Infectious complications after percutaneous
malignancy. Clin Radiol 2007;62:324332. radiofrequency ablation of renal cell carcinoma in patients with ileal
40. Horstman WG, McFarland RM, Gorman JD. Color Doppler conduit. J Vasc Interv Radiol 2008;19(9):13821385.
sonographic findings in patients with transitional cell carcinoma of the 61. Poon RT, Ng KK, Lam CM, et al. Learning curve for radiofrequency
bladder and renal pelvis. J Ultrasound Med 1995;14:129133. ablation of liver tumors: prospective analysis of initial 100 patients in
41. Papatsoris AG, Chrisofos M, Skolarikos A, et al. Upper urinary tract a tertiary institution. Ann Surg 2004;239(4):441449.
transitional cell carcinoma: a 10-year experience. Tumori 2008;94:
7578.
527
CHAPTER
Renal transplantation
Grant M. Baxter
28
DEVELOPMENT OF RENAL TRANSPLANTATION 528 Ciclosporin and tacrolimus toxicity 536
Infection 536
BACKGROUND 528
LATE COMPLICATIONS 537
INDICATIONS AND CONTRAINDICATIONS TO Ureteric stenosis 537
TRANSPLANTATION 529 Transplant artery stenosis 537
DONOR SUPPLY 529 Arteriovenous fistulae 538
Ciclosporin and tacrolimus toxicity 539
HISTOCOMPATIBILITY TESTING 529 Acute rejection 539
Chronic rejection 539
PREOPERATIVE MANAGEMENT 529 Urinary tract infection 540
SURGERY 529 Recurrent disease 540
Other complications 540
IMMUNOSUPPRESSION 529
COMBINED RENAL AND PANCREATIC
IMAGING THE TRANSPLANTED KIDNEY 530 TRANSPLANTATION 541
There are a number of treatment options for end-stage renal and prognosis. A number of small technical differences exist in
disease and these include haemodialysis, peritoneal dialysis and terms of the surgical technique and recipient outcome between
renal transplantation. Of these, there is no doubt that transplanta- cadaveric and live donor transplants; however, the overall manage-
tion is the treatment of choice; however, there are limitations to the ment of the recipient can be regarded as similar in both types.
number of operations that can be performed. These are well recog-
nised, not just by the medical staff involved, but also by the general
public and the many and diverse public health campaigns which
highlight the continuing shortage of suitable donor kidneys.11
HISTOCOMPATIBILITY TESTING
Thankfully, improvements including better donor recipient match-
ing,12,13 the use of more potent immunosuppressive regimens, In order to reduce to a minimum the risk of rejection, the detection
together with improved surgical techniques, have all resulted in of donor-specific antibodies in the lymphocyte cross-match test is a
improved outcomes. The 1- and 5-year graft survival in Europe has contraindication to transplantation.
been improving since the mid-1990s and current figures show a The risk of subsequent episodes of acute rejection is partially
1-year graft survival of 90% with a 5-year survival of 80%; there dependent upon the degree of HLA matching between donor and
are slightly higher values for living donor kidneys and recipient. The genes that determine the HLA antigens are located
slightly lower values for second and subsequent transplants on chromosome 6.14,15 The importance of such HLA matching is
(www.uktransplant.org). reflected in the improved graft survival of a fully HLA matched
There is universal agreement that renal transplantation is the graft (T-half 17.3 years), compared with an incomplete HLA miss
treatment of choice for end-stage renal failure. A successful renal matched graft (T-half 7.8 years),16,17 where T-half is the time taken
transplant will provide a glomerular infiltration rate (GFR) of up to for 50% of transplants that are functioning at one year to fail.
5060mL per minute, which although only half of the normal adult
value, is nevertheless sufficient to return the vast majority of
patients to a normal, independent lifestyle. Such an improvement PREOPERATIVE MANAGEMENT
in the quality of life is difficult and some would say impossible to
measure; however, in the harsh world of health economics, it is The transplant procedure should ideally be performed within 24
clear that the cost benefits of successful transplantation far out- hours of organ retrieval and at worst, 48 hours. During this period
weigh those of failure. This is one reason why resources are tar- the recipient will have been chosen, appropriately prepared for the
geted on the pre-, peri- and immediate post-transplantation period operation with screening for infection and cardiorespiratory reserve
in order to help ensure as positive an outcome as possible. The assessment, and initial dialysis undertaken, if any fluid or metabo-
average life expectancy of a transplant kidney is approximately lite imbalance requires recorrection.
710 years, increasing to 1520 years with a live donor organ. A live related donor, who can be either a family member or close
Although there are many and varied imaging techniques used friend, is screened with a combination of clinical history, examina-
when dealing with the transplant patient, there is no doubt that tion and HLA status assessment. Other assessment tests for live
ultrasound remains central and crucial to the management of these donors will vary from centre to centre but will include a 24-hour
patients and is very useful both in the early postoperative period creatinine clearance, serology, liver function tests, DMSA scan and
as a non-invasive indicator of renal transplant dysfunction and in either MRI or CT to assess anatomy; renal arteriography is largely
the long-term follow-up of many of these patients, particularly reserved for difficult cases.
those with suspected renal artery stenosis.
A B
Figure 28.3 A and B: Normal colour Doppler scan of the transplant kidney. The intrarenal vessels are well visualised and extend to
the periphery of the cortex. The arterial (red) and venous (blue) branches can be easily distinguished. C: Normal spectral Doppler waveform
from an interlobar artery. Having selected and drawn around an appropriate arterial waveform the machine has automatically calculated
both the PI and RI (1.11 and 0.63 respectively). D: Normal colour Doppler scan of the origin of the transplant renal artery (thin arrows) as it
arises from the external iliac artery (thick arrows). E: Spectral Doppler waveform of the transplant renal artery just distal to its origin. The
normal renal artery waveform is well demonstrated and has a peak systolic velocity of 1.50m/s.
Primarily it provides an instantaneous appreciation of the intrare- (Fig. 28.3A, B). As with all Doppler techniques, in order to acquire
nal vasculature and therefore gives a global impression of overall quantitative information spectral Doppler analysis is required (Fig.
transplant perfusion. In addition, it can easily identify the trans- 28.3C). The technique of using colour Doppler and spectral Doppler
plant artery and vein and track these back to their anastomoses with analysis in the transplanted kidney has much in common with
the iliac vessels. Although such information is purely visual and techniques used elsewhere in the vascular tree: the vessel is first
qualitative in many circumstances, it is both helpful and reassuring identified using colour Doppler, the spectral gate is placed over the
531
CHAPTER 28 Renal transplantation
with acute rejection and, although acute tubular necrosis has been an RI greater than 0.7 should be regarded as abnormal. It is well
described as causing a minimal increase in renal length, these fea- recognised that both acute tubular necrosis and acute rejection can
tures are much less marked when compared with those of acute elevate both these values.41,42 However, the higher the ratio, the
rejection. Irrespective of these observations, none of these measure- greater is the likelihood of acute rejection.43 Complete absence, or
ments have been adopted in routine clinical practice. reversal of diastolic flow is likely to be due to acute rejection in the
With regard to Doppler ultrasound, there have been a significant majority of cases. A normal resistive index or pulsatility index,
number of studies performed testing the potential value of this however, does not exclude graft dysfunction and has been noted in
technique in differentiating acute rejection from acute tubular up to 50% of patients with biopsy-proven rejection. Once a histo-
necrosis, as a non-invasive alternative to renal transplant biopsy. logical diagnosis has been established, monitoring of treatment
Some of these initial results were both confusing and contradictory; regimens can be documented using serial spectral Doppler meas-
the reasons for this have been well recognised and include inhomo- urements31 (Fig. 28.4).
geneous study populations, inadequately defined end points and With regard to the colour flow technique itself, power Doppler
differing diagnostic criteria. In retrospect, the expectation of being ultrasound has been promoted as a synergistic tool to colour
able to ascribe some form of histological value to a non-invasive Doppler, or even a replacement. However, there is no evidence to
ultrasound test was probably, at best, optimistic. However, this date that has shown any improvement of the power Doppler tech-
technique continues to perform a useful clinical role in monitoring nique over conventional colour Doppler,44 and in the opinion of
such patients with delayed function.40 many, the loss of directional flow information in many circum-
The role of colour Doppler in the early postoperative period is stances is disadvantageous for vessel identification, or in the detec-
therefore to help provide an overall qualitative impression of renal tion of renal artery stenosis.
perfusion and on specific spectral Doppler analysis, quantify this Other indices, including the acceleration time, have shown inter-
with serial measurements. At our institution scanning is performed esting results in the early transplant period with a short acceleration
three times per week until renal function is established. Although time on day 1 being associated with a longer duration of delayed
differentiation of pathological entities, such as acute tubular necro- function and an acceleration time of less than 90ms on day 5 being
sis from acute rejection is not possible, serial measurement of the associated with a high risk of rejection.45 However, these results
pulsatility and resistive indices, in conjunction with the many clini- were published a number of years ago and they remain to be sub-
cal and biochemical findings, help the renal physician decide stantiated. Conventional resistive and pulsatility index measure-
whether to proceed or refrain from renal biopsy (Table 28.1). A PI ments remain the mainstay for monitoring transplanted kidneys
less than 1.5 or RI less than 0.7 is normal; a PI greater than 1.8 or using Doppler ultrasound. With regard to renal graft outcomes, it
has also been shown that a resistive index of greater than 80, meas-
ured at least 3 months following transplantation, is associated with
subsequent poor graft performance and failure.46 This work, again,
Table 28.1 Causes of elevation of PI/RI in the early
has still to be substantiated and indeed an earlier prognostic value
transplant period within 1 or 2 weeks of transplantation would be clinically more
Acute rejection useful than a post 3-month assessment.
Acute tubular necrosis
Hydronephrosis Arterial thrombosis
Pyelonephritis
Arterial thrombosis is rare and affects less than 1% of transplants.47
Extrarenal collection; in up to 50%; lymphocele commonest
It is often clinically silent and occurs in the early transplant period.
Ciclosporin toxicity; normally no effect on RI/PI It may be discovered either incidentally at a routine isotope reno-
Renal vein thrombosis; reverse diastolic flow gram or on colour Doppler imaging scan in a patient with
A B
Figure 28.4 Delayed function. A: Spectral Doppler waveform from a kidney with delayed function in the first week of transplantation.
This shows complete absence of flow in diastole with a only a small segment remaining. The PI was markedly elevated at 4.01. This
prompted renal biopsy, which showed acute rejection. Appropriate anti-rejection treatment was started; the scan a few days later (B)
showed restoration of normal diastolic flow and a PI of 1.27 consistent with a favourable response to treatment.
533
CHAPTER 28 Renal transplantation
presumed delayed function. Predisposing factors include multiple colour Doppler will show flow in the main transplant artery, which
renal vessels, paediatric donor kidneys and atherosclerosis in either on spectral Doppler analysis will show reversed diastolic flow.48 On
the donor or recipient. The process is generally irreversible, result- occasion, trauma may be the cause of acute arterial occlusion sec-
ing in graft infarction and subsequent nephrectomy. If the graft has ondary to intimal dissection. This is, however, generally outside the
multiple arteries, it is possible for one vessel to thrombose resulting early transplant period and the clinical history is normally highly
in focal segmental infarction but renal function may remain stable suggestive.
and satisfactory in the long term, depending upon the volume of
kidney spared.
The ultrasonic features of main artery thrombosis are striking,
with complete absence of flow in both the kidney and the renal Venous thrombosis
artery both on colour Doppler and spectral Doppler analysis. In this
situation it is important to confirm that the ultrasound machine Venous thrombosis normally causes acute pain and swelling of the
settings are optimised and adjusted for maximum sensitivity for the graft, often in association with an abrupt cessation of renal function
detection of low velocity flow. A good way of confirming thrombo- and urine output. It is more common than arterial occlusion. A
sis is to search for flow in alternative vessels either at similar depth typical patient may be between the third and eighth postoperative
to the transplant kidney or deeper to it, such as demonstrating flow day; if the patient has delayed graft function then pain and tender-
within the deeper iliac artery and vein (Fig. 28.5). On occasion, a ness will predominate, if the kidney is functioning then the sudden
Doppler waveform may still be obtained from the main transplant onset of anuria with or without pain will cause clinical concern.49
artery; if this is the case, it is usually very abnormal with absent Although withholding ciclosporin and tacrolimus in the early post-
diastolic flow and significantly reduced amplitude. Assuming the operative period and the use of subcutaneous heparin or aspirin are
colour features are as described above, this should not alter the thought to help avoid this complication, none of these options have
suspected diagnosis. been proven in clinical trials. Ideally a high index of suspicion is
It is important to remember that absent intrarenal flow may also required in order that early diagnosis and intervention may salvage
be seen in a number of other conditions, including hyperacute rejec- the transplant kidney. However, nephrectomy is still required in
tion or renal vein thrombosis. In both of these scenarios, however, the vast majority of these cases.
A B
Figure 28.5 Absent intrarenal flow. A: B-mode image showing a normal looking transplant kidney. B: Colour Doppler scan of the same
kidney. The PRF or colour velocity scale is set low for increased sensitivity. Despite this there is complete absence of intrarenal flow. Flow,
however, can be visualised in the iliac artery (arrow) with some flash artefact in the surrounding tissues. The appearances are those of
renal artery occlusion. C: The same kidney following the injection of intravenous microbubble contrast agent. This confirms patency of the
iliac artery (arrow) but complete absence of intrarenal flow.
534
Early complications
A B
Figure 28.6 Colour Doppler ultrasound from a patient who had graft tenderness and absent urine output in the early
postoperative period. Significantly reduced flow is noted within the kidney (A) with only one definite arterial vessel seen in the upper pole.
Venous flow was absent throughout the kidney and the main transplant vein. Spectral Doppler sampled from an intrarenal artery (B)
showed reverse diastolic flow (arrows). The features are those of renal vein thrombosis. A graft nephrectomy was performed.
The most common collection is a lymphocele, occurring in 0.6 irreversible chronic damage to the transplant kidney. Furthermore,
18% (Fig. 28.9). Although these can be treated with various sclero- a diagnosis of nephrotoxicity in the acute setting of a non-
sants in an attempt to cure, the success of this approach has been functioning graft is notoriously difficult and therefore many clini-
mixed. Recognised treatment options are now based on laparo- cians avoid the use of these drugs if possible. Serum drug levels
scopic marsupialisation, which is both safe and effective.55,56 and renal biopsy are traditional but imperfect methods of diagnosis
of toxicity. Ultrasound is generally unremarkable, as these drugs
Ciclosporin and tacrolimus toxicity do not produce any significant change in diastolic flow.58 Occasion-
ally a reduction in diastolic flow has been noted, but this is
non-specific.
Both of the above agents are calcineurin inhibitors and represent a
major advance in organ transplantation. Unfortunately there are
side effects with both these agents as they are nephrotoxic, produc- Infection
ing a reversible renovascular constriction acutely and an interstitial
fibrosis chronically.57 As a result of this, recovery from acute tubular The transplant patient is prone to a number of infections, particu-
necrosis may be delayed and, indeed, these drugs may induce larly those of the chest, wound and urinary tract, in the early post-
operative period. Wound infections are likely to be due to
Staphylococcus, whereas urinary catheters and reflux predispose to
urinary tract infections. The latter can cause a deterioration in renal
function which may be indistinguishable from acute rejection and,
although rare, it is not unknown for pyelonephritis to be diagnosed
on transplant biopsy in patients with suspected acute rejection.
Ultrasound has little or no role in the diagnosis of infection,
although it is important to remember that infection may adversely
affect the pulsatility and resistive ratios.
Acute complications
1030% of patients require dialysis for ATN following
transplantation.
Acute rejection can develop in up to 40% of patients following
transplantation.
Colour and spectral Doppler are necessary for graft monitoring; a
PI <1.5 or RI <0.7 is normal.
Vascular occlusions, ureteric obstruction, collections and infection
can all elevate the PI and RI indices.
Arterial and venous occlusions carry a poor prognosis and often
result in transplant nephrectomy.
Most transplant collections are benign; drainage is only
Figure 28.7. Longitudinal scan of a large cystic collection just performed when appropriate.
superior to the bladder. An 8F pigtail catheter was inserted and can Ciclosporin toxicity has no effect on Doppler indices; diagnosis is
be easily identified (arrows). Analysis of the drainage fluid showed suspected on blood levels or at biopsy.
this to be urine, i.e. the collection was a urinoma.
A B
Figure 28.8 A: A large postoperative psoas collection is noted. This is of mixed echogenicity. The patients haemoglobin had fallen
significantly. The appearances are consistent with haematoma. B: The transplant kidney (arrows) lies inferior to the psoas haematoma
(thick arrows).
536
Late complications
A B
Figure 28.9 A: A peri-transplant collection (thick arrows) superior to the bladder had been unchanged over a number of years. A ureteric
stent is also noted within the bladder (thin arrows). B: This collection (arrows) was partially septated and presumed to be a lymphocele.
The patient was asymptomatic and therefore no treatment was indicated.
A B
Figure 28.10 A: Colour Doppler scan of the transplant artery (arrows) at its origin from the external iliac artery (thick arrow). The change in
direction of flow within the transplant artery is easily appreciated. The external iliac vein (arrowhead) is also clearly visualised and
differentiated due to the colour coding. B: Power Doppler scan of the same area as in A with exactly the same labelling for comparison.
There is no sense of flow direction and vessel identification is harder as a consequence.
group of lower risk patients. Clearly, exact cut-off levels will depend Arteriovenous fistulae
upon many factors and departments should review and audit the
level that is appropriate for their practice. Arteriovenous fistulae (AVF) can result from previous renal trans-
Secondary Doppler findings of renal artery stenosis include plant biopsy and have an incidence of approximately 12%. In
marked downstream turbulence (Fig. 28.12C), spectral broadening general most are of little clinical significance and resolve spontane-
and flow reversal, all of which may be seen distal to the primary ously as reflected in one study where, with an incidence of up to
stenotic site and help add weight and confidence to the primary 10% following biopsy, all but one of the ten fistulae had resolved
diagnostic findings. The transplant kidney, being superficial in on follow-up scans.66 In another study the incidence was 16.7%,
position, contributes to the relative ease of examination of the main with 75% closing within a month and 25% persisting longer than
transplant vessels, which can almost invariably be identified in all one year (three patients).67 Those AVFs that persist normally give
patients. Reliance on the secondary signs of stenosis, such as the rise to very pathognomonic and spectacular colour Doppler appear-
parvus tardus effect within the intrarenal arterial vessels (Fig. ances. Clinically they have been considered to be a potential cause
28.12D), as an aid to primary diagnosis is therefore less important of both hypertension and impaired renal function but neither of
than it would be in the native kidney.28 Kidneys with dual arteries these scenarios is a common problem. In practice, these lesions are
may have a stenosis affecting only one of the vessels and care must often simply observed and radiological intervention is only consid-
be taken to examine both components (Fig. 28.13). As well as main ered if a fistula is actively bleeding or significantly increasing in size
transplant vessel lesions, intrarenal branch stenoses have been and causing a steal syndrome from the kidney, when the benefits
described although these are difficult to diagnose with all modali- of embolisation may be considered to outweigh those of conserva-
ties, even angiography. tive management.
538
Late complications
A B
C D
Figure 28.12 Transplant artery stenosis. A: Colour Doppler image at the origin of the transplant renal artery demonstrating an area of
aliasing (arrow) within the proximal transplant artery with normal laminar flow within the iliac artery (thick arrow). The aliasing was focal and
the colour velocity scale was set high. The appearances are those of a transplant artery stenosis. B: Spectral Doppler waveform through
the area of aliasing in the transplant artery showed a markedly elevated peak systolic velocity of 5m/s and spectral broadening, all
features of a renal artery stenosis. C: Spectral Doppler downstream from the main stenosis showing marked turbulence as demonstrated
by the marked and varied irregularity of the waveform itself. D: Spectral Doppler waveform from a segmental renal artery in the same
patient showing the parvus tardus effect indicative of a more proximal stenosis.
The ultrasonic appearances of an AVF include a focus of high can be difficult to differentiate from chronic rejection and therefore
flow on colour Doppler with spectral Doppler showing both arterial often a therapeutic trial of dose reduction or conversion to an
and venous components. This is easily differentiated from high alternative immunosuppressive agent may be required. Following
flow that may be present in other parts of the transplant kidney by this, a small but significant number of patients may respond
the simple manoeuvre of increasing the pulse repetition frequency positively.
(PRF) to a level that results in non-visualisation of the normal intra-
renal vasculature on colour Doppler, with only the pathological Acute rejection
high flow in the fistula being observed. This simple manoeuvre is
in itself diagnostic (Fig. 28.14). On further analysis the spectral
Acute rejection is an unusual late complication. If present, non-
Doppler arterial waveform shows an increase in both systolic and
compliance with drug therapy should be strongly considered. Diag-
diastolic flow within the affected area of the fistula and as a result
nosis and treatment are as previously discussed for acute rejection
the pulsatility index or resistive index will either remain normal or
in the postoperative period.
will be slightly reduced when compared with that of the normal
surrounding vessels.68 Venous flow can be either normal or turbu-
lent and a large draining vein with arterialised flow may also be Chronic rejection
visualised.
Chronic rejection leads to a gradual deterioration of renal function
beginning at least 3 months following transplantation with biopsy
Ciclosporin and tacrolimus toxicity appearances of fibrous intimal thickening, interstitial fibrosis and
tubular atrophy. The most consistent predisposing factor is that of
Both these drugs have been discussed previously and their toxic previous episodes of acute rejection. There is no effective treatment
effects on renal function are well recognised. Continued adminis- and all efforts are concentrated towards preventing episodes of
tration may lead to a progressive deterioration in function, which acute rejection as a method to retard the progress of chronic
539
CHAPTER 28 Renal transplantation
B
A
A B
C D
Figure 28.14 A: Colour flow image of a transplant kidney demonstrates a focus of high flow (arrow); the velocity scale is set at a low level.
Another area of apparent focal flow is also noted (arrowhead). B: The same patient as in A; however, this time the velocity scale has been
significantly increased. Now, only the pathological high flow of the AVF persists (arrow). These appearances are pathognomonic of an AVF.
C: Spectral Doppler of the feeding artery to the AVF shows markedly elevated peak systolic (3m/s) and diastolic values (1.5m/s). D: A
normal intrarenal Doppler waveform from a different area of the kidney for comparison.
Table 28.4 Late complications of renal transplantation COMBINED RENAL AND PANCREATIC
Renal artery stenosis TRANSPLANTATION
Arteriovenous fistula
Hydronephrosis A detailed description of combined organ transplantation is beyond
the scope of this chapter. As for the renal transplantation, patient
Recurrence of disease
selection is crucial and depends upon a multidisciplinary pre-
Chronic rejection transplantation evaluation team. A successful outcome will restore
Malignancy blood glucose levels to normal, improve neuropathy in most
Infection patients and prevent recurrence of diabetic nephropathy in the new
kidney. It may also prevent the secondary complications of diabetes
but the effect on established lesions is not clear.
The standard surgical technique results in anastomosis of the
and improved targeting of these agents in combination with an pancreatic veins, and thus pancreatic endocrine production, to the
increased awareness of the different types of infection that may iliac vein with exocrine drainage via the pancreatic duct drained to
occur have all contributed to improved outcomes. the bladder.71 However, this is gradually being replaced in many
Malignancy remains an issue and with the increased longevity of centres by endocrine drainage to the portal system and drainage of
transplanted kidneys, the number of malignancies developing is the exocrine secretions to the bowel. The transplant kidney is dealt
slowly increasing (Fig. 28.19). The most likely lesions following with in the standard surgical manner.
transplantation are skin-related malignancy, cervical cancer and Vascular complications are the most common and occur in 12%
non-Hodgkins lymphoma. It is therefore obvious that careful of patients; 5% of vascular complications are arterial and 7% venous.
supervision of the transplant population is required so that earlier Other complications include rejection, infection and allograft pan-
diagnosis may result in improved prognosis for each of these creatitis. The overall survival of a combined pancreatic renal trans-
disorders.70 plant is 83%, 72.9% and 65.5% at 1, 3 and 5 years respectively.
541
CHAPTER 28 Renal transplantation
B
A
B
A
543
CHAPTER 28 Renal transplantation
A
B
Figure 28.19 A: Real-time image of a normal transplant kidney with a sharply defined echogenic lesion (arrow) at its pole. The
appearances are those of a benign angiomyolipoma. B: A chronic non-functioning transplant kidney with extensive internal calcification and
distal acoustic shadowing akin to autonephrectomy. C: The same patient as in B. The patient presented with haematuria. It is important to
check not only the transplant kidney(s) in this situation but also the native kidneys. A scan of the right kidney showed a renal tumour
(arrows) accounting for his symptomatology.
C D
544
Use of microbubble contrast agents
30
4 1 Delay
2 Time to peak
3 Max
25 4 Gradient
5 Area under curve
3
20
15
Baseline
10
1 2
0
0
2.41
4.82
7.24
9.65
12.1
14.5
16.9
19.3
21.7
24.1
26.5
28.9
31.4
33.8
36.2
38.6
41
43.4
45.8
48.3
50.7
53.1
55.5
57.9
A Time (seconds)
60
50
40
Mean echo (db)
Cortex
30
20
Pyramid
10
0
60
B Time (seconds)
Figure 28.21 A: A time intensity curve from the renal cortex during dynamic microbubble injection. Various parameters can be measured
including the arrival time from injection, the gradient of the curve, time to peak and peak value, and the area under the curve. B: Graph of
uptake following microbubble injection showing cortical and pyramidal time intensity curves.
545
CHAPTER 28 Renal transplantation
A B
Figure 28.22 A: Baseline colour Doppler scan shows minimal flow to the pole of the transplant kidney (arrows). It was not clear if this was
a technical problem, or an area of infarction. B: Following injection of microbubbles it is clear that the agent has been evenly distributed to
all areas of the transplant kidney (arrows). There is no evidence of focal infarction and the appearances on colour Doppler were
presumably therefore technical in origin.
Vascular occlusion
The diagnosis of renal artery occlusion is a catastrophic event for circumstances when the vessel is difficult to visualise due to patient
any transplant patient. It is rare that a contrast-enhanced study build, deeply situated vessels, bowel gas etc., microbubbles may
would be required to confirm this diagnosis. Sometimes, however, have a limited role.
multiple renal arteries are transplanted with the kidney and one
may suffer damage in the early postoperative period. It is useful to
know if there has been segmental infarction and the extent of such Renal masses
involvement. This can be a difficult diagnosis to make confidently
in some patients on conventional colour Doppler scanning and a Transplant kidneys, like the native kidney, may develop cysts or
more dynamic analysis of the renal circulation following the injec- tumours. With increased longevity of the transplant kidney, a defi-
tion of a microbubble contrast agent is much more revealing in this nite but small increase in the incidence of tumours has been noted
clinical situation (Fig. 28.22). It has been shown that use of such an in the transplant population. These can occur at multiple sites;
agent can quantify both total and regional blood flow in dogs;77 this however, the differentiation of a cyst from a tumour, or clarification
may be one of the more clinically useful applications of these agents of the nature of a complicated cyst can be helped with the use of
in relation to renal transplantation. In some circumstances such as microbubble agents78 (Fig. 28.24). It is important to remember,
with patients with reduced renal function in the early transplant however, that complementary imaging also includes CT and on
period for unknown reasons, it has occasionally been enlightening occasion MRI.
to see focal areas of unsuspected renal infarction (Fig. 28.23).
Potential applications
Renal artery stenosis A number of other potential applications of microbubble time inten-
The vast majority of transplant artery stenoses can be diagnosed sity curves can be considered for the future. These may address
with conventional colour Doppler. The routine use of a micro issues including their relationship with eGFR and creatinine and
bubble agent is not normally required but in the relatively rare any potential predictive value for the overall prognosis for the
546
References
A B
Figure 28.23 A: Colour Doppler ultrasound of a transplant kidney in the early postoperative period showing a lack of colour flow from the
cortex anteriorly (arrows). It was not clear if this was technical, or if the vascular supply to this area was compromised. B: Following the
injection of microbubbles, it can be seen that the anterior cortex is devoid of perfusion (arrows). This wedge-shaped defect is in keeping
with an area of infarction.
A B
Figure 28.24 A: Real-time scan of a native kidney in a patient with loin pain, hypotension and falling haemoglobin. A large inhomogeneous
mass was visualised (arrows). The diagnosis was either one of a bleed into a cyst or tumour. B: Following the injection of a microbubble
agent it was obvious that the lesion was not simple. Focal areas of contrast enhancement (arrows) were seen around the wall of the lesion.
The appearances were therefore those of a cystic tumour with internal haemorrhage.
transplant kidney, prediction of chronic rejection, or indeed any 6. Baxter GM. Ultrasound of renal transplantation. Clin Radiol
potential applications in the monitoring of drug-related studies. All 2001;56:802818.
of these areas remain potential fruitful areas of clinical research. 7. Sandhu C, Patel U. Renal transplantation dysfunction: the role of
interventional radiology. Clin Radiol 2002;57: 772783.
8. Charra B, Calemerd E, Ruffet M, et al. Survival as an index of the
REFERENCES adequacy of dialysis. Kidney Int 1992;41:12861291.
9. Vincenti F. A decade of progress in kidney transplantation.
1. Hamilton D. Alexis Carrel and the early days of tissue transplantation. Transplantation 2004;77:S52S61.
Transplant Rev 1987;2:115. 10. Valderrabano F, Jones EHP, Mallick NP. Report on the management of
2. Murray JE, Merrill JP, Harrison JH. Kidney transplantation between renal failure in Europe XXIV, 1993. Nephrol Dial Transplant
seven pairs of identical twins. Ann Surg 1958;148:343359. 1995;10(suppl 51):125.
3. Starzl TE. Experience in renal transplantation. Philadelphia: Saunders; 11. Gore SM, Cable DJ, Holland AJ. Organ donation from intensive care
1964. units in England and Wales two year confidential audit of deaths in
4. Calne RY, White DJG, Thiru S, et al. Cyclosporin A in patients receiving intensive care. Br Med J 1992;304:349355.
renal allografts from cadaveric donors. Lancet 1978;ii:13231327. 12. Takemoto S, Terasaki PI, Cecka JM, et al. Survival of nationally shared
5. Akbar SA, Jafri SZ, Amendola MA, et al. Complications of renal HLA-matched kidney transplants from cadaveric donors. N Engl J
transplantation. Radiographics 2005;25:13351356. Med 1992;327:834839.
547
CHAPTER 28 Renal transplantation
13. The Canadian Multicentre Transplant Study Group. A randomised nephrotoxicity and acute rejection on resistive index and renal length.
clinical trial of cyclosporin in cadaveric renal transplantation: analysis AJR Am J Roentgenol 1992;158:791797.
at three years. N Engl J Med 1986;314:12191220. 39. Parvin SD, Rees Y, Veitch PS, et al. Objective measurement by
14. Robinson MT, Kindt TJ. Major histocompatibility complex antigens ultrasound to distinguish Cyclosporin A toxicity from rejection. Br J
and genes. In: Paul W, ed. Fundamental immunology. New York: Surg 1986;73:10091011.
Raven Press; 1989. p. 489539. 40. Jakobsen JA, Brabrand K, Egge TS, Hartmann A. Doppler examination
15. Krensky AM. Transplant immunobiology in paediatric of the allografted kidney. Acta Radiol 2003;44(1): 312.
nephrology. 3rd edn. Baltimore: Williams & Wilkins; 1993. p. 41. Chudek J, Kolonko A, Krol R, et al. The intrarenal resistance
13731389. parameters measured by duplex Doppler ultrasound shortly after
16. Jamison RL, Wilkinson R. The pretransplant selection and evaluation kidney transplantation in patients with immediate, slow and delayed
of donor and recipient. In: Nephrology. New York: Chapman & Hall; graft function. Transplant Proc 2006;38:4245.
1997. p. 10721082. 42. Datta R, Sandhu M, Saxena AK, et al. Role of duplex Doppler and
17. Opelz G. Correlation of HLA matching with kidney graft survival in power Doppler sonography in transplanted kidneys with acute renal
patients with or without cyclosporine treatment. Transplant parenchymal dysfunction. Australas Radiol 2005;49:1520.
1985;40:240243. 43. Hillburn MD, Bude RO, Murphy KJ, et al. Renal transplant evaluation
18. Basaran O, Moray G, Emiroglu R, et al. Graft and patient outcomes with power Doppler ultrasound. Br J Radiol 1997;70:3942.
among recipients of renal grafts with multiple arteries. Transplant 44. Chow L, Sommer FG, Huang J, Li KC. Power Doppler imaging and
Proc 2004;36:102104. resistance index measurement in the evaluation of acute renal
19. Robles J, Errasti P, Abad J, et al. Surgical complications in renal transplant rejection. J Clin Ultrasound 2001;29(9):483490.
transplantation: determinant factors. Transplant Proc 45. Merkus JWS, Hoitsma AJ, van Asten WNJC, et al. Doppler spectrum
1995;27:22582259. analysis to diagnose rejection during post transplant acute renal
20. Lai M, Huang C, Chu S, et al. Surgical complications in renal failure. Transplantation 1994;58:570576.
transplantation. Transplant Proc 1994;26:21652166. 46. Radermacher J, Mengel M, Ellis S, et al. The renal arterial resistive
21. Gruber S, Chavers B, Payne W, et al. Allograft renal vascular index and renal allograft survival. N Engl J Med 2003;349(2):
thrombosis lack of increase with cyclosporin immunnosuppression. 115124.
Transplantation 1989;47:475478. 47. Orlic P, Vukas D, Drescik I, et al. Vascular complications after 725
22. Hakim N, Benedetti E, Pirenne J, et al. Complications of ureterovesical kidney transplantations during 3 decades. Transplant Proc
anastomosis in kidney transplant patients: the Minnesota experience. 2003;35:13811384.
Clin Transplant 1994;8:504507. 48. Kaveggia LP, Perella RR, Grant EG, et al. Duplex Doppler sonography
23. Vincenti F, Laskow DA, Neylan JF, et al. One year follow up of an in renal allografts: the significance of reversed flow in diastole. AJR
open label trial of FK506 for primary kidney transplantation. Am J Roentgenol 1990;155:295298.
Transplantation 1996;61:15761581. 49. Penny MJ, Nankivell BJ, Disney APS, et al. Renal graft thrombosis: A
24. European Mycophenolate Mofetil Cooperative Study Group. Placebo survey of 134 consecutive cases. Transplantation 1994;58:565569.
controlled study of mycophenolate mofetil combined with cyclosporin 50. Baxter GM, Morley P, Dall B. Acute renal vein thrombosis in renal
and corticosteroids for prevention of acute rejection. Lancet allografts: new doppler ultrasonic findings. Clin Radiol
1995;345:13211325. 1991;43:125127.
25. de Morais RH, Muglia VF, Mamere AE, et al. Duplex Doppler 51. Reuther G, Wanjura D, Bauer H. Acute renal vein thrombosis in renal
sonography of transplant renal artery stenosis. J Clin Ultrasound allografts: detection with duplex Doppler ultrasound. Radiology
2003;31:135141. 1989;170:557558.
26. Li J, Ji Z, Cai S, et al. Evaluation of severe transplant renal artery 52. MacLennan AC, Baxter GM, Harden P, Rowe PA. Renal
stenosis with Doppler sonography. J Clin Ultrasound 2005;33: transplant vein occlusion; an early diagnostic sign? Clin Radiol
261269. 1995;50:251253.
27. Patel U, Khaw KK, Highes NC. Doppler ultrasound for the detection 53. Kocak T, Nane I, Ander H, et al. Urologic and surgical complications
of renal transplant artery stenosis threshold peak systolic velocity in 362 consecutive living related donor renal transplantations. Urol Int
needs to be higher in low-risk or surveillance population. Clin Radiol 2004;72:252256.
2003;58:772777. 54. Karam G, Maillet F, Parant S, et al. Ureteral necrosis after kidney
28. Baxter GM, Ireland H, Moss JG, et al. Colour Doppler ultrasound in transplantation: risk factors and impact on graft and patient survival.
renal transplant artery stenosis: which Doppler index? Clin Radiol Transplantation 2004;78:725729.
1995;50:618622. 55. Duepree HJ, Fornara P, Lewejohann JC, et al. Laparoscopic treatment
29. Genkins SM, Sanfilippo FP, Carroll BA. Duplex Doppler sonography of lymphoceles in patients after renal transplantation. Clin Transplant
of renal transplants: lack of sensitivity and specificity in establishing 2001;15(6):375379.
pathologic diagnosis. AJR Am J Roentgenol 1989;152: 535539. 56. Risaliti A, Corno V, Donini A, et al. Laparoscopic treatment of
30. Rigsby CM, Taylor KJW, Weltin G, et al. Renal allografts in acute symptomatic lymphoceles after kidney transplantation. Surg Endosc
rejection: evaluation using duplex sonography. Radiology 2000;14(3):293295.
1986;158:375378. 57. Myers BD, Sibley R, Newton L, et al. The long term course of
31. Hollenbeck M, Hilbet N, Meusel F, et al. Increasing sensitivity and cyclosporin associated chronic nephropathy. Kidney Int
specificity of Doppler sonographic detection of renal transplant 1988;33:590600.
rejection with serial investigative technique. Clin Invest 58. Heine GH, Girndt M, Sester U, Kohler H. No rise in renal Doppler
1994;72:609615. resistance indices at peak serum levels of cyclosporin A in stable
32. Wilczek HE. Percutaneous needle biopsy of the renal allograft. kidney transplant patients. Nephrol Dial Transplant
Transplantation 1990;50:790797. 2003;18(8):16391643.
33. Tang S, Li JH, Lui SL, et al. Free hand, ultrasound guided 59. Gray DWR. Graft renal artery stenosis in the transplanted kidney.
percutaneous renal biopsy: experience from a single operator. Eur J Transplant Rev 1994;8:1521.
Radiol 2002;41(1):6569. 60. Erley CM, Duda SH, Wakat JP, et al. Non invasive procedures for
34. Freda A, Van Dijk LC, Van Oostaijen JA, Pattynama PM. Complication diagnosis of renovascular hypertension in renal transplant recipients
rate and diagnostic yield of 515 consecutive ultrasound guided and prospective analysis. Transplantation 1992;54:863867.
biopsies of renal allografts and native kidneys using a 14-gauge 61. Gedroyc WM, Negus R, al Kautoubi A, et al. Magnetic resonance
Biopsy gun. Eur Radiol 2003;13(3):527530. angiography of renal transplants. Lancet 1992;339:789791.
35. Chan R, Common AA, Marcuzzi D. Ultrasound guided renal biopsy: 62. Voiculescu A, Hollenbeck M, Plum J, et al. Iliac artery stenosis
experience using an automated core biopsy. Can Assoc Radiol J proximal to a kidney transplant: clinical findings, duplex
2000;51(2):107113. sonographic criteria, treatment and outcome. Transplantation
36. Pirsch JD, Ploeg RJ, Gange S, et al. Determinants of graft survival after 2003;76(2):332339.
renal transplantation. Transplantation 1996;61:15811585. 63. Butorovic-Ponikvar J. Renal transplant artery stenosis. Nephrol Dial
37. Cochlin DLL, Wake A, Salaman JR, Griffin PJA. Ultrasound changes in Transplant 2003;18(Suppl. 5):7477.
the transplant kidney. Clin Radiol 1988;39:373376. 64. Geddes CC, McManus SK, Koteeswaran S, Baxter GM. Long term
38. Pozniak MA, Kelcz F, DAlessandro A, et al. Sonography of renal outcome of transplant renal artery stenosis managed conservatively or
transplants in dogs: the effect of acute tubular necrosis, cyclosporin by radiological intervention. Clin Transplant 2008;22:572578.
548
References
65. Ruggenenti P, Mosconi L, Bruno S, et al. Post transplant renal artery assessment of the contrast replenishment? Ultrasound Med Biol
stenosis: the hemodynamic response to revascularisation. Kidney Int 2001;27(7):937944.
2001;60(1):309318. 73. Cosgrove D, Eckersley R, Blomley M, Harvey C. Quantification of
66. Merkus JWS, Zeebregts CJAM, Hoitsma AJ, et al. High incidence of blood flow. Eur Radiol 2001;11(8):13381344.
arteriovenous fistula after biopsy of kidney allografts. Br J Surg 74. Claudon M, Barnevolt CE, Taylor GA, et al. Renal blood flow in pigs:
1993;80:310312. changes depicted with contrast enhanced harmonic US imaging
67. Brandenburg VM, Frank RD, Riehl J. Color coded duplex sonography during acute urinary obstruction. Radiology 1999;212:725731.
of arteriovenous fisulae and pseudoaneurysms complicating 75. Hosotani Y, Takahashi N, Kiyomoto H, et al. A new method for
percutaneous renal allograft biopsy. Clin Nephrol 2002;58(6):398404. evaluation of split renal cortical blood flow with contrast echography.
68. Renowden SA, Blethyn J, Cochlin DLL. Duplex and color flow Hypertension Res 2002;25(1):7783.
sonography in the diagnosis of post biopsy arteriovenous fistulae in 76. Lefevre F, Correas JM, Briancon S, et al. Contrast enhanced
the transplant kidney. Clin Radiol 1992;45:233237. sonography of the renal transplant using triggered pulse inversion
69. Matthew TH. Recurrent disease after transplantation. Transplant Rev imaging: preliminary results. Ultrasound Med Biol 2002;28(3):
1991;5:3145. 303314.
70. Penn I. Cancer is a complication of severe immunosuppression. Surg 77. Wei K, Le E, Bin JP, Coggins M, et al. Quantification of renal blood
Gynaecol Obstet 1986;162:603610. flow with contrast enhanced ultrasound. J Am Coll Cardiol
71. Sidhu PS, Baxter GM. Pancreas transplantation. In: Ultrasound of 2001;37(4):11351140.
abdominal transplantation. Stuttgart: Thieme International; 78. Correas J, Claudon M, Tranquart F, Helenon O. Contrast enhanced
2002:125130. ultrasonography: renal applications. J Radiol 2003;84(12 pt 2):
72. Schlosser T, Pohl C, Veltmann C, et al. Feasibility of the flash- 20412054.
replenishment concept in renal tissue: which parameters affect the
549
CHAPTER
Microscopic anatomy
The bladder wall is formed of four layers: the serosa (outermost,
formed from the peritoneum), the muscular layer, the submucosa
and the mucosa. The muscular layer (detrusor muscle) comprises
550
Techniques
three bands of smooth muscle fibres arranged variously in longitu- ureter. Turbulence will only be detected if the specific gravity of the
dinal and circular array. The layers cannot be distinguished on urine in the bladder and the urine from the ureter are different.
ultrasound. The muscle fibres form the involuntary internal sphinc- Fortunately, most patients for bladder ultrasound have been asked
ter at the bladder neck. to drink sufficient amount of fluid to fill their bladder, and the urine
The deep muscle fibres are bound by the submucosa to the excreted by the kidneys is likely to be more dilute than that in the
mucosa, in the most part a loose affiliation so that the mucosa can bladder.
ruck up when the bladder is empty, becoming stretched and With regard to the jets on colour duplex imaging:2,3
smooth as the bladder distends. The mucosa is continuous with that n They assist in identifying the ureteric orifice.
of the ureters (and therefore with the mucosa of the collecting n Their duration varies 0.4s to 7.5s and depends largely on
systems of the kidneys) and with that of the urethra. Transitional fluid intake.2,3 Duration can vary in an individual by up to 2s
cell epithelium lines the mucosa. from one jet to another.2 The interval between jets can be as
The base is the most complex part of the bladder, the sensitive low as 2s or up to 2.5min.3
trigone being triangular in shape and receiving the left and right n The direction of a normal jet is anteromedial and upward.
ureter posteriorly, and opening to the urethra anteriorly. The n Several flow patterns may be observed, including discrete jets,
mucosa over the trigone is always smooth, even when the bladder ureteric streaming, and rest periods.3
is empty because uniquely it is firmly attached to the muscular n Absence of jets in patients with acute obstruction from
layer. The distal ureters pass obliquely through the bladder wall, ureteric calculus suggests high-grade obstruction.4 Indeed, in
the ureteric openings marking the posterior border of the trigone. children, unilateral absence of a jet from the dilated side or
Their course is visible on ultrasound. significant asymmetry in jet frequency indicates upper tract
The urothelium is not just a barrier, but is active in bladder func- obstruction.4 A recent study has shown that when there is less
tion, having an afferent innervation with an important role in the than one jet detected from the dilated side in comparison to
reflex responses to bladder filling and distension. Within the four (combined jets from both ureters), there is an 87%
urothelium, there is a dense muscarinic receptor population, which sensitivity and 96% specificity for obstruction in children with
mediates the release of a diffusible inhibitory factor that inhibits unilateral hydronephrosis.5
smooth muscle contraction.1 n In the stented ureter, looking for ureteric jets is not helpful.6
The bladder derives its blood supply from the internal iliac arter-
The detection of ureteric jets, especially when the jet frequency is
ies, predominantly via the superior, middle and inferior vesical
comparable between the left and right side when scanning for
arteries, supplemented by the obturator and inferior gluteal
several minutes, helps to exclude significant obstruction to the
branches of the internal iliac arteries. The venous drainage forms a
ureter. However, analysing ureteric jets is only an adjunct to urinary
rich plexus of vessels around the inferior and fundal surfaces.
tract ultrasound and must be interpreted alongside evidence of
renal obstruction.7 In particular, failure to detect jets bilaterally does
not usually imply obstruction to both kidneys, but rather that the
difference in specific gravity of the urine from the kidneys com-
TECHNIQUES pared with that in the bladder is too insignificant for turbulence to
be detected.
Transabdominal imaging
Endocavity ultrasound
The default examination of the bladder is via a suprapubic or lower
abdominal window (Fig. 29.1). Modern ultrasound platforms will In rare circumstances, the base of the bladder is best assessed by
give excellent views of the whole viscus and information about the transrectal ultrasound (TRUS). This can be helpful if there is concern
posterior vesical space at frequencies of 5MHz, using a curvilinear about pathology at the trigone or when a mass may be invading the
array. Adjusting the time gain curve (TGC) so that it is flat or even urethra from the bladder. Likewise, TRUS is invaluable when there
j shaped reduces reverberation artefact. Use of compound har- is invasion between the prostate and the bladder, irrespective of the
monic imaging is advocated for a similar reason. origin of the tumour.
The bladder must be moderately full, typically 300400mL Transvaginal ultrasound has a role in evaluating the mobility of
volume, for a meaningful examination. Scans are conducted from the bladder neck. Techniques have been developed that ensure the
the dome down to the base of the bladder and by angling the trans- endocavity probe does not affect the pelvic floor motion.8,9 The
ducer posteriorly and inferiorly, reasonable views of the prostate bladder neck tends to lie more inferiorly and more posteriorly at
should be obtained in male patients. This provides an approximate rest in incontinent women when compared to continent women,
estimation of prostate volume. with more descent on straining and less elevation on squeezing.8 In
In patients with retention, notably chronic retention, the bladder a large study of women with primary stress incontinence, ultra-
may hold up to 1000mL and scanning necessarily is periumbilical sound revealed bladder neck funnelling in just over one-third of
or even more cranially. In these cases, reporting the anatomical subjects, and this correlated with low pressure incontinence; the
level for the dome of the bladder (e.g. centimetres above the umbili- worth of the study is in the high negative predictive value (93%),
cus) is very helpful. so that absence of bladder neck funnelling more or less excludes
The ultrasound examination should include views of the trigone the detection of low pressure leak on formal urodynamics.10
to show the vesico-ureteric junctions and the bladder neck (Fig. Endovaginal US is performed routinely in women presenting
29.1C and D). with postmenopausal bleeding, and in this population, it can detect
unsuspected bladder tumours11 indeed, a small proportion of
those scanned for postmenopausal bleeding may have macro-
Colour duplex imaging: ureteric jets scopic haematuria rather than blood loss per vaginam, emphasising
the worth of transabdominal and transvaginal ultrasound of the
With the peristalsis of the ureter, the urine is propelled from the bladder in this patient group.
kidney to the bladder, emptying sporadically through the vesico-
ureteric junction into the bladder lumen. This may be seen during
real-time ultrasound as a shimmer on greyscale imaging, much Harmonic imaging
more easily appreciated as a jet or flame using colour duplex
imaging (Fig. 29.2). The duplex imaging detects the turbulence of Harmonic imaging is increasingly being used as the default
the intravesical urine caused by the urine being squirted from the setting in renal tract imaging, many platforms performing the
551
CHAPTER 29 Ultrasound of the bladder
C
D
Figure 29.1 Transabdominal scan of bladder in axial (A) and sagittal (B) section. The wall thickness is best estimated on the sagittal
section. The bladder base is the point of entry of both ureters and the point of exit for the urethra; in men, the bladder base may be
elevated because of prostatic hypertrophy. In the axial (C) and sagittal (D) images of the bladder base, the displaced left ureteric orifice is
shown by the black arrow.
post-processing of the fundamental image unless the harmonic mode ultrasound has been the use of gadolinium-based contrast agents
is actively turned off. This is because in children12 and adults harmonic in MRI to evaluate enhancement of lesions and thereby provide
imaging has been proven superior in visualising the renal tract.13 functional as well as structural information.
For two reasons, the contrast argument looks set to swing back
in favour of ultrasound, at least in a select group of patients. The
Contrast media: caution and new horizons first reason is the recognition of a new condition by Cowper etal.
in 2000, called nephrogenic systemic fibrosis (NSF).14 This is a rare
Ultrasound has one incontrovertible and significant advantage over but disabling condition in which the skin becomes indurated and
computed tomography (CT): the absence of ionising radiation. It painful, resulting in contractures. It is also associated with visceral
cannot trump magnetic resonance imaging (MRI) in the same way, sclerosis. The development of NSF is strongly linked to the usage
and MRI has had the ascendancy over ultrasound in bladder mass of gadolinium contrast agents in patients with advanced renal
imaging for a decade or so. One of the benefits of MRI over impairment.15 Thus, recognising that iodinated contrast media are
552
Functional aspects of bladder ultrasound
Figure 29.2 Ureteric jets on colour duplex imaging: from the right ureter (A), both ureters (B) and on (C) CT from both ureters. Note
the displacement of the right ureteric orifice in A by prostatic hyperplasia.
V = ( L A T ) C mL
where V = volume, L = longitudinal length, A = maximum anteropos-
terior diameter, T = maximum transverse diameter and C is a
coefficient.
C ranges from 0.5 to 0.625 based on differing algorithms and
essentially assuming that the bladder is spherical.
Sphere volume = 4/3 r3 where r is the radius equivalent to half
the diameter. The measurements L, A and T are all diameters so the
formula can be rewritten:
3
Sphere volume = 4 3 ( d 2)
= 4 3 d3 8
= 1 6 d3
= 0.52 d 3
C can be up to 0.625; more usually in practice the formula would
Figure 29.3 Bladder volume estimation: orthogonal diameters of
be:
the bladder shown on split screen; the maximum diameters are
used, the image being frozen first in the axial and then in the
V = ( L A T ) 0.6 mL sagittal plane. Most ultrasound platforms automatically calculate the
bladder volume (in this case >100mL).
See Dicuio etal.28 and Yip etal.29 for a more complete mathematical
treatment of the formulae for bladder volume calculation. The conclu-
sion from these papers is that the more simplistic formulae (as above)
are as precise as more complex methods such as the double area a more accurate volume estimation is not warranted in the majority
method and the double ellipsoid method. of clinical settings.
In augmented bladders, ultrasound is not accurate in estimating
urinary volume, because there is no reliable geometry to the neo-
bladder. Ultrasound can provide an idea of the degree of filling,
and more relevant, retention in the augmented bladder, but in
this specialist postoperative group, catheterisation through the ileal
conduit, with confirmation of complete drainage by ultrasound,
symptoms. Often patients have drunk exuberantly prior to the is the recommended method by which residual volume is
scan, so that the bladder fills up rapidly after first void measured.32
n >150mL: indicates retention.
Clearly the latitude in most cases is wide enough for the ultra- Comparison of differing technologies in
sound-predicted bladder volume to be clinically relevant. In 80
postoperative patients, ultrasound (against catheter volume) was bladder volume estimation
97.7% specific, with a negative predictive outcome of 89.5%, obviat- Voided volume measurements or catheter volume measurements
ing the use of catheterisation in those with a bladder residual are taken as the gold standard in studies that set out to determine
volume of <150mL.27 the accuracy of various ultrasound methods for calculating the
volume of the bladder.
A recent comparison of a dedicated bladder, non-real-time
Accuracy of volume estimation at different volume calculator (BladderScan BVI 3000) with a real-time three-
volumes and in bladder shapes dimensional (3D) ultrasound system and with a real-time portable
Once ultrasound has been performed, the bladder volume can be 2D ultrasound platform with iterative bladder volume calculation
estimated by a number of formulae.28 The most common method is (Bardscan II) has been undertaken on 34 patients. Significant cor-
to measure the longitudinal, the transverse and the anteroposterior relation between the voided and calculated bladder volumes were
diameter. These are best captured by splitting the screen into two achieved with each method, but the accuracy and level of clinical
halves, the left screen revealing the transverse image of the bladder agreement was greatest when using the 3D ultrasound system to
at its widest point, the right screen the sagittal image (Fig. 29.3). calculate the bladder volume; the portable 2D ultrasound system
The straightforward method of measuring the three linear, tended to underestimate the bladder volume by 510%.33 In post-
orthogonal diameters, and multiplying the values together, is as operative patients in the urodynamics clinic, Bardscan II performed
precise in estimating bladder volume as more mathematically well against catheter volume measurements with a correlation coef-
complex techniques, notably the ellipsoid and area methods, ficient >0.98.34 In the paediatric setting, however, where the volumes
although the tendency is to underestimate the true volume.30 The are much lower, conventional ultrasound measurements should be
limitations of ultrasound-based bladder volume remain even when used in preference to the BladderScan automated system.35
the bladder contains more than 150mL of fluid, so the predicted The use of 3D ultrasound over bladder volumes 100400mL
bladder volume must be interpreted with a degree of caution and appears accurate with only a minor underestimation of volume
only ever offered as an estimate, not a true value. Because of this (~3%).36
tendency to underestimation, of up to 20% in calculated bladder
volume, some institutions advocate the use of individually deter- Ultrasound and flowmetry
mined proportionality constants to improve the accuracy of resid-
ual bladder volume determinations.31 However, each institution The quantification of bladder volume alone is limited. Ultrasound
needs to define a specific algorithm, and this may be dependent not of the urinary tract (that is, the kidneys as well as the bladder)
simply on the hospital setting but on the specific ultrasound plat- should be augmented by data from a flowmeter.37 The majority of
form used; moreover, a personal computer has to be connected to flowmeters in hospital practice are spinning disc types (rather than
the ultrasound imaging unit. The increased complexity albeit with weight transducer flowmeters). The urine flow rate is charted by
554
Functional aspects of bladder ultrasound
attaching the flowmeter to a chart recorder. A graph is produced Complete bladder emptying and low flow
for each micturition episode, from which peak flow rate (mL per
second), mean flow rate (mL per second), time to peak flow When the flow rate is reduced, the inference is that either there is
(seconds), voiding time (seconds), and time of micturition (seconds) outflow obstruction or there is a weakened, poorly functioning
can all be derived. These data can then be interpreted with the detrusor muscle.
residual volume, derived from ultrasound of the bladder immedi- Outflow obstruction may be mechanical or neurological. The
ately post void, along with visual analysis of the shape of the flow- former is most commonly due to prostatic hyperplasia, and the
meter tracing. bladder wall will be thickened and the bladder base elevated. Ure-
Overall, the ultrasound and uroflowmeter examination is non- thral strictures may also result in thickening of the bladder wall
invasive and provides information about bladder function, bladder with low flow. The mean flow rate is more than 50% of the value
anatomy, bladder anomalies and bladder capacity. There are a
couple of caveats:
n Flow charts where the total voided is less than 125150mL
are limited; it is better to ultrasound the patient as a matter of
routine before sending for flow rate measurement, ensuring Urine flow rates
that the pre-micturition volume (by ultrasound measurement)
is larger than 200mL. In an Italian study, on 67 men in their Post-void residual40
60s and 70s, a voided volume of greater than 125mL Population: 477 randomly selected community-dwelling white men.
(>150mL) necessitated a pre-voiding bladder scan volume Median post-void residual 9.5mL (2.535.4mL 2575%).
greater than 200mL (>250mL), which in the study decreased Post-void residual 50mL much more likely as prostate >30mL.
the number of non-eligible flow rate recordings from 23.9% to Post-void residual urine volume poorly correlates with peak urinary
4.5% (31.3% to 4.5%).38 flow rate.
n Similarly, sending patients with abnormally distended
bladders for physiological flow measurements is ill advised, Urine flow rate41
as the normal innervation that triggers micturition can be Population 514 men (1784 years) who subjectively felt that their
upset with abnormally full bladders, especially in the clinic urination was normal and were objectively demonstrated to be
setting. without prostatic hyperplasia.
n If residual volume exceeds 100mL, the patient should be sent Maximum flow rate: 20.7 7.3mL/s in a mean voided volume of
to urinate again, and a repeat post (second) micturition 290.7 123.2mL.
bladder volume calculated. Voided volume decreases with age; with declining maximum flow
rate bladder capacity diminishes with age.
Of the various parameters, post-micturition residue and
maximum flow rate (as well as prostate volume that can be easily
Functional bladder capacity (FBC)42
estimated by transabdominal ultrasound) are the most useful in
Functional bladder capacity defined as largest voided volume in
the prediction of urodynamically proven bladder outflow
24-hour period.
obstruction.39
Population: 1688 men 50 to 78 years old.
Strongly related to LUTS.
Flow patterns Lower in men with a reduced maximum flow rate (less than 15mL/s)
independent of the post-void residual volume.
In normal subjects the flow tracing is bell-jar shaped.44,45 The delay
to peak flow is between 3 and 8 seconds, and the peak rate 35 LUTS42
40mL/s (men), and approximately 50mL/s in women (Fig. 29.4). Dependent on age.
The abnormal traces low, high or intermittent flow patterns Correlates with a reduced flow rate.
signify defined pathologies, but the classification also relies on the Associated with large post-void residual volume.
volume of post-micturition residue. More frequent as FBC falls.
555
CHAPTER 29 Ultrasound of the bladder
Figure 29.6 Bladder stones. Two large (>1cm) stones and debris
settling out in a dependent fashion in the bladder of a patient with
spina bifida, resulting from a neuropathic bladder. The stones are
echogenic and cast acoustic shadows. On real-time imaging, the
stones were mobile.
A B
Figure 29.7 Bladder stones. A: Stone (45mm) in the distal ureter with proximal dilation of the ureter. At this size and site, the patient
can be managed expectantly. The stone is likely to pass spontaneously. Serial ultrasound can be employed to document passage of the
stone into the bladder. Intervention would be indicated only if the stone failed to pass over 48 hours, the patient suffered intractable pain,
or urosepsis. Contrast advocacy of conservative management with (B) a steinstrasse multiple stone fragments in the distal ureter
following extracorporeal shock-wave lithotripsy treatment to a renal calculus. In the steinstrasse, urgent retrograde JJ ureteric stent 557
placement is advised.
CHAPTER 29 Ultrasound of the bladder
A B
C D
Figure 29.8 Typical appearances of Foley balloon catheters (per-urethral), with saline-filled balloon lying on the trigone (A) and the
catheter lying more proximally the balloon filled with unknown fluid of moderately high echogenicity (B). Occasionally, the Foley catheter
may be inserted short, the balloon inflated in the urethra. In this case, axial (C) and sagittal (D) images confirm that the catheter has not
entered the bladder lumen, the retaining balloon visible in the prostatic urethra.
Less commonly, patients may insert foreign bodies perurethrally part projects into the bladder neck or urethra, it is defined as
into the bladder. These are usually detected by plain radiography, ectopic; when the ureterocele and its orifice are contained by the
but ultrasound may be useful, especially if the object is not radi- bladder, it is defined as intravesical. The latter, due to herniation of
odense (e.g. a plastic drinking straw) (Fig. 29.10). Naturally, the the lower ureter and opening through the bladder wall, are seen on
sonographic findings will depend on the particular foreign body ultrasound as a cystic mass within the bladder, defined by a smooth
inserted. and thin wall (Fig. 29.11). The ureterocele can be seen on real-time
imaging to peristalse, intermittently discharging and then refill-
ing. The intravesical ureterocele is usually an incidental finding, but
it can be complicated by stone formation or it can, occasionally,
Ureteroceles cause obstruction to the upper tract (Fig. 29.12). Most are discov-
The term ureterocele refers to the ballooning of the distal ureter. ered on ultrasound or other imaging by chance, being bilateral in
When the ureterocele is mostly within the submucosa, and only a 3040% of cases.
558
Structural aspects of bladder ultrasound
A B
Figure 29.9 Bilateral ureteric JJ stents shown on KUB X-ray (A). The stent in the bladder on ultrasound (B) appears as a pair of
parallel lines which are echogenic (white arrowheads). In this image, the stent is forming a J and therefore is seen in the anterior and
posterior half of the bladder. Note also the Foley balloon catheter lying posteriorly. Unfortunately, despite insertion of bilateral JJ stents
and long-term bladder catheterisation, the patient went into end-stage renal failure from chronic bladder outflow obstruction (uropathy).
The peritoneal dialysate is manifest as anechoic fluid within the abdominal cavity (thin white arrow).
Urachus
The urachus is an embryonic remnant resulting from involution of
the allantoic duct and the ventral cloaca.48 Attaching the bladder
dome to the umbilicus, the urachus should close during gestation.
Failure of closure is not uncommon, the urachus being reported as
present in up to 30% of adults.48 In children under 16, the urachus
may be present in up to two-thirds of studies.49 On ultrasound, the
urachus presents as a cystic tubular structure in the midline, infe-
rior to the rectus muscle (Fig. 29.13). When patent it can have a
length up to 15cm, and occasionally may exhibit pathology includ-
ing a diverticulum, cyst (a small part of the duct is pinched off, with
closure superiorly and inferiorly),50 and very occasionally, a tumour
Figure 29.10 Radiograph to show a glass bracelet within the can develop within a patent urachus. These are invariably adeno-
bladder lumen. When radio lucent foreign bodies are suspected, carcinomas with a poor prognosis. Their diagnosis is vexatious,
such as drinking straws, ultrasound of the bladder is advised as the presenting as a mass superior to the bladder dome in the anterior
first line of investigation. abdomen. They are best assessed by CT.51
559
CHAPTER 29 Ultrasound of the bladder
A
B
Figure 29.11 Transabdominal ultrasound views (A, B, C, D) showing simple ureteroceles in different patients. Note the mild
dilatation of the ureter in images (B) and (C). There are bilateral ureteroceles in image (D). In all cases, the uretrocele has a smooth and
thin wall.
A B
Figure 29.12 Ureterocele. A: A small stone complicates an otherwise simple ureterocele. B: Concern that mild ureteric dilatation signifies
obstruction associated with a ureterocele is allayed by the prominent and episodic ureteric jet well shown on colour duplex imaging.
A B
Figure 29.13 Urachal cyst. A: Transabdominal ultrasound reveals a cystic structure anterior to the bladder and deep to the abdominal
wall. The differential diagnosis includes a urachal element, a bladder wall tumour such as a leiomyoma or, in women, an endometrial
deposit. Note the mass effect, suggesting the lesion is extrinsic to the bladder. A non-enhanced CT (B) indicates that the lesion (white
arrow) has increased density, suggesting the contents might be haemorrhagic or contain (as in this case) slightly calcific fluid, within a
closed off urachal cyst.
Tumours and bladder masses patients were diagnosed with bladder cancer in the United States,
and 12700 of those patients died from the disease (http://www.
emedicine.com/med/topic2344.htm.), indicating that the frequency
Cancer involving the bladder may be primary, secondary or a mani- of the disease is increasing. Men are affected three to four times
festation of local invasion from adjacent organs. Primary carcinoma more commonly than women, but women tend to fare worse from
is a relatively common condition, with, according to the National the disease. The median age for diagnosis is 6070 years. For data
Cancer Institute, 68810 estimated new cases and 14100 deaths from relevant to the United Kingdom, see Table 29.1.
bladder cancer in the United States in 2008 (http://www.cancer. In the developed world, urothelial cancer, more commonly
gov/cancertopics/types/bladder). In 2004, an estimated 60200 new referred to as transitional cell cancer, comprises 90% of these cases,
561
CHAPTER 29 Ultrasound of the bladder
Tumour detection
The accuracy of transabdominal ultrasound in detecting superficial
Figure 29.14 This patient has bladder outflow obstruction bladder tumours was assessed more than 20 years ago,53,54 with a
secondary to prostatic hyperplasia. The bladder wall is globally reported detection rate of 5094% and false positive rate of 11% at
hypertrophied, with trabeculation, as a consequence, ensuring that that time. The detection rate for tumours greater than 5mm (82%)
the intravesical pressure is sufficient for the bladder to empty was unsurprisingly far better than for tumours less than 5mm
through the compromised urethra. (38%). In fact, the place of ultrasound of the bladder in cancer detec-
tion became firmly established more from clinical and cost drivers
than from somewhat artificial audits of ultrasound detection rates.
The majority of patients with bladder cancer present with haema-
turia,52 and the first-line investigations for haematuria are widely
Table 29.1 Number of deaths from bladder cancer in the accepted nowadays as ultrasound of the urinary tract and cystos-
United Kingdom, 2006 copy, with computed tomography (CT), notably CT urography
(having replaced intravenous urography), a second-line investiga-
England Wales Scotland N. Ireland UK tion. Strategies using cystoscopy or ultrasound as the initial diag-
nostic test have repeatedly been shown to minimise cost and
Males 2675 165 281 56 3,177
morbidity while maintaining diagnostic accuracy.5557
Females 1371 84 144 37 1,636 By the beginning of this millennium, detection of bladder cancer
Persons 4046 249 425 93 4,813 by transvesical ultrasound in patients with haematuria, has reported
sensitivity of 63%, and specificity of 99%. These figures come from
Source: http://info.cancerresearchuk.org/cancerstats/types/bladder/ a series of just over 1000 patients in whom 83% had macroscopic
mortality/. haematuria, 15% had microscopic haematuria and 2% had unspeci-
fied haematuria.58
Patients with bladder cancer may also present, in the absence of
haematuria, with lower urinary tract symptoms. This group, too, is
routinely sent for ultrasound and therefore by default, ultrasound
is frequently the first investigation offered to a patient with bladder
Causes of outflow obstruction cancer: the symptoms appropriately dictate the best investigation
Mechanical and ultrasound provides the opportunity to detect the tumour.
Prostate mostly benign hyperplasia, occasionally prostate The detection rate of bladder cancer by ultrasound depends on
cancer size of tumour, and on location. Detection by ultrasound may fall
Urethral strictures to less than 50% for tumours on the anterior and inferior bladder
Bladder neck stenosis wall,59 and generally anterior wall tumours are poorly detected:
the near-field images are less conspicuous being usually adjacent
Functional to more echogenic material in the pre-vesical space, as opposed to
Bladder neck dyssynergia the stark contrast of a soft tissue echogenic lesion on the side or
Anticholinergics and other drugs posterior wall, outlined by poorly echogenic urine (Figs 29.15
Peripheral neuropathy diabetes mellitus, spinal cord/cauda and 29.16).
equine disease Needless to say, with variable detection rates and a weakness of
Central nervous system multiple sclerosis, trauma, tumours ultrasound to note anterior wall lesions, the ultrasound examina-
tion should always be complemented by cystoscopy. In addition to
improving evaluation of the entire bladder lumen, cystoscopy can
confirm the findings, allow histological sampling, and permit exam-
ination of the urothelium for sessile lesions or carcinoma in situ
which ultrasound cannot detect.59,60 Most bladder transitional cell
with squamous (5%) and adenocarcinoma (2%) forms less common. tumours are superficial, i.e. there is no muscle invasion (Ta, T1 or
Worldwide, squamous cell cancer (SCC) of the bladder predomi- carcinoma in situ). A recently published small prospective study
nates (75%), being associated with chronic infection and inflamma- suggests that virtual cystoscopy (reformatted thin slice CT images)
tion and associated with bladder infection by Schistosoma is nearly as accurate as conventional cystoscopy, being notably
haematobium in the tropics. In Europe, SCC is again a consequence better than transabdominal ultrasound in the detection of
of long-term inflammation associated with bladder catheters and/ polypoid tumours, or tumours less than 1cm in diameter.61 This
or stones. Urothelial cancer the subtype most commonly resonates with a study of 69 patients with urinary bladder
562
Structural aspects of bladder ultrasound
TNM staging
CIS carcinoma in situ, high-grade dysplasia, confined to the
epithelium
Tx primary tumor cannot be evaluated
T0 no primary tumour
Ta papillary tumour confined to the epithelium
T1 tumour invasion into the lamina propria
T1a superficial submucosal invasion
T1b deep submucosal invasion
T2 tumour invasion into the muscularis propria
T2a superficial muscle affected
T2b deep muscle affected
T3 tumour involvement of the perivesical fat
T3a microscopic perivesical invasion
T3b macroscopic invasion
T4 tumour involvement of adjacent organs such as prostate,
rectum or pelvic side wall
T4a prostate, uterus or vagina invaded
T4b pelvic side wall or abdominal wall invaded
N+ lymph node metastasis
M+ metastasis
A B
C D
Figure 29.17 Tumour staging. A: Extensive bladder cancer on the lateral and anterior walls. On the left lateral wall, ultrasound suggests
muscle invasion (T2 at least), but it is unlikely that there is macroscopic extension into the perivesical fat (T3). B: Non-enhanced CT in the
same patient confirms T2 rather than T3 disease. C: Compare with the CT in another patient (urographic phase, contrast in bladder, with
Foley balloon catheter); here there is stranding of the perivesical fat at 4 oclock indicating T3 disease. D: Post-cystectomy specimen,
bladder opened, showing the large malignancy on the lateral wall.
A B
Figure 29.18 Tumour staging: low specificity. A: Mass in bladder in patient with macroscopic haematuria. Cystoscopy found bladder
clot, but no tumour. B: Use of colour duplex imaging shows flow in the periphery of a mass in another patient: the flow would not be seen
in blood clot, and cystoscopy confirmed a mass adjacent to the trigone.
developing in the urethra is relatively rare, and when there is con- Having no muscle coat, diverticula do not empty reliably during
tiguous TCC between the bladder base and proximal urethra, micturition. They therefore predispose to infection, secondary to
usually the primary will have developed in the bladder; the distinc- the urinary stasis. Stones are also liable to become trapped in a
tion, in any case, is academic. diverticulum. Bladder cancer can, of course, develop with the
Transrectal ultrasound (TRUS) is the primary imaging modality mucosa of a diverticulum, and because of the potential for local
of choice for assessing prostate tumours that may have invaded the chronic inflammation from infection or stone entrapment, it is not
bladder base. Magnetic resonance imaging (MRI) has an important unreasonable to proffer that squamous cell cancer may have a
role in secondary investigation of these low pelvic masses. The higher incidence in bladder diverticula than in normal bladder
provenance of the primary (urothelial tumour or prostatic adeno- mucosa.
carcinoma) is established by transurethral resection or transrectal Ultrasound is an ideal modality to detect bladder diverticula.
ultrasound-guided biopsy, with staining for urothelial tumour Real-time scanning in limitless planes means that the communica-
markers and for prostate-specific antigen (PSA). In a similar vein, tion between the bladder and the para-vesical cystic collection can
transvaginal ultrasound (TVUS), supplemented if necessary by be located, the so-called neck of the diverticulum (Fig. 29.21A).
MRI, is the best way to evaluate local invasion of the bladder by Moreover, scanning post void, the degree of urinary retention
cancer of the cervix.81 The parameters to be noted include morphol- within the diverticulum can be readily assessed. Endovaginal
ogy and bulk of the cervical tumour, thickening and echogenicity views, and colour Doppler interrogation can also assist in diagnos-
of the bladder wall, and mobility of the cervix over the lower ing bladder diverticula, specifically in distinguishing it from other
bladder wall. This last feature is feasible because ultrasound is a pelvic cystic masses.82 Once identified, ultrasound will determine
real-time examination, unlike MRI. MRI, on the other hand, is supe- whether there is debris or stones within the diverticulum, and will
rior in elucidating tumour morphology and size. On both TVUS and prompt the clinician to perform directed cystoscopy if focal wall
MRI, progressive involvement of the bladder is apparent as: disrup- thickening is suggested by ultrasound (Fig. 29.21B). Ultrasound is
tion of the endopelvic fascia, focal mural thickening, changes in the also useful in suggesting that a diverticulum may contain tumour.83
bladder mucosa and interruption of the entire bladder wall.81
Transvesical ultrasound is accurate in detecting posterior bladder
wall invasion by rectal cancer, but contrast-enhanced CT and Fistula to the bladder
contrast-enhanced MRI are universally acknowledged as the
gold standard in imaging rectal cancer, and in assessing changes A fistula is defined as an abnormal communication between two
in the posterior pelvis (Fig. 29.20). epithelialised surfaces. Fistulae to the bladder can therefore be to
the vagina or uterine cavity in women, or to the bowel or abdominal
wall in men or women. A fistula is not, in itself, pathology: it may
Diverticula of the bladder be as a consequence of malignancy, infection, trauma, including
iatrogenic trauma, or inflammatory conditions (Table 29.2).
A diverticulum (plural: diverticula) is an out-pouching of the The clinical pointers that a patient may have a bladder fistula are
mucous and submucous membranes through the muscle wall. They offensive urine/faeculent urine, pneumaturia, or, in fistulation to
result from prolonged elevation of the intravesical pressure. Their the female genital tract, constant wetness/passing fluid per vagina.
most common associations are: Pneumaturia or gas in the urine is a very specific finding, strongly
n benign prostatic hypertrophy suggestive of a fistula between the bowel and bladder. It is a
n urethral stricture symptom that needs to be specifically enquired of when a fistula is
n neuropathic (high pressure) bladder. suspected clinically. In the case of fistula to the skin, the symptoms
and signs will be self-evident. The ultrasound findings in fistulation
to the bladder include (when the fistula is to bowel) echogenic gas
in the anterior part of the lumen, casting a dirty shadow and
severely attenuating the beam, limiting evaluation of the deeper
part of the bladder.84 When the posterior bladder is visualised, the
urine will be echogenic. The responsible pathology may be visible
a tumour mass or a diverticular abscess, for example.
The ultrasound findings of fistula between bladder and the
female genital tract are less dramatic.85TVUS may locate the tract to
the vagina, and the presence of fluid within the upper vagina may
also be a clue.86,87 A report from Munich assessing the efficacy of
ultrasound contrast media in the diagnosis of vesico-vaginal fistu-
lae concluded that observation of a jet through the bladder wall
reliably pinpointed the fistula in over 90% of cases,88 stressing that
the examination is less invasive than cystoscopy and the lack of
radiation exposure.
Vesico-uterine fistulae are rare, usually secondary to gynaeco-
logical or obstetric procedures. MRI is the method of choice in the
diagnosis and preoperative assessment of these fistulae, but ultra-
sound may detect echogenic bubbles in the tract between the
bladder and uterus.89 Sonography is also useful by scanning with a
full and empty bladder, demonstrating a focal area of proximity
between bladder and uterus regardless of the degree of bladder
filling.
A B
Figure 29.21 Bladder diverticula. A: Wide-necked posterior wall bladder diverticulum containing sludge and debris. B: Bladder
diverticulum complicated by small echogenic stone.
the bladder taking on the shape of an inverted fir cone. The dif-
ferential for this appearance is easy to resolve with clinical history:
in the well patient, almost always male, pelvic lipomatosis is sus-
pected; following trauma, the diagnosis is pelvic haematoma; when
there is a longstanding history of LUTS, consider chronic cystitis.
Extrinsic masses
Ultrasound is very sensitive in detecting physiological and patho-
logical enlargement of the solid pelvic organs (Fig. 29.22). Thus, the
gravid uterus or a subserosal leiomyoma can be detected readily,
and the extrinsic mass effect on the bladder assessed. The common-
est cause of pressure on the bladder from an adjacent organ is
benign prostatic hypertrophy. In addition to possible bladder
outflow obstruction, with wall thickening, the median lobe of the
prostate may enlarge and indent the base of the bladder.
Malignant involvement of the bladder can be seen in cancers of
the rectosigmoid, when the invasion may be complicated by a
fistula. Loss of the normal separation between the rectum and pos-
terior bladder wall, coupled with a soft tissue mass and air in the Figure 29.22 Extrinsic compression of the posterolateral
bladder (manifest by an echogenic layer in the non-dependent part bladder wall by an enlarged ovary in a patient with confirmed
of the lumen which casts a dirty shadow), are highly suggestive polycystic ovarian syndrome.
567
CHAPTER 29 Ultrasound of the bladder
of a gastrointestinal malignancy invading the bladder. The same or myotubular disease. If there is sigmoid diverticulitis, a
findings can be seen in local invasion of the bowel by a bladder fistula may develop in which case the ultrasound examination
mass, but this is much less commonly encountered than bowel may reveal gas in the bladder, and debris/faeces lying in the
invading bladder. dependent portion of the bladder.
Prostate cancer can invade the bladder base, frequently progres- n It is important to stress that the findings are non-specific,
sively occluding the ureteric orifices. In these cases, the patient may and ultrasound must be interpreted in the wider clinical
present in acute renal failure with bilateral asymmetric hydroneph- picture, as malignancy and cystitis have a broad overlap on
rosis. In women, cervical cancer can behave in the same way. When imaging.91
the bladder base is involved, the ultrasound findings include uret-
eric and pelvicaliceal dilation, inferior bladder wall focal thickening
and a soft tissue mass in the lower pelvis. Transrectal ultrasound Pregnancy-related pathology of
for prostate cancer and transvaginal ultrasound for cervical cancer the bladder
are more sensitive in demonstrating the primary origin of disease
and the invasive soft tissue mass than transvesical imaging. The most important pregnancy-related problem in the urinary tract,
by an order of magnitude, is infection (UTI). This is mostly managed
without the need for imaging. In some cases, renal tract ultrasound
is indicated, mostly concentrating on the upper tracts, seeking out
SPECIFIC CONDITIONS stones, undue hydronephrosis or complications of the UTI. Bladder
ultrasound is generally not critical in this setting.
There are two pathologies related to pregnancy and birth that can
Inflammatory/infective affect the bladder. These are:
Cystitis has several causes. Ultrasound cannot distinguish between 1. Fistula between the bladder and the uterus post caesarean
the different aetiologies. Indeed, the bladder usually appears section. Ultrasound in this case may hint at the problem,
normal in acute cystitis; and when there is abnormality, the appear- with the posterior wall of the uterus adherent to the bladder
ances are non-specific, being seen also in patients with tumour. In regardless of the time of filling of the bladder. A small
short, the clinical diagnosis of cystitis is confirmed by urine analysis convexity of the bladder wall where it is closely apposed to the
and cystoscopy.90 uterus can sometimes be detected. Nevertheless, the diagnosis
There are a number of features that can be seen in cystitis that is reliant on cystoscopy, cystography or sagittal T2 MRI.
can suggest the diagnosis: 2. Placenta percreta.
n Calcification in the bladder wall this is most commonly an
indicator of schistosomiasis infection, and can also be seen in Placenta percreta
tuberculosis or following radiation.
n Gas in the bladder wall, often associated with gas in the lumen: Rarely, the placenta invades through the decidual lining of the
this is a significant finding with a relatively grave prognosis, uterine cavity, into the uterine muscle (placenta accreta). More
signifying emphysematous cystitis. The condition is almost rarely still, trophoblastic tissues penetrate the serosa of the uterus
exclusive to those with a long history of diabetes mellitus. and may extend directly into the bladder.9294 With the ubiquitous
n Multiple echoes within the urine, especially in the clinical use of prenatal ultrasound, this uncommon but potentially fatal
setting of a patient with signs of infection, suggest infective condition may be detected by ultrasound, especially as 3D ultra-
cystitis or even pyocystitis. sound becomes more commonplace.92,95,96
n In chronic cystitis, the bladder wall becomes thickened,
bladder capacity is reduced and the detrusor irritable. Endometriosis of the bladder
n Infection in adjacent organs can result in sympathetic cystitis
in the bladder: ultrasound may reveal an inflamed appendix
Occasionally the endometrial glands and stroma can implant in the
urinary bladder wall. The patient will then present with cyclical
haematuria, coinciding with menstruation. Bladder wall endome-
Causes of cystitis triomas are usually hyperechoic, with internal septations.9799 While
clinical presentation and ultrasound findings may suggest the diag-
Infective
nosis, the diagnosis is made by cystoscopy and biopsy.100
Viral
Fungal
Protozoal schistosomiasis Postoperative
Tuberculosis
Malacoplakia
Conduits and partial resections
Iatrogenic
Post radiotherapy or chemotherapy There are several operations to augment the urinary bladder, either
Medications in patients with low capacity bladders, or as part of neo-bladder
Catheters formation following cystectomy. In the cystectomised patient, the
neo-bladder may be formed by attaching a pouch fashioned from
Other bowel onto the trigone, resulting in a functional unit with preserved
Vasculitis micturition. Alternatively, a pouch may be drained via a conduit to
Eosinophilic the abdominal wall, the stoma being continent (drained by inter-
Interstitial mittent catheterisation) or incontinent (urostomy and stoma bag).
Granulomatous Regardless of the surgical variance, the augmented bladder tends
to have an irregular shape, with irregular, fronded mucosal mem-
Emphysematous brane forming the wall.101 Because of the irregularity, ultrasound is
Gangrenous mostly limited to estimating post-micturition volumes, gauging
Empyema roughly the capacity of the neo-bladder, and looking for stones
within the lumen.102
568
Procedures
Nature Injury to the lower urinary tract often as part of more widespread
Penetrating injury: bullet or knife abdominal/pelvic trauma.
Iatrogenic The most important message is: avoid compounding the initial
Obstetric trauma with iatrogenic injury (injudicious passage of a urethral
Pressure necrosis: bladder neck fistula catheter).
Caesarean section If the patient develops retention and a urethral injury cannot be
Puncture by bone spicule in pelvic fracture (road traffic accident, excluded: insert suprapubic catheter.
fall, riding or sporting injury, etc.) If the urethra is damaged, suprapubic catheterisation is indicated
Radiation and definitive treatment of the urethra deferred for 6 or more
Spontaneous weeks.
Ultrasonography is not a routine investigation in the initial
Type assessment of urethral injuries but can be useful in determining
Simple: the position of pelvic haematoma and the high riding bladder,
Intraperitoneal when a suprapubic catheter is indicated.
Extraperitoneal In polytrauma, CT of the pelvis is usually available, and this can
Combined suggest with surprising accuracy the extent and type of urethral
With urethral involvement injury and bladder injury.
With rectal involvement The MRI suite is no place for the acute trauma patient.
ultrasound in detecting and staging bladder carcinoma. Urol Radiol cancer. AJR Am J Roentgenol 1988;150:10551059.
1985;7:121131. 78. Davies AH, et al. Flexible cystoscopy compared with ultrasound in
55. Corwin HL, Silverstein MD. The diagnosis of neoplasia in patients the detection of recurrent bladder tumours. Br J Urol
with asymptomatic microscopic hematuria: a decision analysis. J Urol 1991;67:491492.
1988;139:10021006. 79. Davies AH, Cranston D, Turner WH, et al. The role of abdominal and
56. Jaffe JS, Ginsberg PC, Gill R, Harkaway RC. A new diagnostic transrectal ultrasound and cytology in the detection of recurrent
algorithm for the evaluation of microscopic hematuria. Urology bladder tumours. Eur Urol 1990;18:124126.
2001;57:889894. 80. Rosenkilde OP, Jrgensen PM, Roed-Petersen K, et al. Control for
57. Brehmer M. Imaging for microscopic haematuria. Curr Opin Urol recurrences of urinary bladder tumours by transabdominal ultrasonic
2002;12:155159. scanning. Scand J Urol Nephrol 1985;19:105107.
58. Datta SN, Allen GM, Evans R, et al. Urinary tract ultrasonography in 81. Huang WC, Yang JM, Yang YC, Yang SH. Ultrasonographic
the evaluation of haematuria a report of over 1,000 cases. Ann R characteristics and cystoscopic correlates of bladder wall invasion by
Coll Surg Engl 2002;84:203205. endophytic cervical cancer. Ultrasound Obstet Gynecol
59. Ozden E, Turgut AT, Turkolmez K, et al. Effect of bladder carcinoma 2006;27:680686.
location on detection rates by ultrasonography and computed 82. Maynor CH, Kliewer MA, Hertzberg BS, et al. Urinary bladder
tomography. Urology 2007;69:889892. diverticula: sonographic diagnosis and interpretive pitfalls.
60. Khadra MH, Pickard RS, Charlton M, et al. A prospective analysis of J Ultrasound Med 1996;15:189194.
1,930 patients with hematuria to evaluate current diagnostic practice. 83. Saez F, Pea JM, Martinez A, et al. Carcinomas in vesical diverticula:
J Urol 2000;163:524527. the role of ultrasound. J Clin Ultrasound 1985;13:4548.
61. Lopes RI, Nogueira L, Albertotti CJ, et al. Comparison of virtual 84. Long MA, Boultbee JE. Case report: the transabdominal ultrasound
cystoscopy and transabdominal ultrasonography with conventional appearances of a colovesical fistula. Br J Radiol 1993;66:465467.
cystoscopy for bladder tumor detection. J Endourol 2008;22: 85. Ramamurthy S, Vijayan P, Rajendran S. Sonographic diagnosis of a
17251729. uterovesical fistula. J Ultrasound Med 2002;21:817819.
62. Mazo EB, Gazhonova VE, Chepurov DA. [Three-dimentional 86. Carrington BM, Johnson RJ. Vesicovaginal fistula: ultrasound
echography in diagnosis and staging of urinary bladder cancer]. delineation and pathological correlation. J Clin Ultrasound
Urologiia 2005;612. 1990;18:674677.
63. Nakamura S, Niijima T. Staging of bladder cancer by 87. Yang JM, Su TH, Wang KG. Transvaginal sonographic findings in
ultrasonography: a new technique by transurethral intravesical vesicovaginal fistula. J Clin Ultrasound 1994;22:201203.
scanning. J Urol 1980;124:341344. 88. Volkmer BG, Kuefer R, Nesslauer T, et al. Colour Doppler ultrasound
64. Abu-Yousef MM, Narayana AS, Franken EA Jr, Brown RC. Urinary in vesicovaginal fistulas. Ultrasound Med Biol 2000;26:771775.
bladder tumours studied by cystosonography. Radiology 89. Huang SC, Yao BL, Chou CY. Transvaginal ultrasonographic findings
1984;153:223226. in vesico-uterine fistula. J Clin Ultrasound 1996;24:209212.
65. Wagner B, Nesslauer T, Bartsch G Jr, et al. Staging bladder carcinoma 90. Browne RF, Zwirewich C, Torreggiani WC. Imaging of urinary tract
by three-dimensional ultrasound rendering. Ultrasound Med Biol infection in the adult. Eur Radiol 2004;4(Suppl 3):E168E183.
2005;31:301305. 91. Afroz S, Taher MA. Cystitis mimicking bladder cancer on
66. Braeckman J, Denis L. The practice and pitfalls of ultrasonography in sonography. AJR Am J Roentgenol 1988;151:12521253.
the lower urinary tract. Eur Urol 1983;9:193201. 92. Litwin MS, Loughlin KR, Benson CB, et al. Placenta percreta
67. Holm HH, Juul N, Torp-Pedersen S, et al. Bladder tumor staging by invading the urinary bladder. Br J Urol 1989;64:283286.
transurethral ultrasonic scanning. Eur Urol 1988;15:3133. 93. Silber SJ, Breakey B, Campbell D, et al. Placenta percreta invading
68. Devonec M, Chapelon JY, Codas H, et al. Evaluation of bladder bladder. J Urol 1973;109:615618.
cancer with a miniature high frequency transurethral 94. Teo RE, Ahmed M, Chilton CP. Placenta percreta involving urinary
ultrasonography probe. Br J Urol 1987;59:550553. bladder. Br J Urol 1996;78:140.
69. Jaeger N, Radeke HW, Adolphs HD, et al. Value of intravesical 95. Campani R, Bottinelli O, Calliada F, Coscia D. The latest in
sonography in tumor classification of bladder carcinoma. Eur Urol ultrasound: three-dimensional imaging. Part II. Eur J Radiol
1986;12:7684. 1998;27(Suppl 2):S183S187.
70. Schulze S, Holm-Nielsen A, Mogensen P. Transurethral ultrasound 96. Hull AD, Salerno CC, Saenz CC, Pretorius DH. Three-dimensional
scanning in the evaluation of invasive bladder cancer. Scand J Urol ultrasonography and diagnosis of placenta percreta with bladder
Nephrol 1991;25:215217. involvement. J Ultrasound Med 1999;18:853856.
71. Saga Y, Numata A, Tokumitsu M, et al. Comparative study of novel 97. Kinkel K, Frei KA, Balleyguier C, Chapron C. Diagnosis of
endoluminal ultrasonography and conventional transurethral endometriosis with imaging: a review. Eur Radiol 2006;16n:285298.
ultrasonography in staging of bladder cancer. Int J Urol 98. Goodman JD, Macchia RJ, Macasaet MA, Schneider M. Endometriosis
2004;11:597601. of the urinary bladder: sonographic findings. AJR Am J Roentgenol
72. Salo JO. Intravesical ultrasound for staging bladder tumours. Scand J 1980;135:625626.
Urol Nephrol 1987;21:203207. 99. Park SB, Kim JK, Cho KS. Sonography of endometriosis in infrequent
73. Horiuchi K, Tsuboi N, Shimizu H, et al. High-frequency endoluminal sites. J Clin Ultrasound 2008;36:9197.
ultrasonography for staging transitional cell carcinoma of the 100. Pastor NH, Donate MMJ, Gimnez BJM, et al. [Bladder
bladder. Urology 2000;56:404407. endometriosis. Report of two cases and bibliographic review, with
74. Horiuchi K, Shimizu H, Yoshida K, Nishimura T. New ultrasonic special focus on Spanish articles.] Arch Esp Urol 2006;59:111122.
cystofiberscope for staging bladder tumors. J Endourol 101. Ralls PW, Barakos JA, Skinner DG, et al. Imaging of the Kock
2005;19:130132. continent ileal urinary reservoir. Radiology 1986;161:477483.
75. Malone PR. Transabdominal ultrasound surveillance for bladder 102. McInerney PD, DeSouza N, Thomas PJ, Mundy AR. The role of
cancer. Urol Clin North Am 1989;16:823827. urodynamic studies in the evaluation of patients with augmentation
76. Vera-Donoso CD, Llopis B, Oliveet F, et al. Follow-up of superficial cystoplasties. Br J Urol 1995;76:475478.
bladder cancer: how to spare cystoscopies? Eur Urol 1990;17:1719.
77. Dershaw DD, Scher HI. Serial transabdominal sonography of bladder
571
CHAPTER
THE SEMINAL VESICLES, EJACULATORY DUCTS AND The prostate originates from the urogenital sinus, as outpouchings
SPHINCTERS 574 from the prostatic part of the urethra between the 9th and 12th
weeks of fetal life. This develops into the glandular, stroma and
TRANSRECTAL ULTRASOUND OF THE PROSTATE AND
smooth muscles of the gland; but the seminal vesicles and ejacula-
ACCESSORY STRUCTURES 574
tory ducts (and possibly the central zone, see below) are of Wolffian
SONOGRAPHIC APPEARANCES OF THE NORMAL PROSTATE duct origin. Skenes glands found in the female urethra are the
GLAND 576 female homologue of the prostate.
Normal prostate vascularity 576
Bladder
Symphysis pubis
Vas deferens Seminal vesicle
Anterior
Obturator internus Prostate
fibromuscular stroma
Urethra Transition zone Opening of the
Peripheral zone Central zone Levator ani ejaculatory duct at
Urogenital the verumontanum
Puborectalis Seminal
vesicle diaphragm
Obturator internus
Rectum Inferior pubis
ramus Crus of corpus
cavernosum and
Corpus spongiosus ischiocavernosa
Ischiorectal and bulbospongiosus muscle muscle
fossa
A B
Anterior Lateral lobes Prostatic Anterior fibromuscular stroma Transitional zone Levator ani Prostatic
lobe capsule muscle fascia
Levator AFS Prostatic
fascia capsule
TZ TZ
U Neuro-
CZ ED vascular
ED CZ A
bundle
PZ
V N
Figure 30.1 The anatomy of the prostate gland and surrounding structures. A and B: Axial and coronal line illustrations of the
prostate gland and its immediate anatomical relationships (modified from Patel U, Rickards D, Handbook of Transrectal Ultrasound and
Biopsy of the Prostate, Martin Dunitz 2002). C: Line illustration of the classical lobar anatomical model, which is now known to be
inaccurate, although certain terminological derivations are still sometimes used, e.g. median lobe enlargement. D: The zonal model of the
gland (modified from Patel U, Diseases of the bladder and prostate, in Ultrasound of the Urogenital System, Baxter G, Sidhu P, Eds,
Thieme, 2006). As well as being more accurate, this has clinical correlates (see text) and the zones can be differentiated on imaging.
E: The fascial planes around the gland. These planes are not generally identifiable on ultrasound, except for the capsule (AFS, anterior
fibromuscular stroma; TZ, transition zone; CZ, central zone; PZ, peripheral zone; ED, ejaculatory duct; A, artery; V, vein; N, nerve).
30.1). Five lobes were described the anterior, middle, posterior This posterior venous outlet, coupled with the propensity of early
and two lateral lobes. The anterior lobe was that small area of periprostatic tumour spread because of the deficient prostate
the gland anterior to the urethra; the median lobe the region capsule (as described above), accounts for the early spread of pros-
between the ejaculatory ducts and the proximal urethra. The tate cancer to the pelvic and lumbar bones.
remaining gland at the back and to the sides represented the pos-
terior and lateral lobes. In reality, clear lobar anatomical distinction
is not demonstrable in the adult gland, and the model has now PROSTATIC NERVE SUPPLY
fallen into disuse, to be replaced by a zonal model1 based on
glandular differentiation (Fig. 30.1). These zones also closely cor-
relate with radiological and histological anatomy. Three zones are From an imaging perspective, the vascular bundles act as a land-
described the peripheral, central and transition zones though mark for the neural plexus as the nerves are not otherwise identifi-
some texts, inaccurately, consider the peri-urethral glands as a able. They contain fibres from the inferior hypogastric plexus,
further zone. parasympathetic fibres from the pelvic splanchnic nerves (S2, 3 and
The peripheral zone (PZ) accounts for most of the gland in the 4) and sympathetic fibres from the sacral sympathetic trunks. The
young adult (>70%). It lies behind the urethra and is bulkier around resulting plexus runs along the pelvic side wall, and at the level of
the base. Its lateral margins project substantially anterior, such that the prostate is situated within the lateral pelvic fascia, superficial to
this zone is seen to cup the gland on axial TRUS. These cups are the prostatic fascia, intimately related to and inseparable from the
termed the posterolateral margins or the anterior horns, adjacent to vascular bundles.
the neurovascular bundles. The second largest glandular portion is The major relevance of the prostatic nerves to the imager is
the central zone (CZ, about 25% of the non-enlarged gland), which merely to appreciate that the gland is to a degree sensate, and that
lies anterior to the PZ and behind the proximal urethra (similar to local anaesthetic is of benefit during prostate biopsy.
the median lobe of the old lobar model). The ejaculatory ducts
traverse the CZ. The transition zones (TZ) are two glandular areas
adjacent to the urethra, and account for less than 5% of the gland PROSTATIC LYMPHATIC DRAINAGE
in the absence of benign prostatic hyperplasia (BPH). Histologi-
cally, the zones demonstrate subtle microscopic differences and it Prostatic lymphatics drain into the periprostatic subcapsular
is believed that the CZ may be of Wolffian duct origin as it partly network, and then to the internal iliac, external iliac and obturator
resembles the seminal vesicle epithelium. Further histological com- chains. There is no constant sentinel node described for prostate
ponents of the gland are the fibromuscular stroma, which lie most cancer spread, but the commonest affected is the obturator node.
anterior to the urethra. Unlike the zones, neither the anterior fibro- Although theoretically within reach of TRUS, the periprostatic
muscular stroma nor the peri-urethral glands are clearly identifia- nodes are in practice rarely visualised on US.
ble on US or of much clinical importance. Terminologically, the
gland is sometimes also divided into an outer and inner gland,2
with the outer gland comprising the PZ and CZ and the inner gland THE SEMINAL VESICLES, EJACULATORY
the TZ and peri-urethral glands. This nomenclature is often used
loosely in clinical practice to differentiate that part of the gland DUCTS AND SPHINCTERS
more likely to harbour cancer (i.e. the PZ) from the rest of the gland.
For the radiologist, the value of the zonal model is that it corre- The seminal vesicles, ejaculatory ducts and urethral sphincters (Fig.
lates with the common prostate pathologies.3 For unknown reasons, 30.1) are important para-prostatic structures as they may be either
cancer most commonly originates in the PZ, whilst benign prostatic individually diseased or involved as a part of prostate disease. The
hyperplasia (BPH) is principally a disease of the TZ and the peri- seminal vesicles (SVs) are positioned above the prostate, against the
urethral glands. Prostatitis, the third commonest prostate disease, posterior wall of the bladder. The ureter passes superomedial to
can affect any zone.2 the seminal vesicles and the neurovascular bundles lie in the groove
between the prostate and vesicle. Blood supply to the vesicles is
from branches of the middle rectal and inferior vesical arteries.
Anterior to, and eventually medial to, each vesicle lies the ductus
BLOOD SUPPLY OF THE PROSTATE AND (or vas) deferens. The ampulla (or duct) of the seminal vesicle fuses
SEMINAL VESICLES with the ampulla of the vas to form the ejaculatory duct (ED), which
punctures the base of the gland, traverses anteroinferioly through
The main arterial supply to the prostate and seminal vesicles arises the central zone and empties into the prostatic urethra at the veru-
from the inferior vesical artery, which is a branch of the anterior montanum. The duct is a potential pathway for local tumour exten-
division of the internal iliac artery. The distal arterial branches can sion into the seminal vesicles.
be grouped into capsular and urethral branches. The capsular Urinary continence is dependent on the bladder neck and the
branches are located in the lateral pelvic fascia, posterolateral to the external urethral sphincter. The bladder neck has smooth muscle
bladder, and supply the outer prostate. The urethral branches of fibres contiguous with those of the prostate and seminal vesicles
the inferior vesical artery enter the prostate at the junction of the (the bladder neck is sometimes termed the internal sphincter). The
bladder and prostate, and supply the central portion. This arterial external sphincter is composed of striated muscle, responsible for
distribution is recognisable on TRUS, with normal flow being voluntary control of continence. Its preservation is of prime concern
greatest around the periphery and the urethra. during prostatic surgery. On US, the position of both sphincters is
Venous drainage is more complex, and their surgical control is identifiable, as they are more hypoechoic than prostate, or of mixed
an important step during prostatectomy. The dorsal vein of the echogenicity.
penis divides into three branches that also drain the prostate. A
single superficial branch lies anterior to the prostatic fascia. The
right and left lateral deep branches pass posterolaterally, beneath TRANSRECTAL ULTRASOUND OF
the prostatic fascia. These veins are not clearly separable during
TRUS. All of the major branches interconnect with adjacent venous THE PROSTATE AND ACCESSORY
complexes, particularly the lateral pelvic plexi (e.g. the internal STRUCTURES
pudendal vein, obturator and pelvic plexi), and this ramifying
venous system finally drains into the iliac veins; in addition some Although the gland may be visualised on transabdominal scanning,
veins also communicate with the lumbar venous complex of Batson. the views are too poor for diagnosis but the dimensions may be
574
Transrectal ultrasound of the prostate and accessory structures
Urethra
Urethra
Prostate
Prostate
Bladder
Bladder
Seminal
Seminal vesicle
vesicle
Rectum
Rectum TRUS
probe
TRUS
probe
B
A
measured, albeit imprecisely. In contrast, the prostate can be seen scan at a frequency of 510MHz, but are also capable of multifre-
with sub-millimetre precision using a transrectal probe.4 Varieties quency scanning and prostate biopsy as well. For most glands
of probe designs are available. Radiology departments favour the 7.510MHz is adequate, but large glands require 5MHz to inspect
more versatile end-firing probe which requires a fanning or rocking the anterior structures or the bladder neck.
motion (Fig. 30.2), unlike the simple advancement or rotation move- The left lateral position is best for scanning, and the higher the
ments necessary for true axial/longitudinal probes. Modern probes knees are flexed the easier the examination for both patient and
575
CHAPTER 30 The prostate and seminal vesicles
SONOGRAPHIC APPEARANCES OF
operator. No special preparation is necessary. Some urine in the THE NORMAL PROSTATE GLAND
bladder is helpful, but over-distension will lead to urinary urge
as the probe is moved around. The lubricated, condom- In the young man, the gland is homogeneous2,4 and the zones dif-
covered probe is inserted into the anus and directed slightly poste- ficult to differentiate, but generally the peripheral zone is hypere-
rior, to follow the natural contour of the lower rectum. Deep choic relative to the central and transition zones (Figs 30.3 and 30.4).
breathing through an open mouth helps to relax the anal sphincter This echo-differentiation is further boosted by glandular enlarge-
and the probe is incrementally advanced, during each expiration. ment, because of compression of the peripheral zone, but normally
This manoeuvre is especially useful in those with a narrow anus or the central and transition zones cannot be separated from each
tight sphincter. other (the position of the CZ can usually only be inferred from the
The probe should be advanced till the gland is seen anteriorly location of the ejaculatory ducts).
about 10cm beyond the anal margin and the gland scanned in a The anterior fibromuscular stroma is not easily defined either.
systematic manner (summarised in Fig. 30.2). Magnification should Although there is no histological prostate capsule, the distinction
be adjusted until the entire gland is visualised on the screen.2 Mul- between the gland and surrounding fat is so distinct that a sono-
tiple focal zones are more useful with modern probes, and the focal graphic capsule can be seen. The levator ani muscles are seen as
depth adjusted to encompass the whole gland. linear mixed echogenic lateral boundaries of the prostatic bed. The
First the gland size should be measured (Fig. 30.3). Studies have urethra is seen as a line, also of mixed echogenicity, but has no
shown that the correlation between the volume and true prostate lumen at rest. With muscular hypertrophy the urethra, and bladder
weight is between 0.82 and 0.99.5 The correlation is poorer for large neck, become increasingly hypoechoic and sound attenuating, a
glands (>80mL) as they deviate from the semi-ellipsoid shape, common finding with prostate gland enlargement. Just beyond the
assumed by the formula used for volume calculation. Next the apex can be seen the hypoechoic external urethral sphincter. In
gland should be examined in the axial plane from the base to the longitudinal plane, the non-enlarged gland should not elevate
the apex. the bladder base. Elevation is seen with glandular enlargement,
The echogenicity of the glandular zones should be compared especially if the CZ is enlarged, and the term median lobe enlarge-
between the two sides and note made of any asymmetry. The ment still has some loose clinical value.
gland should then be scanned in the longitudinal plane and asym- Highly reflectile, non-shadowing foci may be seen within the
metry again noted. Any suspected abnormality should be ducts of the inner gland, so-called corpora amylacea (Fig. 30.5)
examined in two planes, as only those seen on both will be true representing mucoproteins. They have no clinical significance. Scat-
abnormalities. This is especially useful near the gland base and tered calcification is also sufficiently common to be considered a
apex, as otherwise partial voluming of adjacent seminal vesicles or normal finding. Heavier focal calcification may represent prosta-
urethra can be misinterpreted as hypoechoic abnormalities. The far titis (see below) or calculi within the ejaculatory ducts or urethra;
lateral edge of the gland is another blind spot that should also be and only very rarely is prostate cancer calcified.
scrutinised in both planes. Finally, the seminal vesicles, ejaculatory
ducts, vasa and the external urethral sphincter should be Normal prostate vascularity
examined.
Colour flow imaging can be of some diagnostic value6 and should
On colour Doppler US,6,7 the normal gland has strong vascular
be used routinely. The colour window should be enlarged to signals from the neurovascular bundles, the pericapsular arteries
encompass the entire gland in the axial view. The gain should be and the peri-urethral branches (Fig. 30.6) but there is little internal
reduced till there is no flow, and then slowly increased till flow or parenchymal flow. Importantly, like the overall gland echogenic-
commences around the capsule and the urethra. A low flow setting ity, normal parenchymal vascularity is broadly symmetrical.
is useful. This is normal prostate vascularity (see under Blood
supply of the prostate and seminal vesicles above for explana-
tion). Flow characteristics should be slowly evaluated in the axial SONOGRAPHIC APPEARANCES OF
plane, from the base to the apex of the gland, and any focal intra-
parenchymal flow asymmetry noted. Intravenous contrast will THE NORMAL SEMINAL VESICLES AND
augment flow,7 normal or abnormal, but is not yet used routinely. EJACULATORY DUCTS
Duplex Doppler US has no diagnostic role in the prostate and
sonoelastic imaging, or elastography, is still being explored. The For seminal vesicles, both transverse and longitudinal scans are
accepted indications for TRUS are well described. helpful (Fig. 30.7). Ejaculatory ducts are best seen in the
576
Sonographic appearances of the normal seminal vesicles and ejaculatory ducts
B
A
577
CHAPTER 30 The prostate and seminal vesicles
A B
Figure 30.6 A: Normal prostate vascularity on colour Doppler ultrasound, with strong signals in the capsular and peri-urethral vessels but
no substantial focal parenchymal or intra-prostatic flow. In comparison, B shows increased focal flow from the right inner gland. There is
no focal nodule in this area on the greyscale image, but this area should be targeted during biopsy, especially in those with previous
negative biopsies.
578
Acquired abnormalities
A
B
On vascular imaging, normal flow is barely seen in the epithe- haematospermia and obstructive infertility. Giant cysts may
lium, even on high sensitivity settings. Abnormal flows are asym- obstruct urinary flow (usually seen in teenagers) and bilateral
metric and involve the lumen and surrounding fat planes and Mllerian cysts may be associated with unilateral renal agenesis.9
infiltrated tissue. However, the diagnostic value of seminal vesicle Tumours of these structures are rarely seen.
colour Doppler has also not been extensively studied or reported. Mllerian cysts (Fig. 30.8) do not communicate with the urethra,
unlike a persistent prostatic utricle (or utricle cyst) which may
communicate. Persistent utricles, sometimes mega-utricles, are
often associated with hypospadias or genital anomalies. Seminal
CONGENITAL OR vesicle cysts are rare. In isolation they are inconsequential, but
DEVELOPMENTAL ANOMALIES multiple SV cysts are associated with adult polycystic kidney
disease.10
The prostate gland is absent in hermaphrodites. There are no other In practice it may be difficult to differentiate Mllerian from
described congenital or developmental anomalies of the prostate utricle cysts, but the latter are smaller and do not extend beyond
gland, but very rarely, the prostate may be hypoplastic, e.g. with the gland. Cyst content, which can be sampled via the transrectal
prune belly syndrome or in those with low testosterone levels or route (see below), may be helpful. Mllerian duct cysts should have
retarded sexual development. The seminal vesicles, vasa and/or no prostate-specific antigen (PSA) expression. Utricle cyst fluid may
ejaculatory duct may be absent as a combined maldevelopment of or may not contain sperm, depending on whether they communi-
the Wolffian duct (additionally the bladder trigone and the CZ may cate with the urethra and ejaculatory ducts.
be deficient with a wide bladder neck).
These abnormalities are rare but those of the Mllerian duct or,
more commonly, utricle development are often seen on TRUS (5
8.6%), as midline cystic structures.8 They are round in the axial ACQUIRED ABNORMALITIES
plane and teardrop shaped on longitudinal scanning, and may
extend above the prostate gland. The majority are incidental find-
ings and may be slightly thick-walled but are always transonic, Benign prostate hyperplasia or
unless after internal bleeding or infection. Small amounts of internal hypertrophy (BPH)
debris may be mistaken for wall thickening. If there is doubt, then
a re-scan in the other lateral position will often clarify. Occasion After the 40th year, the prostate hypertrophies and above the age
ally they may be calcified and clinical presentations include of 50 years, over 50% will have some degree of BPH. The glandular
579
CHAPTER 30 The prostate and seminal vesicles
580
Acquired abnormalities
A B
Figure 30.9 Benign prostate hyperplasia. A and B: Axial scans of patients with BPH. Note the heterogeneous echotexture of the inner
gland (arrow) representing BPH affecting the transition zone. Note also how the naturally hyperechoic quality of the peripheral zone is
further accentuated by compression due to inner gland enlargement. An extreme example of this is seen in B (arrow points to the
compressed PZ).
A B
Figure 30.10 Benign prostate hyperplasia. A: This image demonstrates many of the typical anatomical findings of a gland with BPH.
The star indicates asymmetrical enlargement, with a disproportionately larger left lobe. The arrowheads point to a deviated prostatic urethra
and the thin arrow to the elevated bladder base. The size has been measured (bottom left of image). Note also that the entire peripheral
zone is hypoechoic, which proved to be malignant on biopsy. B: This gland is nominally of normal size (25mL) but BPH has resulted in
disproportionate enlargement of the median lobe (arrow), which is protruding into the bladder
adenomas can be seen in the PZ, again distinguished by a well- TRUS guidance to relieve obstructive symptoms but the benefit is
defined edge, mixed echogenicity and peripheral flow. temporary.
TRUS has not been proven to add much useful information in the The value of TRUS for evaluating recurrent outflow obstruction
evaluation of the patient presenting with suspected BPH, reduced has also not been proven. On scanning, regrowth and restriction of
flow rates or LUTS, apart from prostate sizing. Recent data suggest the bladder neck may be seen, but does not influence management
that there is a link between size and eventual bladder retention, and as much as urinary flowmetry and post-void residues. TRUS also
need for surgery. Another use for size estimation is that glands tends to underestimate the size of the cavity after transurethral
>100mL may be better treated by retropubic prostatectomy, rather resection of the prostate (TURP), unless examined with a moder-
than transurethral resection. TRUS is also not of proven value in ately full bladder. A good cavity is 12cm in diameter and extends
the follow-up of the patient on conservative or pharmacological towards the apex of the gland (Fig. 30.12). Compromised cavities
management of known BPH. 5-Alpha reductase agents can decrease occur because of inadequate resection, when TRUS will show a tiny
the gland size by up to 25%, but repeated TRUS for size estimation cavity or none at all, and bladder neck stricture will show a mid-
does not directly influence management. Rarely, TRUS may provide prostatic cavity with a closed echogenic bladder neck. In recurrent
useful diagnostic information. Occasionally, an obstructing cyst at hyperplasia, an adenoma may be seen reducing the TURP cavity
the bladder neck may be seen. Such cysts can be aspirated under (Fig. 30.13).
581
CHAPTER 30 The prostate and seminal vesicles
A B
Figure 30.11 Prostate gland with background BPH. A: Cystic changes are present anteriorly (arrow). These are believed to represent
degenerative adenomas rather than obstructed ducts or gland structures. B: Bilateral hyperechoic nodules in the inner gland, consistent
with adenomas (arrows), and a solitary hypoechoic adenoma in the left lobe (short arrow).
Prostatitis
The clinical, pathological and sonographic features of prostatitis
vary widely (Table 30.1). Acute prostatitis is uncommon but can
occur in the young man, and is due to infection by the usual urinary
tract organisms. Systemic signs of infection are present, and the
prostate gland is tender on rectal examination. On TRUS, the gland
may show increased generalised or focal vascularity (Fig. 30.14).
The gland is of focal or generalised decreased echogenicity and the
capsule is thick or ill defined.11 An abscess may be seen as focal
Figure 30.13 Longitudinal TRUS view showing regrowth of cystic degeneration (Fig. 30.15), with a thick capsule and/or air,12
benign prostate hyperplasia, with a prominent adenoma (arrow) and may be drained by TRUS-guided aspiration (see below).
protruding into the TURP cavity. However, the gland may also be entirely unremarkable.
582
Acquired abnormalities
Acquired
1. Duct ectasia mild distension of normal ducts. Very
Figure 30.16 Axial image of one of the described common
appearances of chronic prostatitis, with heavy inner gland 2. Ejaculatory duct cysts just lateral to midline. Post
calcification. inflammation or TURP. Contain sperm or calculi with seminal
vesicle dilatation
3. Cystic degeneration of BPH nodules commonest cysts.
In transition zone
4. Retention cysts due to dilatation of gland acini. May
cause obstruction if located close to the bladder neck (ball
valve obstruction)
5. Cavitary prostatitis rare, due to prolonged inflammation.
Multiple cysts
6. Abscess post prostatitis, commoner in diabetics and after
bladder catheterisation. Thick-walled and septated
7. Cystic prostate cancer (very rare)
Figure 30.18 Cysts. A: Axial and longitudinal images of a typical utricle cyst (arrow). Note its midline position, good definition, and
transonic nature. It is entirely intra-prostatic and of teardrop shape on the longitudinal image. B: Axial image showing normal ductal ectasia
of the peripheral zone (arrow). This has no clinical significance. C: An example of a cystic prostate carcinoma. These are rare.
Carcinoma of prostate
Study of gland vascularity improves the specificity by about
510%,17 and this performance is only slightly further improved by
TRUS diagnosis of prostate cancer the use of power (or colour energy) Doppler or the use of ultra-
Now the commonest non-cutaneous male cancer over 80% originate sound contrast media.7 Three general flow patterns have been
in the peripheral zone.3 The remainder arise in the central/transi- described (Fig. 30.25) focal flow, increased flow around a nodule
tion zone or are anteriorly infiltrating peripheral zone cancers. As or asymmetric flow with increased number and size of vessels on
the peripheral zone is the most homogeneous of the zones, even in the side harbouring tumour. When seen in association with a hyp-
the presence of marked hyperplasia, most cancers should be easily oechoic nodule, all three are highly suggestive of cancer; but in the
visible. Yet this is not so. Although highly variable appearances more difficult area of isoechoic tumour, flow is disappointingly
have been described (illustrated in Fig. 30.25, and also see Figs 30.26 often normal or unhelpful. Simple 3D TRUS systems and elastog-
and 30.27),4 ranging from hypoechoic to hyperechoic, in modern raphy are now becoming available, but their value is unproven. In
practice most cancers are isoechoic or barely visible; a reflection of current practice, TRUS is accurate if the described changes are seen
the downward stage migration of prostate cancer at presentation. in the presence of a significantly elevated prostate-specific antigen
Table 30.3 illustrates the various types and locations of abnormality (PSA) level, but not accurate for confident exclusion of prostate
that may be seen with prostate cancer, and their diagnostic cancer in those with mildly elevated PSA (especially if <10ng/mL).
reliability. Prostate biopsy (covered below) is necessary to confirm suspected
Often the abnormality is subtle, and careful examination is malignancy or to confidently exclude low-volume or isoechoic
important. The posterolateral horns, apices and the base of the cancer in all patients with clinical suspicion of tumour.
gland close to the seminal vesicles are areas of higher cancer inci-
dence and also relative blind areas; they should be scrutinised in
multiple orientations and the two sides compared. Even then,
Staging of prostate cancer
described abnormalities are not specific enough as inflammation, As most tumours in contemporary practice are isoechoic, staging
hyperplasia, prostatic intra-epithelial neoplasia and necrosis can all by TRUS is only applicable in the minority with visible cancers
look similar.2,4 (Table 30.3). Tumour volume T2 staging is inaccurately assessed
585
CHAPTER 30 The prostate and seminal vesicles
Figure 30.25 Prostate cancer. A: A diffuse mixed echotexture abnormality (arrow) affecting the right peripheral zone that proved to be a
Gleason 3+3 cancer on biopsy. B: A well-defined hypoechoic abnormality in the midline peripheral zone of mildly increased vascularity
(arrow), extending into the left inner gland. This proved to be a Gleason 3+3 cancer on biopsy. C: The arrow points to a mixed echotexture
nodule in the right inner gland, extending into the periprostatic fat, and of increased vascularity. This proved to be Gleason 4+4 tumour on
biopsy. D: Note the asymmetry and enlargement of the right lobes. The differentiation between the right peripheral zone and inner gland is
lost (outlined by arrows). This area is also of increased vascularity. This proved to be a Gleason 5+5 tumour on biopsy. E: A subtle cancer
located in the left peripheral zone (arrow), but of increased vascularity. This proved to be a Gleason 3+3 tumour on biopsy. F: A large
tumour of mixed echogenicity located in the right peripheral zone.
on TRUS, but bilateral nodules imply stage T2C disease. Regarding Extracapsular extension (ECE) T3A disease is best seen on
T3/4 staging,2,4,18 the areas of the prostate gland where local inva- axial scans. Early ECE is seen as an irregular hypoechoic bulge of
sion is more likely are the neurovascular bundles, the seminal vesi- the capsule, but a long line of contact is a surrogate indicator of a
cles (Figs 30.26, 30.27), the ejaculatory ducts, the apex of the gland high likelihood of local invasion. If tumour is seen to extend into
and the prostate capsule, immediately adjacent to the tumour. All the periprostatic fat, then advanced ECE is diagnosed. Neurovas-
are areas of relative weakness of the prostate capsule, where struc- cular bundle involvement will create an asymmetry of these struc-
tures pierce through the capsule, which is consequently thin or tures, best appreciated on axial views. The sign of seminal vesicle
deficient. involvement T3B disease is loss of the acute angle between the
586
TRUS-guided intervention
Prostate cancer
The commonest non-cutaneous cancer in males.
Over 80% originate in the peripheral zone.
In modern practice the majority of cancers are isoechoic.
The commonest sonographic sign is a hypoechoic nodule or
region in the peripheral zone with internal vascularity.
Colour Doppler imaging further improves specificity by about 10%
when compared to greyscale TRUS.
Figure 30.26 A locally advanced prostate cancer. On the Staging by TRUS is only 5686% accurate.
left-hand image the hypoechoic tumour (arrows) is seen to involve Current practice favours 10- or 12-core biopsy pattern.
both peripheral zones and on the right-hand (longitudinal) image the
hypoechoic change extends into the seminal vesicle (arrow). This is
therefore a T3b tumour.
Figure 30.27 Prostate cancer. Note that the fat plane between UNUSUAL TRUS ABNORMALITIES
the prostate gland and the rectal wall (arrowhead) is lost adjacent
to the tumour in the right peripheral zone (arrow). This is therefore a Other rare prostate abnormalities may be seen (Fig. 30.30) and their
T3a tumour. sonographic findings are described in Table 30.4.
TRUS-GUIDED INTERVENTION
vesicle and the prostate base in the longitudinal plane. Extension
inferiorly from the gland apex into the membranous urethra T4
disease is very difficult to recognise; but tumour reaching up to Prostate biopsy
the levator muscles also T4 disease can be recognised. Enlarged
nodes are seldom seen as the focal length of TRUS is restricted. For
this pelvic US is better, and MRI or CT best. Principles of prostate biopsy
The accuracy of TRUS in local staging is only modest. Reported
sensitivity, specificity and accuracy ranges are 5092%, 4691% and Uniquely among image-guided biopsies, prostate biopsy is not
5886% respectively for ECE. For seminal vesicle involvement the (generally) lesion directed. As discussed, most prostate cancers in
sensitivity is 2260%, specificity about 88% and accuracy 78%; but contemporary practice are isoechoic or diagnostically non-specific.
it should be understood that these are historical figures and modern Being invisible, targeted biopsies are naturally not feasible. So pros-
TRUS staging may perform more poorly still, as contemporary tate biopsy is a sampling technique,21 but sampling is systematic,
cancers are isoechoic. Colour Doppler is not of proven value and not random, and biopsies are targeted onto the portion of the pros-
for non-invasive staging magnetic resonance imaging is most accu- tate most likely to harbour cancer i.e. the peripheral zone.
rate, and a sensitivity of 91% and specificity of 96% for MRI with Modern probe biopsy is via the transrectal route and the transper-
spectroscopy have been reported,19 although modern studies report ineal route is reserved for brachytherapy implantation or template-
lower figures of 78% and 88% respectively.20 based biopsy techniques. The advantage of the transrectal route is
Clinical outcome of prostate cancer is also dependent on the its convenience, but there is a higher risk of infection and per-rectal
histological score (the Gleason score) and this is determined from bleeding range of 04% and 1.358% respectively in pooled data.22
the prostate biopsies; and further, less specific, measures of clinical Thus antibiotic prophylaxis is necessary; the agent of choice varies
outcome include the number of prostate biopsies that reveal cancer, but a 5-quinolone is most often used, e.g. ciprofloxacin. The comfort
the percentage of the core length involved by cancer and whether level of the procedure has also been improved by the use of local
biopsies from both lobes were positive. anaesthesia.23
The number of biopsies necessary to confidently exclude clini-
cally significant prostate cancer undergoes constant change.21 This
Follow-up of prostate cancer or assessment reflects the changing demographics of tumours at presentation.
Early stage tumours are smaller in volume and naturally only iden-
of suspected recurrent tumour tifiable by wider sampling. Six cores, targeted onto the peripheral
TRUS is of limited value2 and cannot replace PSA estimation for zone, was the historical practice standard, but as this missed many
disease monitoring. After radiotherapy, the gland can vary from cancers (1931%) 10 or 12 cores are now recommended in the UK24
587
CHAPTER 30 The prostate and seminal vesicles
Table 30.3 Prostate cancer illustration of the various features described on transrectal ultrasound (figure modified from
Patel U, Rickards D, Handbook of Transrectal Ultrasound and Biopsy of the Prostate, Martin Dunitz, 2002)
Staging
Accuracy 5092% for extracapsular Extracapsular extension:
extension, 78% for seminal vesicle Irregular hypoechoic bulge of capsule
extension; but these are historical figures. Infiltration into periprostatic fat
There are no modern data available, but Neurovascular bundle:
modern accuracy is likely to be poorer Asymmetry
still, as most cancers diagnosed now are Enlargement
early stage, with PSA <10ng/mL Seminal vesicle (SV) involvement:
Loss of angle between SV and base of gland
Enlargement of SV
High Gleason grade:
High flow on Doppler US may signify higher Gleason grades
Focal nodule
increased vascularity
surrounding
hypoechoic area Focal area
of increased
vascularity
Hypoechoic nodule
with elevated capsule Focal Irregular or Diffuse hypoechoic
elevation ill-defined area
B of capsule capsule
588
TRUS-guided intervention
TRUS findings
Tuberculosis May be Like prostatitis
secondary to
intravesical BCG
for treatment of
bladder cancer
Sarcoidosis Non-specific
Infarction Particularly after Hypoechoic
catheterisation nodules
Lymphoma Usually Large hypoechoic
non-Hodgkins masses
throughout the
Figure 30.28 An example of recurrent tumour post gland with
radiotherapy. The appearances of the gland after radiotherapy periprostatic
(or brachytherapy) are highly variable but normally uniform be it infiltration
hypoechoic or isoechoic and symmetrical. Residual tumour can only Leukaemia Non-specific
be identified on biopsy. This example shows clear asymmetry of
Metastasis Lung, melanoma Non-specific
appearances, with hypoechoic change in the left lobe with mildly
increased vascularity. Recurrent tumour was confirmed on biopsy. Comedocarcinoma Hypoechoic
nodules with
multiple small
hyperechoic foci
Primitive Multilobulated,
neuroectodermal multinodular
tumour
Cystic adenoid Normal or
carcinoma hypoechoic
nodule
Sarcoma Huge
heterogeneous
mass between
bladder and
rectum
Solitary fibrous Hypoechoic
tumour nodule
Rhabdomyosarcoma Isoechoic
Other rare cancers Non-specific
Figure 30.29 Longitudinal view of a recurrent tumour, seen as Note: the data on many of these are sparse. Usually merely a few case
reports.
a hypoechoic nodule (arrow), after radical prostatectomy. These
appearances are non-specific and postoperative fibrosis can look
the same. If increased vascularity is seen then tumour is more likely.
Apex
Rectum wall
Rectum
C (1) (2) (3)
Figure 30.31 The principles behind prostate biopsy (or more accurately prostate gland sampling) and the method of prostate
anaesthesia. The first row (A) illustrates the various biopsy schemes used, in the coronal plane. The first is the classical sextant pattern.
This misses about 25% of cancers. The next three schemes illustrate the octant, 10-core and 12-core regimes respectively. In current
practice the 10- or 12-core regime is favoured, but this may change in the future with further down-migration of prostate cancer at
presentation.
Prostate biopsy is a systematic sampling technique, and this is further emphasised in the second row (B) showing that cores are
preferentially targeted onto the peripheral zone as most cancers arise here. Note how the needle trajectories have been aimed
anterolaterally to maximise peripheral zone sampling.
The last row (C) illustrates the various methods for anaesthetising the gland. In (1) the needle is advanced to just outside the apex and
the local anaesthetic injected to create a pool around it. In (2) the injection has been made into Denonvilliers fascia, just beyond the rectal
wall. In the last example (3), the local anaesthetic has been introduced around the neurovascular bundle, between the base of the gland
and the seminal vesicle. Any of these three sites can be used, as none is of proven superiority, but both sides should be injected for
maximum effect. Injection directly into the gland is of no benefit. (Note that image C is inverted, with the apex of the gland on the left-hand
side, as this is the orientation used during TRUS-guided interventions on most machines.)
but there are no firm recommendations by other national bodies puncture using a template,26 under sedation or general anaesthesia.
though some have made a case for 1418, or more.21 Figure 30.31 The relative safety of both methods has been described, but either
illustrates the principles of targeting and summarises the method is associated with a significant risk of temporary outflow
technique. obstruction (510%), which may require bladder catheterisation for
In a minority, in spite of repeated negative 12-core biopsies, there a few days.
continues to be a suspicion of an undisclosed cancer, e.g. rising PSA
levels. In this case saturation biopsy can be carried out.25 The defini-
tion of saturation is subjective, but most agree that at least 24 (and
Biopsy of the post-prostatectomy bed
up to 40) cores should be taken and that the entire gland, both inner After total prostatectomy the PSA level should be near undetecta-
and outer portions, should be sampled. This can be carried out via ble. If not, or if the PSA later starts rising, there is the possibility of
the transrectal route, or more precisely by transperineal needle residual prostate cancer. This is more likely if there were positive
590
References
Pubic symphisis
Pubic bones
Bladder Urethra
Levator ani
Perianastomotic
tissues
Figure 30.33 Needle targeting when the prostate bed is biopsied following radical prostatectomy.
surgical margins post-prostatectomy which occurs in 1040% of simplest and can be carried out safely, the transperineal route will
cases, depending on surgical expertise and patient selection. If reduce the risk of introduced infection or contamination.
appropriate investigations (bone scan and CT/MRI) are negative Injection of seminal vesicles or ejaculatory ducts with iodinated
for occult metastatic disease, residual/recurrent disease at the anas- contrast under combined TRUS/fluoroscopic guidance is an elegant
tomosis needs to be excluded. method for confirming obstructive infertility, or to show communi-
On TRUS, the anastomosis and its surrounding tissues are nor- cation between a utricle cyst and the urethra.28
mally symmetric and of mixed echotexture (Fig. 30.32), represent-
ing postoperative fibrosis and normal tissues. Recurrent tumour is
more likely to be hypoechoic and of (mildly) increased vascular- REFERENCES
ity.2,25 The seminal vesicle beds should also be examined, as this 1. McNeal JE. The zonal anatomy of the prostate. Prostate 1981;2:3549.
may be the site of residual cancer in some cases, especially in those 2. Patel U, Rickards D. Handbook of transrectal ultrasound and biopsy
with basal positive margins. In either case biopsy confirmation may of the prostate. London: Martin Dunitz; 2002.
be necessary. This is easily carried out under TRUS guidance (Fig. 3. McNeal JE, Redwine EA, Freiha FS, et al. Zonal distribution of
30.33).27 Local anaesthetic can be used and is effective, but injection prostatic adenocarcinoma. Correlation with histologic pattern and
may be difficult because of the fibrosis. Also, this may lead to tem- direction of spread. Am J Surg Pathol 1988;12(12):897906.
porary loss of bladder control as the external sphincter may become 4. Coakley FV, Hricak H. Radiologic anatomy of the prostate gland: a
anaesthetised. The bladder should be emptied before biopsy. There clinical approach. Radiol Clin North Am 2000;38:1530.
5. Terris MK, Stamey TA. Determination of prostate volume by
are few data regarding complications, but these are believed to be
transrectal ultrasound. J Urol 1991;145(5):984987.
no greater than after conventional prostate biopsy and antibiotics 6. Kelly IM, Lees WR, Rickards D. Prostate cancer and the role of color
should be given. At least two cores, but ideally four, should be Doppler US. Radiology 1993;189:153.
taken, one from either side and just above the anastomosis. 7. Halpern EJ, Rosenberg M, Gomella LG. Prostate cancer: contrast-
enhanced US for detection. Radiology 2001;219(1):219225.
8. Nghiem HT, Kellman GM, Sandberg SA, et al. Cystic lesions of the
Drainage of prostate abscess, cyst or prostate. Radiographics 1990;10:635650.
seminal vesicles 9. Gilsanz V. Duplicated Mullerian duct remnants: unilateral occlusion
and ipsilateral renal agenesis in a male. AJR Am J Roentgenol
1981;137:174175.
Prostate abscesses are generally treated with antibiotics, but drain-
10. Danaci M, Alpolat T, Bastemir M, et al. The prevalence of seminal
age should be considered if clinical response is poor. In such a case vesicle cysts in autosomal dominant polycystic kidney disease.
simple TRUS-guided needle aspiration can be performed. Occa- Nephrol Dial Transplant 1998;13:28252828.
sionally, cyst drainage of utricle or Mllerian remnants may be 11. Langer JE, Cornud F. Inflammatory disorders of the prostate and the
performed to sample contents. Although the transrectal route is distal genital tract. Radiol Clin North Am 2006;44(5):665677.
591
CHAPTER 30 The prostate and seminal vesicles
12. Papanicolaou N, Pfister R, Stafford S, et al. Prostate abscess: imaging 22. Ghani KR, Dundas D, Patel U. Bleeding after transrectal
with transrectal sonography and MRI. AJR Am J Roentgenol ultrasonography-guided prostate biopsy: a study of 7-day morbidity
1987;149:981982. after a 6, 8 and 12 core protocol. BJU Int 2004;94:10141020.
13. Clements R, Thomas KG, Griffiths GJ, Peeling WB. Transrectal 23. Lee-Elliott CE, Dundas D, Patel U. Randomized trial of lidocaine vs
ultrasound appearances of granulomatous prostatitis. Clin Radiol lidocaine/bupivacaine periprostatic injection on longitudinal pain
1993;47(3):174176. scores after prostate biopsy. J Urol 2004;171(1):247250.
14. Kuligowska E, Fenlon HM. Transrectal US in male infertility: spectrum 24. http://www.cancerscreening.nhs.uk/prostate/pcrmp01.pdf (accessed
of findings and role in patient care. Radiology 1998;207(1): 20 September 2008).
173181. 25. Stewart CS, Leibovich BC, Weaver AL, Lieber MM. Prostate cancer
15. Meacham RB, Townsend RR, Drose JA. Ejaculatory duct obstruction: diagnosis using a saturation needle biopsy technique after previous
diagnosis and treatment with transrectal sonography. AJR Am J negative sextant biopsies. J Urol 2001;166:8692.
Roentgenol 1995;165:14631466. 26. Bott SR, Henderson A, Halls JE, et al. Extensive transperineal template
16. Torigian DA, Ramchandani P. Hematospermia: imaging findings. biopsies of prostate: modified technique and results. Urology
Abdom Imaging 2007;32(1):2949. 2006;68(5):10371041.
17. Pallwein L, Mitterberger M, Pelzer A, et al. Ultrasound of prostate 27. Wasserman NF, Kapoor DA, Hildebrandt WC, et al. Transrectal
cancer: recent advances. Eur Radiol 2008;18(4):707715. ultrasound in evaluation of patients after radical prostatectomy. Part
18. Presti JC Jr, Hricak H, Narayan PA, et al. Local staging of prostatic 1: Normal post-operative anatomy. Part 2: TRUS and biopsy findings
carcinoma: comparison of transrectal sonography and endorectal MR in the presence of residual and early recurrent prostatic cancer.
imaging. AJR Am J Roentgenol 1996;166(1):103108. Radiology 1992;185:361377.
19. Choi YJ, Kim KJ, Kim N, et al. Functional MR imaging of prostate 28. Lawler LP, Cosin O, Jarow JP, Kim HS. Transrectal US-guided seminal
cancer. Radiographics 2007;27:6377. vesiculography and ejaculatory duct recanalization and balloon
20. Ocak I, Bernardo M, Metzger G, et al. Dynamic contrast enhanced dilation for treatment of chronic pelvic pain. J Vasc Interv Radiol
MRI of prostate cancer at 3T: a study of pharmacokinetic parameters. 2006;17(1):169173.
AJR Am J Roentgenol 2007;189:W192W201.
21. Raja J, Ramachandran N, Munneke G, Patel U. Current status of
transrectal ultrasound-guided prostate biopsy in the diagnosis of
prostate cancer. Clin Radiol 2006;61(2):142153.
592
CHAPTER
beneath the sac and stabilised by the patient crossing his ankles.
INTRODUCTION The penis is held against the anterior abdominal wall by the patient
and covered with a towel. A high-frequency linear array probe
Despite the widespread use of more sophisticated imaging tech- (712MHz) should be used, with sensitive colour and spectral
niques, delineation of the contents of the scrotum remains firmly Doppler capabilities. Usually the probe length (>5cm) should allow
within the domain of ultrasound. As a consequence, ultrasound is accurate longitudinal length measurements of the testis. Initially
recognised as the first-line and often only imaging modality both testes are examined in the transverse plane, in order to produce
employed in the assessment of scrotal abnormalities. The superficial the spectacle view to allow comparison of testicular parenchyma
nature of the scrotal sac and contents lends itself to thorough and features; important if a unilateral global testicular problem is sus-
accurate imaging with ultrasound. Technical advances in trans- pected (Fig. 31.1). The examination of the entire scrotal sac should
ducer design and image processing have further improved ultra- include both the transverse and longitudinal planes, documenting
sound diagnosis of diseases of the scrotal contents, with colour any abnormalities present. Testicular volume may be calculated
Doppler adding important information. This chapter will deal and colour Doppler ultrasound will confirm vascular supply. If the
with aspects related to the testis and epididymis, detailing both ultrasound examination fails to detect a lump as felt by the patient,
normal ultrasound features and those features related to disease the patient should palpate the lesion and hold this between two
processes. fingers to be re-examined with ultrasound.
Tunica albuginea
Tunica vaginalis
(visceral layer)
Tunica vaginalis
(parietal layer)
Cremasteric muscle
Dartos muscle
Figure 31.1 Normal testis. A transverse view through both the
testes, the spectacle view allows comparison of the reflectivity of Skin
the two testes, normal in this patient. A spectacle view is of
particular importance in infiltrative lymphoma and leukaemia.
Figure 31.2 The anatomical layers surrounding the normal
testis. The blue shaded area between the two layers of the tunica
vaginalis is the area of fluid accumulation which gives rise to a
hydrocele (from Sidhu PS, Clinical Radiology 1999; 54:343352).
tunica albuginea, forms a capsule that covers the testis. The testis
is then further covered by a reflected fold of the processus vaginalis
that becomes the visceral layer of the tunica vaginalis, with the
remainder of the peritoneal sac forming the parietal layer of the
tunica vaginalis. The visceral layer of the tunica vaginalis covers
the testes and the epididymis, whereas the parietal reflection covers
the anterior and lateral parts of the testes and the epididymis
leaving a bare area to which the mesentery of the testis is attached;
this is important in understanding the bell-clapper deformity and
spermatic cord torsion. A reflection of the tunica albuginea forms
the mediastinum testis, within which the rete testis forms.1
Trans-mediastinal artery
Pampiniform plexus
A large branch of the testicular artery may split off and traverse the
testis to form capsular branches at the opposite aspect: the trans-
mediastinal artery. An intra-testicular artery traverses the testis in
a centrifugal direction in a reported 52% of patients, unilateral in
half.8 The artery is readily identified with colour Doppler ultra-
Figure 31.4 Normal venous drainage of the testis (from Sidhu sound, returns a low resistance spectral Doppler waveform and is
PS, Clinical Radiology 1999; 54:343352). accompanied by the trans-mediastinal vein (Fig. 31.11).
595
CHAPTER 31 Diseases of the testis and epididymis
Figure 31.5 Spermatic cord Doppler ultrasound. A: A transverse image through the spermatic cord, demonstrating the testicular vein
(long arrow) and the three arteries (short arrows) that are present in the spermatic cord: the testicular artery, the cremasteric artery and the
artery to the ductus deferens. B: Spectral Doppler analysis of one of the arteries in the spermatic cord demonstrates a high resistance
pattern (resistance index 0.88), implying that this is either the cremasteric artery or the artery to the ductus deferens. C: Spectral Doppler
analysis of one of the arteries in the spermatic cord demonstrates a low resistance pattern (resistance index 0.73), implying that this is the
testicular artery.
Figure 31.8 Normal rete testis. The rete testis (RT) is a low
reflective area at the hilum of the testis with finger-like projections Figure 31.10 Normal epididymal head. The normal triangular
into the parenchyma (arrow). shaped epididymal head. The changes in reflectivity of the epididymis
are demonstrated; the low reflectivity of the body (long arrow) alters
in the head of the epididymis (short arrow) to a higher reflectivity.
Two-tone testis
The term two-tone describes the appearances of an artefact within
the testis where an intra-testicular artery produces acoustic shad-
owing resulting in a discrete uniform area of decreased reflectivity
posterior to the artery (Fig. 31.12). This artefact is caused by refrac-
tive shadowing at both edges of the intra-testicular artery. The
reflectivity of the remainder of the testis is normal. The use of colour
Doppler ultrasound readily confirms the presence of the intra-
testicular artery as being the source of the artefact.9
Rete testis
The rete testis is located in the mediastinum testis. Microscopically
the rete testis is composed of three parts: the septal (interlobular)
portion containing the tubuli recti, the tunical (mediastinal) portion Figure 31.12 Two-tone testis. There is a well-demarcated low
consisting of a network of channels, and the extra-testicular rete, reflective appearance generated through the testis (arrows) which
does not appear to be related to a pathological cause.
597
CHAPTER 31 Diseases of the testis and epididymis
Teratoma
Teratoma constitutes 510% of primary testicular tumours, divided
into mature, immature and teratoma with malignant transforma-
tion according to the presence of derivatives of the different germi-
Figure 31.17 Embryonal cell tumour. Often a component of
nal layers (endoderm, mesoderm and ectoderm). Teratoma is the
mixed germ cell tumours, this is an example of a pure embryonal
second most common testicular tumour in children (<4 years), and
cell tumour that is ill defined, lobulated and partly cystic (arrow).
teratoma cells occur in over 50% of adult cases of mixed germ cell
tumours. A teratoma tends to be a complex tumour, and the ultra-
sound features are those of a well-defined complex mass with cystic
change (Fig. 31.19). Calcification may be present. Malignant trans-
formation into a teratocarcinoma occurs (Fig. 31.20). In the prepu-
Embryonal cell carcinoma bertal testes a pure teratoma runs a benign course and testis-sparing
This is the second most common tumour after seminoma; embryo- surgery may be undertaken. This is not true for the postpubertal
nal carcinoma is present in 87% of mixed germ cell tumours, but in teratoma, which will metastasise irrespective of the histological
the pure form accounts for 2% of all testicular tumours. Embryonal features. Spread is via the lymphatic route and the 5-year survival
carcinoma affects younger men (2535 years) and tends to be more rate is 70%.
aggressive; a significant number will present with metastases.
These tumours are often heterogeneous, ill defined and blend Regressed or burnt-out germ cell tumours
imperceptibly into adjacent testicular parenchyma (Fig. 31.17). Patients may present with widespread metastases but no primary
tumour except for an area of calcification or fibrosis within an often
Choriocarcinoma atrophic testis.18 The pathogenesis of this phenomenon may be the
Choriocarcinoma is a rare tumour, occurring in a pure form in <1% result of a high metabolic rate of the tumour, which outgrows its
of patients but in a mixed germ cell tumour in 8% of patients, where blood supply and involutes (Fig. 31.21).
it is highly malignant. Choriocarcinoma carries the worst prognosis
of any germ cell tumour; a high level of human chorionic gonado-
trophin confers a poor prognosis and often results in gynaecomas-
Non-germ cell tumours
tia. Ultrasound will demonstrate a heterogeneous solid mass with Non-germ cell tumours (gonadal stromal tumours) account for
areas of haemorrhage, necrosis and calcification. These tumours 36% of all testicular tumours. The prevalence of non-germ cell
show a tendency to haematogenous spread. tumours is higher in the paediatric age group, constituting 30% of
600
Intra-testicular abnormalities
Metastasis
Metastasis to the testis is unusual, with the most frequent primary
sites being the prostate, lung, melanoma, colon and kidney.21 Metas-
tases occur most commonly in patients over 50 years of age. Metas-
Figure 31.24 Leukaemia. A larger right testis with the suggestion tasis usually occurs in advanced disease and is indistinguishable on
of areas of lower reflectivity (arrows) in a patient with acute myeloid ultrasound from a primary tumour (Fig. 31.25).
leukaemia.
Focal lesions: non-neoplastic lesions
affect the testis is non-Hodgkins lymphoma, usually of the diffuse
histiocytic type. The ultrasound appearances of testicular lym- Epidermoid cyst
phoma are similar to germ cell tumours, particularly a seminoma: The pathogenesis of an epidermoid cyst is uncertain. It is likely it
discrete low reflective lesions with increased colour Doppler flow. either arises from monodermal development of a teratoma or as a
However, complete testicular involvement may be seen, emphasis- result of squamous metaplasia of surface mesothelium. These are
ing the need to compare the reflectivity of both testes (Fig. 31.23). benign lesions with no malignant potential. Epidermoid cysts com-
prise 1% of all testicular tumours and are true cysts, containing a
cheesy laminated material. Patients are usually between 20 and 40
Leukaemia years at presentation. Classically on ultrasound, epidermoid cysts
Testicular involvement in acute leukaemia is estimated at 64% and are well circumscribed with a high reflective border and internal
in chronic leukaemia at 25%. Primary leukaemia of the testis is rare, laminations giving an onion-ring appearance (Fig. 31.26). These
although it is a common site of recurrence in children. The blood lesions are avascular on colour Doppler ultrasound. There are four
testis barrier prevents chemotherapy agents from dealing with types of appearance documented on ultrasound: (i) classic onion
intra-testicular leukaemia cells. The ultrasound appearances are ring configuration; (ii) densely calcified mass; (iii) peripheral rim or
very variable, being unilateral or bilateral, diffuse or focal, low or central calcification; and (iv) mixed pattern.22 The treatment for
high reflectivity with increased colour Doppler flow (Fig. 31.24).20 epidermoid cyst is either enucleation or orchidectomy and as the
Differentiation from inflammatory disease is difficult without a full ultrasound findings are frequently non-specific, orchidectomy is
clinical history. often performed.
602
Intra-testicular abnormalities
Splenogonadal fusion
Splenogonadal fusion is a rare condition where an accessory spleen
exists within the scrotum or pelvis fused to the gonadal organs; the
majority of cases occur on the left side. Splenogonadal fusion is far
more common in males, where presentation is usually with a scrotal
mass.23 There are two types described, continuous and discontinu-
ous. In the more common continuous type, a cord connects the
normal and ectopic spleen; this cord may be beaded with small
splenunculi. In the discontinuous type there is no cord present.
There are several recognised associations with splenogonadal
fusion; inguinal hernia and cryptorchidism are the most common,
with micrognathia, peromelia, cleft palate, cardiac defects and
several other rarer congenital anomalies also reported. The appear-
ance of splenogonadal fusion on ultrasound resembles a mass Figure 31.28 Adrenal rest cells. A focal low reflective area in the
within the scrotal sac of low reflectivity in comparison to the normal central aspect of the testis (arrow); adrenal rest cells (reproduced
testicular parenchyma. The mass may not be seen separate to the with permission from Giles Rottenberg, London and the Editor.
testis and as such will be readily confused with a primary testicular Houghton R, Rottenberg G. Testicular lumps. Imaging 2005;
tumour (Fig. 31.27). Colour Doppler ultrasound flow in the abnor- 17:101112).
mal tissue assumes a pattern similar to that seen in the central
aspect of the normal testis or that seen in splenic tissue.24 Should
the diagnosis be considered, a 99mTc-sulphur colloid scan will
demonstrate uptake within the ectopic splenic tissue. Segmental infarction
Global testicular infarction is well recognised, usually as a result of
torsion of the spermatic cord, severe epididymo-orchitis or trauma.26
Adrenal rest cells Segmental testicular infarction is, however, rare and is usually diag-
Testicular adrenal rest tumours are benign adenocorticotrophic nosed following orchidectomy. The predisposing factors to segmen-
hormone (ACTH)-dependent lesions that are asymptomatic and tal infarction include polycythaemia, intimal fibroplasia of the
occur in patients with congenital adrenal hyperplasia. Increased spermatic artery, sickle cell disease, hypersensitivity angiitis and
ACTH levels prevent involution of aberrant adrenal cortical cells trauma, although the majority are idiopathic in origin.27 Patients
that migrate with gonadal tissues in fetal life. The testicular adrenal with segmental infarction tend to be older than those with global
rests are usually less than 5mm and can normally be found in the testicular infarction arising from spermatic cord torsion, usually
testis and surrounding tissues in 7.515% of neonates and 1.6% of between 20 and 40 years. Segmental testicular infarction is charac-
adults. Ectopic adrenal rest cells within the testis develop as a terised by poor or absent flow on colour Doppler ultrasound in a
tumour-like abnormality in response to elevated circulating ACTH. focal low reflective area with no posterior acoustic enhancement.
The intra-testicular nodules of adrenal rests can gradually expand The low reflective area may be wedge-shaped or assume a more
and destroy the testicular parenchyma, resulting in low testosterone rounded appearance.27 Focal expansion of a pole of the testis may
production and infertility. Treatment with steroid therapy can sta- mimic a primary testicular tumour and colour Doppler ultrasound
bilise or regress these lesions, and aids the diagnosis. These tumours provides a useful discriminatory tool (Fig. 31.29).28 Serial ultra-
usually appear as focal low reflective abnormalities with abnormal sound examinations of an area of infarction will demonstrate reduc-
colour flow and are often bilateral (Fig. 31.28).25 tion in size of the lesion.
603
CHAPTER 31 Diseases of the testis and epididymis
A B
Figure 31.29 Segmental infarction. A: Two focal areas of low reflectivity (arrows) in a testis of a patient complaining of acute testicular
pain with no evidence of inflammatory disease. B: The colour Doppler appearances (arrows) demonstrate absence of flow to the area,
suggesting a segmental infarction as the cause of the appearances.
Sarcoidosis
Sarcoidosis is a multisystem disorder characterised by non-
caseating epithelioid granulomas. Sarcoid most commonly involves
the epididymis; solitary testicular involvement is uncommon. Dif-
ferentiation from a primary testicular malignancy is challenging.
However, if there is clinical evidence of sarcoid elsewhere, if the
intra-testicular lesions are multifocal or if there is associated epidi-
dymal involvement, a more confident ultrasound diagnosis may be
offered (Fig. 31.30). The reported incidence of genital involvement
at postmortem is 44.5% but only 0.5% of these patients had clinical
symptoms. Testicular sarcoid presents with a mass which may be
painful. On ultrasound sarcoid appears as a low reflective focal Figure 31.30 Testicular sarcoid. Three focal lesions within the
lesion.29,30 Without these associated symptoms or features, tissue testis in a patient with sarcoidosis (reproduced with permission from
biopsy for pathological evaluation may be required. Stewart VR, Sidhu PS. The testis: the unusual, the rare and the
bizarre. Clinical Radiology 2007; 62:289302).
Focal orchitis and abscess formation
Pure orchitis is uncommon; the testis is frequently involved when
epididymitis occurs resulting in epididymo-orchitis. Pure orchitis enlargement of a testis and is indistinguishable from a tumour at
most often arises as a result of the paramyxovirus causing mumps. ultrasound.
On ultrasound, the testis is enlarged with either diffuse low reflec-
tivity with pure orchitis or more commonly focal areas of low Intra-testicular haematoma
reflectivity when associated with epididymitis. On occasion a focal
abnormality may be produced that mimics a tumour, which should Testicular rupture, extra-testicular haematoma and a haematocele
regress with serial ultrasound examinations (Fig. 31.31). Abscess are the most common sequelae of testicular trauma. An uncommon
formation may occur, particularly with severe epididymo-orchitis, finding is an isolated intra-testicular haematoma, which has a vari-
where the abscess demonstrates low reflectivity with peripheral but able appearance on ultrasound with a temporal change in charac-
no internal colour Doppler signals (Fig. 31.32).31 The internal echoes teristics on repeat ultrasound.32 A history of trauma to the scrotum
of the abscess may vary depending on the age, but should be pre- should prompt the diagnosis. Acutely the haematoma appears as
dominantly fluid-filled with septations (Fig. 31.33). If an abscess patchy increased reflectivity that becomes darker and decreases in
ruptures through the tunica albuginea, a pyocele may develop and size as the haematoma retracts, to eventually resolve completely.
this may further form a fistula to the skin surface. Idiopathic granu- The haematoma demonstrates no colour Doppler flow, a low reflec-
lomatous orchitis can also present as a focal mass or diffuse tive rim thought to represent surrounding oedema, and internal
604
Intra-testicular abnormalities
A B
Figure 31.31 Focal orchitis. A: An area of low reflectivity at the upper aspect of the testis (arrow) in a patient with focal orchitis.
B: The colour Doppler image demonstrates increased colour flow (arrow) to the area with vessels arranged in a uniform pattern conforming
to the normal anatomical distribution of vessels.
Intra-testicular cysts
Figure 31.34 Intra-testicular haematomas. Two areas of
Intra-testicular cysts were thought to be rare but are now seen as predominantly low reflectivity (arrows) but with central high
incidental findings in 810% of ultrasound examinations.33 These reflectivity in a patient following a motorcycle accident.
605
CHAPTER 31 Diseases of the testis and epididymis
Figure 31.36 Tunica albuginea cyst. A small cyst (arrow) is Figure 31.38 Dilated cystic rete testis. The central aspect of the
situated in the line of the echogenic tunica albuginea. These tunica testis; along the line of the mediastinum testis are multiple areas of
albuginea cysts are frequently palpated by the patient and give rise cystic dilatation (arrows) of varying size in keeping with dilatation of
to concern. the rete testis.
cysts are rarely palpated and even if large are not firm. Simple cysts Tunica vaginalis cyst
are well-delineated anechoic round structures, with a thin smooth
wall and posterior acoustic enhancement (Fig. 31.35). The origin of A tunica vaginalis cyst arises from either the visceral or parietal
the intra-testicular cyst is uncertain: congenital, traumatic or post- layer of the tunica vaginalis (Fig. 31.37).
inflammatory. These cysts are often near the mediastinum testis
and may arise from an anomalous efferent duct. The cysts may be
Dilatation of the rete testis
as large as 30mm and careful examination is required to exclude
any wall irregularity which may suggest a cystic tumour. Cystic ectasia of the rete testis results from the partial or complete
obstruction of the efferent ducts often by inflammation or trauma,
and causes dilatation of the rete testis in an asymmetrical unilateral
Tunica albuginea cyst distribution (Fig. 31.38). However, cystic ectasia of the rete testis
Tunica albuginea cysts are located within the dense tissue of the often occurs in a bilateral and symmetrical distribution in the older
closely adherent tunica albuginea (Fig. 31.36). The origin is unknown patient. The differential diagnosis is of a malignant cystic testicular
but may be mesothelial. These cysts are usually solitary, unilocular tumour although the bilateral nature of ectasia usually suggests the
and readily palpated by the patient as a firm nodule on the surface diagnosis. The ultrasound appearances of a dilated rete testis are
of the testis giving concern. These lesions are often difficult to see multiple low reflective oval or rounded structures, which do not
with ultrasound and the patients cooperation is invaluable in locat- demonstrate vascular flow within the mediastinum testes.6 The
ing the lesion. cysts usually measure a few millimetres in diameter but may be as
606
Intra-testicular abnormalities
Atrophy
Testicular atrophy may occur following cryptorchidism, inflamma-
tion, torsion of trauma, hypothyroidism, oestrogen treatment, liver arbitrarily classified into limited, defined as fewer than five micro-
cirrhosis, hypopituitary disease and ageing. The testis is globally liths per ultrasound field, or classical, defined as more than five
reduced in size, usually unilateral with changes in testicular reflec- microliths per field.36 A further definition, florid, where there are
tivity related to the underlying cause, but usually of lower reflectiv- innumerable microliths per ultrasound field, has also been sug-
ity. While volume and vascularity of the testis are reduced, the gested.37 The prevalence of all forms of testicular microlithiasis is
epididymis remains normal. Atrophy is a natural phenomenon of reported at 0.6%9.0%.38,39 Testicular microlithiasis is characterised
ageing where changes in the normal testis reflectivity, usually of a by the formation of microliths from degenerating cells in the
heterogeneous nature, may occur (Fig. 31.40).35 seminiferous tubules. Acoustic shadowing is not seen, probably
due to the small size of the calcifications. Although usually an
incidental finding during the investigation of testicular symptoms,
Testicular microlithiasis and testicular microlithiasis has been associated with various medical
macrocalcification conditions, including infertility, cryptorchidism, Klinefelters syn-
drome, Downs syndrome and pulmonary alveolar microlithiasis.
Testicular microlithiasis describes the appearance of multiple Testicular microlithiasis has also been found in association with
tiny bright foci, measuring 12mm in diameter, which may be benign and malignant tumours in the testis, with reports indicating
unilateral or bilateral (Fig. 31.41). The number of calcified foci and seminoma as the commonest tumour to occur in association with
the pattern of distribution can vary, being either very diffuse or testicular microlithiasis (Fig. 31.42).40 Furthermore a high number
more peripherally clustered.36 Testicular microlithiasis has been of patients with intra-tubular germ cell neoplasia have testicular
607
CHAPTER 31 Diseases of the testis and epididymis
microlithiasis; approximately 50% of patients with intra-tubular solid tumours of the extra-testicular tissues are normally benign
germ cell neoplasia develop testicular cancer within 5 years.41 As a although malignant lesions are seen. The reported prevalence of
consequence, the significance of finding isolated testicular micro- extra-testicular solid tumours varies between 3% and 16% of all
lithiasis is as yet uncertain; surveillance with ultrasound on an patients referred for scrotal ultrasound.45 Metastases may also occur
annual basis is advocated.38 A number of case reports have detailed in the extra-testicular space.
the development of a primary testicular tumour whilst on an ultra-
sound surveillance programme.39,42
The association of testicular macrocalcification within benign tes- Epididymal cysts and spermatoceles
ticular lesions is well documented and can be found in association
Extra-testicular cysts are commonly found in the spermatic cord,
with intra-testicular cysts and epidermoid tumours. Benign intra-
epididymis (Fig. 31.44), tunica albuginea or tunica vaginalis. Epidi-
testicular tumours, commonly derived from the Sertoli and Leydig
dymal cysts are most commonly found in the epididymal head,
cells of the seminiferous tubules, are difficult to distinguish from
contain clear serous fluid and on ultrasound demonstrate typical
malignant tumours and these too demonstrate calcification. Large
features of a cyst with posterior acoustic enhancement and may be
smooth curvilinear calcification at the periphery of a tissue mass
seen in up to 40% of patients. A spermatocele consists of cystic dila-
has been shown in Sertoli cell tumours. Granulomatous disease
tation of tubules of the efferent ductules and occurs in the epididy-
within the testes can also present with a low reflective mass and
mal head (Fig. 31.45), often containing low reflective debris
areas of calcification within.43 The presence of macrocalcification in
representing spermatozoa, lymphocytes, cellular debris, fat and
association with malignant tumours has also been noted, particu-
proteinaceous fluid.46 The differentiation between a spermatocele
larly with the entity of burnt-out tumours, and recently macrocal-
and a simple cyst is unimportant and they may be indistinguishable
cification has been associated with a higher prevalence of primary
on ultrasound. Spermatocele is though to be more common than an
testicular tumours (Fig. 31.43).44
epididymal cyst and more frequent in the epididymal head. These
cystic structures are normally painless unless inflamed, a rare
occurrence (Fig. 31.46). Spermatocele may be large (>4cm) and
Testicular microlithiasis mimic a hydrocele; differentiation is usually attained by demon-
strating fluid anterior to the testis in a hydrocele.
Small 12mm highly reflective areas with no posterior acoustic
shadowing.
May be bilateral or unilateral. Tubular ectasia and vasectomy
Associated with an increased prevalence of testicular malignancy.
High numbers of patients with testicular microlithiasis have
Following vasectomy, the epididymis has a characteristic appear-
intra-germ cell neoplasia.
ance of dilatation, with an inhomogeneous appearance on ultra-
Annual ultrasound surveillance is suggested.
sound described as ectasia of the epididymis. These appearances
are unrelated to symptoms and are seen in 45% of patients
(Fig. 31.47). There may be an associated spermatocele and sperm
granuloma.
A B
Figure 31.44 Epididymal head cysts. A: Two cysts are present in the epididymal head (short and long arrows). B: A septated
epididymal head cyst (arrow).
Figure 31.45 Spermatocele. A cyst in the epididymal tail Figure 31.47 Post-vasectomy. The epididymis is dilated (between
demonstrates debris (long arrow) that is layering and produces arrows, >4mm) in a patient who has undergone a vasectomy, with
posterior acoustic enhancement (short arrow): a spermatocele. a characteristic reflective pattern demonstrated.
Lipoma
This is the most common benign tumour of the extra-testicular
space and it is commonly found in the spermatic cord.48 Patients of
all ages are affected, with the tumour manifesting as a non-tender
scrotal lump. At ultrasound a lipoma has a homogenous high to
iso-reflective appearance, and varies in size (Fig. 31.49). Magnetic
resonance (MR) imaging will confirm the fat content of the lesion,
Figure 31.46 Inflamed spermatocele. On colour Doppler prior to excision if necessary.
ultrasound there is increased colour Doppler flow to the periphery
of the spermatocele (arrow) in keeping with inflammatory change. 609
CHAPTER 31 Diseases of the testis and epididymis
Malignant
Rhabdomyosarcoma
Liposarcoma
Leiomyosarcoma
Malignant schwannoma
Malignant fibrous histiocytoma
Pleomorphic hyalinising angiectatic tumour
Varicocele
A varicocele is present in up to 15% of adult male patients. Varic-
oceles are caused by incompetent valves in the internal spermatic
vein. Impaired drainage is more evident when standing upright or
during a Valsalva manoeuvre, which renders the varicocele more
prominent. Varicoceles are left-sided in 78%, right-sided in 6% and
bilateral in 15%. This abnormal dilatation of veins arises more often
on the left as a consequence of the angle at which the left testicular
vein enters the left renal vein. The normal veins of the pampiniform
plexus measure 0.51.5mm and a vein diameter of greater than
Figure 31.55 Scrotal pearl. The high reflective area (arrow) lying 2mm should be considered abnormal.56 On ultrasound, a varicocele
free within a small hydrocele within the scrotal sac represents a consists of multiple low reflective serpiginous tubular structures of
scrotal pearl, and causes posterior acoustic shadowing. varying size, best seen superior and lateral to the testis. If large the
varicocele may extend to the inferior aspect of the testis (Fig. 31.57).
Tumbling low-level echoes may be identified on real-time imaging,
Extra-testicular lesions
secondary to low flow. Ultrasound in the supine and erect positions
as well as following the Valsalva manoeuvre will help identify the
Nearly all are benign abnormalities. varicocele and document retrograde filling. Examination of the left
The majority are epididymal head cysts. kidney is advocated in the presence of a varicocele to exclude a
Lipomas occur commonly. renal tumour in all patients by many clinicians, without much sup-
Adenomatoid lesions are commonest in the epididymis. porting evidence as to the prevalence of this association.57 This is
Rhabdomyosarcoma occurs between the ages of 5 and 16 probably only really indicated in the presence of a varicocele that
years. has recently arisen in patients over the age of 40 years. Occasionally
an intra-testicular varicocele may occur (Fig. 31.58) with an inci-
dence quoted at <2% in a symptomatic population.58 The ultrasound
appearances of an intra-testicular varicocele are anechoic serpigi-
nous or cystic structures radiating from the mediastinum testis. The
by their characteristic position and shape.43 Calcifications present appearance on colour and spectral Doppler examination is charac-
in between the two layers of the tunica vaginalis have a character- teristic, as an intra-testicular varicocele demonstrates vascular flow,
istic appearance and are termed scrotal pearls, often best seen in differentiating this from other cystic structures such as a prominent
the presence of a hydrocele (Fig. 31.55). A scrotal pearl, often pal- rete testis or an intra-testicular cyst. An intra-testicular varicocele
pated by the patient, is usually freely mobile within a hydrocele. will behave in a similar fashion to an extra-testicular varicocele,
They may arise from inflammation of the tunica vaginalis or from increasing in size and demonstrating retrograde flow on Valsalva
remnants of an appendix testis or epididymis. manoeuvre. A common clinical presentation is with testicular pain
attributed to stretching of the tunica albuginea secondary to venous
Extra-testicular non-focal lesions congestion.
A classification of varicoceles based on clinical features is as
follows: grade 1, varicocele is palpable only during the Valsalva
Inguinal hernia manoeuvre; grade 2, readily palpable without the need for the
Valsalva manoeuvre; and grade 3, visible on inspection.59 Identifica-
Inguinal hernias are a common cause of a scrotal swelling. Physical tion of a varicocele in patients being investigated for infertility may
examination is normally sufficient to arrive at the diagnosis of an be of relevance, although testicular volume, ultrasound appear-
intra-scrotal inguinal hernia; ultrasound may be useful in the dif- ances and Doppler studies may also be of importance.
ficult cases. On ultrasound the hernia contains bowel or omentum
giving rise to peristalsis of fluid-filled loops of bowel, air within
bowel or high reflective omental fat.
ACUTE SCROTUM
Fluid collections
Acute scrotal pain is a common urological emergency for which
epididymo-orchitis is the commonest cause. The most important
Hydrocele, pyocele and haematocele
diagnostic distinction to be made in patients presenting with acute
Between the two layers of the tunica vaginalis, there is normally a scrotal pain is between acute spermatic cord torsion and the other
little serous fluid present, and this may be visualised in up to 85% causes of acute scrotal pain (Table 31.3). The treatment for acute
of asymptomatic men. When the collection of fluid becomes large, spermatic cord torsion is urgent surgical exploration to maintain
a hydrocele develops, the commonest cause of a painless scrotal viability of the testis and avoid testicular infarction. Diagnostic
swelling. The fluid accumulation is confined to the anterior and accuracy is therefore imperative in order to identify those patients
lateral aspects of the scrotum, sparing the bare area of the testis; the that require immediate surgical intervention as well as avoiding
testis appears to lie in a posterior location within the scrotal sac. A unnecessary surgery in patients with a non-surgical cause for acute
hydrocele is normally of low reflectivity, with posterior acoustic testicular pain. In the emergency setting, the ready availability of
enhancement, but may contain multiple echoes in the presence of greyscale ultrasound, with the ability to assess testicular vascula-
cholesterol crystals (Fig. 31.56).55 Hydroceles may be idiopathic or ture on colour Doppler, allows ultrasound to remain the imaging
develop secondary to trauma (haematocele), infection (pyocele), modality of choice. Clinical examination can be notoriously
612
Acute scrotum
C D
Figure 31.56 Extra-testicular fluid collections. A: The testis is displaced inferiorly by a large hydrocele without any echogenic debris
visible: a simple hydrocele. B: A pyocele in a patient with severe epididymo-orchitis with echogenic debris (arrow) representing pus. C: A
haematocele in a patient following blunt testicular trauma, with layering of echogenic debris seen (arrow). D: Extensive highly reflective
material within a chronic hydrocele representing cholesterol crystals (arrow).
Figure 31.57 Extra-testicular varicocele. Serpiginous dilated Figure 31.58 Intra-testicular varicocele. With the Valsalva
(>2mm) veins at the lower aspect of the testis; a testicular manoeuvre there is filling of the tubular structure with colour: an 613
varicocele. LT, left testis. intra-testicular varicocele (arrow).
CHAPTER 31 Diseases of the testis and epididymis
inaccurate in distinguishing the causes of acute scrotal pain. In enlargement, decreased reflectivity and increased colour Doppler
particular, the clinical discrimination between acute epididymo- flow (Fig. 31.59).61,62 The presence of increased colour Doppler flow
orchitis and spermatic cord torsion can be virtually unachievable; to the inflamed epididymis is the hallmark of hyperaemia and use-
imaging may play an important role. Familiarity with the ultra- fully aids the diagnosis of epididymitis and epididymo-orchitis. On
sound features of common causes of acute scrotal pain is therefore spectral Doppler ultrasound, there is a high-flow, low resistance
a necessity for the emergency on-call radiologist in order to provide waveform.63 There is often a reactive hydrocele, with septations if
complementary information for the clinical team to aid accurate a pyocele develops and scrotal wall thickening. The infection often
diagnosis in these patients. spreads to the adjacent testis (epididymo-orchitis), seen as patchy
areas of low reflectivity and increased colour Doppler signal, an
Inflammatory disease appearance that may persist for several months following treat-
ment.64 In addition, with focal ultrasound changes of the testes it is
difficult to exclude a malignant lesion. It is therefore important that
Epididymo-orchitis and epididymitis diffuse heterogeneous hyper-reflectivity and focal changes of the
testes in suspected orchitis be followed up to ensure complete reso-
Epididymo-orchitis and epididymitis predominantly affects the lution and rule out neoplasm.65
sexually active male of less than 40 years, the older patient with Venous infarction of the testis may occur in patients with severe
urological disease and the prepubertal boy with an associated epididymo-orchitis where localised oedema occludes the venous
urogenital anomaly.60 The main causative organisms in sexually drainage of portions of the testis or the entire testis (Fig. 31.60). The
transmitted diseases are Chlamydia trachomatis and Neisseria gonor-
rhoeae, whereas in prepubertal boys and in men over the age of 40
years, the organisms responsible are Escherichia coli and Proteus
mirabilis. Epididymitis causes acute scrotal pain of varying intensity
and pyuria with fever; at clinical examination the epididymis may
be palpated as a thickened tender structure separate from the testis.
On ultrasound, the epididymis may be involved in focal areas
(often the lower is affected first) or in a global pattern, with
A B
Figure 31.60 Venous infarction. A: There is an area of irregularity and mixed reflectivity present in the posterior aspect of the testis
(arrow) in a patient with severe epididymitis. B: Colour Doppler ultrasound demonstrates absence of flow signal in the mixed reflective
region of the testis (arrow): testicular venous infarction following severe acute epididymitis. There is usually increased colour Doppler flow in
orchitis.
614
Acute scrotum
Epididymo-orchitis
Acute onset of pain.
Focal or diffuse enlargement of the epididymis.
Increased colour Doppler flow to the affected areas.
Orchitis is a common occurrence.
Abscess is a potential complication.
Orchitis Trauma
Usually the testis is affected in patients with epididymitis giving Testicular trauma is commonly seen following motor vehicle acci-
rise to epididymo-orchitis. Primary orchitis without associated dents, athletic injury or a straddle injury. The mobility and elasticity
epididymitis is relatively rare but may be caused by HIV or mumps of the scrotal tissues provides protection for the testis in the event
615
CHAPTER 31 Diseases of the testis and epididymis
A B
Figure 31.64 Testicular trauma. A: Spectacle view of trauma to the right testis (short arrow) with a heterogeneous appearance and loss
of clarity of the tunica albuginea (long arrow) suggesting a testicular rupture. B: Ultrasound of the testis following trauma demonstrating a
fracture line (short arrow) through the mid-aspect of the testis and disruption of the lower testicular pole with a heterogeneous appearance
of haemorrhage (long arrow).
of trauma. However, forceful compression of the scrotal contents the duration of the torsion. The initial disruption will be to the
against the pubic ramus or impact with objects moving at high venous and lymphatic drainage, rather than to the arterial input of
velocity can result in serious injury. the testes, and venous infarction occurs earlier. Scrotal oedema is
Blunt trauma accounts for 85% of testicular injuries and penetrat- an early feature as the lower pressure cremasteric plexus is the first
ing injuries for 15%. Blunt scrotal trauma may result in a variety of vascular channel to be affected. Areas of testicular infarction begin
injuries including testicular rupture, torsion, dislocation, hae- to appear within 2 hours of complete occlusion of the testicular
matoma or contusion. Epididymal, scrotal wall and urethral injury artery, irreversible ischemia occurs after 6 hours and complete inf-
may also be seen. Pain and swelling of the scrotum following arction is established by 24 hours.73 Intra-vaginal torsion most com-
trauma makes clinical examination extremely difficult. Ultrasound monly occurs between the ages of 12 and 18 years, with a reported
is useful in the context of trauma and can help to exclude or confirm incidence of 1 in 4000 males younger than 25 years.74 Torsion com-
testicular rupture and differentiate testicular haematoma from hae- monly arises as puberty approaches, when testicular volume may
matocele (Fig. 31.64). Testicular rupture is a surgical emergency. On increase by a factor of five, thereby increasing the propensity of the
ultrasound, in testicular rupture, there is discontinuity of the tunica testis to fall forward and rotate.
albuginea, irregular heterogeneous testicular margins, a haema- Clinically intra-vaginal torsion presents with pain of sudden or
tocele and diminished colour Doppler flow to the affected area.70 insidious onset and is followed by swelling of the ipsilateral
Direct visualisation of a fracture site is unusual; more often paren- scrotum. The main clinical dilemma remains the distinction between
chymal heterogeneous areas are seen. A haematoma will initially spermatic cord torsion and acute epididymo-orchitis. Establishing
be seen as a high reflective area but with evolution over time, the diagnosis is important since in acute epididymo-orchitis, resolu-
will subsequently manifest as a low reflective complex cystic tion with minimal intervention is the rule unless complications,
structure. such as an abscess, supervene; by contrast surgery is mandatory for
torsion. The diagnostic dilemma is compounded by the occasional
similarity in clinical presentation: fever and pyuria may occur in
Spermatic cord torsion both conditions.
In spermatic cord torsion, the ultrasound appearances are vari-
Testicular torsion occurs when the spermatic cord is twisted and able depending on the time elapsed from the onset of symptoms.
the correct term is spermatic cord torsion. A narrow mesenteric With the development of congestion and infarction, the testes
attachment from the spermatic cord to the testes and epididymis is appear abnormally enlarged with decreased reflectivity75 (Fig.
regarded as the dominant cause, a slender attachment occurring as 31.65). The tunica albuginea and the mediastinum testis appear of
a result of a small testicular bare area. This allows the testes to fall relatively high reflectivity, and a small amount of fluid may pool
forward within the cavity of the tunica vaginalis and then to rotate in the lower pole of the sac of the tunica vaginalis. Later, as inf-
like a bell-clapper: the intravaginal type of torsion, as the guber- arction is established, haemorrhage may cause increased reflectiv-
naculum is fixed to the scrotal wall preventing the rotation of the ity and heterogeneity; this is particularly true in missed torsion
tunica vaginalis.71 In neonates, the gubernaculum is not attached to and chronic torsion (symptoms present for more than 10 days).
the scrotal wall and the entire testes, epididymis and the tunica Enlarged, thrombosed pampiniform plexus veins, within the sper-
vaginalis twist in a vertical axis on the spermatic cord, termed matic cord, may be visible and there may be an abrupt change in
extravaginal torsion.72 Neonatal torsion is rare, occurring in the calibre of the spermatic cord below the point of torsion. This
prenatal period and associated with an inguinal hernia. Factors results in an enlarged, twisted spermatic cord superior and poste-
other than an anatomical anomaly may predispose to spermatic rior to the epididymal head, containing round anechoic structures
cord torsion since the incidence of torsion (0.025%) is far less than representing veins.76 This may resemble the whirlpool pattern
the incidence of bell-clapper deformities. encountered with MR imaging77 (Fig. 31.66). Skin thickening of
Two factors are of importance in spermatic cord torsion: the the scrotum may be present as a manifestation of venous
extent of the spermatic cord twist (90 to three complete twists) and congestion.
616
Acute scrotum
Spontaneous de-torsion
A pitfall of the use of colour Doppler ultrasound in the assessment
Figure 31.65 Missed spermatic cord torsion. The testis is
of the acute scrotum, and in the desire to exclude the presence of
enlarged and heterogeneous (arrow) with a surrounding hydrocele.
spermatic cord torsion, is the entity of a spontaneous de-torsion.
No colour Doppler flow is identified within the testis but there is
The susceptible testis undergoes torsion, and then spontaneously
colour Doppler signal within the para-testicular tissues. The
untwists, resulting in hyperaemia of the previously ischaemic testis.
ultrasound was performed 24 hours after the onset of symptoms.
On ultrasound, the B-mode appearances may be unremarkable, but
an increase in colour Doppler flow may resemble acute epididymo-
orchitis, resulting in a misinterpretation and possibly severe conse-
quences for the patient.
Torsion of an appendage
Torsion of the testicular (or epididymal) appendage is considered
to be more common than spermatic cord torsion and an important
differential diagnosis among boys under the age of 13 years who
present acutely with a painful scrotum. Although most frequently
presenting in patients between 7 and 13 years of age, torsion of a
testicular appendage can occur at any age. The onset may be associ-
ated with trauma or exercise, with pain, erythema, tenderness and
scrotal swelling common presenting symptoms.26 In light-skinned
individuals the palpable, infarcted, tender appendage may be
visible at the upper pole of the testis; this blue-dot sign is reported
to occur in up to 21% of patients presenting with torsion of an
appendage.79
With torsion of a testicular appendage, the testis itself usually
appears normal on ultrasound with a normal low resistance arterial
supply. There is often an associated localised upper pole hydrocele
Figure 31.66 Whirlpool sign of spermatic cord torsion. The and an inflammatory reaction in the epididymis, which is often
appearance of a whirlpool above the testis (arrow), and separate enlarged. The torted appendage may have a variable appearance
from the epididymis, which represents the torted spermatic cord. most commonly of increased homogeneous reflectivity, although
up to 30% are reported as being of low reflectivity surrounded by
an area of increased perfusion (Fig. 31.67).80 Colour Doppler studies
may demonstrate an avascular mass separate from the testis and
The basis for the ultrasound diagnosis of spermatic cord torsion epididymis and an inflammatory reaction with increased blood
is the absence or decreased flow in the symptomatic testis com- flow in adjacent structures. With time the appendix becomes
pared to the asymptomatic testis. Colour Doppler ultrasound increasingly of higher reflectivity, indicating the onset of calcifica-
allows visualisation of intra-testicular blood flow; in torsion blood tion, eventually completely detaching itself.
flow is either reduced or absent, whereas it may be increased in
epididymo-orchitis.61 Therefore colour Doppler ultrasound is most
useful in rapidly differentiating acute spermatic cord torsion from
epididymo-orchitis. Although colour Doppler ultrasound is of
value in the adult testes it is less sensitive for the detection of blood
Torsion of an appendage
flow in children, since symmetry of blood flow is less well estab-
lished and is dependent on testicular size.5 A further limitation with More common in 713-year-old age group.
colour Doppler ultrasound is the entity of epididymo-orchitis The testis is normal on ultrasound.
complicated by testicular infarction.66 In these cases, a reversal of Ultrasound demonstrates a highly reflective appendage with a
diastolic flow in the testicular artery is thought to be characteristic surrounding hydrocele.
of venous thrombosis, and when combined with the greyscale and Surgical exploration is not indicated; treatment is conservative.
colour Doppler ultrasound appearances of the inflamed epididymis,
617
CHAPTER 31 Diseases of the testis and epididymis
REFERENCES 30. Eraso CE, Vrachliotis TG, Cunningham JJ. Sonographic findings in
testicular sarcoidosis simulating malignant nodule. J Clin Ultrasound
1. Langman J. Genital system. Medical embryology. 3rd edn. Baltimore: 1999;27:8183.
Williams and Wilkins; 1975. p. 175200. 31. Mevorach RA, Lerner RM, Dvoretsky PM, Rabinowitz R. Testicular
2. The reproductive organs of the male. In: Williams PL, Warwick R, abscess: diagnosis by ultrasonography. J Urol 1986;136:12131216.
Dyson M, Bannister LH, editors. Grays anatomy. 37th edn. London: 32. Purushothaman H, Sellars ME, Clarke JL, Sidhu PS. Intra-testicular
Churchill Livingstone; 1989. p. 14241434. haematoma: differentiation from tumour on clinical history and
3. Aziz ZA, Satchithananda K, Khan M, Sidhu PS. High-frequency color ultrasound appearances in two cases. Br J Radiol 2007;80:e184e187.
Doppler ultrasonography of the spermatic cord arteries: resistive 33. Hamm B, Fobbe F, Loy V. Testicular cysts: differentiation with US and
index variation in a cohort of 51 healthy men. J Ultrasound Med clinical findings. Radiology 1988;168:1923.
2005;24:905909. 34. Rouviere O, Bouvier R, Pangaud C, et al. Tubular ectasia of the rete
4. Paltiel HJ, Diamond DA, Di Canzio J, et al. Testicular volume: testis: a potential pitfall in scrotal imaging. Eur Radiol 1999;9:
comparison of orchidometer and US measurements in dogs. Radiology 18621868.
2002;222:114119. 35. Harris RD, Chouteau C, Patrick M, Schned A. Prevalence and
5. Ingram S, Hollman AS. Colour Doppler sonography of the normal significance of heterogeneous testes revealed on sonography: ex vivo
paediatric testis. Clin Radiol 1994;49:266267. sonographic-pathologic correlation. AJR Am J Roentgenol 2000;175:
6. Sellars MEK, Sidhu PS. Pictorial review: ultrasound appearances of the 347352.
rete testis. Eur J Ultrasound 2001;14:115120. 36. Backus ML, Mack LA, Middleton WD, et al. Testicular microlithiasis:
7. Sellars MEK, Sidhu PS. Ultrasound appearances of the testicular imaging appearances and pathologic correlation. Radiology 1994;192:
appendages: pictorial review. Eur Radiol 2003;13:127135. 781785.
8. Middleton WD, Meredith MW. Analysis of intratesticular arterial 37. Amaechi I, Sidhu PS. Testicular microlithiasis and macrocalcification:
anatomy with emphasis on transmediastinal arteries. Radiology prevalence of tumors and follow-up in a single center over 10 years.
1993;189:157160. Eur Radiol Suppl 2008;18:175.
9. Bushby LH, Sellars ME, Sidhu PS. The two-tone testis: spectrum of 38. Miller FNAC, Sidhu PS. Does testicular microlithiasis matter? A
ultrasound appearances. Clin Radiol 2007;62:11191123. review. Clin Radiol 2002;57:883890.
10. Rifkin MD, Kurtz AB, Pasto ME, Goldberg BB. Polyorchidism 39. Poulsen J, Sidhu PS, Holm M. Testicular microlithiasis a sinister
diagnosed preoperatively by ultrasonography. J Ultrasound Med condition? In: Dawson C, Muir GH, editors. The evidence for urology.
1983;2:9394. Shrewsbury, UK: TFM Publishing; 2005. p. 3138.
11. Leung AK. Polyorchidism. Am Fam Physician 1988;38:153156. 40. Ganem JP, Workman KR, Shaban SF. Testicular microlithiasis is
12. Rajbabu K, Morel JC, Thompson PM, Sidhu PS. Multi-cystic (rete associated with testicular pathology. Urology 1999;53:209213.
testis) supernumerary testis in polyorchidism with underlying 41. Skakkebaek NE, Berthelsen JG, Giwercman A, Muller J. Carcinoma-in-
microlithiasis: ultrasound appearances. Aust Radiol 2007;51: situ of the testis: possible origin from gonocytes and precursor of all
B56B58. types of germ cell tumours except spermatocytoma. Int J Androl
13. Greenlee RT, Hill-Harmon MB, Murray T, Thun M. Cancer Statistics, 1987;10:1928.
2001. CA Cancer J Clin 2001;51:1536. 42. Gilbert S, Nuttall MC, Sidhu PS, Ravi R. Metachronous testicular
14. Grantham JG, Charboneau JW, James EM, et al. Testicular neoplasms: tumors developing 5 and 9 years after the diagnosis of testicular
29 tumors studied by high-resolution US. Radiology 1985;157: microlithiasis. J Ultrasound Med 2007;26:981984.
775780. 43. Bushby LH, Miller FNAC, Rosairo S, et al. Scrotal calcification:
15. Horstman WG, Melson GL, Middleton WD, Andriole GL. Testicular ultrasound appearances, distribution and aetiology. Br J Radiol
tumours: Findings with color Doppler US. Radiology 1992;185: 2002;75:283288.
733737. 44. Miller FNAC, Rosairo S, Clarke JL, et al. Testicular calcification and
16. Sidhu PS, Sriprasad S, Bushby LH, et al. Impalpable testis cancer. microlithiasis: association with primary intra-testicular malignancy in
BJU Int 2004;93:888. 3,477 patients. Eur Radiol 2006;17:363369.
17. Woodward PJ, Schwab CM, Sesterhenn IA. Extratesticular scrotal 45. Frates MC, Benson CB, DiSalvo DN, et al. Solid extratesticular masses
masses: radiologic-pathologic correlation. Radiographics 2003;23: evaluated with sonography: pathologic correlation. Radiology
215240. 1997;204:4346.
18. Comiter CV, Renshaw AA, Benson CB, Loughlin KR. Burned-out 46. Rifkin MD, Kurtz AB, Goldberg BB. Epididymis examined by
primary testicular cancer: sonographic and pathological characteristics. ultrasound: correlation with pathology. Radiology 1984;151:187190.
J Urol 1996;156:8588. 47. Ramanathan K, Yaghoobian J, Pinck RL. Sperm granuloma. J Clin
19. Carmignani L, Gadda F, Gazzano G, et al. High incidence of benign Ultrasound 1986;14:155156.
testicular neoplasms diagnosed by ultrasound. J Urol 2003;170: 48. Lioe TF, Biggart JD. Tumours of the spermatic cord and paratesticular
17831786. tissue. A clinicopathological study. Br J Urol 1993;71:600606.
20. Rayor RA, Scheible W, Brock WA, Leopold GR. High resolution 49. Makarainen HP, Tammela TL, Karttunen TJ, et al. Intrascrotal
ultrasonography in the diagnosis of testicular relapse in patients with adenomatoid tumors and their ultrasound findings. J Clin Ultrasound
acute lymphoblastic leukaemia. J Urol 1982;128:602603. 1993;21:3337.
21. Garcia-Gonzalez R, Pinto J, Val-Bernal JF. Testicular metastases from 50. Hertzberg BS, Kliewer MA, Hertzberg MA, Distell BM. Epididymal
solid tumours: an autopsy study. Ann Diagn Pathol 2000;4:397400. leiomyoma: sonographic features. J Ultrasound Med 1996;15:797799.
22. Atchley JTM, Dewbury KC. Ultrasound appearances of testicular 51. Stewart VR, Sriprasad S, Pomplun S, et al. Sonographic features of a
epidermoid cysts. Clin Radiol 2000;55:493502. spermatic cord capillary hemangioma. J Ultrasound Med 2007;26:
23. Carragher AM. One hundred years of splenogonadal fusion. Urology 139142.
1990;35:471475. 52. Wood A, Dewbury KC. Case report: paratesticular rhabdomyosarcoma
24. Stewart VR, Sellars ME, Somers S, et al. Splenogonadal fusion: B-mode colour Doppler appearances. Clin Radiol 1995;50:130131.
and color Doppler sonographic appearances. J Ultrasound Med 53. Stein A, Kaplun A, Sova Y, et al. Leiomyosarcoma of the spermatic
2004;23:10871090. cord: report of two cases and review of the literature. World J Urol
25. Avila NA, Premkumar A, Shawker TH, et al. Testicular adrenal rest 1996;14:5961.
tissue in congenital adrenal hyperplasia: findings at gray-scale and 54. Kuwabara H, Uda H, Sakamoto H, Sato A. Malignant mesothelioma of
color Doppler US. Radiology 1996;198:99104. the tunica vaginalis testis. Report of a case and review of the
26. Sidhu PS. Clinical and imaging features of testicular torsion: role of literature. Acta Pathol Jpn 1991;41:857863.
ultrasound. Clin Radiol 1999;54:343352. 55. Gooding GA, Leonhardt WC, Marshall G, et al. Cholesterol crystals in
27. Bilagi P, Sriprasad S, Clarke J, et al. Clinical and ultrasound features of hydrocoeles; sonographic detection and possible significance. AJR Am
segmental testicular infarction: six-year experience from a single J Roentgenol 1997;169:527529.
centre. Eur Radiol 2007;17:28102818. 56. Dogra VS, Gottlieb RH, Oka M, Rubens DJ. Sonography of the
28. Sriprasad SI, Kooiman GG, Muir GH, Sidhu PS. Acute segmental scrotum. Radiology 2003;227:1836.
testicular infarction: differentiation from tumour using high frequency 57. El-Saeity NS, Sidhu PS. Scrotal varicocele, exclude a renal tumour. Is
colour Doppler ultrasound. Br J Radiol 2001;74:965967. this evidence based? Clin Radiol 2006;61:593599.
29. Rehman J, Rizkala ER, Chughtai B, Khan SA. Hypoechoic testicular 58. Das KM, Prasad K, Szmigielski W, Noorani N. Intratesticular
mass: a case of testicular and epididymal sarcoidosis. Urology varicocele: evaluation using conventional and Doppler sonography.
2005;66:e9e10. AJR Am J Roentgenol 1999;173:10791083.
619
CHAPTER 31 Diseases of the testis and epididymis
59. Dublin L, Amelar RD. Varicocele size and results of varicocelectomy in 74. Williamson RCN. Torsion of the testis and allied conditions. Br J Surg
selected subfertile men with varicocele. Fertil Steril 1970;21:606609. 1976;63:465476.
60. Siegal A, Snyder H, Duckett JW. Epididymitis in infants and boys: 75. Hricak H, Lue TF, Filly RA, et al. Experimental study of the
underlying anomalies and efficacy of imaging modalities. J Urol sonographic diagnosis of testicular torsion. J Ultrasound Med
1987;138:11001103. 1983;2:349356.
61. Horstman WG, Middleton WD, Melson GL. Scrotal inflammatory 76. van Dijk R, Karthaus HFM. Ultrasonography of the spermatic cord in
disease: Color Doppler US findings. Radiology 1991;179:5559. testicular torsion. Eur J Radiol 1994;18:220223.
62. Fitzgerald SW, Erickson SJ, Dewire DM, et al. Color sonography in the 77. Vijayaraghavan SB. Sonographic differential diagnosis of acute
evaluation of the adult acute scrotum. J Ultrasound Med 1992;11: scrotum: real-time whirlpool sign, a key sign of torsion. J Ultrasound
543548. Med 2006;25:563574.
63. Brown JM, Hammers LW, Barton JW, et al. Quantitative Doppler 78. Dogra VS, Rubens DJ, Gottlieb RH, Bhatt S. Torsion and beyond: new
assessment of acute scrotal inflammation. Radiology 1995;197:427431. twists in spectral doppler evaluation of the scrotum. J Ultrasound Med
64. Cook JL, Dewbury K. The changes seen on high-resolution ultrasound 2004;23:10771085.
in orchitis. Clin Radiol 2000;55:1318. 79. McCombe AW, Scobie WG. Torsion of scrotal contents in children.
65. Amaechi I, Sidhu PS. Ultrasound in the assessment of the on-call Br J Urol 1988;61:148150.
acute scrotum. Imaging 2008;20:131138. 80. Lerner RG, Mevorach RA, Hulbert WC, Rabinowitz R. Color Doppler
66. Eisner DJ, Goldman SM, Petronis J, Millmond SH. Bilateral testicular US in the evaluation of acute scrotal disease. Radiology 1990;176:
infarction caused by epididymitis. AJR Am J Roentgenol 1991;157: 355358.
517519. 81. Stamenkovic I, Lew PD. Early recognition of potentially fatal
67. Sanders LM, Haber S, Dembner A, Aquino A. Significance of reversal necrotizing fasciitis. The use of frozen-section biopsy. N Engl J Med
of diastolic flow in the acute scrotum. J Ultrasound Med 1994;13: 1984;28:16891693.
137139. 82. Paty R, Smith AD. Gangrene and Fourniers gangrene. Urol Clin
68. Drudi FM, Laghi A, Iannicelli E, et al. Tubercular epididymitis and North Am 1992;19:149162.
orchitis: US patterns. Eur J Radiol 1997;7:10761078. 83. Kane CJ, Nash P, McAninch JW. Ultrasonographic appearance of
69. Dogra VS, Bhatt S. Acute painful scrotum. Radiol Clin North Am necrotizing gangrene: aid in early diagnosis. Urology 1996;48:142144.
2004;42:349363. 84. Rajan DK, Scharer A. Radiology of Fourniers gangrene. AJR Am J
70. Herbener TE. Ultrasound in the assessment of the acute scrotum. Roentgenol 1998;170:163168.
J Clin Ultrasound 1996;24:405421. 85. Grainger AJ, Hide IG, Elliot ST. The ultrasound appearances of scrotal
71. Corriere JN. Horizontal lie of the testicle: a diagnostic sign and torsion oedema. Eur J Ultrasound 1998;8:3337.
of the testis. J Urol 1972;107:616617. 86. Stewart VR, Sidhu PS. The testis: the unusual, the rare and the bizarre.
72. Blackhouse KM. Embryology of testicular descent and maldescent. Clin Radiol 2007;62:289302.
Urol Clin North Am 1982;9:315.
73. Luker GD, Siegel MJ. Color Doppler sonography of the scrotum in
children. AJR Am J Roentgenol 1994;163:649655.
620
CHAPTER
Anatomy
INTRODUCTION
Ventral highly reflective corpus spongiosum expands to form the
Ultrasound plays an important role in the evaluation of penile glans penis.
pathology. High-frequency small parts linear transducers allow Dorsal paired low reflective corpora cavernosa
interrogation of the greyscale anatomy and dynamic vascular enveloped by the thin highly reflective tunica albuginea
imaging of the normal and diseased penis. Diagnostic images can distensible sinusoidal tissue essential for erectile function.
be obtained with few artefacts in a non-invasive manner and Internal pudendal artery divides into
without exposure to ionising radiation. Ultrasound of the penis has dorsal penile artery, bulbar artery and the cavernosal arteries.
been useful in the assessment of erectile dysfunction, but is also Venous drainage via the superficial and deep dorsal veins
valuable in the assessment of Peyronies disease, penile masses, emissary veins pierce the tunica albuginea, draining into dorsal
priapism and following trauma. veins via cavernosal, spongiosal and circumflex veins
the emissary vein/tunica region is the site of the veno-
occlusive mechanism.
Bucks fascia
Cavernosal artery
Corpus cavernosa
Corpus spongiosum Urethra Urethral artery
Corpus spongiosum
Figure 32.1 Anatomy of the penis. (Modified from Baxter GM
and Sidhu PS. Ultrasound of the Urogenital System. Thieme,
Stuttgart, 2006, Ch. 12, Diseases of the penis with functional
Glans
evaluation by Wilkins CJ, Sidhu PS.)
A B
Figure 32.3 Ultrasound appearances of the penis. A: In the flaccid state, the paired corpora cavernosa (long arrows) are of low
reflectivity and contain the cavernosal arteries (short arrows). The higher reflective corpora spongiosum (arrowhead) contains the urethra.
B: During tumescence, the corpora cavernosa expand with blood resulting in pockets of low reflectivity forming (short arrows). The
cavernosal arteries are more prominent (long arrow).
treatment of venous leaks have poor long-term clinical outcomes. absence of diastolic flow is a frequent occurrence in the normal
Despite this, patient pressure means that surgical correction for responder, and is not a sinister finding.13 More recent work has
venous leak, whilst controversial, is still carried out in some centres. found that the absence of systolic flow at 1 hour following intra-
The use of arterial reconstructive surgery is indicated only in a cavernosal injection of a stimulant is a more useful predictor and
small group of patients with new onset focal arterial occlusion with warrants immediate treatment and admission.14 Imaging all patients
few or no features of systemic vascular disease.7,8 at 1 hour post procedure would be impractical and a 4-hour return
However, a CDUS examination remains useful; experience shows to receive prompt treatment based on patient self-assessment has
that many patients benefit psychologically from a normal test been shown to work well.3
result. Additionally, CDUS imaging of the penis is important in the
pre-assessment of patients due to undergo revascularisation surgery Technique
following penile trauma, and to document vascularity prior to
surgery for Peyronies disease.9 There is also evidence that erectile
The stimulated CDUS examination should be performed with a
dysfunction may be an early marker of peripheral and coronary
chaperone, in a setting that offers patient privacy with little possi-
atherosclerotic disease.10 Pooled data suggests that a normal arterial
bility of interruption. A high-frequency linear small parts trans-
response to prostaglandin E1 has a negative predictive value for the
ducer with a small footprint is required. Intra-cavernosal injection
presence of coronary artery disease of 84%, whilst a diminished
of PGE-1 is performed with a small-bore needle (typically 30G). The
response has a positive predictive value of 32%.
ideal injection site is between the proximal and mid thirds of the
shaft at the dorsolateral aspect. Following injection of the vasoactive
Physiology of the erectile process substance the angle-corrected velocity of either the left or the right
cavernosal artery is recorded at 5-minute intervals from baseline up
Penile erection is the consequence of neurovascular events trig- to 30 minutes.15 Tumescence and rigidity are documented.
gered by a combination of psychological and hormonal factors. Colour flow Doppler ultrasound of the cavernosal arteries should
Increased cavernosal artery blood flow results in filling of the sinu- be performed with the probe positioned at the base of the penis on
soids of the corpora cavernosa. This leads to an elevation of pres- the ventral surface. The angle for Doppler analysis needs to be
sure in the corpora as the sinusoids distend within the non-compliant optimised (<60) with box-steering, angle correction and orientation
tunica albuginea. The rise in intra-tunica pressure compresses the of the probe to ensure reproducible, valid measurements. The peak
sub-tunica venous plexuses between the trabecula and tunica systolic velocity (PSV) of the cavernosal artery varies according to
albuginea. In turn, this partially occludes venous drainage from the the location of sampling, with higher velocities more proximally.16
penis and results in tumescence. Complete occlusion of venous Measurement of the spectral Doppler trace is most reproducible at
outflow is achieved during sexual activity by compression of the the base of penis where the angle of the cavernosal vessel is not
engorged corpora cavernosa at their base by contraction of the parallel with the probe.9 Self-stimulation has been advocated as an
ischio-cavernosal muscles. This final stage results in rigidity. During adjunct to pharmacological stimulation in order to obtain a maximal
tumescence intra-cavernous pressures reach approximately response, although the risk of ejaculation (which would necessitate
100mmHg and when rigid the pressure may rise to several hundred a repeat of the test on a separate occasion) needs to be considered
mmHg. and patients should be advised to stop prior to this.17
Erectile dysfunction is the result of a failure of this process and
may be due to neurogenic, psychogenic, vascular (arterial or Baseline imaging
venous) causes, or as the result of disruption of the tunica albug-
inea, post-traumatic or more commonly due to Peyronies disease. Baseline B-mode US imaging is performed in longitudinal and
Alternatively it may be due to patient medication or systemic dis- transverse planes with the penis held by the patient in the anatomi-
orders such as diabetes mellitus with multifactorial causes not cal position. Before injection of the stimulant detailed ultrasound
uncommon. examination of the penis is required. This allows selection of an
appropriate site for injection. Significant abnormalities such as
fibrotic plaque disease, focal cavernosal fibrosis, arterial calcifica-
tion or tunica disruption may be detected. Ultrasound imaging
STIMULATED COLOUR DOPPLER prior to injection allows the observer to distinguish between true
ULTRASOUND calcification/fibrosis abnormalities and the spurious appearance of
calcification/fibrosis of the corpora which may occur following
inadvertent intra-cavernosal injection of air bubbles18 (Fig. 32.5).
Pharmacological agents The cavernosal arteries range in diameter from 0.3mm in the flaccid
Prostaglandin E-1 (PGE-1) is the most widely used agent for phar-
macological stimulation of the penis. The normal dosage of PGE-1
is between 10 and 20g. Practice varies, but most commonly 20g
is administered at the outset of the test. An alternative is to assess
the erectile response after an initial dose of 10g and if inadequate
a second 10g injection is administered. However, the examination
is significantly shortened with the single dose method and use of a
single dose minimises patient discomfort and anxiety. PGE-1 is
widely reported as a safe treatment but there is a small risk of pria-
pism (less than 1%).11 Papaverine, the second most commonly used
stimulant, has a reported incidence of iatrogenic priapism of up to
18%.12 Regardless, patients should be fully informed of the risks and
given appropriate advice. One possible strategy is that patients with
an erection lasting longer than 4 hours be given direct access to an
on-site urology opinion to ensure prompt treatment. During stimu- Figure 32.5 Air in the corpora cavernosa. Following the
lated CDUS, absence of cavernosal artery flow or a resistance index intra-cavernosal injection of a vasoactive substance, air (arrows)
greater than 1.00 (absent diastolic flow) was thought to be highly causing acoustic shadowing is present at the injection site in the
specific in predicting priapism. However, experience suggests that corpora cavernosa.
623
CHAPTER 32 Ultrasound of the penis
state to 1.0mm during erection.6,7,19 The PSV of the cavernosal development of tumescence and subsequent veno-occlusion
artery in the flaccid penis in normal patients is 1015cm/s. This results in a reduction in diastolic flow.
value should be documented and further sampling during the n Phase 3: Corresponds to no diastolic flow.
study should be performed in the same location. n Phase 4: Characterised by reversal of diastolic flow and
represents full erection (Fig. 32.8).
Normal response n Phase 5: The final stage of rigidity, usually not seen in clinical
practice, shows a decrease in systolic velocities, which may
approach zero.22
During the pharmacologically induced erection, dynamic assess-
ment of the spectral Doppler waveform is performed. Maximal This sequence of events has a variable time course. Assessment
arterial engorgement occurs early in tumescence and allows colour over 30 minutes is occasionally required to ensure that the maximal
mapping of the vessels. Variations such as bifurcation, duplication effect has been attained, although 20 minutes is normally
and a common origin of the cavernosal arteries are often seen20 (Fig. sufficient.23
32.6). Cross communications between left and right cavernosal
arteries are present in virtually all patients.19 Anomalies may lead Arteriogenic erectile dysfunction
to a reduction in the PSV in the absence of significant arterial insuf-
ficiency and therefore measurements obtained may result in false
Maximal PSV of the cavernosal artery following injection of vasoac-
positive results.21 If there is definite asymmetry of the cavernosal
tive agents is the most accurate indicator of arterial disease. The
arteries, this should be documented and both arteries sampled
average PSV in normal volunteers is between 30 and 40cm/s.24 A
during the course of the assessment. A focal stenosis may result in
PSV of 35cm/s is unequivocally normal, whilst a PSV of <25cm/s
high-velocity jets at the site of narrowing on colour Doppler US
following adequate stimulation indicates definite arterial insuffi-
and, more distally, in damped pulsatility. The helicine arteries are
ciency.18 Intermediate values are not specific and in this group
not visible in the flaccid penis but become apparent during the
sildenafil is often used as some will have mild to moderate arterial
onset of erection and branch in a radial direction from the cavern-
insufficiency and may benefit25 (Fig. 32.9).
osal arteries (Fig. 32.7). During the course of tumescence, erection
Some authors suggest that arteriogenic erectile dysfunction can
and full rigidity the helicine arteries become less visible as progres-
be diagnosed on the basis of the PSV in the flaccid penis. One study
sive venous occlusion leads to a reduction and finally cessation of
showed that a cut-off value of 10cm/s for the PSV in the non-erect
penile inflow.19
penis was 96% sensitive and 92% specific in the diagnosis of arterio-
Pharmacologically induced erection follows a predictable
genic erectile dysfunction.26 The degree of change in the diameter
sequence of changes on CDUS in patients without erectile dysfunc-
of the cavernosal artery during the erectile process provides some
tion. Schwartz etal.22 divided this sequence into stages.
insight into the degree of arterial insufficiency. In normal patients
n Phase 0: Prior to injection the dorsal arteries of the penis are the vessel increases in size by 75100%, whereas in patients with
more clearly identified than the cavernosal arteries. In about arteriogenic erectile dysfunction this figure is usually less than
one-third of patients colour and spectral Doppler analysis of 75%.23 However, the increase in the baseline diameter following
the cavernosal artery prior to stimulation is not possible. The pharmacological stimulation does not correlate with either the
normal spectral waveform at this stage is monophasic with a measured PSV or clinical grading of erection and it is not routine
high resistance pattern showing minimal or no diastolic flow. to measure arterial diameters.27
n Phase 1: Follows pharmaco-stimulation and marks the onset
of erection. During phase 1 the systolic and diastolic flow
increase results in continuous flow throughout the cardiac Veno-occlusive erectile dysfunction
cycle. In normal volunteers PSV is usually greater than
35cm/s and the peak end-diastolic velocity (EDV) is greater Ultrasound may be used to diagnose veno-occlusive dysfunction in
then 8cm/s. patients with normal arterial inflow. Having established a normal
n Phase 2: As pressure increases within the corpora cavernosa arterial response with a PSV >35cm/s, an EDV of >5cm/s is
there is a progressive decrease in the diastolic flow. The usually accepted as the level above which a venous leak is
624
Stimulated colour Doppler ultrasound
A B
Further imaging
The diagnosis of venous incompetence on ultrasound requires
normal arterial inflow. In cases with mixed aetiology of erectile
dysfunction an indeterminate result may be obtained and reflects
both arterial inflow insufficiency and venous leak. In this group of
patients, cavernosography and arteriography may be required.
Cavernosography with cavernosometry remains the diagnostic ref-
Figure 32.9 Arterial erectile dysfunction. The peak systolic erence standard for the diagnosis of venous leak, as this technique
velocity remains at 27.5cm/s despite three doses of PGE-1. The measures outflow resistance without the need for adequate arterial
end-diastolic velocity remains elevated at 6.7cm/s; venous integrity inflow as well as mapping the sites of incompetence.31 Therefore,
cannot be assessed in the presence of arterial erectile dysfunction. following a positive CDUS for venous leak, cavernosography is
625
CHAPTER 32 Ultrasound of the penis
usually required if surgical venous ligation is planned. As previ- smooth muscle in the corpora cavernosa and result in a failure of
ously discussed, surgical intervention for venous leak has a limited the normal veno-occlusive mechanism required for an erection. On
success rate and its effects may be short-lived. However, it is a rela- CDUS this is characterised by forward flow in the cavernosal artery
tively minor surgical procedure and may be the treatment option throughout the cardiac cycle and is indistinguishable from a posi-
of choice for young patients, providing a temporary improvement tive finding of venous incompetence. In patients with a suboptimal
in symptoms. An alternative treatment is coil embolisation via a response to PGE-1 injection and features of venous incompetence
direct approach using a draining vein.32 the study may be supplemented by an intra-cavernosal injection of
phentolamine. Phentolamine is an alpha-adrenoreceptor antagonist
False venous leak and has been found to be safe at an intra-cavernosal dose of 2mg
with no significant impact on systemic blood pressure. In a study
by Aversa etal.33 phentolamine normalised erectile response in
Anxiety following injection of PGE-1 may lead to a false positive
20/26 patients initially diagnosed with venous leak following injec-
result for venous leak due to elevated adrenergic tone.11 Increased
tion with PGE-1 (Fig. 32.11). Phentolamine led to a statistically
levels of adrenaline prevent complete relaxation of the sinusoidal
significant increase in the grade of erection, PSV and a decrease in
EDV in this study.33 Similar results have been reported in other
studies.11 The concern that intra-cavernosal injection of multiple
vasoactive agents may lead to an increased risk of priapism is
unfounded.11,33
The marked reduction in false positive results has led many
authors to recommend that intra-cavernosal phentolamine is neces-
sary before a venous leak can be diagnosed by CDUS assessment
in the younger patient. Furthermore, phentolamine, as an oral prep-
aration, may offer a therapeutic approach in this very specific group
of patients.34,35 Venous leak not reversed by phentolamine is highly
predictive of a structurally based abnormality.
A B
Figure 32.11 Colour Doppler ultrasound response to intra-cavernosal phentolamine. A: Following pharmaco-stimulation with
PGE-1 in this young patient, the peak systolic velocity and the end-diastolic velocity are difficult to interpret; arterial input may be
insufficient to prevent a venous leak. B: At 25 minutes, 5 minutes after a 2mg dose of phentolamine, the peak systolic velocity increases
to 75.7cm/s and the end-diastolic velocity is negative at 5.4cm/s; the arterial and venous mechanisms are intact.
626
Peyronies disease
Figure 32.13 Peyronies disease. Linear calcification (arrows) in Figure 32.15 Malignant tumour of the penis. A poorly
the corpora cavernosa, causing acoustic shadowing; likely vascularised mass (arrow) in the distal shaft of the penis; a
Peyronies disease. squamous cell carcinoma.
plaque may encase the cavernosal arteries and cause arterial erectile
dysfunction.48 Furthermore, there is also an increased incidence of
arterial and mixed vascular abnormalities.49 B-mode assessment of
calcification allows patient selection for lithotripsy therapy, and
CDUS examination is important prior to possible corrective surgery,
to ascertain the course of the cavernosal arteries in relation to
plaques.50
PENILE FIBROSIS
Penile fibrosis may result from a number of causes. Without prompt
treatment ischaemic priapism will cause fibrosis of the cavernosal
tissue, producing diffuse cavernosal fibrosis. On ultrasound this is
recognisable as replacement of normal sinusoidal tissue in the
corpora cavernosa by ill-defined hyperechoic regions. Regular self-
injection with intra-cavernosal stimulation therapy for erectile dys-
function, in particular papaverine, may cause focal areas of penile
fibrosis to develop.51 Ultrasound examination can delineate areas of
Figure 32.14 Peyronies disease. Focal area of altered reflectivity
fibrosis allowing follow-up and guiding decisions on therapy.52 In
(arrows) in the corpora cavernosa; likely Peyronies disease.
some patients there may be intra-corporal calcification without any
associated plaque and this is thought to result from regions of focal
fibrosis or possibly previous trauma.53
Peyronies disease
Plaques may or may not be calcified.
In the flaccid state plaques can be difficult to visualise, but may PENILE MASSES
become apparent during tumescence; image at the site of
maximal curvature.
Both arterial and venous diseases are more common in
Primary penile malignancies are rare. Squamous cell carcinoma
Peyronies disease mixed aetiology is often present requiring
accounts for up to 95% of malignancies of the penis and is most
careful assessment to guide therapy.
commonly located at the glans (Fig. 32.15). Squamous cell carci-
Plaques and/or fibrosis may occur following treatment with
noma is associated with human papilloma virus (types 16 and 18)
PGE-1 and can necessitate cessation of treatment.
and is more common in the developing world. Other primary
malignancies include melanomas, basal cell carcinoma and lym-
phoma.54 Metastatic spread of malignancy to the penis may be
either haematogenous or lymphatic. Metastases should be sus-
may extend beyond those that are palpable to involve the corporal pected in patients with a known primary malignancy and new
tissue or the inter-cavernosal septum and these may be visible on onset priapism. Ultrasound is the preferred imaging modality for
ultrasound.46 Focal or diffuse thickening of the tunica (which penile malignancy.21,55 Ideally, it should be performed following
becomes more apparent following pharmacological stimulation) injection of PGE-1. Ultrasound can assist in identifying the depth
may be the only ultrasound feature.47 of tumour invasion and, specifically, allows evaluation of corpora
Distortion of the tunica albuginea results in a higher incidence of cavernosal infiltration. It has been shown to be more accurate than
venous erectile dysfunction than in the general population. Rarely, clinical examination in determining the extent and size of the
628
References
Figure 32.16 Penile prosthesis. The low reflective area (arrow) Figure 32.17 Penile fracture. A transverse image through the
within the shaft of the penis is clearly of an artificial nature. penis demonstrating a haematoma (short arrows) displacing the
normal structures of the penis (long arrow) as a consequence of a
fracture.
tumour.56 Detection of local lymph nodes is readily performed
using ultrasound; however, assessment of microscopic infiltration
is not possible.21,55
On ultrasound squamous cell carcinoma tends to be hypoechoic,
relatively heterogeneous and typically poorly vascularised on Urethrography involves ionising radiation, whilst urethroscopy is
CDUS. Interruption of the echogenic tunica albuginea indicates invasive and may introduce infection. Ultrasound allows visualisa-
malignant infiltration.57 Ultrasound is of limited value in large tion of the structures around the urethra whilst these other tech-
tumours and MR imaging is generally indicated in this context. The niques essentially provide luminal views. Some practitioners have
appearances of secondary disease are similar to those of primary advocated the use of ultrasound for evaluating the urethra. Using
penile cancer involving the corpora.58 high-frequency linear probes the normal anterior (bulbar and
Other masses occurring in the penis include those found in the penile) urethra is visualised when distended with fluid. Lidocaine
skin and subcutaneous tissues elsewhere including cysts, lipomas gel or normal saline may be used to obtain urethral distension in a
and neurofibromas. A further unusual mass which may be encoun- retrograde direction via the urethral meatus in a manner analogous
tered is a penile prosthesis, easily identifiable by parallel highly reflec- to conventional urethrography. Alternatively, antegrade passage of
tive walls and the man-made symmetrical structure (Fig. 32.16). urine with constriction of outflow at the glans by means of a clamp
or the patients fingers during the ultrasound examination may be
utilised. Images are acquired in longitudinal and transverse planes.
Imaging of the posterior urethra is more problematic but may be
PENILE TRAUMA performed with a transrectal probe. Micturating images of the pos-
terior urethra with the probe in situ allow high-resolution images
Blunt trauma to the flaccid penis rarely causes a fracture, but may of the posterior urethra. However, the self-evident problems of
result in extra-tunica or cavernosal haematoma formation. Penile micturition with the probe in place limit the value of this
fractures most commonly occur as a result of compression of the technique.
erect penile shaft against the pubic symphysis during sexual inter- The anterior (bulbar and penile) urethra is of relatively uniform
course. Presentation is usually acute with a history of pain, swelling diameter and measures up to 1.0cm across. The walls are smooth
and sudden loss of tumescence during intercourse.43 The principal and highly reflective. Strictures, intra-luminal masses and calculi
role of ultrasound in the acute setting is to identify defects in the are well visualised.
tunica albuginea and to allow assessment of the extent of acute Ultrasound of the urethra serves as an important adjunct to other
haematoma formation (Fig. 32.17). Ultrasound aids diagnosis in imaging modalities in the evaluation of stricturing disease. In par-
cases where the history or clinical findings are atypical. Identifica- ticular, bulbar urethral strictures, which tend to be focal, benefit
tion of a tunica defect should prompt immediate surgical repair as from ultrasound evaluation in order to determine the best treat-
delay in treatment of over 24 hours following the initial injury ment. The presence of abnormal peri-urethral tissue, which meas-
significantly increases the risk of long-term sequelae.59 ures more than 3mm, is predictive of poor outcome unless surgical
Complications of penile fracture include corporal fibrosis with or resection is performed.63 Ultrasound has been shown to be more
without plaque formation, disruption of the tunica albuginea and accurate in the measurement of the length of strictures in the bulbar
urethral disruption.59,60 Urethral injury may be present in up to 20% urethra than conventional urethrography.64 Accurate evaluation of
of cases.61 If there is clinical concern about a urethral injury then stricture length is important as it in part determines the decision to
formal urethrography is required. Erectile dysfunction due to graft or excise a stricture.63
impairment of the veno-occlusive mechanism may also occur.62
REFERENCES
URETHRAL ULTRASOUND 1. Williams PL, Warwick R, Dyson M, Bannister LH. Splanchnology. In:
Williams PL, Warwick R, Dyson M, Bannister LH, editors. Grays
anatomy. 37th edn. London: Churchill Livingstone; 1989. p. 14321433.
Formal urethrography supplemented by urethroscopy remains the 2. Bella AJ, Brant WO, Lue TF. Penile anatomy. In: Bertolotto M, editor.
imaging modality of choice for the assessment of the male urethra. Color Doppler US of the penis. Berlin: Springer; 2008. p. 1114.
629
CHAPTER 32 Ultrasound of the penis
3. Wilkins CJ, Sidhu PS. Diseases of the penis with functional evaluation. 30. Kassouf W, Carrier S. A comparison of the International Index of
In: Baxter GM, Sidhu PS, editors. Ultrasound of the urogenital system. Erectile Function and erectile dysfunction studies. BJU Int
Stuttgart: Thieme; 2006. p. 181192. 2003;91:667669.
4. Feldman HA, Goldstein I, Hatzichristou DG, et al. Impotence and its 31. Lue TF, Hricak H, Schmidt RA, Tanagho EA. Functional evaluation of
medical and psychosocial correlates: results of the Massachusetts Male penile veins by cavernosgraphy in papaverine-induced erection. J Urol
Aging Study. J Urol 1994;151:5461. 1986;135:479482.
5. Benet AE, Melman A. The epidemiology of erectile dysfunction. Urol 32. Fowlis GA, Sidhu PS, Jager HR, et al. Preliminary report: combined
Clin North Am 1995;22:699709. surgical and radiological penile vein occlusion for the management of
6. Virag R. Intracavernous injection of papaverine for erectile failure. impotence caused by venous-sinusoidal incompetence. Br J Urol
Lancet 1982;2(8304):938. 1994;74:492496.
7. Montague DK, Jarow J, Broderick GA, et al. American Urological 33. Aversa A, Rocchietti-March M, Caprio M, et al. Anxiety-induced
Association guideline on the management of priapism. J Urol failure in erectile response to intracorporeal prostaglandin-E1 in
2003;170:13181324. non-organic male impotence: a new diagnostic approach. Int J Androl
8. Montague DK, Jarow JP, Broderick GA, et al. Chapter 1: The 1996;19:307313.
management of erectile dysfunction: an AUA update. J Urol 34. Goldstein I. Oral phentolamine: an alpha-1, alpha-2 adrenergic
2005;174:230239. antagonist for the treatment of erectile dysfunction. Int J Impot Res
9. Golijanin D, Singer E, Davis R, et al. Doppler evaluation of erectile 2000;12(Suppl. 1):S75S80.
dysfunction part 1. Int J Impot Res 2007;19:3742. 35. Wespes E, Rondeux C, Schulmann CC. Effect of phentolamine on
10. Montorsi P, Ravagnani PM, Galli S, et al. Association between erectile venous return in human erection. Br J Urol 1989;63:9597.
dysfunction and coronary artery disease: matching the right target 36. Muneer A, Minhas S, Arya M, Ralph DJ. Stuttering priapism a
with the right test in the right patient. Eur Urol 2006;50:721731. review of the therapeutic options. Int J Clin Pract 2008;62:12651270.
11. Gontero P, Sriprasad S, Wilkins CJ, et al. Phentolamine re-dosing 37. Gordon S, Marsh P, Day A, Chappell B. Priapism as the presenting
during penile dynamic colour Doppler ultrasound: a practical method symptom of an aortocaval fistula. Emerg Med J 2004;21:265.
to abolish a false diagnosis of venous leakage in patients with erectile 38. Bertolotto M, Mucelli FP, Liguori G, Sanabor D. Imaging priapism: the
dysfunction. Br J Radiol 2004;77:922926. diagnostic role of color Doppler US. Color Doppler US of the penis.
12. Lomas GM, Jarow JP. Risk factors for papaverine-induced priapism. Berlin: Springer; 2008. p. 7988.
J Urol 1992;147:12801281. 39. Bertolotto M, Mucelli RP. Nonpenetrating penile traumas: sonographic
13. Cormio L, Bettocchi C, Ricapito V, et al. Resistance index as a and Doppler features. AJR Am J Roentgenol 2004;183:10851089.
prognostic factor for prolonged erection after penile dynamic colour 40. Walker TG, Grant PW, Goldstein I, et al. High-flow priapism:
Doppler ultrasonography. Eur Urol 1998;33:9497. treatment with superselective transcatheter embolization. Radiology
14. Shamloul R, Ghanem HM, Salem A, et al. The value of penile duplex 1990;174:10531054.
in the prediction of intracavernous drug-induced priapism. Int J Impot 41. Kang BC, Lee DY, Byun JY, et al. Post-traumatic arterial priapism:
Res 2004;16:7879. colour Doppler examination and superselective arterial embolization.
15. Govier FE, Asase D, Hefty TR, et al. Timing of penile color flow Clin Radiol 1998;53:830834.
duplex ultrasonography using a triple drug mixture. J Urol 42. Brant WO, Bella AJ, Lue TF. Peyronies disease: etiology and
1995;153:14721475. treatment. In: Bertolotto M, editor. Color Doppler US of the penis.
16. Kim SH, Paick JS, Lee SE, et al. Doppler sonography of deep Berlin: Springer; 2008. p. 5560.
cavernosal artery of the penis: variation of peak systolic velocity 43. Zargooshi J. Penile fracture in Kermanshah, Iran: report of 172 cases.
according to sampling location. J Ultrasound Med 1994;13:591594. J Urol 2000;164:364366.
17. Mihmanli I, Kantarci M. Erectile dysfunction. Semin Ultrasound CT 44. Bertolotto M, Coss M, Neumaier CE. US evaluation of patients with
MRI 2007;28:274286. Peyronies disease. In: Bertolotto M, editor. Color Doppler US of the
18. Wilkins CJ, Sriprasad S, Sidhu PS. Colour Doppler ultrasound of the penis. Berlin: Springer; 2008. p. 6170.
penis. Clin Radiol 2003;58:514523. 45. Bekos A, Arvaniti M, Hatzimouratidis K, et al. The natural history of
19. Bertolotto M, Lissiani A, Pizzolato R, Fute MD. US anatomy of the Peyronies disease: an ultrasonography-based study. Eur Urol
penis: common findings and anatomical variations. In: Bertolotto M, 2008;53:644650.
editor. Color Doppler US of the penis. Berlin: Springer; 2008. 46. Brant WO, Bella AJ, Garcia MM, et al. Isolated septal fibrosis or
p. 2538. hematoma atypical Peyronies disease? Eur Urol 2007;177:179182.
20. Jarrow JP, Pugh VW, Routh WD, Dyer RB. Comparison of penile 47. Brock G, Hsu GL, Nunes L, et al. The anatomy of the tunica albuginea
duplex ultrasonography to pudendal arteriography. Variant penile in the normal penis and Peyronies disease. J Urol 1997;157:276281.
arterial anatomy affects interpretation of duplex ultrasonography. 48. Bertolotto M, de Stefani S, Martinoli C, et al. Color Doppler
Invest Radiol 1993;28:806810. appearance of penile cavernosal-spongiosal communications in
21. Mancini M, Bartolini M, Maggi M, et al. The presence of arterial patients with severe Peyronies disease. Eur Radiol 2002;12:
anatomical variations can affect the results of duplex sonographic 25252531.
evaluation of penile vessels in impotent patients. J Urol 1996;155: 49. Kadioglu A, Tefekli A, Erol H, et al. Color Doppler ultrasound
19191923. assessment of penile vascular system in men with Peyronies disease.
22. Schwartz AN, Wang KY, Mack LA, et al. Evaluation of normal erectile Int J Impot Res 2000;12:263267.
function with color flow Doppler sonography. AJR Am J Roentgenol 50. Levine LA, Coogan CL. Penile vascular assessment using color duplex
1989;153:11551160. sonography in men with Peyronies disease. J Urol 1996;155:
23. Chiou RK, Alberts GL, Pomeroy BD, et al. Study of cavernosal arterial 12701273.
anatomy using color and power Doppler sonography: impact on 51. Pery M, Rosenberger A, Kaftori JK, Vardi Y. Intracorporeal
hemodynamic parameter measurement. J Urol 1999;162:358360. calcifications after self-injection of papaverine. Radiology 1990;176:
24. Golijanin D, Singer E, Davis R, et al. Doppler evaluation of erectile 8183.
dysfunction part 2. Int J Impot Res 2007;19:4348. 52. Chew KK, Stuckey BG, Earle CM, et al. Penile fibrosis in
25. Benson CB, Aruny JE, Vickers MA. Correlation of duplex sonography intracavernosal prostaglandin E1 injection therapy for erectile
with arteriography in patients with erectile dysfunction. AJR Am J dysfunction. Int J Impot Res 1997;9:225229.
Roentgenol 1993;160:7173. 53. Doubilet PM, Benson CB, Silverman SG, Gluck CD. The penis. Semin
26. Roy C, Saussine C, Tuchmann C, et al. Duplex Doppler sonography of Ultrasound, CT, MRI 1991;12:157175.
the flaccid penis: potential role in the evaluation of impotence. J Clin 54. Kayes O, Ahmed HU, Arya M, Minhas S. Molecular and genetic
Ultrasound 2000;28:290294. pathways in penile cancer. Lancet Oncol 2007;8:420429.
27. Patel U, Lees WR. Penile sonography. In: Solibiati L, Rizzatto G, 55. Algaba A, Horenblas S, Pizzocaro-Luigi PG, et al. EAU guidelines on
editors. Ultrasound of superficial structures. London: Churchill penile cancer. Eur Urol 2002;42:199293.
Livingstone; 1995. p. 229242. 56. Agrawal A, Pai D, Ananthakrishnan N, et al. Clinical and sonographic
28. Quam JP, King BF, James EM, et al. Duplex and color Doppler findings in carcinoma of the penis. J Clin Ultrasound 2000;28:
sonographic evaluation of vasculogenic impotence. AJR Am J 399406.
Roentgenol 1989;153:11411147. 57. Bertolotto M, Serafini G, Dogliotti L, et al. Primary and secondary
29. Bassiouny HS, Levine LA. Penile duplex sonography in the diagnosis malignancies of the penis: ultrasound features. Abdom Imaging
of venogenic impotence. J Vasc Surg 1991;13:7582. 2005;30:108112.
630
References
58. Vapnek JM, Hricak H, Carroll PR. Recent advances in imaging studies 61. Fergany AF, Angermeier KW, Montague DK. Review of Cleveland
for staging of penile and urethral carcinoma. Urol Clin North Am Clinic experience with penile fracture. Urology 1999;54:352355.
1992;19:257266. 62. Gontero P, Sidhu PS, Muir GH. Penile fracture repair: assessment of
59. El Bahnasawy MS, Gomha MA. Penile fractures: the successful early results and complications using color Doppler ultrasound. Int J
outcome of immediate surgical intervention. Int J Impot Res Impot Res 2000;12:125129.
2000;12:273277. 63. Morey AF, McAninch JW. Sonographic staging of anterior urethral
60. Asgari MA, Hosseini SY, Safarinejad MR, et al. Penile fractures: strictures. J Urol 2000;163:10701075.
evaluation, therapeutic approaches and long-term results. J Urol 64. Nash PA, McAnich JW, Bruce JE, Hanks DK. Sono-urethrography in
1996;155:148149. the evaluation of anterior urethral strictures. J Urol 1995;154:7276.
631
CHAPTER
Adrenals
Keith Dewbury and Elizabeth E. Rutherford
33
INTRODUCTION 632 ANATOMY AND SCANNING TECHNIQUES
ANATOMY AND SCANNING TECHNIQUES 632
Embryologically, the adrenal cortex is of mesodermal origin and the
NORMAL APPEARANCES 633 medulla develops from neuroectodermal tissue. The cortex pro-
CONGENITAL ANOMALIES 634 duces hormones including cortisol, aldosterone and androgens and
Agenesis 634 consists of three layers: the zona glomerulosa (outermost layer),
Hyperplasia (adrenogenital syndromes) 634 zona fasciculata (largest, middle layer) and the zona reticularis
Discoid adrenal 634 (innermost layer). The more central adrenal medulla is smaller and
secretes adrenaline, noradrenaline and dopamine. The adrenal
ADRENAL CYSTS 634
glands are yellowish in colour, weigh approximately 4g each and
ADRENAL HAEMORRHAGE 635 measure 36cm in length, 23cm in width and 26mm in thick-
ness. Each consists of an anteromedial ridge from which two thin
HYPERPLASIA 635
limbs extend posteriorly.
ADRENAL CALCIFICATION 635 The right adrenal is pyramidal in shape, lying between the infe-
rior vena cava (IVC) and right crus of diaphragm. The inferior
TUMOURS 635
Benign 636
aspect of the gland never extends caudally to the level of the renal
Adenomas 636 vessels.3 The left adrenal is crescentic in shape and lies more crani-
Myelolipomas 636 ally than its counterpart. The medial and lateral limbs are also
Phaeochromocytoma 637 shorter than those on the right. It lies lateral or slightly posterior to
Malignant 637 the aorta and lateral to the left crus of diaphragm. Superiorly, it lies
Adrenal cortical carcinoma 637 posterior to the lesser sac, and more inferiorly, it is posterior to the
Neuroblastoma 637 pancreas. The glands receive their blood supply from the inferior
Metastases 640 phrenic arteries, renal arteries and directly from the aorta. There is
ROLE OF CT AND MRI IN CHARACTERISATION OF usually a single adrenal vein that drains into the vena cava on the
ADRENAL LESIONS 642 right and into the left renal vein on the left.4
The position of the adrenals as described requires an intercostal
scanning approach using the acoustic window of the liver on the
right and the spleen on the left. To visualise the right adrenal, the
transducer is placed in the ninth or tenth intercostal space in
the mid or anterior axillary line. Scanning transversely, the trans-
INTRODUCTION ducer is gently rotated to move the field of view from the renal
hilum upwards to a few centimetres above the kidney, concentrat-
The adrenal glands are small, paired organs which lie anteromedial ing on the region behind the IVC and directly adjacent to the right
to the upper pole of the kidneys and may therefore be challenging diaphragmatic crus. In the upper transverse section on the right a
to visualise with ultrasound. Initial descriptions of adrenal ultra- vertical linear or curvilinear structure corresponding to the antero-
sound reported that the right adrenal was easier to visualise than medial ridge and medial limb is seen. In the middle section both
the left.1,2 Recent improvements in ultrasound technology have limbs are seen as an inverted V or Y. Through the inferior portion
increased the sensitivity of abdominal ultrasound in the detection of the gland only the lateral limb may be seen as a horizontal band.
of adrenal lesions such that lesions less than 1cm may be identified. Coronal or longitudinal sections are obtained by rotating the trans-
Lesion detection, however, depends on a number of factors, in ducer through 90. The upper pole of the right kidney is located and
particular patient habitus, and whilst lesions as small as 5mm can the transducer angled medially. Both limbs of the gland may be
be detected if visualisation is good, when imaging is suboptimal, simultaneously displayed as a thin, long inverted V- or Y-shaped
lesions under 2cm in diameter may not be identified. In cases structure up to 6cm in length. A further small medial angulation is
where there is doubt as to the presence of a lesion or in obese necessary to visualise the anteromedial ridge of the gland in this
patients where an adrenal lesion is suspected, computed tomogra- plane where it lies posterior to the IVC.
phy (CT) is the initial imaging modality of choice. Whilst magnetic The left adrenal gland is more difficult to image because of the
resonance (MR) and CT imaging are undoubtedly better imaging smaller acoustic window available through the spleen. The trans-
modalities for characterisation of adrenal masses, there are certain ducer is placed on the eighth or ninth intercostal space in the pos-
lesions that have characteristic ultrasound appearances. Adrenal terior axillary line, avoiding stomach or bowel gas, to give a coronal
lesions detected at ultrasound may be the first manifestation of scan. The upper pole of the kidney should first be located through
malignancy or may be benign and incidental. Ultrasound of the the spleen. A small angulation of the transducer towards the ante-
adrenal glands is also particularly useful in children, when radia- rior aspect of the kidney will demonstrate the left adrenal gland in
tion dose reduction is paramount and the glands are more readily the perirenal space between spleen, kidney and left diaphragmatic
visualised than in adults. crus. This is best recognised when both limbs are shown, displaying
632
Normal appearances
A B
Figure 33.2 Normal neonatal adrenal glands. A: Longitudinal view of the right adrenal gland in a neonate. Note the clear distinction
between the low reflectivity cortex and higher reflectivity medulla. B: Transverse image showing both adrenal glands (arrows) in a neonate.
633
CHAPTER 33 Adrenals
Figure 33.3 Congenital adrenal hyperplasia. Note the large size Figure 33.4 Discoid adrenal. Longitudinal image in a neonate.
of the gland (compared with the normal neonatal adrenal Fig. There is left renal agenesis. The flattened elongated left adrenal
33.2A) and pronounced corticomedullary differentiation. gland is well visualised through the spleen. Note the marked
corticomedullary differentiation.
A B
folding of the adrenal gland into a medial and lateral wing. The
CONGENITAL ANOMALIES gland becomes flattened and elongated, producing a typical discoid
shape. This may be particularly well seen in neonates when the
gland is proportionally larger and the zonal architecture is still seen
Agenesis (Fig. 33.4).
A B
Figure 33.6 Subacute right adrenal haemorrhage in a neonate. A: The ultrasound appearances are of a solid mixed reflectivity mass.
B: CT image in the same child confirms the presence of mixed attenuation within the right adrenal, with higher attenuation areas signifying
recent haemorrhage.
635
CHAPTER 33 Adrenals
homogeneous, focal areas of necrosis or haemorrhage are more malities and biochemical tests reveal hypokalaemia, hypernatrae-
likely to occur in larger masses, resulting in a more heterogeneous mia and raised urine and serum aldosterone levels.
appearance.21 The majority of adrenal adenomas are found incidentally at CT
examination, although routine abdominal ultrasound may also
detect them. The intracytoplasmic lipid content of adrenal adeno-
Benign mas allows their diagnosis by unenhanced CT imaging25 or opposed
phase chemical shift MRI.26 At unenhanced CT imaging, 98% of
homogeneous adrenal masses with a CT attenuation value of 10
Adenomas Hounsfield units or less will be benign, with the majority of these
being adenomas, although 29% of adenomas will have a greater
These tumours are common incidental findings, being reported in attenuation value and are hence indistinguishable from non-
up to 3% of adult autopsies.22 Approximately 10% of adrenal adeno- adenomas, including metastases.27 At ultrasound, adrenal adeno-
mas are bilateral and their incidence increases with age. They are mas appear solid, rounded (Fig. 33.7) or slightly flattened (Fig. 33.8)
usually small and measure 12cm in diameter. Whilst most adeno- and well defined. They are homogeneous and of low reflectivity.
mas are non-functioning and detected incidentally, they may be
hyperfunctioning and present with symptoms related to excessive
hormone (cortisol or aldosterone) secretion.
Adenomas that secrete excessive amounts of cortisol result in
Myelolipomas
Cushings syndrome, which is characterised by truncal obesity, hir- Adrenal myelolipoma is a rare cortical tumour composed of
sutism, amenorrhoea, hypertension and weakness and can also be varying proportions of fat and bone marrow elements.28,29 There is
caused by adrenal hyperplasia, adrenal carcinoma or exogenous no malignant potential and the lesions are endocrinologically non-
corticosteroid administration. Conns syndrome results from the functioning. They arise in the zona fasciculata of the gland. Myelol-
excessive secretion of aldosterone, which is due to an adrenal ipomas are usually asymptomatic and discovered incidentally
adenoma in 70% of cases. Women are more likely to have hyperal- although they may cause symptoms if they undergo haemorrhage
dosteronism due to an adenoma, whereas men with hyperaldos- or become large and exert a local pressure effect on adjacent struc-
teronism are more likely to have underlying adrenal hyperplasia.23,24 tures. They have a prevalence at postmortem of 0.08% to 0.2%.30 On
Symptoms include hypertension, weakness, tetany and ECG abnor- ultrasound these rare tumours are characteristically highly reflective,
A B
A B
Figure 33.8 Flattened adrenal adenoma. A: Well-defined, low reflectivity right adrenal lesion with a more linear morphology (arrow).
B: CT in the same patient confirmed a right adrenal adenoma (arrow).
636
Tumours
due to their fat content (Fig. 33.9A). They may also contain calcifica- Other rare benign adrenal lesions include ganglioneuromas,
tion. If discovered incidentally at ultrasound, CT should be per- haemangiomas32 and lipomas. The ultrasound features of these
formed to confirm the presence of fat in these lesions (Fig. 33.9B). tumours are non-specific and hence the diagnosis is usually made
histologically.
Phaeochromocytoma
Phaeochromocytomas are endocrinologically active tumours that Malignant
secrete adrenaline and noradrenaline, causing paroxysmal head-
ache, palpitations, excessive perspiration and hypertension. They
are found in up to 1% of patients with hypertension. The majority Adrenal cortical carcinoma
arise within the chromaffin cells of the adrenal medulla but up to
10% arise in the autonomic nervous tissue, particularly in the Primary adrenal cortical carcinoma is rare, accounting for 0.2% of
organs of Zuckerkandl.31 The majority of adrenal phaeochromocy- all cancer deaths. It can arise from any of the layers of the adrenal
tomas are benign but 510% are malignant and up to 5% are cortex. Approximately half of tumours are endocrinologically
multiple. Multiple lesions are frequently associated with various active33 and therefore present earlier with features of excess
hereditary syndromes, e.g. multiple endocrine neoplasia (MEN) hormone production such as Cushings syndrome. Non-
type IIa and IIb, von HippelLindau syndrome, neurofibromatosis functioning tumours are often therefore large and have invaded the
and tuberous sclerosis. The diagnosis may be confirmed by bio- adrenal vein and IVC by presentation. Colour Doppler examination
chemical assay for urinary catecholamines and metabolites, e.g. may therefore be useful to assess for venous invasion. Nodal and
vanillylmandelic acid (VMA). blood-borne metastases are common and tumour recurrence fol-
Phaeochromocytomas may be large or small at presentation. The lowing surgery is common. Adrenal carcinoma has a variable
right adrenal is more commonly affected than the left. Typically, appearance at ultrasound with larger lesions often exhibiting
when small they are well-defined, round or oval masses with a central necrosis or haemorrhage. Tumours are usually well defined
uniform reflectivity. Larger tumours frequently undergo necrosis and some lesions may contain calcification (Fig. 33.12).
or haemorrhage with loss of homogeneity, and calcification may be
seen (Figs 33.10 and 33.11). Neuroblastoma
Neuroblastoma is the second most common abdominal tumour of
childhood (after Wilms tumour), with 80% occurring in children
under 5 years of age and one-third under 2 years of age. It accounts
for approximately 15% of childhood cancer deaths.34 Under 1 year
Benign adrenal lesions
of age the tumour may spontaneously regress or differentiate into
Adenomas (solid, low reflectivity, rounded or flattened). a ganglioneuroma. Approximately 35% of neuroblastomas arise in
Myelolipomas (highly reflective due to fat content). the adrenal medulla, with the extra-adrenal paraspinal ganglia and
Phaeochromocytoma (90% benign, variable appearance posterior mediastinum being other common sites.35 Neuroblastoma
calcification). may present as an asymptomatic abdominal mass or present with
Lipomas. symptoms related to metastases or the secretion of catecholamines.
Cysts. There may be generalised debility with weight loss and fever. Up
Ganglioneuromas. to three-quarters of patients have metastases at the time of presenta-
Haemangiomas. tion, with the most commonly affected sites being the bone marrow,
lymph nodes, liver and skin.36
A B
Figure 33.9 Myelolipoma. A: Longitudinal ultrasound image showing homogeneously highly reflective right adrenal mass, typical of a
myelolipoma. B: Coronal CT reformat in the same patient confirms the presence of fat in the right adrenal lesion (arrow), which also
contains some linear calcification medially. The left adrenal gland (arrowhead) is normal.
637
CHAPTER 33 Adrenals
A B
638
Tumours
A B
Figure 33.11 Phaeochromocytoma. A: Well-defined rounded right adrenal lesion. Note the slightly increased reflectivity of the lesion
compared to the adjacent liver. There is also a small necrotic area (arrow), which is a typical finding in phaeochromocytomas. B: Note how
the lesion (arrow) indents the posterior aspect of the IVC (arrowheads) this is a typical finding with adrenal lesions.
A
B
Figure 33.12 Adrenal cortical carcinoma. A: Large solid right adrenal mass, which is invading
the adjacent liver (arrows). The areas of increased reflectivity within it probably represent
haemorrhage. B: The mass is displacing the right kidney (arrowheads) inferiorly. C: Sagittal CT
C reformat in the same patient confirms liver invasion (arrows) and inferior displacement of the
kidney (arrowhead). 639
CHAPTER 33 Adrenals
A B
Figure 33.13 Neuroblastoma in a child. A: Ultrasound image showing a mixed reflectivity rounded 13cm left adrenal lesion that is
slightly ill defined. A small left pleural effusion is present. B: CT scan in the same patient confirms the mixed attenuation nature of the
lesion and helps in planning subsequent management.
A B
Figure 33.14 Adrenal metastasis. A: Ultrasound imaging revealed a well-defined low reflectivity with central necrotic areas. B: Coronal
CT reformat showing the right adrenal lesion (arrow) with a normal contralateral gland. The primary tumour in this case was unknown.
Ultrasound is useful for assessing the local extent of the primary Ultrasound is particularly valuable in the follow-up of those chil-
tumour and for the detection of liver metastases, although further dren who undergo chemotherapy to monitor the response of the
imaging with CT or MR is performed for initial tumour staging. tumour whilst minimising radiation dose.
Neuroblastomas are typically heterogeneous and predominantly of
high reflectivity although sometimes cystic areas are seen within
the lesion, corresponding to areas of haemorrhage or necrosis (Fig.
Metastases
33.13). Calcification is present in at least 30%.34 The margins of the The adrenal glands are the fourth most common site in the body
tumour are usually ill defined. Neuroblastoma will often cross for metastases after the lungs, liver and bones. Common primaries
the midline and displace the ipsilateral kidney.37 It is important to metastasise to the adrenals include bronchial, renal, colonic and
to delineate the relationship of the mass to the IVC and aorta breast carcinomas in addition to melanoma. The adrenals may also
before surgery is planned as they may be encased by tumour, and be involved with non-Hodgkins lymphoma. Metastases are usually
colour Doppler examination is useful to evaluate their patency. rounded or oval and poorly reflective38,39 (Figs 33.14 and 33.15).
640
Tumours
A B
Figure 33.15 Adrenal metastasis. A: Right adrenal metastasis with central areas of increased reflectivity, likely to reflect haemorrhage.
B: Axial CT image in the same patient confirms the heterogeneous nature of the adrenal metastasis (arrow). The left adrenal is normal in
appearance.
A B
Figure 33.16 Adrenal metastasis. A: Ultrasound image of a huge right adrenal lesion in a patient who had undergone a previous
right nephrectomy for renal cell carcinoma. Note the irregular soft tissue around the periphery and central anechoic necrotic component.
B: Coronal CT reformat in the same patient confirms the presence of a large, predominantly cystic right adrenal lesion (arrow). The left
adrenal is normal (arrowhead). Note the previous right nephrectomy.
641
CHAPTER 33 Adrenals
642
CHAPTER
compromised in women with a raised body mass index. Tissue It is a medicolegal requirement that all ultrasound examinations
harmonics often optimises the images by reducing noise and rever- be reported. Ideally this should be within a radiology information
beration artefact. system (RIS) but failing this a report should be written in the
TV scanning is performed using a 48MHz curved array trans- patients medical records. Similarly all images captured during the
ducer. As such the images are of high resolution with a small field course of a scan should be archived within a picture archiving and
of view. The detail of the endometrium and internal architecture of communication system (PACS). Both these measures serve as a
the ovaries is often exquisite. Thus a TV scan should never be permanent record that an examination has taken place and allow
omitted if the clinical indication suggests gynaecological pathology the ultrasonographer to compare old with new studies. Reporting
and the pelvic anatomy has not been well seen on TA scanning, or and archiving also facilitates audit.
if endometrial pathology is suspected. The bladder should be
emptied prior to a TV scan. It is imperative to explain clearly to the
woman what the examination entails and to obtain verbal consent.
Complete privacy must be guaranteed and a female chaperone PELVIC ANATOMY
should be present. In general women are quite accepting of this
examination technique and are relieved to empty their bladder, par-
ticularly if they have initially undergone a TA scan. When the exami- Skeleton
nation is complete it is mandatory to clean the transducer with an
antimicrobial agent. This is also true of the transabdominal probe The skeleton and attached muscles provide the framework upon
following a TA scan. which the pelvic viscera are supported. Knowledge of them pro-
Both a TA and a TV scan may be necessary to obtain the maximum vides a fuller understanding of pelvic anatomy as a whole. The
amount of information from a single examination. Both techniques articulated hip bone, sacrum and coccyx enclose the pelvic cavity.
lend themselves to guided biopsies, aspirations and drainages. The brim of this cavity, the pelvic brim, is formed by the pubic crest,
the pectineal line of the pubis, the arcuate line of the ilium and the
ala and promontory of the sacrum. The plane of the pelvic brim is
oblique, being 3550 up from the horizontal. It is also known as
the pelvic inlet and is orientated anteriorly. Below the level of the
Transabdominal and transvaginal scanning
pelvic brim is called the true pelvis. The long posterior wall of the
Transabdominal scanning true pelvis is formed by the concavity of the sacrum and coccyx.
Full bladder The short anterior wall consists of the pubic symphysis and the
25MHz curved array transducer bodies of the paired pubic bones and their rami. It is bound laterally
Large field of view by the inner aspects of the quadrangular area of the fused ilium and
Upper abdomen may be assessed ischium (Fig. 34.1). The outlet to the true pelvis faces posteriorly.
The greater pelvis or false pelvis lies above the pelvic brim. It
Transvaginal scanning consists of the paired iliac wings, the inner surfaces of which form
Empty bladder the iliac fossae and the posterior abdominal wall. Anteriorly there
48MHz curved array endovaginal transducer is no bony wall to the greater pelvis. Instead it is formed by the
High resolution, small field of view aponeuroses of the anterolateral abdominal wall muscles and
Verbal consent the rectus abdominis. The cavity of the greater pelvis is effectively
the lower abdominal cavity.1
Sacrum
Inguinal
ligament
Greater
sciatic
Acetabulum foramen Ischial
tuberosity
Obturator Sacro-tuberous
Superior ligament
Pubic rami Pubis Symphysis Ischium foramen
and inferior
Spinal Sacrum Sacrospinous Coccyx Lesser sciatic
A B canal ligament foramen
Figure 34.1 The bony pelvis. A: A frontal view showing the pelvic brim. B: A view from the right of the medial aspect of the left pelvic
bones.
646
Pelvic anatomy
Muscles mobile and their position varies with parity and degree of bladder
and intestinal filling. During pregnancy they are lifted high in the
There are four paired muscles of the true pelvis. The lateral group pelvis, becoming entirely abdominal by the third trimester.
are obturator internus and piriformis. These are also lower limb In the nulliparous woman the ovaries occupy the ovarian fossae
muscles. The medial group are levator ani and coccygeus. These on the pelvic side walls. The upper pole is tilted laterally and is
latter two muscles constitute the pelvic floor and in the midline are overlapped by the infundibulum of the uterine tube. The lower pole
slung around the urethra, vagina and anal canal. These three efflu- is tilted medially towards the uterus to which it is attached by the
ent channels pierce the pelvic floor to enter the perineum. suspensory ligament of the ovary. The ovaries are suspended from
Obturator internus has a broad origin from the body of the the anterior border by a fold of peritoneum, the mesovarium, which
ischium and the obturator membrane which covers most of the attaches it to the broad ligament. The lateral ovarian surface con-
obturator foramen of the ischium. It extends upwards to the pelvic tacts parietal peritoneum behind which lies the angle between the
brim. The fibres of obturator internus converge towards the lesser internal and external iliac vessels, the ureter, obturator vessels and
sciatic notch where they leave the pelvis to attach to the greater nerves and the origin of the uterine artery. Thus the iliac vessels
trochanter of the femur. This muscle is covered by the obturator
fascia. Posterior and superior to obturator internus is piriformis,
which arises from the middle three sacral segments. It runs trans- External iliac
versely to the greater sciatic foramen, exiting the pelvis to attach to Ureter Iliacus m. Psoas m. vessels Tendinous arch
the greater trochanter (Fig. 34.2).
The levator ani consists of three main parts: puborectalis, pubo-
coccygeus and iliococcygeus. Their fibres are continuous and arise
from the body of the pubis, the obturator fascia and the ischial
spine. The muscle fibres run posteroinferiorly to the midline to
insert in the coccyx, the levator raphe and the anococcygeal
ligament.
Coccygeus arises from the ischial spine. From here its fibres fan
out to be inserted into the coccyx and the lowest sacral segment
(Fig. 34.3).
The muscles of the greater pelvis are those of the posterior Ov
abdominal wall, psoas major and iliacus. The psoas muscle arises
from the five lumbar vertebrae. It passes downwards along the
pelvic brim, beneath the inguinal ligament in the groin to attach to
the lesser trochanter. Iliacus arises from the iliac bone and passes
under the inguinal ligament. Its tendon fuses with that of the psoas
muscle to insert into the lesser trochanter2 (Fig. 34.4).
Pelvic viscera
Obturator
Internal iliac vessels Pyriformis m. Coccygeus m. internus m.
The ovaries
Figure 34.2 Left pelvic side wall viewed from the right showing
The ovaries are the paired female sex organs. They are composed the lateral group of muscles of the true pelvis. Coccygeus and the
of fibrous tissue in which ova are embedded. In the embryo and muscles of the false pelvis are also shown. The iliac vessels are
fetus the ovaries are sited in the lumbar region near kidneys and superimposed along with the left ovary in the left ovarian fossa.
gradually descend into the true pelvis. In the adult the ovaries are Note the location of the ureter.
Ala of sacrum
Fascia on
piriformis
Pelvic brim
Coccygeus
Anococcygeal
ligament
Iliococcygeus Obturator internus
fascia
Pubococcygeus
Rectum
Tendinous arch Vagina
Urethra Puborectalis
Figure 34.3 The female pelvic floor viewed from above (modified from Sinnatamby CS, Lasts Anatomy, Regional and Applied,
11th edn, 2006, Churchill Livingstone).
647
CHAPTER 34 Pelvic anatomy and scanning techniques
serve as a useful landmark when trying to locate the ovaries during Blood supply
an ultrasound examination. The medial ovarian surface faces the
uterus and the uterine vessels within the broad ligament (Figs 34.2 The ovarian artery is a branch of the abdominal aorta arising just
and 34.5). below the origin of the renal arteries. It runs down behind perito-
On the right side superolateral to the ovary are the ileocaecal neum in the paracolic gutter and crosses the ureter and psoas
junction, the caecum and the appendix. On the left is the sigmoid muscle. Crossing the pelvic brim the vessel enters the suspensory
colon and rectosigmoid junction. This is important to bear in mind ligament of the ovary to enter the lateral end of the broad ligament
when scanning a woman presenting with iliac fossa pain in terms below the uterine tube. It divides into branches that supply the
of a differential diagnosis.3 ovary, the uterine tube and the skin of the labium majus.
Ovarian veins form a plexus in the mesovarium and suspensory
ligament, draining into paired ovarian veins that accompany the
Psoas Quadratus ovarian artery and drain into the inferior vena cava on the right and
Inferior vena cava Aorta muscle lumborum muscle the renal vein on the left.3
The uterus
Whilst described as midline, the uterus is rarely exactly in the
midline, particularly in parous women. The non-pregnant uterus
has a slit-like cavity and lies within the true pelvis. Superolaterally
the cavity is continuous with the uterine tubes. Inferiorly it leads
into the endocervical canal and on into the vagina. The overall
tubular anatomy may be referred to as the uterovaginal canal.
The uterus is likened to a flattened pear. It is made up of the
fundus, body, isthmus and cervix. The fundus is the broadest com-
ponent and projects above the entry points of the paired uterine
tubes. The bilateral upper angles into which the tubes feed are the
cornua. The uterine body tapers below this to the cervix, the junc-
Iliacus
tion between the body and cervix being the isthmus. The cervix
muscle
projects into the vaginal vault, forming the vaginal fornix; this is
deepest posteriorly.
The uterine body and the posterior surface of the cervix are
enclosed in peritoneum. Laterally this fold of peritoneum becomes
the broad ligament. When anteverted the anterior uterine surface
rests on the bladder and the peritoneal covering reflects off it at the
level of the internal cervical os onto the bladder, forming the vesico-
External iliac Ilio-psoas uterine pouch. The posterior uterine and cervical surface faces
artery and vein muscle upwards, having loops of bowel lying upon it. The peritoneum
reflects off this at the level of the posterior vaginal fornix onto the
Figure 34.4 Frontal view of the pelvis showing the muscles of rectum, forming the recto-uterine pouch or the pouch of Douglas
the false pelvis. The major blood vessels are shown. (Fig. 34.5).
External
Ovarian iliac artery
artery Round
Round Ampulla Isthmus Uterine Bladder Fundus ligament
ligament body of uterus
Ovarian
Suspensory artery
ligament
Ligament
Infundibulum
of ovary
Ovary
Broad ligament
Obturator
internus
Ureter
Isthmus
Uterine artery
Cervix
Recto-uterine pouch
Levator ani
Vault of vagina
Figure 34.5 Coronal view of the female pelvis viewed from behind showing the uterus, tubes, ovaries and related structures. The
broad ligament has been removed on the right side (modified from Sinnatamby CS, Lasts Anatomy, Regional and Applied, 11th edn,
2006, Churchill Livingstone).
648
Technique and ultrasound anatomy
Table 34.1 Variation in uterine size and cervical:fundal ratio with age
The long axis of the uterus relative to the vagina describes uterine brim at 60 to the horizontal. It is an H-shaped slit in the transverse
version while the long axis of the uterine body relative to the cervix plane, its anterior and posterior walls being in apposition. The
describes uterine flexion. The normal position of the long axis of vagina serves as a useful landmark when performing a TA scan.
the uterus relative to the vagina is anteversion but up to 20% of The upper vagina expands to receive the cervix, which projects into
nulliparous females may have a retroverted uterus. it. Surrounding the cervix is the vaginal fornix, which is deepest
The outer uterine layer is the myometrium. It is a fibromuscular posteriorly, and this generally is where the tip of the transducer
layer composed of smooth muscle and connective tissue. There would be positioned when examining the uterus during a TV scan.
is an inner layer of longitudinal smooth muscle and a circular
outer layer.
The innermost uterine layer is a mucous membrane, the
endometrium. This is subject to hormonal influences and cyclical PHYSIOLOGY OF THE FEMALE
changes.4 SEXUAL CYCLE
The variation in uterine size with age, parity and menopausal
status is shown in Table 34.1.57 The size of the uterine body relative The female sexual cycle is often a 28-day cycle but this is variable,
to the cervix is subject to change throughout a females lifetime. In with some women having shorter and others longer cycles. Day one
the neonate the uterus is only slightly smaller than that of a prepu- of the cycle is the first day of menstruation. In a postpubertal female
bertal child. The cervix and fundus are approximately equal in size. the ovarian changes are dependent upon two hormones secreted by
The endometrium is hypertrophied in response to maternal hor- the anterior pituitary gland, follicle-stimulating hormone (FSH) and
mones and is seen as an echogenic bilayer on ultrasound.5 A pre- luteinising hormone (LH). In the first few days of the cycle there is
pubertal cervix is larger than the uterine body and fundus by a ratio a modest increase in FSH and LH levels. This stimulates growth of
of 2:1. Endometrial echoes are absent and only the echogenic 612 primary follicles within the ovary and is called the follicular
midline interface is visible.6 After puberty the fundus enlarges such phase. The follicles grow and secrete oestrogen. After a week or so
that in the reproductive years the cervix to body ratio is 1:2 in nul- of growth one follicle becomes dominant while the others involute.
liparous women and 1:3 in parous women. After the menopause During this time the levels of LH and, to a lesser extent FSH, rise
the uterus atrophies and the ratio becomes 1:1. sharply, stimulating rapid follicular growth, decreasing oestrogen
production and increasing progesterone secretion. A mid-cycle LH
surge promotes ovulation and the follicle ruptures. This would
Uterine tubes occur at day 14 in a regular 28-day cycle. Following ovulation LH
The uterine tubes are approximately 10cm in length and divided causes luteinisation of the ruptured follicle, converting it into the
into four segments. The medial extremity is the short intramural corpus luteum. This is the luteal phase. The corpus luteum secretes
component. It is surrounded by myometrium. Next is a narrow, progesterone and oestrogen, which prepare the endometrium to
straight segment, the isthmus. This lies in the upper edge of the receive a fertilised ovum. If fertilisation does not occur the corpus
broad ligament. Beyond this is the wider ampulla. The lateral luteum, which has a lifespan of around 12 days, involutes. Conse-
extremity is the expanded open end, the infundibulum, which quently progesterone and oestrogen levels fall and menstruation
lies behind the broad ligament adjacent to the pelvic side wall takes place.
(Fig. 34.5). Following menstruation there is a thin residual layer of
endometrium. Rising oestrogen levels cause endometrial regenera-
tion and proliferation, hence this is known as the proliferative
Blood supply phase. The endometrial proliferative phase coincides with the fol-
licular phase of the ovary. After ovulation and the development of
The uterus and tubes receive their blood supply from the uterine the corpus luteum, oestrogen and progesterone levels rise, causing
artery and ovarian artery, branches of the internal iliac artery and further endometrial proliferation and secretory development. This
the aorta, respectively. The uterine artery runs in the base of the is called the secretory phase and it coincides with the ovarian luteal
broad ligament medially to the cervix. Here it gives branches to the phase8 (Fig. 34.6).
upper vagina and cervix. It ascends in the broad ligament giving
off branches to the myometrium and reaches the cornua, where it
turns laterally. It then anastomoses with branches of the ovarian
artery supplying the uterine tube. TECHNIQUE AND ULTRASOUND
The uterine vein follows a similar course to the artery, ultimately ANATOMY
draining into the internal iliac veins.4
structure. The walls are hypoechoic and the apposed anterior and With less caudal angulation the uterus occupies the field of view.
posterior walls produce a hyperechoic midline stripe. In the trans- In the longitudinal plane the hypoechoic myometrium surrounds
verse plane the vagina appears as a flattened rectangle with a the endometrium. The endometrium coats the uterine cavity and
hyperechoic midline stripe. The upper vagina is seen to expand to is generally hyperechoic relative to the myometrium. In the non-
accommodate the cervix (Fig. 34.7). pregnant uterus the cavity is a potential space that is represented
by the echogenic line of the apposed anterior and posterior endome-
trial surfaces.
By turning the transducer 90 the uterus becomes ovoid. The
Ovulation myometrium surrounds the inner oval of the endometrium in the
Follicular phase Luteal phase
body. Angling cephalad towards fundus the endometrium elon-
Proliferative phase Secretory phase
gates as it extends to the cornua. The serosal surface of the uterus
should be smooth (Fig. 34.8).
The position of the ovaries is variable. With the transducer orien-
Anterior pituitary
LH
tated in the transverse plane and the uterine fundus in the centre of
the field of view, if the ovaries are in their usual anatomical location,
each may be visualised next to the iliac vessels and the pelvic side
FSH wall. A degree of angulation to each side may be necessary. Imaging
Ovary
Oestrogen
A B
Figure 34.8 TA scan (A) longitudinal/sagittal and (B) transverse images of the uterus. The serosal surface is smooth (red dot).
The myometrium is homogeneous and hypoechoic relative to the endometrium (white dot). The midline stripe is hyperechoic (yellow dot).
650
Technique and ultrasound anatomy
the ovaries in the longitudinal plane often requires insonating from covered with a clean probe cover containing coupling gel. This is
the contralateral side of the bladder. Thus to image the right ovary also used on the outside surface of the probe cover at its tip. The
the transducer is placed on the skin to the left of the midline on the positioning of the woman must allow the operator to have adequate
lower anterior abdominal wall. It is angled obliquely such that the leverage of the probe handle. This can be achieved in a number of
ultrasound beam passes through the bladder towards the right iliac ways. A useful manoeuvre is to ask the patient to lie supine on the
vessels and pelvic side wall, where the ovary should come into examination couch so that her bottom is right at the foot end of the
view. The opposite is true for the left ovary (Fig. 34.9). couch and her head is at its centre. A chair is placed at a lower level
TA scanning provides an overview of the ovarian position. It is than the couch at the foot end. The woman bends her legs at the
complementary to TV scanning when the ovaries are not in their knees in order that her feet can rest on the chair.
normal anatomical position such as in the pouch of Douglas or The transducer is gently introduced into the vagina and advanced
when they are lifted out of the true pelvis in the presence of an until it meets resistance. At this point the tip is in the posterior
enlarged, fibroid uterus. fornix. In the presence of an anteverted uterus the handle of the
The pelvic musculature is best appreciated on TA scanning. probe often requires lowering towards the floor so that the ultra-
The muscles lie posterior and lateral to the uterus and are depicted sound beam passes through the entire organ. When the uterus is
as well-defined, linear structures of homogeneous, low-level retroverted the handle may require elevation. Once the uterus has
echogenicity. been located and the operator has centred it on the monitor, a fre-
quent mistake of novices to the technique is that of moving the
Transvaginal scanning transducer too quickly and too far. Movements of the transducer
should be small, otherwise the uterus will no longer be in the centre
of the field of view, and slow so that the region of interest is sys-
To master the technique of transvaginal scanning requires practice
tematically interrogated. Individuals with a radiology background
and patience. Prior to scanning a patient, the transducer must be
usually view the image with the apex of the scan sector positioned
at the top of the screen. As such, in anteversion in the sagittal plane
the fundus will be on the left-hand side of the monitor and in ret-
roversion it will be on the right (Fig. 34.10). A perfect, though not
always achievable, sagittal midline image should have an uninter-
rupted echogenic midline stripe. Ideally this should extend from
the fundus to the external cervical os, and represents the apposed
anterior and posterior endometrial and endocervical mucosal sur-
faces. It is from this midline image that endometrial thickness is
measured. It ensures an accurate measurement with no obliquity.
Effectively the two endometrial layers are measured from the ante-
rior interface between the myometrium and endometrium to the
posterior interface (Fig. 34.10). It is entirely normal to have a tiny
volume of fluid in the uterine cavity in pre- and postmenopausal
women. In premenopausal women this may be around the time of
ovulation and during menstruation. If fluid is present, the endome-
trial thickness measurement should not include the fluid. The single
endometrial layers are measured and added together. If it is not
possible to define the echogenic midline stripe within the
endometrium or if the stripe is interrupted, it may be a sign of
pathology within the uterine cavity. Such pathology might include
an endometrial polyp or a polypoid fibroid.
In the sagittal plane it is important to pan from side to side (par-
Figure 34.9 TA scan of right ovary. The image is achieved by asagittal to parasagittal) so that the entire uterus is assessed.
insonating obliquely from the left through the bladder to the right Turning the transducer 90 with the leading edge towards the
pelvic side wall. operator produces a transverse image of the uterus. When the
A B
Figure 34.10 TV scan sagittal midline image of (A) an anteverted uterus with the fundus (red dot) to left and the cervix (yellow dot) to the
right. The callipers are measuring the endometrial thickness. B: The fundus to right in retroversion.
651
CHAPTER 34 Pelvic anatomy and scanning techniques
uterus is anteverted, panning through it from fundus to cervix echo-poor inner layer of inner myometrium. It has been described
requires the probe handle to be gradually elevated from a position as the subendometrial halo and is composed of tightly packed
of relative depression. The opposite is true in retroversion. The muscle cells with an increased vascularity. This myometrial layer
transverse plane allows full assessment of the myometrium from may play a role in stripping the endometrium during menstruation
serosa to endometrial interface. It also allows visualisation of the and promoting sperm transport.10 It corresponds to the junctional
endometrium as it extends out to the cornua (Fig. 34.11). Careful zone of subendometrial myometrium demonstrated on magnetic
attention should be paid here as the cornua are a hysteroscopic resonance imaging11 (Fig. 34.13).
blind spot. The endometrium should be well defined with a smooth, clear
interface between it and the underlying myometrium. In addition,
its echogenicity should be uniform throughout.
During the early proliferative phase of the reproductive cycle the
Ultrasound anatomy endometrium is isoechoic or slightly hyperechoic to the outer myo-
metrium. As this phase progresses, the endometrium develops a
multilayered configuration. Viewing from anterior to posterior,
Uterus adjacent to the inner myometrium, the anterior endometrium
The serosal surface of the uterus is smooth. The myometrium has an outer hyperechoic basal layer. Next is an inner hypoechoic
returns intermediate level homogeneous echoes. Vessels are seen functional layer. This appearance is repeated in the posterior
penetrating the outer myometrium and these correspond to the endometrium, the two being separated by the midline echo repre-
arcuate branches of the uterine circulation9 (Fig. 34.12). There is an senting the apposed anterior and posterior surfaces. This has been
Figure 34.11 TV scan transverse image of the uterus showing a Figure 34.12 Uterus. TV scan sagittal image showing linear
smooth serosal surface (red dot), homogeneous myometrium anechoic structures (red dot) in the periphery of the posterior
(yellow dot) and the endometrium elongating out towards the myometrium. These represent the arcuate branches of the uterine
cornua (green dots). circulation.
A B
Figure 34.13 Uterus. A: TV scan sagittal plane. Retroverted uterus with a hypoechoic subendometrial halo (red dots) representing the
inner myometrium. The callipers are measuring the endometrial thickness. B: T2-weighted midline sagittal magnetic resonance image of
the uterus showing the hypointense subendometrial junctional zone (red dots) of the myometrium.
652
Technique and ultrasound anatomy
Figure 34.14 TV scan sagittal image of an anteverted uterus. Figure 34.15 TV scan midline sagittal image of an anteverted
The endometrium exhibits the multilayered appearance of a uterus. The endometrium is secretory and is uniformly hyperechoic.
proliferative phase endometrium. There is an outer, basal
hyperechoic layer (red dots) and an inner hypoechoic functional
layer (yellow dots). The midline stripe is hyperechoic. This is the
triple line sign.
The ultrasound contrast agent is a positive contrast agent consisting followed laterally to its outer limit where the ovary should be
of microbubbles. The contrast is instilled whilst performing a TV located adjacent to the iliac vessels. By applying gentle pressure on
scan and tubal patency is assessed. The National Institute for Health the skin in the relevant iliac fossa the image of the ovary may
and Clinical Excellence (NICE) recommend HyCoSy as an initial become clearer as bowel loops are displaced. In addition, the ovary
investigation of tubal patency in the assessment of women with is pushed downwards towards the transducer tip. This technique
fertility problems.16 is akin to a gynaecological bimanual examination. Ovaries in
women of reproductive age are generally straightforward to locate
Ovaries because of the presence of anechoic follicles. If an ovary is not in
the expected anatomical location, it may be found in the pouch of
Douglas or around the peripheries of the uterus. When the uterus
Technique is enlarged the ovaries may have been lifted out of the true pelvis
and therefore beyond the range of a TV probe.
A useful technique to localise the ovaries with TV ultrasound is to
position the transducer in the transverse plane at the level of the
uterine fundus. From here follow the endometrium laterally as it Anatomy
extends out towards the cornua. Beyond the cornua it is often pos- Ovarian shape is variable, ranging from almond shaped to spheri-
sible to visualise a hypoechoic, linear structure. This represents the cal. An outer cortex of the ovary contains immature follicles and it
broad ligament and its contents (Fig. 34.17). This should be is here that cyclical changes are observed. During the follicular
phase the follicles grow, appearing as peripheral anechoic struc-
tures. Usually only one will reach 10mm becoming the dominant
follicle (Fig. 34.18). As it matures the dominant follicle may reach
25mm in diameter. Within it, it is possible to depict the cumulus
oophorus, which represents the oocyte surrounded by a cluster of
granulosa cells. It gives rise to a cyst within a cyst appearance and
is a sign of impending ovulation.9 Following ovulation the ovary
enters the luteal phase. The follicle deflates and the wall becomes
irregular.17 This is the corpus luteum, the appearance of which
ranges from a cystic structure with an irregular, echogenic wall to
a cystic structure containing a fine latticework of septations (Fig.
34.19). The variability represents haemorrhage in its different mani-
festations.18 It is normal to see a small volume of free fluid in the
pouch of Douglas following ovulation.
Ovarian volume changes with age, menopausal status, phase of
menstrual cycle and external hormonal influences. It is calculated
using the formula for an ellipse:
A B
Figure 34.18 Ovarian follicle. A: TV scan longitudinal image through the right ovary during the follicular phase. Note the iliac vessels
posterior to the ovary (red dot). B: The dominant follicle.
654
Congenital anomalies of the female genital tract
655
CHAPTER 34 Pelvic anatomy and scanning techniques
A B
Figure 34.20 Uterine arteries. TV scan transverse image through the cervix (red dot) demonstrating (A) the uterine arteries laterally
(yellow dots). B: Uterine arteries with colour flow Doppler. C: Uterine arteries with both colour flow and pulsed wave Doppler. There is a
diastolic notch (white dot) in the pulsed wave Doppler trace.
a Complete b Partial
V Septate VI Arcuate VII DES drug-related
Figure 34.22 Mllerian anomalies: the American Fertility Society classification (reproduced with permission from Fertility and Sterility
1988; 47(6):952).
limitations are in part due to the overlap in the findings of some a haematometrocolpos. A further complication of this is retrograde
anomalies. It should be noted that three-dimensional ultrasound menstruation from the blood-filled uterine cavity down the uterine
has been shown to be superior to conventional two-dimensional tube. As a consequence haematosalpinx, endometriosis and pelvic
ultrasound in the assessment of uterine anomalies. Its superiority adhesions have been described. On ultrasound two separate, diver-
lies in its ability to better delineate the fundal contour and to calcu- gent uterine horns are identifiable with a deep cleft between them.
late uterine volume.23,25 Within these are two separate, non-communicating endometrial
Class I anomalies constitute agenesis or hypoplasia and comprise cavities and two cervices are present23,27 (Fig. 34.23).
510% of MDAs. The hypoplasia may be vaginal, cervical, fundal, The class IV anomaly is the bicornuate uterus, which constitutes
tubal or combined. The ovaries, however, are normal as they are 10% of MDAs. It results from incomplete fusion of the superior
not Mllerian in origin. MayerRokitanskyKusterHauser syn- segments of the uterovaginal canal. There are two symmetrical
drome is the most common variant, comprising complete vaginal uterine horns with an intervening cleft. The horns are most often
agenesis and a 90% association with uterine agenesis. On ultra- fused at the isthmus, giving rise to the bicornuate unicollis uterus.
sound the uterus is absent whilst the ovaries are in their usual In a bicornuate bicollis uterus there is cervical duplication. In both
anatomical location.23 types the two endometrial cavities communicate (Fig. 34.24). There
Class II anomalies comprise the unicornuate uterus and is an increased risk of spontaneous abortion (2835%) and preterm
its variants. These account for 20% of MDAs and result from com- labour (1423%). In addition, this anomaly is associated with the
plete or incomplete development of one of the Mllerian ducts. highest incidence of cervical incompetence in comparison to other
There may be: (a) a communicating rudimentary horn, (b) a non- MDAs. Ultrasonically a large fundal cleft is present and the uterine
communicating rudimentary horn, (c) a rudimentary horn with no horns are widely divergent23,27,28 (Fig. 34.25).
endometrial cavity or (d) no rudimentary horn. A solitary uterine Class V anomalies are most common, comprising 55% of MDAs.
horn accounts for 35% of unicornuate uteri while the remainder The septate uterus results from complete or partial failure of resorp-
have a rudimentary horn. In the presence of a cavitary, non- tion of the midline septum. This anomaly has the highest associa-
communicating rudimentary horn, there is an association with tion with recurrent abortions and premature delivery. The septum
dysmenorrhoea and haematometra at menarche, and also endome- is midline, arising from the fundus. A complete septum extends to
triosis. Women with a class II anomaly can sustain a normal preg- the external cervical os and a partial septum is of variable length.
nancy but there is an increased risk of spontaneous abortion All partial septa contain myometrium, whereas complete septa
(4162%) and premature delivery (1020%). These anomalies are contain myometrium in the upper segment and fibrous tissue in the
not easily recognised ultrasonically. The uterine body in subtype d lower segment. Ultrasonically the fundal contour is flat, convex or
is usually smaller than a normal, nulliparous corpus but this size mildly concave. In the fundal region the septum has a similar echo-
discrepancy may not be noticeable on ultrasound. The corpus may genicity to myometrium and in the presence of a complete septum
appear asymmetric, ellipsoidal and laterally deviated. In the other the caudal portion is hypoechoic23,27,28 (Fig. 34.26).
subtypes the rudimentary horn may be mistaken for an adnexal The class VI anomaly is the arcuate uterus. It differs only slightly
mass.23,2628 from the normal uterine morphology and has no clinically
Class III anomalies are characterised by complete duplication of significant implications. It is characterised by a mild indentation
the uterus and cervix. Uterus didelphys accounts for 5% of MDAs of the endometrium at the fundus due to near complete resorp
and is due to non-fusion of the Mllerian ducts. There is often both tion of the uterovaginal septum. Ultrasonically there is a
a vertical and a transverse vaginal septum. The latter may cause normal fundal contour and smooth indentation of the fundal
obstruction of the ipsilateral vagina and uterus that can give rise to myometrium.23,27
657
CHAPTER 34 Pelvic anatomy and scanning techniques
C D
Figure 34.23 Uterus didelphys. A: TA scan sagittal image of a right haematometrocolpos in a uterus didelphys. The red dot indicates
the haematocolpos and the yellow dot indicates the haematometra. B: Non-distended left uterus with haematocolpos (red dot) still visible.
C: Transverse image of both non-distended, widely divergent, uteri. The black dot indicates the deep cleft between them. This image has
been acquired following excision of a transverse vaginal septum. D: Axial T2-weighted magnetic resonance image showing divergent,
non-distended uteri.
658
References
2. Mundy RA, Healy JC, editors. True pelvis, pelvic floor and perineum.
In: Grays anatomy: the anatomical basis of clinical practice. 39th edn.
Edinburgh: Elsevier Churchill Livingstone; 2005.
3. Ind T, Healy JC, editors. Ovaries. In: Grays anatomy: the anatomical
basis of clinical practice. 39th edn. Edinburgh: Elsevier Churchill
Livingstone; 2005.
4. Ind T, Healy JC, editors. Uterus. In: Grays anatomy: the anatomical
basis of clinical practice. 39th edn. Edinburgh: Elsevier Churchill
Livingstone; 2005.
5. Nussbaum AR, Sanders RC, Douglas Jones M. Neonatal uterine
morphology as seen on real-time US. Radiology 1986;160:641643.
6. Hernanz-Schulman M. Pediatric gynecologic imaging. In: Clinical
gynecologic imaging. Philadelphia: Lippincott-Raven; 1997.
7. Platt JF, Bree RL, Davidson D. Ultrasound of the normal nongravid
uterus: correlation with gross and histopathology. J Clin Ultrasound
1990;18:1519.
8. Guyton AC. Female physiology before pregnancy and the female
hormones. In: Textbook of medical physiology. 8th edn. Philadelphia:
WB Saunders; 1991.
9. Gratton D, Harrington C, Holt SC, Lyons EA. Normal pelvic anatomy
using transvaginal scanning. Obstet Gynecol Clin North Am 1991;18:4.
Figure 34.25 TA scan transverse image demonstrating 10. NICE Clinical Guidelines. Fertility: assessment and treatment for
diverging uterine horns (red dots) in a bicornuate uterus. people with fertility problems. 2004.
11. Fleischer AC, Kepple DM. Normal pelvic anatomy as depicted by
various sonographic techniques. In: Clinical gynaecologic imaging.
Philadelphia: Lippincott-Raven; 1997.
12. Tetlow RL, Richmond I, Manton DJ, et al. Histological analysis of the
uterine junctional zone as seen by transvaginal ultrasound. Ultrasound
Obstet Gynecol 1999;14:188193.
13. Nalaboff KM, Pellerito JS, Ben-Levi E. Imaging the endometrium:
disease and normal variants. Radiographics 2001;21:14091424.
14. Epstein E, Valentin L. Managing women with post-menopausal
bleeding. Best Practice and Research: Clinical Obstetrics and
Gynaecology 2004;18(1):125143.
15. Gupta JK, Chien FW, Voit D, et al. Ultrasonographic endometrial
thickness for diagnosing endometrial pathology in women with
postmenopausal bleeding: a meta-analysis. Acta Obstet Gynaecol
Scand 2002;81:799816.
16. Gull B, Karlsson B, Milsom I, et al. Transvaginal sonography of the
endometrium in a representative sample of postmenopausal women.
Ultrasound Obstet Gynecol 1996;7:322327.
17. Fleischer AC, Vasquez JM, Kepple DM. Transvaginal sonography in
gynaecologic fertility disorders. In: Clinical gynaecologic imaging.
Philadelphia: Lippincott-Raven; 1997.
18. Timor-Tritsch IE. Relevant pelvic anatomy. In: Ultrasound in
gynecology. 2nd edn. Philadelphia: Churchill Livingstone Elsevier;
2007.
19. Cohen HL, Tice HM, Mandel FS. Ovarian volumes measured by US:
Bigger than we think. Radiology 1990;160:641643.
Figure 34.26 TV scan transverse image through uterine body 20. Timor-Tritsch IE. Color Doppler mapping in gynecology. In:
demonstrating a septate uterus with two discrete, echogenic Ultrasound in gynecology. 2nd edn. Philadelphia: Churchill
endometria (red dots) separated by a hypoechoic structure (yellow Livingstone Elsevier; 2007.
dot). This is either a muscular or fibrous septum. 21. Sladkevicius P, Valentin L, Marsal K. Blood flow velocity in the
ovarian and uterine arteries during the normal menstrual cycle.
Ultrasound Obstet Gynecol 1993;3:199208.
22. Scholtes MCW, Wladimiroff JW, van Rijen HJM. Uterine and ovarian
Class VII anomalies represent the consequences of in-utero expo- flow velocity waveforms in the normal menstrual cycle: a transvaginal
sure of the female fetus to diethylstilbesterol (DES). DES is a syn- Doppler study. Fertil Steril 1989;52(6):981985.
thetic oestrogen introduced in 1948 and given to women experiencing 23. Triano RN, McCarthy SM. State of the art: Mullerian duct anomalies:
recurrent spontaneous abortions and premature deliveries up until imaging and clinical issues. Radiology 2004;233:1934.
1971. The structural anomalies described in women who were 24. The American Fertility Society. The American Fertility Society
classification of adnexal adhesions, distal tubal occlusion secondary to
exposed in utero to DES include a hypoplastic uterine cavity, short-
tubal ligation, tubal pregnancies. Mullerian anomalies and intrauterine
ened upper uterine segment, T-shaped uterus, hypoplastic cervix, adhesions. Fertil Steril 1988;49:944955.
transverse septa, circumferential vaginal or cervical ridges, and 25. Wu HM, Hsu CC, Huang KE. Detection of congenital Mullerian duct
cervical hood or collar. Tubal anomalies have also been described anomalies using three dimensional ultrasound. J Clin Ultrasound
including tubal shortening and fimbrial abnormalities. Women 1997;25:487492.
exposed to DES in utero also have an increased risk of developing 26. Brody JM, Koelliker SL, Frishman GN. Unicornuate uterus: imaging
vaginal clear cell carcinoma.23 appearance, associated anomalies and clinical implications. AJR Am J
Roentgenol 1998;171:13411347.
27. Pellerito JS, McCaarthy SM, Doyle MB, et al. Diagnosis of uterine
REFERENCES anomalies: relative accuracy of MR imaging, endovaginal sonography,
and hysterosalpingography. Radiology 1992;183:795800.
1. Newell RLM, Williams A, editors. Pelvic girdle, gluteal region and hip 28. Dykes TM, Siegel C, Dodson W. Imaging of congenital uterine
joint. In: Grays anatomy: the anatomical basis of clinical practice. 39th anomalies: review and self-assessment module. AJR Am J Roentgenol
edn. Edinburgh: Elsevier Churchill Livingstone; 2005. 2007;189(3):S1S10.
659
CHAPTER
Ovaries
Diane DeFriend
35
the menstrual cycle and it is essential to appreciate the range of
NORMAL SIZE AND APPEARANCES 660 normal appearances in order to correctly identify and characterise
Position 660 pathology.
Size 660
Appearances 661
Cyclical variations 661 Position
FUNCTIONAL CYSTS 663
The ovaries are paired, oval structures which usually lie posterola-
Follicular cysts 663
Corpus luteal cysts 663 teral to the uterus, attached to the posterior leaf of the broad liga-
Haemorrhagic cysts 663 ment by a double fold of peritoneum, the mesovarium, which
Paraovarian cysts 664 conveys the ovarian vessels. The ovary usually has a craniocaudal
Peritoneal inclusion cysts 664 axis, with its tubal extremity uppermost, and its uterine extremity
Ovarian remnant syndrome 666 attached to the upper angle of the uterus by the ovarian ligament,
Postmenopausal cysts 666 also known as the round ligament of the ovary. This is continuous
Polycystic ovary syndrome (PCOS) 666 with the round ligament (of the uterus), which extends from the
Hyperreactio luteinalis and ovarian hyperstimulation syndrome 667 uterine cornua to the pelvic wall and crosses forwards to traverse
Theca lutein cysts 667
the inguinal canal and terminate in the labium majus (Fig. 35.1).
Ovarian hyperstimulation syndrome 667
These ligaments are remnants of the fetal gubernaculum and are
OVARIAN TORSION 668 not generally visualised by ultrasound unless outlined by ascites
(Fig. 35.2). The part of the broad ligament extending between the
CHARACTERISATION OF AN ADNEXAL MASS 668
attachment of the mesovarium and the lateral wall of the pelvis is
BENIGN VERSUS MALIGNANT OVARIAN LESIONS 670 sometimes called the suspensory ligament of the ovary.
The ovary usually lies on the peritoneum of the pelvic side wall,
OVARIAN TUMOURS 670
Symptoms 671 in the angle between the internal and external iliac vessels, and its
Classification 671 position anterior to the internal iliac vessels serves as a useful refer-
Epithelial neoplasms 671 ence for its identification (Fig. 35.3). The position of the ovaries may
Serous tumours serous cystadenoma and be variable, however, due to factors such as laxity of the ligaments
cystadenocarcinoma 671 and in practice, a search for the ovaries should be made from the
Mucinous tumours mucinous cystadenoma and pouch of Douglas (Fig. 35.4) to the superolateral aspect of the
cystadenocarcinoma 672 uterus. Previous surgery can also alter the position, and after hys-
Pseudomyxoma peritonei 672 terectomy the ovaries may lie medially, directly superior to the
Endometrioid tumours 673
vaginal vault.1
Clear cell tumours 674
Brenner (transitional cell) tumours 674
Germ cell tumours 674 Size
Mature teratoma (dermoid) 674
Immature teratomas 676 The ovaries vary in size according to age and also in relation to the
Dysgerminomas 676
stage of the menstrual cycle.
Yolk sac tumours (endodermal sinus tumours) 676
Sex cord stromal tumours 677
Ovarian volume is considered to be the best method for deter-
Granulosa cell tumours 677 mining ovarian size. The volume of the ovary can be calculated
Fibromas/thecomas 678 using the formula, length width anteroposterior diameter
SertoliLeydig cell tumours (androblastoma) 678 0.523 (i.e. the formula for a prolate ellipse).
Metastatic tumours 678 The reported normal range of ovarian volumes for adult men-
Lymphoma 680 struating females has varied between series. This may reflect a
Screening 680 number of factors, such as the scan technique used (transabdominal
ENDOMETRIOSIS 680 versus transvaginal) and the different populations studied (asymp-
tomatic versus symptomatic). Furthermore, fluctuation in ovarian
PELVIC INFLAMMATORY DISEASE 682 size throughout the menstrual cycle makes defining normal ovarian
volumes difficult. Merz et al. recorded a mean ovarian volume of
78cm3 with a standard deviation of approximately 2.5 in pre-
menopausal women using transvaginal ultrasound.2
In postmenopausal women, ovarian size depends on the time
NORMAL SIZE AND APPEARANCES since the menopause, with a number of studies showing that
ovarian volume decreases with increasing time elapsed.2,3 Tepper
Despite technological advances in other imaging techniques, ultra- et al. have established normal values for ovarian volume, according
sound remains the initial investigation of choice for evaluation of to menopausal age, in healthy postmenopausal women and found
the ovaries. The ovaries vary in appearance in relation to age and that mean ovarian volume decreased from 8.6cm3, in the first year
660
Normal size and appearances
Ovary
Suspensory ligament
of the ovary
Broad ligament
Ovarian ligament of uterus
(Round ligament
of ovary)
B
A
Figure 35.1 A: Diagram showing the uterus and ovaries and their related ligaments. B: Left adnexa. Transverse, transvaginal ultrasound
image, demonstrating the superior aspect of the broad ligament (arrowheads), and the left ovary (arrows).
post menopause, to 2.2cm3, after 15 years (Table 35.1).3 Tepper, in relatively homogeneous echotexture. The follicles, which help in
association with others, has also tried to determine whether differ- the identification of the ovary, are seen as echo-free areas, predomi-
ent ovarian volume cut-off values can distinguish between normal, nantly in the cortex, while the central medulla is more echogenic.
benign and malignant lesions in postmenopausal women. In a The size of the follicles varies with the stage of the menstrual cycle
study of 362 postmenopausal women prior to gynaecological and with age, and in practice, the postmenopausal ovary is harder
surgery, an ovarian volume of less than 8cm3 had a 100% negative to find because of its small size and the fact that it contains fewer
predictive value for ovarian cancer. They concluded, however, that or no follicles (Fig. 35.5). Ability to visualise both ovaries in post-
it was not possible to define a cutoff value to distinguish between menopausal women with transvaginal scanning has been reported
benign and malignant lesions and that any enlarged ovary, >8cm3, to be possible in between 60% and 97% cases.2,3 However, if a thor-
in a postmenopausal woman may contain a malignancy.4 ough examination with a transvaginal probe fails to identify a post-
menopausal ovary it is unlikely that a significant pathology will
remain undetected.
Appearances
The ovary consists of a fibrous stroma covered by a single layer of Cyclical variations
cuboidal epithelium. The tunica albuginea is a layer of fibrous tissue
immediately deep to the epithelium. The stroma is made up of a The appearance of the premenopausal ovary varies in response to
peripheral cortex and central medulla. The cortex contains numer- the gonadotrophic hormones, follicule-stimulating hormone (FSH)
ous follicles, which contain female gametes in various stages of and luteinising hormone (LH) secreted by the anterior pituitary.
development, while the central medulla is highly vascular and Three phases of the ovarian cycle are recognised ultrasonically, the
contains few follicles. Ultrasonically the normal ovary is of follicular phase, ovulation and the luteal phase.
661
CHAPTER 35 Ovaries
A B
Figure 35.3 Position of the ovary in relation to the iliac vessels. A: Transvaginal scan showing the position of a normal ovary
(arrowhead) anterior to the iliac vessels (arrow). B: Transabdominal scan showing a normal ovary (O) visualised between the internal and
external iliac vessels.
Figure 35.4 Transvaginal image showing a normal ovary Figure 35.6 Transvaginal image of an ovary, containing a
(arrow), lying within the pouch of Douglas. dominant follicle (arrow), in the follicular phase of the ovarian cycle.
The follicular phase begins on the first day of menses and con-
tinues to ovulation, 1014 days later. During the follicular phase,
the ovaries contain several immature follicles, typically less than
1cm, with a dominant follicle becoming evident by day 812 (Fig.
35.6). The dominant follicle reaches a pre-ovulation, mean diameter
of between 2023mm.
There are no reproducible sonographic signs which reliably
predict ovulation, but a cumulus oophorus may be seen, as an
eccentric, echogenic or cyst-like mural protrusion, 1224 hours
prior to ovulation. Some fluid may be present in the pouch of
Douglas, particularly after ovulation, with the fluid formed pre-
dominantly from the active ovary.
In the luteal phase, a corpus luteum, which forms from the rup-
tured follicle, can be seen in most cases. The function of the corpus
luteum is to produce hormones to support the early pregnancy
prior to the placenta taking over. The corpus luteum may have a
varied appearance on ultrasound, reflecting its maturation and
involution. It may appear hypoechoic with thick walls. Haemor-
rhage is common and it often appears as an irregular or crenated
Figure 35.5 Transvaginal image showing a normal cyst with low-level echoes and circumferential flow (Fig. 35.7A, B).
postmenopausal ovary (arrow). The ovary lies adjacent to bowel, In the absence of fertilisation, the corpus luteum begins to undergo
which is causing acoustic shadowing. involution and is eventually replaced by scar tissue to form a corpus
662
Functional cysts
A B
Figure 35.7 Corpus luteum. Transvaginal images showing (A) characteristic appearance of a crenated cyst (callipers) with internal
echoes, (B) characteristic circumferential flow, and (C) the endometrium in the secretory phase of the cycle (callipers) of the same patient.
The presence of a corpus luteum should correlate with an endometrium in the secretory phase.
FUNCTIONAL CYSTS
Follicular cysts
The development of physiological follicles is a normal function of
the ovary. Follicular cysts occur as a result of failure of ovulation, Figure 35.8 Transabdominal ultrasound image of a simple
or failure of involution of a mature follicle. They are commonly seen ovarian cyst (arrow), which contains anechoic fluid, has an
at ultrasound, although their true incidence is unknown, as they are imperceptible wall and shows posterior acoustic enhancement
often asymptomatic. Most follicles are small, but as they mature can (arrowhead).
reach sizes of 2.53.0cm. The term follicular cyst should therefore
be reserved for cystic structures greater than this size, which can
become as large as 20cm. The typical appearance is of a unilocular the corpus luteum. They are prone to haemorrhage and rupture,
cyst with no internal echoes, a thin smooth wall, and posterior tending to be more symptomatic than follicular cysts, and patients
acoustic enhancement. Follicular cysts are often detected inciden- often present with pain. Complex luteal cysts can mimic malignant
tally and usually regress spontaneously (Fig. 35.8). lesions and follow-up may be required to ensure resolution.
A B
Figure 35.12 A and B: Clot retraction in haemorrhagic cysts. The clot in each of these haemorrhagic cysts has a concave margin
(arrowhead), helping to distinguish it from a mural nodule.
Figure 35.13 Transvaginal ultrasound image of a Figure 35.15 Transvaginal ultrasound image shows a cystic
haemorrhagic cyst (arrow). This contains apparent septa due to lesion (arrow) separate from the right ovary (arrowhead), which was
clot retraction but these resolved on follow-up imaging. proven at histology to be a paraovarian cyst.
Ultrasonic appearances
Peritoneal inclusion cysts typically appear as multicystic, adnexal
masses (Fig. 35.16). They are extra-ovarian, with fluid surrounding
the ovary, without involvement of the parenchyma, and a key
feature for their diagnosis is the presence of a normal, albeit some-
times distorted, ovary surrounded by septa and fluid. The ovary is
not always identified, however, and may lie within the periphery
Figure 35.14 Haemorrhagic cyst with clot retraction. The of the cyst.13,14 The walls of the cyst are formed by adjacent pelvic
internal echoes give the appearance of a thick wall and a septum structures and acute angular margins are a characteristic feature.
(arrow), but these echoes showed movement on real-time scanning, The differential diagnosis includes a paraovarian cyst or a hydros-
did not show colour flow and resolved on follow-up imaging. alpinx.13 Occasionally the entrapped ovary can be mistaken for a
solid nodule, and dense adhesions may form thick septa, which
may show vascularity, making distinction from an ovarian tumour
represent an accumulation of fluid, produced by the ovary, which difficult. A recent prospective study reports the sensitivity of trans-
fails to be resorbed by abnormal peritoneum and becomes con- vaginal sonography in the diagnosis of peritoneal inclusion cysts as
tained by peritoneal adhesions. Their formation requires a function- 62%, with a specificity of 96%.12 A stable appearance on follow-up
ing ovary and the presence of adhesions, and they therefore imaging, and the use of other imaging techniques, such as magnetic
occur predominantly in premenopausal women with a history of resonance imaging (MRI), may be helpful.
665
CHAPTER 35 Ovaries
A single polycystic ovary is sufficient for the diagnosis, but if other conditions resulting in high levels of hCG, such as multiple
there is a follicle more than 10mm in diameter, the scan should be pregnancy. It has also been recorded with otherwise normal
repeated at a time of ovarian inactivity. A peripheral distribution pregnancies.
of follicles and bright ovarian stroma are no longer required for the This condition is usually asymptomatic or presents with mild
diagnosis. Other factors regarding optimal technique for scanning abdominal symptoms. Ultrasound features are of bilaterally, or
are outlined in the guidelines and include that: rarely unilaterally, enlarged ovaries which range in size from 3 to
n the transvaginal route should be used wherever possible, 20cm. Multiple cysts and minimal stroma are said to give a spoke
particularly with obese women wheel appearance.24 Rarely, haemorrhage may occur into the cysts.
n the scan should ideally be performed in the first 3 days of the Torsion or rupture can also occur and presentation in such cases is
menstrual cycle, if practical, or at random if there is oligo- or with acute pain. Ascites and pleural effusions are rare, although
amenorrhoea they may be seen in severe cases. Maternal virilisation is an associ-
n the number of follicles should be estimated in both the ated finding in approximately 25% patients.24
longitudinal and anteroposterior cross-sections of the ovary
n the size of follicles less than 10mm should be expressed as
the mean of the diameters measured on two sections. Ovarian hyperstimulation syndrome
It should be stressed that an ultrasound finding of a polycystic Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic
ovary is not by itself diagnostic of PCOS, which is a syndrome and form of HL, following ovulation induction for the treatment of
requires the additional features described.23 Likewise, if the clinical infertility. In addition to the enlarged ovaries (Fig. 35.20), this syn-
and biochemical features are present, an ultrasound is not required drome is characterised by ascites and pleural effusions. Systemic
for the diagnosis. It is believed that 20% of women with polycystic effects are thought to be due to vasoactive products released
ovaries have no symptoms.22 While the previous criteria did not from hyperstimulated ovaries. In severe cases there may be marked
include ovarian appearance, some are concerned that the ultra- fluid shifts with development of renal or liver dysfunction,
sound criteria in the new definition are too broad. This could result acute respiratory distress syndrome (ARDS) and thrombotic
in a low specificity with multifollicular ovaries being considered complications.25
polycystic ovaries.23 Most cases of severe ovarian hyperstimulation syndrome are
The incidental discovery of a polycystic ovary can be an impor- seen following IVF treatment, but the condition can occur following
tant finding to report. For example, in women with ovulatory infer- any supraphysiological ovarian stimulation, including gonado-
tility, where PCOS is not the cause, the presence of a polycystic trophin ovulation induction and also, albeit rarely, with clomiphene
ovary increases the risk of hyperstimulation syndrome if drugs are alone.25 Mild forms of the syndrome are common, affecting up to
administered to stimulate the ovaries for assisted conception.22 33% of IVF cycles, but only 38% of IVF cycles are complicated by
moderate or severe OHSS. Young lean women and those with poly-
Hyperreactio luteinalis and ovarian cystic ovaries are supposedly at increased risk and the severity is
increased in cycles where conception occurs.
hyperstimulation syndrome OHSS has rarely been reported to occur in spontaneously con-
ceived pregnancies.24 In these cases it may be difficult to distinguish
severe HL from spontaneous OHSS. Whilst some authors distin-
Theca lutein cysts guish the two on the basis of aetiology and clinical course, others
These are the largest of the functional cysts, and they result from view the conditions as a continuum.24 In practice, the distinction is
excessive stimulation by gonadotrophins. They are seen primarily not important clinically as the treatment is the same.
in patients with trophoblastic disease or as a result of iatrogenic OHSS has been classified according to severity, into mild, moder-
administration of human chorionic gonadotrophin (hCG) for the ate, severe and critical grades.26 In mild cases the ovaries usually
treatment of infertility. measure less than 8cm in association with mild abdominal symp-
Hyperreactio luteinalis (HL) and ovarian hyperstimulation syn- toms, while in moderate cases the ovaries are larger, between 8 and
drome (OHSS) are both rare conditions during pregnancy. HL 12cm, with ultrasonic evidence of ascites. Severe disease is charac-
occurs during a spontaneous pregnancy and is characterised by terised by clinical ascites, with the ovaries often over 12cm in size.
the presence of multiple luteinised cysts secondary to hyperstimu- With critical OHSS there may be tense ascites or a large hydrotho-
lation by hCG or increased sensitivity to hCG. HL occurs most rax, thromboembolic episodes and ARDS. Paracentesis may be
commonly with hydatidiform mole or choriocarcinoma as well as helpful for the relief of symptoms and should be performed under
667
CHAPTER 35 Ovaries
ultrasound guidance to avoid inadvertent puncture of the enlarged absence or abnormality of venous and/or arterial flow in associa-
ovaries. tion with torsion,34 with some authors reporting the positive predic-
tive value for torsion in the absence of venous flow as 94%.36
However, others have shown normal arterial or arterial and venous
flow in proven cases of torsion,27 thought to be explained by either
OVARIAN TORSION incomplete or intermittent torsion, or the presence of a dual arterial
blood supply to the ovary (Fig. 35.22). Some have described a
Adnexal torsion is the partial or complete rotation of the ovarian twisted vascular pedicle as a feature suggestive of ovarian torsion,37
pedicle on its long axis. It usually involves both the ovary and although this is not a specific finding. A more recent study has
tube27,28 and, if persistent, can result in infarction of the adnexal documented the sonographic whirlpool sign, i.e. the presence of
structures. Early intervention is important to attempt to preserve hypoechoic vessels around the central axis of the twisted pedicle
the ovary, but diagnosis is often difficult with both the clinical seen on greyscale imaging, as a more specific sign of ovarian
symptoms and signs and imaging features being non-specific. torsion, with evidence of colour flow within this whirlpool of
Adnexal torsion has a prevalence of 2.7%.29 It occurs predomi- vessels an indicator of viability of the ovary.31 Whilst the presence
nantly in women of reproductive age or younger, and a pre-existing of this sign may be a good predictor of torsion, there is no indica-
ovarian lesion is common.30 Underlying lesions are usually benign, tion, in this study, as to how often cases of torsion are likely to
with teratoma being the most commonly reported, although under- demonstrate this feature.
lying malignancy has been described. Torsion in the absence of an A recent retrospective review of 39 patients with proven torsion
underlying condition is thought to be more common in children, found that abdominal pain, vomiting, ovarian enlargement and
where the adnexal structures are more mobile. When torsion occurs absence of venous flow were the most common associations with
in postmenopausal women there is a higher incidence of an under- torsion. However, ovarian enlargement, even in the presence of
lying lesion.27 Other predisposing factors for torsion include preg- arterial and venous flow, is the most commonly associated ultra-
nancy and ovulation induction. The right ovary is reported to be sound finding. The authors conclude that suspicion for torsion
affected more frequently than the left in some series,29,30 possibly should be high if a patient presents with the appropriate clinical
related to the position of the colon on the left side. symptoms and ovarian enlargement, regardless of the presence or
The most common clinical presentation of torsion is acute onset absence of flow. In these cases surgical exploration should not be
of severe abdominal or pelvic pain often localised to a lower quad- delayed.35
rant. Associated symptoms and signs include nausea and vomiting,
leucocytosis and fever. A palpable abdominal mass may be present.27
The absence of additional symptoms and signs does not, however,
exclude the diagnosis. CHARACTERISATION OF
The appearances of ovarian torsion are variable depending on AN ADNEXAL MASS
whether it is partial or complete and on the presence or absence of
a pre-existing mass. The most common sonographic finding is Adnexal masses are a common clinical problem, with many women
enlargement of the ovary or the presence of an adnexal mass, which undergoing surgery for suspicious masses, the majority of which
may be cystic, solid or complex and which often reflects the under- turn out to be benign. Ultrasound is usually the first-line investiga-
lying lesion (Fig. 35.21). Pelvic fluid is frequently an associated tion for evaluation of a suspected adnexal mass. It has high sensitiv-
finding.31 Previous reports suggest that the presence of multiple, ity for the detection of pelvic masses and for confirming that a mass
small, peripheral follicles in a unilaterally enlarged ovary is a spe- is of ovarian as opposed to uterine origin, as well as excluding other
cific finding for torsion,32,33 although other authors have failed to pathologies such as bowel-related lesions.
confirm this.34 A recent review suggests that the only consistent The distinction from fibroids can be a particular problem, and not
greyscale finding in torsion is enlargement of the ovary or ovary uncommonly a pedunculated or broad ligament fibroid may mimic
mass complex and that other previously described findings, such an ovarian lesion or vice versa, especially where degeneration of a
as ground glass and cystic changes, are nonspecific.35 fibroid alters the characteristic ultrasonic appearances. In these
Various colour Doppler findings in torsion have been described instances, full assessment, often including further imaging with
but these are often conflicting. A number of studies have reported MRI, is appropriate.
A B
Figure 35.21 Two examples of pathologically proven torsion. A: No underlying cause could be identified. B: Torsion of a cystic
epithelial tumour resulting in infarction. Both cases were associated with free fluid.
668
Characterisation of an adnexal mass
A B
Figure 35.22 Surgically proven torsion of the ovary and tube. A: The enlarged ovary (arrow) shows peripheral follicles. B: Colour
Doppler images show flow within the ovary and arterial flow is demonstrated with spectral Doppler.
Clinical assessment
CA125 assay
US
Image-guided
core biopsy
Figure 35.23 Pathway of imaging and intervention for suspected ovarian cancer. (Redrawn with permission from Investigating women
with suspected ovarian cancer. Spencer JA et al. Gynecologic Oncology 108 (2008) 263. Elsevier.)
Ultrasound also has an important role in characterisation of an Where clinical findings, ultrasound and CA125 levels suggest a
ovarian lesion, in order to inform decisions regarding treatment. benign lesion, follow-up imaging with ultrasound is recommended
The most important distinction is between a non-neoplastic or if symptoms do not require immediate surgery.
benign lesion as opposed to an ovarian cancer. Optimal surgical If they suggest a malignant lesion, either surgical staging or com-
resection for ovarian cancer includes radical hysterectomy, bilateral puted tomography (CT) is generally performed. CT is increasingly
oophorectomy and omentectomy with lymph node sampling, and used to assess the extent of disease and suitability for surgery. In
best results are obtained when such extensive surgery is performed addition, CT can help to exclude other primary sites of tumour such
by specialist gynaecologists in cancer centres.38 In benign or border- as gastric or colonic carcinoma, which can mimic the appearance of
line malignant lesions more limited surgery, such as cystectomy or ovarian cancer with peritoneal disease and ovarian masses. While
oophorectomy, may be appropriate and laparoscopic techniques MRI is superior to CT in assessing local spread of disease and is
may be an option. Optimal characterisation of lesions is therefore probably at least equivalent in terms of staging ovarian cancer, the
important in order to allow appropriate subspecialty referral, avoid limited availability of this technique means that CT remains the
inadequate surgery in malignant disease and likewise avoid inap- primary imaging modality for staging.
propriate radical surgery for benign lesions. Where patients are considered for neoadjuvant chemotherapy,
Whilst ultrasound is useful in the characterisation of an ovarian both ultrasound and CT may be helpful in guiding biopsy to obtain
mass, its limited specificity means that a number of lesions will histology prior to treatment. While it may be appropriate to obtain
remain indeterminate. A combination of clinical information (espe- histology for advanced tumours, biopsy is contraindicated for local-
cially age and menopausal status), ultrasound features and tumour ised ovarian cancer, because of the potential to seed tumour and
markers can be used to make decisions regarding further imaging upstage the disease.
or treatment strategies, with these decisions now generally made in Indeterminate lesions with equivocal or contradictory findings
the setting of the multidisciplinary team meeting (MDT). on US, clinical examination and CA125 are best evaluated with
669
CHAPTER 35 Ovaries
A B
Figure 35.24 Benign serous cystadenoma. Transvaginal images showing (A) a thin-walled loculated lesion with hypoechic fluid. The
septa are thin. B: A unilocular cyst with echo-free fluid and a small papillary nodule (arrow).
As
proportion of
Tumour all ovarian
type tumours Classification
Epithelial 6570% Serous cystadenoma/
carcinoma
Mucinous cystadenoma/
carcinoma
Endometrioid carcinoma
Clear cell carcinoma
Brenner tumour
Germ cell 1520% Mature teratoma/dermoid
Immature teratoma
Dysgerminoma
Yolk sac tumour Figure 35.25 Serous cystadenocarcinoma. Transvaginal image
shows a cystic lesion with prominent soft tissue elements (arrow).
Sex cord 510% Granulosa cell tumour
stromal SertoliLeydig cell tumour Colour flow was seen centrally within the soft tissue on Doppler
Fibroma imaging.
Thecoma
Metastatic 510%
tumours
malignant ovarian neoplasms (85%) are of the epithelial type.51
There is also a borderline category, otherwise known as tumours
of low malignant potential. These tumours have cytological fea-
Symptoms tures of malignancy but show no evidence of stromal invasion.51
They are found in younger patients and have a better prognosis
Symptoms of ovarian cancer are usually non-specific and patients than their malignant counterparts.
may present with a palpable mass, abdominal pain or distension,
weight loss or vague gastrointestinal symptoms. Hormonal activity
may be associated with the sex cord stromal tumours but is rarely Serous tumours serous cystadenoma and
associated with epithelial tumours, with the exception of some cystadenocarcinoma
endometrioid tumours.
Serous tumours are the commonest type of epithelial neoplasms,
Classification comprising 30% of all ovarian neoplasms. Approximately 60% are
benign, 25% malignant and 15% are classified as borderline or of
low malignant potential.51 Serous cystadenocarcinomas represent
Ovarian tumours may be primary or metastatic. They are classified
about 40% of malignant ovarian tumours. Cystadenomas have a
on the basis of cell origin as epithelial, germ cell and sex cord
peak incidence in women aged between 30 and 40 years, whereas
stromal tumours (Table 35.2). While it is not the role of ultrasound
cystadenocarcinomas are more common in perimenopausal and
to characterise tumours on a histological basis, imaging features
postmenopausal women. Approximately 20% of benign, but 50% of
may sometimes suggest a tumour subtype.
malignant serous tumours are bilateral.51
Ultrasonically, these tumours reflect their macroscopic appear-
Epithelial neoplasms ance. They are predominantly cystic and may be either unilocular
or multilocular with thin septa in the benign types (Fig. 35.24A).
Epithelial tumours are the most common type of ovarian neoplasm They contain largely echo-free, serous fluid. These tumours are
(Table 35.2). The majority of them are benign although most characterised by papillary projections and their presence is the
671
CHAPTER 35 Ovaries
A B
Figure 35.31 Pseudomyxoma peritonei. Transverse transabdominal ultrasound image (A) and axial contrast-enhanced CT scan
(B) showing bilateral mucinous ovarian tumours (arrows). Mucinous ascites was present. A low-grade primary mucinous tumour of the
appendix was identified at surgery and histology.
673
CHAPTER 35 Ovaries
Figure 35.33 Clear cell tumour. Transvaginal image showing a Figure 35.34 Brenner tumour in association with a mucinous
cystic lesion with peripheral, solid areas (arrow). These appearances cystadenoma. There is a complex cystic lesion with a solid area
are non-specific. (arrows), which represents the Brenner tumour. These appearances
are non-specific and the Brenner tumour was only identified
histologically.
A B
Figure 35.38 Transvaginal images showing examples of dermoid mesh. A: A dermoid cyst (arrow), with multiple linear
hyperechogenic interfaces or dermoid mesh which is thought to be due to hair fibres. B: A dermoid cyst with echogenic lines and dots
(dermoid mesh) in association with an echogenic nodule, which shows the tip of the iceberg sign.
A B
Figure 35.40 Dermoid cyst. Transvaginal scan (A) shows an echogenic dermoid (arrow) on the left side, which was difficult to distinguish
from bowel. CT scan (B) in the same patient confirms the presence of a fat containing lesion (arrow), which is diagnostic of a dermoid.
MRI, which does not involve ionising radiation, is now the most commonly used imaging modality to further evaluate a suspected dermoid.
(Fig. 35.40) and small, echogenic dermoids may be mistaken for Dysgerminomas
haemorrhagic lesions. Finally, a large dermoid may be identified
but not recognised if some of its borders are obscured, on account Dysgerminomas represent 12% of ovarian neoplasms. They are
of the limited field of view afforded by transvaginal sonography. malignant germ cell tumours, which resemble seminomas and are
This emphasises the importance of including a transabdominal scan most common under 30 years of age. They are usually solid tumours
for pelvic imaging, which is particularly important when a pelvic and are predominantly unilateral.57 They may be associated with
mass can be palpated but not visualised on transvaginal views. elevated serum hCG levels.
Further imaging relies on identification of fat, for which MRI is
now the most widely used imaging modality. Fat appears as high
signal on T1-weighted MRI sequences and shows suppression on Yolk sac tumours (endodermal sinus tumours)
fat saturation sequences. This allows distinction from haemorrhage These are rare malignant tumours, which occur mainly in
and confirmation of the diagnosis of a dermoid (Fig. 35.41). children or young women. At ultrasound they are predominantly
Although CT imaging also allows identification of fat (Fig. 35.40), echogenic, solid masses57 but can contain cystic and solid
it has the disadvantage of using ionising radiation. elements.56 These tumours are associated with an elevated alpha-
Complications of dermoids include torsion, rupture and rarely fetoprotein level.
malignant change. Torsion is the most frequent complication and
is reportedly more common in pregnancy. Large dermoids are
usually removed to prevent torsion. Rupture occurs rarely in
approximately 1%. Malignant change is also rare, occurring in 12%
of cases, with squamous carcinoma being the most common malig-
nancy to develop.57 Malignant transformation usually occurs in Sonographic features of a dermoid cyst (teratoma)
older women and may be recognised by the presence of enhancing The sonographic appearance of dermoids is highly variable. Charac-
nodules on MRI. teristic appearances include:
focal or diffuse high-amplitude echoes that attenuate the acoustic
Immature teratomas beam
echogenic mural nodule, often with acoustic shadowing
Immature teratomas represent less than 1% of all teratomas. They dermoid plug
are rapidly growing malignant tumours, and are most common in tip of the iceberg sign acoustic shadowing posterior to an
the first two decades of life. echogenic focus that obscures the posterior border of the lesion
They tend to be unilateral and are predominantly solid or hyperechoic lines and dots dermoid mesh
have prominent solid elements within a cyst at ultrasound fatfluid levels.
examination.54,57
676
Ovarian tumours
A B
C D
Figure 35.41 Dermoid. Sagittal T1-weighted (A) and T2-weighted (B) MR images and axial T1-weighted (C) and fat suppression
sequences (D). These show a cystic lesion with a fluid level and a central nodule (B, arrowhead). On the sagittal images (A and B) the fat
is high signal on the T1-weighted image (A, white arrow) and intermediate signal on the T2-weighted image (B, white arrow). The signal
intensity is equivalent to subcutaneous fat on both sequences. On the axial images (C and D) the high signal intensity fat (C, white arrow)
on the T1-weighted images shows fat suppression (D, white arrow), confirming the presence of a dermoid. (Williams P & DeFriend D.
Techniques in Gynaecological Imaging: Non Ultrasound Techniques. Radiology Integrated Training Initiative 2010: e-learning session
46_00036. Royal College of Radiologists, London).
Sex cord stromal tumours endometrial hyperplasia73 and up to 25% of patients will have
endometrial carcinoma.72 Granulosa cell tumours can occasionally
Sex cord stromal tumours are derived from the sex cords and spe- be androgenic and present with virilisation.54 They vary in size at
cialised stroma of the developing gonad. They represent 510% of presentation, with hormonally active tumours tending to present
ovarian neoplasms and approximately 2% of malignant ovarian with a smaller size.72 In contrast to epithelial tumours, more than
neoplasms. They include granulosa cell tumours, fibromas, theco- 90% of granulosa cell tumours are confined to the ovary at presenta-
mas/fibrothecomas and SertoliLeydig cell tumours. tion and hence have a better prognosis.72
Ultrasonically the appearances are non-specific and granulosa
Granulosa cell tumours cell tumours may present as large multilocular cystic masses with
solid components or as solid tumours72,73 (Fig. 35.42). A more recent
Granulosa cell tumours are rare, accounting for 3% of all ovarian study suggests two typical patterns: (i) a solid mass with heteroge-
malignancies, but are the most common malignant sex cord stromal neous echogenicity of the solid tissue or (ii) a multilocular-solid
tumour. They include adult granulosa cell and juvenile granulosa mass with large solid areas but only rarely papillary projections.74
cell tumours, with only the former discussed here. Adult granulosa It is reported that the virilising type are more commonly cystic.72
cell tumours occur predominantly in perimenopausal or postmeno- Granulosa cell tumours have a propensity to rupture and up to 15%
pausal women, are unilateral in 95% cases and are generally of may present with haemoperitoneum.54
low-grade malignancy. They are the most common oestrogen- MRI may show more specific features, with high signal on
producing tumour, and manifest clinically as irregular bleeding in T1-weighted imaging reflecting their propensity for haemorrhage
premenopausal women or as postmenopausal bleeding.72 Approxi- and T2-weighted imaging showing a characteristic sponge-like
mately one-third of women with granulosa cell tumours will have appearance.54,72
677
CHAPTER 35 Ovaries
A B
Figure 35.42 Granulosa cell tumour. Transvaginal scan of the left adnexa (A) and uterus (B) in a 62-year-old woman with
postmenopausal bleeding. A: The left ovary (arrow) was enlarged as compared to the right and appeared to contain a solid mass.
B: There is marked endometrial thickening (between callipers). Histology showed a granulosa cell tumour of the ovary and the endometrial
thickening was shown to be endometrial hyperplasia. Granulosa cell tumours vary in size at presentation, with hormonally active tumours
tending to present with a smaller size.
A B
Figure 35.44 Fibrothecoma. Transvaginal ultrasound images (A, B) show an 8cm solid lesion in a postmenopausal woman (A). This
was proven to be a fibrothecoma at histology. There was associated endometrial thickening (B, between callipers).
between them in terms of solidity, and although secondary neo- most common primary site, may also produce solid tumours, but
plasms were more often bilateral than primary neoplasms, this was often produce cystic metastases similar to primary ovarian tumours.
not a significant finding. The only statistically significant feature on In support of this concept, Testa et al. have recently shown that
ultrasound was multilocularity, which was more common in ultrasound features of metastases differ depending on the origin of
primary malignancy.78 Alcazar also found no difference in terms of the primary. They found that metastases from stomach, breast,
bilaterality, but metastatic tumours were significantly more often, lymphoma or uterus were mostly solid while those from the colon,
purely or predominantly solid.79 Overall they conclude that no rectum, appendix or biliary tract were more heterogeneous with a
imaging feature is highly accurate in distinguishing primary from multilocular appearance, with or without solid elements85 (Fig.
secondary tumours. 35.46). A number of authors have acknowledged the difficulties in
These conflicting results may be partly explained by the different distinguishing between primary and secondary tumours. In prac-
primary tumours studied. Pathological studies have shown that tice the presence of bilateral or solid tumours may raise the possibil-
gastric, breast, lymphoma and carcinoid tumours often produce ity of a metastatic tumour and further imaging with CT and biopsy
solid metastases in the ovaries. Colonic tumours, which are the may be helpful.
679
CHAPTER 35 Ovaries
ENDOMETRIOSIS
Endometriosis is defined as the presence of functional endometrial
glands and stroma outside of the uterus. The pathogenesis is
unknown, with theories regarding its aetiology including implanta-
tion from retrograde menstruation and metaplastic differentiation
of serosal surfaces. Endometriosis most commonly affects the
ovaries. Other sites of involvement include the uterine ligaments,
pouch of Douglas, fallopian tubes, rectosigmoid and bladder, in
decreasing order of frequency.86 Endometriosis may be present as
peritoneal implants, adhesions and ovarian lesions with symptoms
Figure 35.46 Transabdominal image, showing metastatic occurring due to cyclical bleeding into the implants. Repeated
involvement of an ovary, secondary to a primary colonic haemorrhage into ovarian implants results in blood-filled ovarian
carcinoma. The lesion is largely cystic with septa and solid cysts known as endometriomas, or chocolate cysts.
elements. Flow was demonstrated within the septa on colour Endometriosis is a common condition, which is thought to affect
Doppler. 510% of all women. It is found predominantly in women of repro-
ductive age and approximately 20% of women presenting with
infertility are thought to have endometriosis.87
Patients usually present with infertility or chronic pelvic pain,
Lymphoma typically dysmenorrhoea or dyspareunia. Some women are asymp-
tomatic and the extent of the disease does not necessarily correlate
Lymphoma of the ovary in the absence of lymph node or bone with the severity of symptoms.
marrow involvement is rare. It is often bilateral and usually appears Small peritoneal implants are difficult to diagnose radiologically
as a solid mass at ultrasound. and ultrasound is of particular use for the identification of endome-
triotic ovarian cysts. Transrectal ultrasound has been used to assess
Screening endometriotic involvement of the rectovaginal septum and utero-
sacral ligaments88 and other imaging modalities such as MRI have
The poor outcome of ovarian cancer is largely related to late pres- more recently been evaluated for detection of peritoneal implants.86
entation and screening has been seen as a means to improve prog- Laparoscopy remains the gold standard for detection of disease.
nosis. Currently screening is not practical due to the relatively low Endometriomas have a variety of appearances at ultrasound,
prevalence of the disease and the limited specificity of the available ranging from anechoic to echogenic cysts.87 Septa and solid areas
techniques. may be present.89 They are often multiple and are bilateral in up to
Measurement of CA125 and transvaginal ultrasound are the main half of cases.86 They are of variable size87,90 and are often thick
techniques that have been evaluated for use in screening. walled, although this is not a distinguishing feature.89
Serum CA125 is the most commonly used tumour marker for The classic description is a cystic lesion with homogeneous low-
ovarian cancer. It is raised in 85% women with epithelial ovarian level echoes, which are more likely to be detected with transvaginal
cancer as opposed to 1% of normal individuals, but its sensitivity than transabdominal scanning91,92 (Fig. 35.47). This characteristic
is limited in early stage disease, and it detects less than 50% of appearance was found to occur in 95% of cases in a retrospective
stage I tumours. It is insensitive for mucinous and germ cell review.89 This review also tried to establish which criteria are most
tumours. It also lacks specificity and can be raised in other important in distinguishing endometriomas from other adnexal
680
Endometriosis
A B
Figure 35.47 Transvaginal images showing typical appearances of an endometrioma. A: Unilocular cystic lesion with
homogeneous low-level echoes (white arrow). B: There is the typical echo pattern with some echogenic layering (black arrow).
A B
Figure 35.50 Pelvic inflammatory disease. Transvaginal images in a 38-year-old woman with clinical signs of PID. A: There is fluid
within the endometrial canal (between callipers) consistent with endometritis. B: The fallopian tube is dilated and contains echoes (arrow),
with no flow seen on colour Doppler, consistent with a pyosalpinx.
A B
Figure 35.53 Tubo-ovarian abscess. Transabdominal ultrasound image (A) and axial contrast-enhanced CT scan (B) in a patient with
clinical signs of infection. Ultrasound (A) shows a tubo-ovarian abscess, containing linear echoes (arrowhead) typical of gas. The tube and
ovary could not be identified separately. CT scan (B) confirms the presence of an abscess with a locule of gas identified (arrowhead). Note
the intrauterine contraceptive device (arrow), which increases the risk of PID.
A B
Figure 35.54 Ovarian abscess. Transvaginal ultrasound and axial CT scan in a patient with signs of infection. The patient had undergone
a hysterectomy several years previously. A: Transvaginal ultrasound image showing a right ovarian lesion with multiple echoes within it.
B: CT scan confirmed the presence of gas. The previous hysterectomy made an ascending infection an unlikely diagnosis. Surgery
showed an ovarian abscess secondary to an inflamed appendix.
683
CHAPTER 35 Ovaries
REFERENCES 27. Chiou S-Y, Lev-Toaff AS, Masuda E, et al. Adnexal torsion: new
clinical and imaging observations by sonography, computed
1. Salem S. The uterus and adnexa. In: Rumack C, Wilson S, Charboneau tomography, and magnetic resonance imaging. J Ultrasound Med
J, editors. Diagnostic ultrasound. 2 edn. St Louis: Mosby; 1998. 2007;26(10):12891301.
p. 519573. 28. Kaakaji Y, Nghiem HV, Nodell C, Winter TC. Sonography of obstetric
2. Merz E, Miric-Tesanic D, Bahlmann F, et al. Sonographic size of uterus and gynecologic emergencies: Part II, gynecologic emergencies. AJR
and ovaries in pre- and postmenopausal women. Ultrasound Obstet Am J Roentgenol 2000;174(3):651656.
Gynecol 1996;7(1):3842. 29. Hibbard L. Adnexal torsion. Am J Obstet Gynecol 1985;152:456461.
3. Tepper R, Zalel Y, Markov S, et al. Ovarian volume in postmenopausal 30. Warner MA, Fleischer AC, Edell SL, et al. Uterine adnexal torsion:
women suggestions to an ovarian size nomogram for menopausal sonographic findings. Radiology 1985;154(3):773775.
age. Acta Obstet Gynecol Scand 1995;(74):208211. 31. Vijayaraghavan SB. Sonographic whirlpool sign in ovarian torsion.
4. Aviram R, Gassner G, Markovitch O, et al. Volumes of normal ovaries, J Ultrasound Med 2004;23(12):16431649.
ovaries with benign lesions, and ovaries with cancer in menopausal 32. Graif M, Itzchak Y. Sonographic evaluation of ovarian torsion in
women: is there an optimal cut-off value to predict malignancy? J Clin childhood and adolescence. AJR Am J Roentgenol 1988;150(3):647649.
Ultrasound 2008;36(1):15. 33. Graif M, Shalev J, Strauss S, et al. Torsion of the ovary: sonographic
5. Patel MD, Feldstein VA, Filly RA. The likelihood ratio of sonographic features. AJR Am J Roentgenol 1984;143(6):13311334.
findings for the diagnosis of hemorrhagic ovarian cysts. J Ultrasound 34. Albayram F, Hamper UM. Ovarian and adnexal torsion: spectrum of
Med 2005;24(5):607614. sonographic findings with pathologic correlation. J Ultrasound Med
6. Athey PA, Cooper NB. Sonographic features of parovarian cysts. AJR 2001;20(10):10831089.
Am J Roentgenol 1985;144:8386. 35. Shadinger LL, Andreotti RF, Kurian RL. Preoperative sonographic and
7. Barloon TJ, Brown BP, Abu-Yousef MM, Warnock NG. Paraovarian clinical characteristics as predictors of ovarian torsion. J Ultrasound
and paratubal cysts: preoperative diagnosis using transabdominal and Med 2008;27(1):713.
transvaginal sonography. J Clin Ultrasound 1996;24(3):117122. 36. Moshe B-A, Yuri P, Sami H. The effectiveness of spectral and color
8. Savelli L, Ghi T, De Iaco P, Ceccaroni M, et al. Paraovarian/paratubal Doppler in predicting ovarian torsion. A prospective study. Eur J
cysts: comparison of transvaginal sonographic and pathological Obstet Gynecol Reprod Biol 2002;104(1):6466.
findings to establish diagnostic criteria. Ultrasound Obstet Gynecol 37. Lee EJ, Kwon HC, Joo HJ, et al. Diagnosis of ovarian torsion with
2006;28(3):330334. color Doppler sonography: depiction of twisted vascular pedicle.
9. Alpern MB, Sandler MA, Madrazo BL. Sonographic features of J Ultrasound Med 1998;17(2):8389.
parovarian cysts and their complications. AJR Am J Roentgenol 38. Spencer JA, Forstner R, Hricak H. Investigating women with
1984;143(1):157160. suspected ovarian cancer. Gynecol Oncol 2008;108(2):262264.
10. Genadry R, Parmley T, Woodruff JD. The origin and clinical behaviour 39. Brown DL, Doubilet PM, Miller FH, et al. Benign and malignant
of the paraovarian tumour. Am J Obstet Gynecol 1977;129:873880. ovarian masses: selection of the most discriminating gray-scale and
11. Kim JS, Woo SK, Suh SJ, Morettin LB. Sonographic diagnosis of Doppler sonographic features. Radiology 1998;208(1):103110.
paraovarian cysts: value of detecting a separate ipsilateral ovary. AJR 40. Stein SM, Laifer-Narin S, Johnson MB, et al. Differentiation of benign
Am J Roentgenol 1995;164(6):14411444. and malignant adnexal masses: relative value of gray-scale, color
12. Guerriero S, Ajossa S, Mais V, et al. Role of transvaginal sonography in Doppler, and spectral Doppler sonography. AJR Am J Roentgenol
the diagnosis of peritoneal inclusion cysts. J Ultrasound Med 1995;164(2):381386.
2004;23(9):11931200. 41. Fleischer AC, Rodgers WH, Kepple DM, et al. Color Doppler
13. Jain KA. Imaging of peritoneal inclusion cysts. AJR Am J Roentgenol sonography of ovarian masses: a multiparameter analysis. J
2000;174(6):15591563. Ultrasound Med 1993;12(1):4148.
14. Savelli L, De Iaco P, Ghi T, et al. Transvaginal sonographic appearance 42. Kurjak A, Zalud I, Alfirevic Z. Evaluation of adnexal masses with
of peritoneal pseudocysts. Ultrasound Obstet Gynecol 2004;23:284288. transvaginal color ultrasound. J Ultrasound Med 1991;10(6):295297.
15. Phillips HE, McGahan JP. Ovarian remnant syndrome. Radiology 43. Fleischer AC, Rodgers WH, Rao BK, et al. Assessment of ovarian
1982;142(2):487488. tumor vascularity with transvaginal color Doppler sonography.
16. Fleischer AC, Tait D, Mayo J, et al. Sonographic features of ovarian J Ultrasound Med 1991;10(10):563568.
remnants. J Ultrasound Med 1998;17(9):551555. 44. Jain KA. Prospective evaluation of adnexal masses with endovaginal
17. Dereska NH, Cornella J, Hibner M, Magrina JF. Mucinous gray-scale and duplex and color Doppler US: correlation with
adenocarcinoma in an ovarian remnant. Int J Gynecol Cancer pathologic findings. Radiology 1994;191(1):6367.
2004;14(4):683686. 45. Salem S, White LM, Lai J. Doppler sonography of adnexal masses: the
18. RCOG. Guideline no 34. Ovarian cysts in postmenopausal predictive value of the pulsatility index in benign and malignant
women. London: Royal College of Obstetricians and Gynaecologists; disease. AJR Am J Roentgenol 1994;163(5):11471150.
2003. 46. Buy JN, Ghossain MA, Hugol D, et al. Characterization of adnexal
19. Patel MD. Practical approach to the adnexal mass. Radiol Clin North masses: combination of color Doppler and conventional sonography
Am 2006;44:879899. compared with spectral Doppler analysis alone and conventional
20. Levine D. What is the significance of the incidental discovery of a sonography alone. AJR Am J Roentgenol 1996;166(2):385393.
unilocular ovarian cyst in a postmenopausal woman (either with or 47. Kinkel K, Hricak H, Lu Y, et al. US characterization of ovarian masses:
without a family history of ovarian cancer) during a pelvic a meta-analysis. Radiology 2000;217(3):803811.
sonographic examination to exclude ovarian carcinoma? AJR Am J 48. Fleischer AC. Recent advances in the sonographic assessment of
Roentgenol 1994;163(1):215216. vascularity and blood flow in gynecologic conditions. Am J Obstet
21. Goldstein SR, Subramanyam B, Snyder JR, et al. The postmenopausal Gynecol 2005;193:294301.
cystic adnexal mass: the potential role of ultrasound in conservative 49. Timmerman D, Schwrzler P, Collins WP, et al. Subjective assessment
management. Obstet Gynecol 1989;73(1):810. of adnexal masses with the use of ultrasonography: an analysis of
22. Balen AH, Laven JSE, Tan S-L, Dewailly D. Ultrasound assessment of interobserver variability and experience. Ultrasound Obstet Gynecol
the polycystic ovary: international consensus definitions. Hum Reprod 1999;13(1):1116.
Update 2003;9(6):505514. 50. Valentin L. Use of morphology to characterize and manage common
23. Belosi C, Selvaggi L, Apa R, et al. Is the PCOS diagnosis solved by adnexal masses. Best Pract Res Clin Obstet Gynaecol 2004;18(1):
ESHRE/ASRM 2003 consensus or could it include ultrasound 7189.
examination of the ovarian stroma? Hum Reprod 2006;21(12): 51. Wagner BJ, Buck JL, Seidman JD, McCabe KM. From the archives of
31083115. the AFIP. Ovarian epithelial neoplasms: radiologic-pathologic
24. Haimov-Kochman R, Yanai N, Yagel S, et al. Spontaneous ovarian correlation. Radiographics 1994;14(6):13511374.
hyperstimulation syndrome and hyperreactio luteinalis are entities in 52. Jacobs I, Menon U. Screening for ovarian cancer. Best Pract Res Clin
continuum. Ultrasound Obstet Gynecol 2004;24(6):675678. Obstet Gynaecol 2002;16(4):469482.
25. RCOG. The management of ovarian hyperstimulation syndrome 53. Cancer Research UK. UK ovarian cancer incidence statistics. 2008.
Green-top guideline No. 5. Royal College Obstetricians and 54. Mironov S, Akin O, Pandit-Taskar N, Hann LE. Ovarian cancer. Radiol
Gynaecologists; 2006. Clin North Am 2007;45(1):149166.
26. Mathur R, Evbuomwan I, Jenkins J. Prevention and management of 55. Sohaib SA, Husband JE, Reznek R. Ovarian cancer. In: Husband JE,
ovarian hyperstimulation syndrome. Curr Obstet Gynaecol Reznek R, editors. Imaging in oncology. London: Taylor and Francis;
2005;15(2):132138. 2004. p. 429466.
684
References
56. Jung SE, Lee JM, Rha SE, et al. CT and MR imaging of ovarian tumors 77. Outwater EK, Marchetto B, Wagner BJ. Virilizing tumors of the ovary:
with emphasis on differential diagnosis. Radiographics 2002;22(6): imaging features. Ultrasound Obstet Gynecol 2000;15(5):365371.
13051325. 78. Brown DL, Zou KH, Tempany CMC, et al. Primary versus secondary
57. Sutton CL, McKinney CD, Jones JE, Gay SB. Ovarian masses revisited: ovarian malignancy: imaging findings of adnexal masses in the
radiologic and pathologic correlation. Radiographics 1992;12(5): Radiology Diagnostic Oncology Group Study. Radiology
853877. 2001;219(1):213218.
58. Tempany CMC, Zou KH, Silverman SG, et al. Staging of advanced 79. Alcazar JL, Galan MJ, Ceamanos C, Garcia-Manero M. Transvaginal
ovarian cancer: comparison of imaging modalities Report from the gray scale and color doppler sonography in primary ovarian cancer
Radiological Diagnostic Oncology Group. Radiology 2000;215(3): and metastatic tumors to the ovary. J Ultrasound Med 2003;22(3):
761767. 243247.
59. Ronnett BM, Shmookler BM, Diener-West M, et al. 80. Cho KC, Gold BM. Computed tomography of Krukenberg tumors.
Immunohistochemical evidence supporting the appendiceal origin of AJR Am J Roentgenol 1985;145(2):285288.
pseudomyxoma peritonei in women. Int J Gynecol Pathol 81. Athey PA, Butters HE. Sonographic and CT appearance of Krukenberg
1997;16(1):19. tumors. J Clin Ultrasound 1984;12(4):205210.
60. Tanaka YO, Yoshizako T, Nishida M, et al. Ovarian carcinoma in 82. Ulbright TM, Roth LM, Stehman FB. Secondary ovarian neoplasia.
patients with endometriosis: MR imaging findings. AJR Am J A clinicopathologic study of 35 cases. Cancer 1984;53:1164.
Roentgenol 2000;175(5):14231430. 83. Hann LE, Lui DM, Shi W, et al. Adnexal masses in women with breast
61. Green GE, Mortele KJ, Glickman JN, Benson CB. Brenner tumors of cancer: US findings with clinical and histopathologic correlation.
the ovary: sonographic and computed tomographic imaging features. J Radiology 2000;216(1):242247.
Ultrasound Med 2006;25(10):12451251. 84. Shimizu H, Yamasaki M, Ohama K, et al. Characteristic
62. Athey PA, Siegel MF. Sonographic features of Brenner tumor of the ultrasonographic appearance of the Krukenberg tumor. J Clin
ovary. J Ultrasound Med 1987;6(7):367372. Ultrasound 1990;18(9):697.
63. Koonings PP, Campbell K, Mishell Jr DR, Grimes DA. Relative 85. Testa A, Ferrandina G, Timmerman D, et al. Imaging in gynecological
frequency of primary ovarian neoplasms: a 10-year review. Obstet disease (1): ultrasound features of metastases in the ovaries differ
Gynecol 1989;74(6):921926. depending on the origin of the primary tumor. Ultrasound Obstet
64. Quinn SF, Erickson S, Black WC. Cystic ovarian teratomas: the Gynecol 2007;29(5):505511.
sonographic appearance of the dermoid plug. Radiology 86. Gougoutas CA, Siegelman ES, Hunt J, Outwater EK. Pelvic
1985;155(2):477478. endometriosis: various manifestations and MR imaging findings. AJR
65. Beller MJ. The tip of the iceberg sign. Radiology 1998;209(2): Am J Roentgenol 2000;175(2):353358.
395396. 87. Suren A, Osmers R, Dietrich M, et al. Sonomorphology of
66. Caspi B, Appelman Z, Rabinerson D, et al. Pathognomonic echo endometriotic cysts. Int J Gynecol Obstet 1998;62:155165.
patterns of benign cystic teratomas of the ovary: classification, 88. Fedele L, Bianchi S, Portuese A, et al. Transrectal ultrasonography in
incidence and accuracy rate of sonographic diagnosis. Ultrasound the assessment of rectovaginal endometriosis. Obstet Gynaecol
Obstet Gynecol 1996;7(4):275279. 1998;91(3):444448.
67. Tongsong T, Wanapirak C, Khunamornpong S, Sukpan K. Numerous 89. Patel MD, Feldstein VA, Chen DC, et al. Endometriomas: diagnostic
intracystic floating balls as a sonographic feature of benign cystic performance of US. Radiology 1999;210(3):739745.
teratoma: report of 5 cases. J Ultrasound Med 2006;25(12):15871591. 90. Woodward PJ, Sohaey R, Mezzetti Jr TP. Endometriosis: Radiologic-
68. Kurjak A, Kupesic S, Babic MM, et al. Preoperative evaluation of cystic Pathologic Correlation. Radiographics 2001;21(1):193216.
teratoma: what does color Doppler add? J Clin Ultrasound 91. Volpi E, De Grandis T, Zuccaro G, et al. Role of transvaginal
1997;25(6):309316. sonography in the detection of endometriomata. J Clin Ultrasound
69. Zalel Y, Caspi B, Tepper R. Doppler flow characteristics of dermoid 1995;23:163167.
cysts: unique appearance of struma ovarii. J Ultrasound Med 92. Spencer JA, Weston MJ. Imaging in endometriosis. Imaging
1997;16(5):355358. 2003;15(2):6371.
70. Hertzberg BS, Kliewer MA. Sonography of benign cystic teratoma of 93. Asch E, Levine D. Variations in appearance of endometriomas.
the ovary: pitfalls in diagnosis. AJR Am J Roentgenol 1996;167(5): J Ultrasound Med 2007;26(8):9931002.
11271133. 94. Alczar JL, Laparte C, Jurado M, Lpez-Garca G. The role of
71. Patel MD, Feldstein VA, Lipson SD, et al. Cystic teratomas of the transvaginal ultrasonography combined with color velocity imaging
ovary: diagnostic value of sonography. AJR Am J Roentgenol and pulsed Doppler in the diagnosis of endometrioma. Fertil Steril
1998;171(4):10611065. 1997;67(3):487491.
72. Outwater EK, Wagner BJ, Mannion C, et al. Sex cord-stromal and 95. Okaro E, Condous G, Khalid A, et al. The use of ultrasound-based
steroid cell tumors of the ovary. Radiographics 1998;18(6):15231546. soft markers for the prediction of pelvic pathology in women with
73. Ko SF, Wan YL, Ng SH, et al. Adult ovarian granulosa cell tumors: chronic pelvic pain can we reduce the need for laparoscopy? BJOG
spectrum of sonographic and CT findings with pathologic correlation. 2006;113(3):251256.
AJR Am J Roentgenol 1999;172(5):12271233. 96. Timor-Tritsch IE, Lerner JP, Monteagudo A, et al. Transvaginal
74. Demidov VN, Lipatenkova J, Vikhareva O, et al. Imaging of sonographic markers of tubal inflammatory disease. Ultrasound
gynecological disease (2): clinical and ultrasound characteristics of Obstet Gynecol 1998;12(1):5666.
Sertoli cell tumors, Sertoli-Leydig cell tumors and Leydig cell tumors. 97. Patel MD, Acord DL, Young SW. Likelihood ratio of sonographic
Ultrasound Obstet Gynecol 2008;31(1):8591. findings in discriminating hydrosalpinx from other adnexal masses.
75. Stephenson WM, Laing FC. Sonography of ovarian fibromas. AJR Am AJR Am J Roentgenol 2006;186(4):10331038.
J Roentgenol 1985;144(6):12391240.
76. Athey PA, Malone RS. Sonography of ovarian fibromas/thecomas.
J Ultrasound Med 1987;6(8):431436.
685
CHAPTER
A B
Figure 36.1 Uterus. A: Normal transvaginal longitudinal image of the uterus. Note the defined thin endometrial echo (arrow) and its dark
myometrial halo (double-headed arrows). The halo should not be confused as being part of a trilaminar proliferative endometrium. Also
note the prominent subserosal myometrial vessels (curved arrows). B: Normal transvaginal longitudinal image of the uterus. The
endometrium is in the proliferative phase and shows a typical trilaminar pattern, between the callipers. The dark myometrial halo is present
around the endometrium. Compare this to A where the endometrium is atrophic.
Other tests
Computed tomography (CT) offers very little in the evaluation of
the uterus. It may coincidentally show a distended uterine cavity
in scans performed for other reasons, but other tests will be required
to determine if there is pathology present. Some authors believe
that modern multidetector CT scanners with their ability to produce
isometric voxels in multiplanar reconstructions may rival MR scans
in their staging of the cervix but this is yet to be reliably proven.
Figure 36.2 Normal transabdominal longitudinal image of the CT does provide useful assessment of lymphadenopathy and
uterus, using the full bladder technique. The uterus is further away distant metastases in women with uterine or cervical cancers and
from the probe than in the transvaginal images but detail of the it can show complications of treatment such as colo-vaginal fistulae
endometrium and myometrial halo is still visible. or abscesses.
Magnetic resonance (MR) provides exquisite images of the
uterus and cervix, demonstrating zonal anatomy on T2-weighted
of the pelvic relations. In slim women, it may not be necessary to images (Fig. 36.3). It has a strong role in the local staging of endome-
have a full bladder in order to obtain good views of the uterus. trial and cervical cancers. Its use is best reserved for imaging once
Gentle pressure with the probe on the abdominal wall will bring the diagnosis of cancer has already been made. Like ultrasound,
the uterus into view within the near field of the probe and allow MR cannot distinguish benign endometrial hyperplasia from cancer
good resolution imaging. This can be especially useful in early even with diffusion-weighted imaging, so biopsy remains neces-
pregnancy scans. The transabdominal approach also allows the sary. Ultrasound is a cheaper and more readily available test to
kidneys to be checked for hydronephrosis, which might be second- assess the endometrium prior to biopsy. MR has a role in the follow-
ary to gynaecological pathology. up of cancers treated with chemo/radiotherapy and is also the best
Some authors advocate using just transvaginal ultrasound for objective test to assess fibroids before and after uterine artery
dedicated clinics. An example might be a postmenopausal bleeding embolisation.
687
CHAPTER 36 Uterus and vagina
Fibroids
Adenomyosis
Endometrial pathology
Hyperplasia
Polyp
Carcinoma
Pelvic inflammatory disease
Endometritis
Chronic
Postmenopausal atrophic
Coagulopathies
Congenital deficiencies
Thrombocytopenia
Leukaemia
Figure 36.6 Transverse transvaginal view of the uterus
Systemic disorders showing two intramural fibroids (marked by callipers).
Hypothyroidism
Systemic lupus erythematosus
Chronic liver failure including control of heavy bleeding. It comprises a slow-release
Obesity cylinder of levonorgestrel around a conventional T-shaped frame.
Levonorgestrel is a progesterone that has local effects on the
Iatrogenic endometrium and prevents proliferation. The system can be left in
place for 5 years.
Intrauterine devices
Surgical management varies from hysterectomy, through submu-
Anticoagulants
Progesterones cous fibroid resection and endometrial resection, to newer tech-
niques of endometrial ablation and radiological techniques of
uterine artery embolisation (UAE), transvaginal radio-frequency
Cervix
ablation (RFA) and high-intensity focused ultrasound (HIFU).
Chronic cervicitis
Polyp
Carcinoma
MYOMETRIUM
Vagina
Atrophic vaginitis Uterine fibroids
Infection
Foreign body Fibroids (also known as myomas, leiomyomas or fibroleiomyomas)
Trauma are a benign uterine smooth muscle proliferation. The smooth
Carcinoma muscle fibres are disposed in smooth concentric rings with a vari-
able amount of fibrous tissue forming whorls of tissue. They are
Vulva usually clearly demarcated and most commonly found in the body
of the uterus (Fig. 36.6) though they may arise in the cervix or broad
Squamous carcinoma ligament and very rarely in the vagina.3
Melanoma Fibroids are common, being present in more than 30% of women
aged 4060 years of age.4 Risk factors for fibroids include nullipar-
Non-gynaecological sources mistaken for vaginal bleeding ity, obesity, family history, black race and hypertension. Interest-
ingly, physical activity is thought to be protective against the
Haematuria
development of fibroids, and not just because women with fibroids
Rectal bleeding
avoid exercise.5 There is an association of polycystic ovary syn-
drome and the development of fibroids in African-American
women.6 There is clearly a relationship with oestrogen stimulation:
nulliparity indicates continuous oestrogen stimulation without the
to identify those women who do not need hysteroscopy by defining interruption of pregnancy or lactation; obesity is associated with
normality. It is less useful as a positive predictor as hysteroscopy increased amounts of endogenous oestrogen being stored in body
will still be needed. fat; tamoxifen and hormone replacement therapy treatment may
Medical treatment can be hormonal or non-hormonal. Progester- result in enlargement of fibroids. Many medical treatments of
one is often used to stabilise menstrual loss. The oral contraceptive fibroids are aimed at interrupting this oestrogen stimulation. Depo-
pill can also be used in those without contraindications and is par- Provera (medroxyprogesterone acetate),7 mifepristone,8 and gona-
ticularly useful in younger women who also require contraception. dotrophin-releasing hormone9 have all been shown to decrease
Non-hormonal treatments such as tranexamic acid (improved hae- fibroid size and improve quality of life. Likewise, the use of a
mostasis) or mefenamic acid (control of prostaglandin production Mirena intrauterine system in women with fibroids and menor-
in the uterus) can be tried. rhagia has been shown to reduce menstrual blood loss and pain,10
The Mirena intrauterine system, although initially marketed as a though the rate of expulsion of the device is higher in women with
contraceptive device, has become used for much wider indications fibroids than in those without.
689
CHAPTER 36 Uterus and vagina
Fibroids change in size with age. They are unknown prior to abnormally adherent placenta (accreta), growth restriction and
puberty, they enlarge with time during the reproductive years and preterm delivery. Very rarely fibroids in the lower segment or
they reduce in size after the menopause.11 Their size can vary from cervix may prevent a normal vaginal delivery. Uterine fibroids of
the imperceptible on ultrasound to lesions that fill the abdominal 5cm in size or larger are independently associated with caesarean
cavity. Size does not necessarily correlate with symptoms, the section performed prior to the onset of labour and the risk increases
largest often being silent. Small fibroids affecting the endometrium with the size of the fibroid.14 Myomectomy at the time of caesarean
can produce disproportionately severe symptoms, possibly by delivery carries a high risk of significant haemorrhage and is best
increasing the surface area of the endometrial cavity. avoided. Pyomyoma is the rare development of an infected fibroid
in the postpartum period. It is uncommon since the advent of anti-
biotics but is potentially lethal. The formation of gas in the fibroid
Pregnancy and fibroids gives a distinctive pattern of increased echogenicity.15
Pregnancy is often quoted as a cause of fibroid enlargement: whilst Uterine contractions in pregnancy (Braxton Hicks) may mimic
it is true that enlargement and central degeneration of fibroids may the presence of a fibroid by distorting the uterine contour, usually
occur, this phenomenon is actually quite rare,12 with the great the inner contour rather than the outer. They can be distinguished
majority of pregnant women showing no change in size of their by their normal echogenicity and because they are transient.
fibroids (Fig. 36.7). Those that do change in size most commonly do Patience is required as it may take up to 20 minutes for them to
so in the first trimester. Fibroids do impact on the management of relax and show that the apparent mass was only a contraction. Rim
some pregnancies13 though most pregnancies are unaffected. Large calcified fibroids may also confuse the sonographer by simulating
(greater than 5cm) submucosal and retroplacental fibroids seem to the fetal head or if the rim is incompletely calcified, other fetal
impart a greater risk for pain, vaginal bleeding, placental abruption, parts.
Figure 36.7 Pregnancy and fibroids. MR scan of the non-gravid uterus (A) shows a large subserosal fibroid arising from the anterior
wall of the uterus and bending the uterus posteriorly. Ultrasound when the woman is pregnant shows the fibroid arising off the fundus of
the uterus on the edge of image (arrow) (B) and it is shown fully in image (C) between the callipers. It has not enlarged or shown central
degeneration.
690
Myometrium
Fertility and fibroids Deep dyspareunia (pelvic pain associated with sexual inter-
course) has been shown to be unrelated to the presence of fibroids.
Fibroids are implicated in subfertility. They may block the tubal Women with fibroids do not have any increased prevalence or
ostia or prevent implantation of the embryo by distorting the severity of deep dyspareunia and their sexual function is
uterine cavity. Endometrial thickness is no different between those unimpaired.25
with fibroids and those without, but in a study of those undergoing
first assisted reproduction cycles, the rate of non-proliferative
endometrial pattern and live birth rates (34% for those with fibroids Ultrasound appearances of fibroids
versus 43% for those without) were significantly different.16 Women
Fibroids produce a variety of ultrasound appearances depending
with fibroids larger than 4cm require an increased number of IVF
on their size, number, position and the relative amount of fibrous
cycles to achieve an ongoing pregnancy.17
tissue, smooth muscle and calcification within them. The typical
appearance of an intramural fibroid is of a well-demarcated, round
Nomenclature of site of fibroids or oval lesion within the normal homogeneous myometrial echo
(Fig. 36.8). Fibroids may be echo-poor, isoechoic to myometrium,
The clinical symptoms that may arise, outside of pregnancy, depend or echo-bright. Increased reflectivity may be due to calcification,
on the site and size of the fibroid. Fibroids that lie entirely within which can be punctuate, amorphous or rim in nature, or due to the
the myometrium are termed intramural; those that distort the outer presence of fat within the lesion; a so-called lipoleiomyoma (Fig.
margin of the uterus are subserosal; and those that distort the 36.9). The uterus can be enlarged by the presence of one or many
endometrial cavity are submucosal. The degree of distortion caused
by submucosal and subserosal fibroids may vary from a minor
bump to a fully pedunculated fibroid.
The European Society of Hysteroscopy has classified submucosal
fibroids into three groups: those that are pedunculated and entirely
within the endometrial cavity are type 0; those that lie mostly
within the cavity such that there is an acute angle between the wall
of the cavity and the wall of the fibroid are type 1; and those that
are mostly within the myometrium such that the angle between the
cavity wall and the wall of the fibroid is obtuse are type 2. The
purpose of the classification is to reflect the suitability for hystero-
scopic resection of the fibroid. Submucosal fibroids may be expelled
vaginally following treatments such as uterine artery embolisation
or gonadotrophin-releasing hormone agonists.18
Subserosal fibroids have the same variety of extension through
the uterine serosa. Fully pedunculated fibroids may provide diag-
nostic difficulty in distinguishing them from other adnexal masses.
Degenerative cystic change in the fibroid may give it an appearance
similar to an ovarian cyst.19 A valuable sign is the bridging vascu-
lar sign whereby the blood supply to the pedunculated mass is
seen to arise from uterine vessels helping to confirm its peduncu-
lated nature.20 A fibroid that has its blood supply through a narrow
pedicle runs the risk of twisting and cutting off the blood supply,
the so-called torted pedunculated fibroid. This produces acute
symptoms of pain and tenderness, not unlike any other cause of an
acute abdomen. Torsion of other adnexal masses or ovaries will
give similar symptoms. CT is usually better than ultrasound in Figure 36.8 Transverse view of a fibroid in the uterine
establishing the diagnosis in the acute setting.21 Those subserosal fundus. The fibroid is between the callipers. Note the streaky
fibroids that extend laterally may lie within the layers of the broad shadowing arising from the fibroid. A characteristic feature.
ligament; indeed fibroids may develop entirely within the broad
ligament, as can other rare variants of fibroids such as an
angioleiomyoma.22
fibroids and the outline of the uterus may become lobulated (Fig. Fibroids can outgrow their blood supply and undergo central
36.10), often most easily seen where it pushes against the full necrosis or cystic change (Fig. 36.13). This cystic change can vary
bladder. Fibroids have a dense nature which impairs the passage from a simple cavity to a complex array of echogenicities with a
of ultrasound so that most show posterior acoustic shadowing even surrounding irregular wall and septations. It is a not-uncommon
without calcification. The whorled nature of a fibroid or internal diagnostic dilemma to distinguish a cystic fibroid from another
calcification can lead to the typical venetian blind pattern of acous- potentially serious adnexal mass such as an ovarian tumour. When
tic shadowing with bands of diverging linear shadows (Fig. 36.11). a mass is large enough it may be impossible to tell on ultrasound
Fibroids may be so dense or calcified that they prevent visualisation whether it is uterine or ovarian in origin. Magnetic resonance plays
of other structures. Dense calcification of a fibroid is commoner in a very useful role here as it gives a better overall anatomical depic-
the postmenopausal age group and may be picked up as an inci- tion of the pelvis26 and may help identify the normal ovaries else-
dental finding on an abdominal radiograph for other reasons. Cal- where. Indeed MR is ultrasounds complement as it can give
cification of the margins alone of a fibroid also occurs (Fig. 36.12). precise fibroid mapping and characterisation:27 because of this MR
The presence of fibroids may prevent adequate examination of the is the favoured imaging tool in the work-up for uterine artery
rest of the pelvic organs; the endometrium and the ovaries may be embolisation and post-embolisation quantification of fibroid
obscured. shrinkage.
A B
Figure 36.12 Calcified fibroids. A dense calcified fibroid with a strong acoustic shadow (A) and a rim calcified fibroid (B) are shown.
692
Myometrium
Submucosal fibroids need to be distinguished from endometrial Magnetic resonance is better able to differentiate the two condi-
polyps. Polyps typically show as homogeneously hyperechoic tions, though of course they often coexist.
masses. Submucous fibroids are more likely to be hypoechoic.
Lesions greater than 20mm in size are much more commonly
fibroids. Fibroids may have more than one feeding vessel whereas Vascularity and malignant change
polyps never do.28 The blood flow through a fibroid can be very varied. The finding
A retroverted uterus on transabdominal ultrasound can produce of central or peripherally placed vessels, their velocities and the
the misleading impression of a fundal fibroid; this is in part due to impedance to flow show a very wide range of variation across
the axial lie of the uterus relative to the ultrasound beam and the benign fibroids. Some authorities believe that fibroids containing
consequent increase in sound attenuation. Transvaginal ultrasound sarcoma are more likely to show increased vascularity and high-
easily resolves this issue. Duplication anomalies of the uterus, typi- velocity flows; others believe that malignant mixed mesodermal
cally a bicornuate uterus, can also confuse as one fundus may tumours are more likely to have low-impedance flow;30 however,
mimic a fibroid. Identification of the endometrium in each horn these features are non-specific. Leiomyosarcomas are more likely to
resolves this issue. This can be more of an issue if there is a preg- be larger than 8cm in diameter (Fig. 36.14) and show central degen-
nancy in one horn and not the other. eration when diagnosed.31 Magnetic resonance is also unable to
Ultrasound has a high sensitivity for fibroids but only a relatively distinguish leiomyosarcomas from cellular fibroids. The most
poor specificity (about 40% in one study) and a low negative predic- useful indicator is a rapid increase in size of the lesion over time. It
tive value. Adenomyosis is the most common final diagnosis in should be borne in mind that sarcomas do not generally arise in
women with inaccurate ultrasound reports for uterine fibroids,29 pre-existing fibroids but develop de novo. Furthermore, most leio-
being found in both false positive and false negative reports. The myosarcomas are diagnosed at postoperative histology rather than
diffusely enlarged uterus without a focal lesion that might in the before resection.
past have been thought to represent numerous small intramural
fibroid changes is more likely to be a manifestation of adenomyosis.
Treatment of fibroids
Hysterectomy used to be the only effective surgical treatment.
Women who wish to preserve or improve their fertility may opt for
myomectomy. Hysteroscopic resection of submucous fibroids is
well recognised. Uterine artery embolisation is well established as
an alternative treatment with many papers reporting a 5060%
reduction in fibroid size32 with up to a 95% rate of symptom relief.
Fibroids
30% of women aged 4060.
Oestrogen stimulation a common causal factor; regression after
menopause.
Position: submucosal, intramural, subserosal and pedunculated.
Symptoms: disorders of menstruation, pelvic pain and urinary
symptoms.
Ultrasound appearance variable but commonly attenuating with a
streaky shadowing.
Rapid growth suggests sarcoma.
Figure 36.13 Central necrosis of a large fibroid. Note the Treatments: medical, surgical, embolisation and ablation.
complex cystic centre with an irregular surrounding wall.
A B
Figure 36.14 Leiomyosarcoma. Ultrasound (A) and pathological specimen (B) of a proven leiomyosarcoma. The only feature of note
was the large size of the fibroid. The diagnosis of sarcoma had not been suspected preoperatively.
693
CHAPTER 36 Uterus and vagina
Other new treatments include: radio-frequency thermal ablation 15mm in size and subendometrial, and not to be confused with
done either transvaginally33 or percutaneously;34 and focused ultra- the normal venous spaces seen in the subserosal layer. Other fea-
sound ablation.35 tures (Fig. 36.16) which are less specific are: asymmetric thickening
Medical treatments (Depo-Provera (medroxyprogesterone of the uterine walls; loss of definition of the endometrial/myome-
acetate),7 mifepristone,8 and gonadotrophin-releasing hormone9) trial interface; and the formation of adenomyomas. Adenomyomas
have all been shown to decrease fibroid size and improve quality are usually poorly defined, echogenic masses that may contain
of life. The use of the Mirena intrauterine system has been discussed cystic spaces, sited near the junctional zone.38 They have features
earlier. The advent of the menopause relieves many women of their that overlap with fibroids but one useful feature is that they do not
fibroid related symptoms. show the rim vascularisation that fibroids may do on colour
Doppler. Bright echogenic subendometrial foci may be artefactually
Adenomyosis
This is a condition of migration of endometrial glands into the Adenomyosis
myometrium, which provokes an associated smooth muscle hyper-
plasia. It is most commonly encountered in the fourth and fifth 80% of women with endometriosis also have adenomyosis.
decades of life and is strongly associated with endometriosis. Up to Many remain asymptomatic.
80% of women with endometriosis will also have adenomyosis Fibroids and adenomyosis may coexist.
(though women with endometriosis as their main complaint usually Diagnosis: subendometrial echogenic striations, globular shape to
present earlier in life, in the third and fourth decades). Adenomyo- uterus and myometrial cysts.
sis is more common in multiparous women. MR is a better diagnostic tool for adenomyosis.
Symptoms of adenomyosis
Adenomyosis has been a difficult condition to diagnose before the
advent of high quality transvaginal ultrasound or magnetic reso-
nance. Consequently, its symptomatology is poorly understood.
Certainly, some women will experience heavy or painful bleeding
and a tender uterus which waxes and wanes through the cycle.36
Many though will remain asymptomatic and the condition is only
found as an incidental finding on imaging. Adenomyosis often
coexists with other conditions and these produce confusion over
related symptoms.
Diagnosis of adenomyosis
There is some overlap with the features in fibroid change, and
fibroids and adenomyosis may coexist. The most specific signs of
adenomyosis on ultrasound37 are: subendometrial echogenic linear
striations; a globular configuration to the uterus; and myometrial
cysts (Fig. 36.15). The subendometrial striations have a high posi- Figure 36.15 Adenomyosis. Three small cysts are seen in the
tive predictive value of 80%. The myometrial cysts are due to the myometrium adjacent to the endometrium (arrows). These are
endometrial glands still showing cyclic function. They are usually strong indicators of adenomyosis.
A B
Figure 36.16 Adenomyosis. A and B: Both images show asymmetrical thickening of the uterine walls (double-headed arrows). There is
also loss of definition of the endometrium in (B).
694
Myometrium
produced by intravasation of air during saline infusion hysterogra- They present with postmenopausal bleeding and are commonly
phy39 so, ideally, ordinary transvaginal ultrasound should be done quite bulky at presentation (Fig. 36.18). There are no distinguishing
prior to any infusion. Overall, the diagnostic sensitivity of ultra- features on ultrasound to separate them from benign fibroids. The
sound is suboptimal, even in the best hands only ranging from 50% most useful sign is that of rapid enlargement. They are often highly
to 87%.40 Magnetic resonance is the better imaging tool,41 showing vascular with central flow visible on colour Doppler. Histology is
thickening of the low-signal junctional zone on T2-weighted required for diagnosis.31
imaging and the presence of foci of high signal in the myometrium
due to haemorrhage (T1) or cystic endometrial glands (T2) (Fig.
36.17). It suffers much less from observer variation. Lymphoma and metastases
Adenomyosis can rarely be the origin of adenocarcinoma arising Lymphomatous involvement of the uterus may occur as part of a
outside the normal endometrium. They may display a more generalised systemic disorder (usually non-Hodgkins type with
aggressive histological subtype than conventional endometrial involvement of liver, spleen or lymph nodes) or as a primary mani-
adenocarcinoma. festation. In the latter case, it invariably arises in the cervix rather
than the uterine body and is usually B-cell in type. Ultrasound
Treatment of adenomyosis shows a uniformly hypoechoic mass which is rarely calcified,
centred on the cervix. Magnetic resonance appearances may suggest
Generally, treatment is aimed at suppressing menstruation. Anti- the diagnosis but biopsy is needed.
prostaglandins, sex hormones, danazol and gonadotrophin-releas- Metastases to the uterus are usually to the endometrium, though
ing hormone analogues have all been tried.42 Surgical procedures they can be to the body or cervix as well. They are rare. Primary
include endometrial ablation, laparoscopic electrocoagulation, sites are often in the breast or stomach. There are no specific fea-
radio-frequency ablation and adenomyoma resection. Uterine tures on ultrasound.
artery embolisation has also been used with promising results. Ulti-
mately, if fertility is not desired, hysterectomy can be offered.
Lipoma
Other myometrial lesions Lipoleiomyomas are fat-rich fibroids, in distinction to pure lipomas.
Both will look bright on ultrasound. Magnetic resonance is useful
to prove the presence of fat. They are benign lesions.
Malignant mixed Mllerian tumours
These rare tumours are usually aggressive and rapidly invasive. Arteriovenous malformation (AVM)
They most commonly present as an intracavitary mass with dilation
These abnormal arterio-vascular communications may arise as a
of the endometrial canal. They tend to look hyperechoic on ultra-
manifestation of abnormal placentation and retained products of
sound; myometrial invasion is common and has a predilection for
conception or as a consequence of surgical curettage or trauma.
the uterine fundus.43 They arise in pluripotential cells in the Mlle-
They characteristically show as areas of intense signal on colour
rian duct system and are at least in part sarcomatous.
Doppler within the endometrium or myometrium (Fig. 36.19).44
Tortuous feeding vessels may be visible on greyscale ultrasound.
Uterine sarcoma There is overlap with the appearances of trophoblastic disease, so
serum beta human chorionic gonadotrophin (beta-hCG) levels
These are rare tumours with a peak incidence at 5060 years of age. should be checked. They usually present with persistent bleeding
They mostly develop de novo rather than in pre-existing fibroids. after miscarriage. Curettage can provoke massive haemorrhage and
is best avoided.45 Transcatheter arterial embolisation has been the
standard treatment; however, the greater use of ultrasound after
A B
Figure 36.19 Arteriovenous malformation. Transverse view (A) of a bright, turbulent blush of colour Doppler signal due to an AVM
following miscarriage, together with an arteriogram (B) demonstrating the tangle of vessels associated with a true AV fistula.
Endometrial ablation
Coagulation of the endometrium using thermal energy is an alter-
native treatment to hysterectomy or medical treatment for dysfunc-
tional uterine bleeding. The aim is to destroy the endometrium and
reduce the cavity to a narrow fibrotic tube. The procedure works
best if done when the endometrium is at its thinnest in the early
part of the cycle. Follow-up ultrasound may show fluid in
the cavity, adhesions and residual or regenerated endometrium
(Fig. 36.23). Haematometrium is a potential complication and may
be focal.
A B
D
C
Figure 36.30 The normal endometrium in different phases of the menstrual cycle: menstrual (A), proliferative (B), peri-ovulatory (C) and
secretory (D).
699
CHAPTER 36 Uterus and vagina
uncommon operation done for early stage cervical cancer when the
Endometrial hyperplasia
woman wishes to retain the ability to carry a pregnancy. The cervix
is removed but the uterine body is left behind. Assisted conception Presents with abnormal bleeding in the perimenopausal age
will be needed if pregnancy is desired. A Manchester repair done group.
for prolapse also removes the cervix and although a passage is left Persistent thickening over 10mm is predictive.
to allow uterine contents to escape, a haematometrium can result Histology is needed to diagnose the presence of atypia.
(Fig. 36.29). Atypia is a precursor to endometrial cancer.
Knowledge of the type and extent of surgery clearly affects the
postoperative features and the likelihood of complications.
A B
Figure 36.32 Endometrial polyp (A) with a single feeding vessel shown on colour Doppler (B), though there are branching vessels within
the polyp itself. Note that the polyp has an ovoid shape.
A B
Figure 36.33 Endometrial polyps are easier to see in the proliferative phase of the cycle. The echogenicity of the ovoid polyp is outlined
against the darker endometrium (A). A single feeding vessel is also shown on colour Doppler (B).
A B
Figure 36.34 Saline infusion hysterography. The polyp is hard to see against the secretory phase endometrium (A) but is clearly
outlined by saline in (B). 701
CHAPTER 36 Uterus and vagina
to be submucosal fibroids. Small cystic areas may develop due to Endometrial cancer
dilated glands within the polyp. Polyps are most easily seen in the
proliferative phase when their echogenicity stands out against the
relatively hypoechoic endometrium (Fig. 36.33). Later, in the secre- Aetiology
tory phase, the echogenicity of the endometrium may match that of
the polyp and make it difficult to see. Occasionally a thin echogenic There are various factors that increase the risk of developing
rim may be seen around a polyp due either to a band of compressed endometrial cancer, namely: nulliparity, obesity, hypertension, dia-
endometrium or to the interface with the cavity. Saline infusion betes, polycystic ovary syndrome, hereditary non-polyposis color-
hysterography can be used to reveal the polyp (Fig. 36.34). This is ectal cancer and pelvic irradiation. A common causative factor is
best done in the early proliferative phase when the endometrium exposure to unopposed oestrogen, either from endogenous produc-
is thin. Later in the cycle when the endometrium is thick, wrinkles tion from hormone-secreting tumours, or exogenous medication
from contractions may simulate sessile polyps. Polyps can be single such as tamoxifen or hormone replacement therapy with oestrogen
or multiple. 3D ultrasound is better at giving a global depiction of and no progestogen. Endometrial hyperplasia with atypia has a
multiple polyps than 2D. 25% risk of developing carcinoma. Most are adenocarcinomas. It is
Blood clots may mimic a polyp but will not be vascularised and the commonest gynaecological malignancy and the fourth com-
will not be constant on repeat examinations. Submucosal fibroids monest cancer in women. The majority of women are postmeno-
are more likely to be round, be hypoechoic and to show shadowing pausal, with the commonest ages being 50 to 65 years.
(Fig. 36.35). Fibroids are more likely to have multiple feeding
vessels which branch over the surface and may also have a layer of
overlying endometrium. A history of pregnancy raises the possibil- Symptoms
ity of other intracavitary masses, namely retained products of con- The most common presentation is with abnormal bleeding, typi-
ception and gestational trophoblastic disease. cally postmenopausal bleeding. About 10% of women with post-
Most polyps are benign, particularly in the premenopausal age menopausal bleeding will have endometrial cancer and the longer
group. Polyps are associated with endometrial cancer, with 10% of the interval between menopause and the onset of bleeding the
cancer patients showing coexistent or malignant polyps. Ultra- greater the likelihood of cancer. Some present with a vaginal dis-
sound cannot distinguish a benign polyp from one with atypia, nor charge rather than bleeding. An obstructed uterine cavity causing
can ultrasound distinguish a benign polyp from coexistent endome- a haematometrium may present with pain.59
trial cancer. Consequently, polyps should be removed and the
endometrium sampled. Tamoxifen use is associated with an
increased incidence of polyps and cancer. Diagnosis
The role of ultrasound falls into two main groups. Firstly, women
who present with postmenopausal bleeding will be investigated
with hysterography. Ultrasound can be used as a negative predic-
tive tool to triage those women who do not need hysteroscopy.
Endometrial polyps
Secondly, asymptomatic women may have ultrasound scans for
Circumscribed overgrowth of endometrium. other reasons and ultrasound can be used to predict which of those
Any age but usually perimenopausal. need further investigation of their endometrium.
Typically oval in shape on ultrasound. The typical feature is that endometrial cancer produces thicken-
Best seen against the proliferative phase endometrium. ing of the endometrium (Fig. 36.36). Focal thickening is more con-
Saline infusion hysterography helps to reveal them. cerning than diffuse and likewise an uneven echogenicity is more
Most are benign, but no imaging features to distinguish them concerning than an even echo. Irregular branching of endometrial
from malignancy. vessels on power Doppler is also a concerning sign60 though addi-
Tamoxifen use is associated with polyp formation. tion of Doppler to the predictive score obtained from greyscale
features barely increases performance (Fig. 36.37). Texture analysis
Figure 36.35 Submucous fibroid. In comparison with endometrial Figure 36.36 Grossly thickened endometrium in a
polyps, a submucous fibroid (between callipers) is more likely to be postmenopausal woman. She was found to have endometrial
round, dark and shadowing. cancer.
702
Endometrium
A B
Figure 36.37 Endometrial cancer. Longitudinal transabdominal image (A) shows a bright irregular endometrium that disrupts the normal
hypoechoic subendometrial layer. These features are strongly indicative of invasive endometrial cancer. The addition of colour Doppler (B)
whilst showing irregular hypervascularity does not increase the predictive power of the scan.
of the endometrium using a computer model has been proposed studies are in accord with the Birmingham experience64 that using
but has not found widespread acceptance.61 a cut-off of 4mm saves hysteroscopy without missing any cancers.
Staging and prognosis of endometrial cancer depends on the An important caveat is that an unmeasurable endometrial thickness
degree of myometrial invasion (Fig. 36.38). Stage 1a is confined to is an indication for hysteroscopy. Loss of the endometrial/myome-
the endometrium, or invades the inner half of the myometrium and trial distinction is potentially a sign of invasion and carries as high
1b the outer half. Ultrasound typically shows a low-echo, suben- a risk of carcinoma as finding a markedly thickened endometrium.
dometrial, myometrial halo around the endometrium. Disruption The transvaginal ultrasound technique must show the entire
of this layer suggests myometrial invasion (Fig. 36.39). However, length of the endometrium. Measurement of thickness is made in
prospective studies have shown that ultrasound is very unreliable the longitudinal plane at the widest point. The hypoechoic inner
at assessing invasion, with one study showing up to 30% incorrectly myometrium (or subendometrial halo) should not be included.
staged.62 Likewise, any intracavitary fluid should not be included in the
Postmenopausal women should have an atrophic endometrium. measurement (Fig. 36.41). The significance of any intracavitary fluid
It has been found that ultrasound has a high negative predictive depends on the coexistent endometrial thickness but also on its
value for endometrial cancer if the double-layer thickness is 4mm echogenicity. Echo-free fluid and a thin endometrium is usually a
or less (Fig. 36.40). Many centres use this as a triage tool to exclude benign condition,65 but the presence of echoes in the fluid confers a
women from unnecessary hysteroscopy. There are dissenting voices greater risk of endometrial cancer66 and both endocervical and
as a small proportion of women with cancer will have a thin endometrial sampling is advised.
endometrium, one study even claiming that up to 10% of women Other ultrasound techniques that are used are saline infusion
with cancer have a thickness less than 4mm.63 However, most hysterography (SIH) and 3D ultrasound. SIH is advocated as a
better way of visualising endometrial abnormalities and it certainly
helps in the delineation of polyps and fibroids. However, it confers
very little advantage over transvaginal ultrasound in the diagnosis
of malignancy.67 If SIH is used in the presence of endometrial cancer
it does not cause any increased risk of extrauterine dissemination
of the disease.68
3D ultrasound by enabling calculation of the endometrial volume
can give higher specificities and better negative predictive values
for endometrial cancer than using the endometrial thickness.
However, there is no agreement between the various studies about
the optimal volume to use as a cut-off. A range of values from
1.35mL,69 to 2.7mL70 to 3.56mL71 have been reported as optimal
values by different authors. It seems that any centre would have to
validate its own volume measurement before applying it. The use
of endometrial thickness is a much more readily reproducible meas-
urement across different centres.
Patient preference for ultrasound or hysteroscopy as the initial
investigation for endometrial cancer differs depending on how the
question is asked. Women asked which procedure they found more
tolerable using a visual analogue pain score opted for ultrasound.72
In contrast, when women were taught about the probability of
finding endometrial cancer and the advantages and disadvantages
of different diagnostic strategies they showed a clear preference for
hysteroscopy and its greater diagnostic certainty.73
Advanced tumours at presentation are relatively rare because
Figure 36.39 Endometrial cancer. Normal endometrium and a bleeding is generally an early symptom. However, some women
subendometrial layer are seen on the right, whereas there is a will present with large uterine masses that can be mistaken for
tumour on the left invading into the myometrium (arrow). fibroids or an ovarian mass. Endometrial cancer can metastasise to
A B
Figure 36.40 Atrophic endometrium: perimenopausal (A) and postmenopausal (B). There are obvious subserosal venous spaces seen
in A and a dense focus of myometrial calcification in B as well. The calcification is probably in an old fibroid.
704
Endometrium
A B
Figure 36.41 If there is fluid in the endometrial cavity (A), this should not be included in the endometrial thickness measurement. The
double layer endometrial thickness in (B) is correctly measured, total 4.4mm.
A B
Figure 36.42 Local staging of endometrial cancer is best done with MR. A large endometrial tumour is seen on ultrasound (A), which
is shown by MR (B) to extend into the outer half of the myometrium stage Ib.
A B
Figure 36.43 Cystic changes associated with tamoxifen usage, with apparently greatly enlarged endometrial width on
transabdominal (A) and transvaginal (B) views. This can be misleading as some of these changes can be in old adenomyosis in the
subendometrial layer.
A B
Figure 36.44 Normal T shaped intrauterine device. Longitudinal image (A) shows the body of the device in the endometrial cavity
and transverse image (B) shows the less echogenic T bar in the fundus.
local inflammatory reaction. This releases fluid into the lumen of of the limitations of the ultrasound beam width. Early versions of
the genital tract that is toxic to eggs and sperm. Far fewer sperm the Mirena coil were poorly reflective and harder to see (Fig. 36.45).
reach the egg, and any resultant fertilised egg is much less likely to The cross bar is often less reflective than the body of the IUD. The
survive the altered milieu of the uterus. The common belief that strings may be seen in the cervical canal. Some IUDs produce very
IUDs act to abort embryos in the uterus is not supported by the characteristic appearances, the Gynaefix appears as a row of six
evidence. spots, the old-fashioned Lippes loop (Fig. 36.46) has a serpentine
The role of ultrasound is to confirm the site of an IUD and to look appearance but may also appear as a row of spots if seen in cross-
for potential complications. The IUD should be visualised as cen- section. Patients from China may show a ring-shaped IUD.
trally located within the endometrial cavity (Fig. 36.44), with the Complications of an IUD include low position, associated infec-
crossbar (if present) in the fundal part of the cavity.83 Typically, the tion, migration into the myometrium, uterine perforation, associ-
IUD shows as a strong reflector casting an acoustic shadow. This is ated intra- or extrauterine pregnancy and fragmentation of the IUD.
more so when viewed in cross-section than longitudinally because If an IUD is known to be present but cannot be seen with
707
CHAPTER 36 Uterus and vagina
Endometritis
Secondary to ascending infection through the cervix.
Causes: iatrogenic (any invasive procedure), pregnancy related or
part of generalised pelvic inflammatory disease (PID).
C. trachomatis and N. gonorrhoeae; common in PID.
Primarily a clinical diagnosis.
There are no specific ultrasound features.
Non-specific signs: thickened endometrium, fluid in cavity, free
pelvic fluid, diffuse enlargement of uterus and loss of definition of
the endometrial border.
Ashermans syndrome/intrauterine
synechiae
Synechiae are intrauterine adhesions that cause the walls of the
endometrial cavity to stick together at various sites. Ashermans
syndrome is usually reserved for the more severe forms, with
partial or complete obliteration of the endometrial cavity. The com-
monest cause is dilatation and curettage, particularly in the post-
partum period when the uterus has a softened myometrium, which
is more prone to damage. Retained placenta also increases the risk
of adhesions.
Clinically, women present with hypo- or amenorrhoea, infertility,
or if the woman does become pregnant, an increased risk of miscar-
riage and postpartum haemorrhage.
Small bright foci on the basal layer of the endometrium are the
clue to the site of adhesions. These may commonly be seen in
asymptomatic postmenopausal women, when they are of no con-
Figure 36.50 MR scan showing an IUD as a dark linear
sequence. However, in the symptomatic infertile woman, adhesions
structure within the bright endometrium on T2-weighted images.
may be commonly missed on ordinary transvaginal sonography.
Sonohysterography is the best way to demonstrate the adhesions.
These vary from fine strands (Fig. 36.52) to thick septa. Dilation of
Endometritis the cavity with saline can cause pain in those with adhesions. Divi-
sion of the adhesions can be achieved at hysteroscopy.
Infection of the endometrium is generally caused by ascending
infection through the cervix. It may form part of a more generalised Haematometrium and other
pelvic inflammatory disease or be localised. Iatrogenic causes
include any invasive procedure, such as cervical biopsy, hysteros- related conditions
alpingogram, IUD insertion or endometrial instrumentation.
Endometritis may also occur as a result of pregnancy, due to pre- Retention of blood or mucus within the genital tract leads to disten-
mature rupture of membranes, abortion, postpartum, or prolonged sion. The obstruction can be congenital or acquired. In children and
labour. The commonest clinical manifestation is pain and fever in adolescents the obstruction is usually congenital, which might be
the postpartum period. due to an intact hymen (1 in 1000) or an atresia or stenosis of the
Microbiologically, postpartum endometritis may be due to group vagina (1 in 5000). These congenital lesions are associated with
B streptococcus alone or it may be polymicrobial with both anaero- renal tract anomalies, so the ultrasound examination needs to be
bic and aerobic organisms. In the setting of non-pregnancy-related extended to include the kidneys. In the adult, the obstruction is
pelvic inflammatory disease, the two commonest organisms are usually at the cervix or high vaginal level.
Chlamydia trachomatis and Neisseria gonorrhoeae. The genital tract becomes dilated above the obstruction. If the
Ultrasound examination may be limited by pain and often dilation contains blood the terms used are:
shows either normal or non-specific findings.86 Endometritis is pre- n haematocolpos: vaginal distension obstruction at vaginal
dominantly a clinical diagnosis as uncomplicated endometritis level
709
CHAPTER 36 Uterus and vagina
A B
Figure 36.51 Endometritis. There are no specific signs on ultrasound for endometritis. Features that may be seen in association are:
(A) retained fluid in the cavity after caesarean section (note the suture material in the fresh scar); (B) retained fluid and echogenic basal foci
of tiny amounts of RPOC; (C) fluid and debris in the endometrial cavity; and (D) hypervascularity of the myometrium.
n haematometrocolpos: vaginal and uterine distension uterus and the adjacent obstructed moiety is misinterpreted as an
obstruction at vaginal level adnexal cyst.
n haematometra: uterine distension obstruction at cervical Treatment of these congenital variants can range from simple
level division of an obstructing membrane through to more extensive
n haematosalpinx: dilation of fallopian tubes obstruction at surgery required for more complicated Mllerian duct anomalies
cornua. or cloacal malformations. MR provides the best anatomical
If the lesion contains pus, substitute pyo for haemato and if it information, although transrectal sonography has been used as
contains only secretions use hydro instead. well.90
The most common presentation of congenital lesions is with Adults who develop secondary genital tract obstruction do so for
primary amenorrhoea. Cyclical pelvic pain, low back pain and a variety of reasons (Table 36.4). Cervical stenosis as a result of
urinary retention are all reported. Acute urinary retention can be endometrial ablation may cause retrograde menstruation, endome-
the presenting complaint in an imperforate hymen.87 Some may triosis and delay in diagnosing endometrial cancer.91 Unexplained
present as a huge paravaginal mass88 this is due to a vaginal postmenopausal haematometra needs to be investigated thor-
septum dividing the vagina lengthways. The syndrome of Herlyn oughly to exclude an underlying malignant cause.92 Post-radiother-
WernerWunderlich comprises uterus didelphys (Fig. 36.53), an apy stenosis usually occurs within a year of treatment. Occasionally,
obstructed hemivagina and ipsilateral renal agenesis.89 Problems the uterus will be so distended that it mimics an adnexal cyst.
with diagnosis can occur when one moiety of a uterus didelphys is Failure to find a normal uterus should always raise the possibility
obstructed. The unobstructed moiety is assumed to be a normal that the abnormal mass is the uterus.
710
Endometrium
Congenital anomalies
Covered in Chapter 34 also.
The genital tract dilates above any congenital obstruction.
An intact hymen is commonest cause.
An MR scan is almost 100% accurate in diagnosing congenital
gynaecological anomalies.
There is an association with renal anomalies.
Primary amenorrhoea commonest presentation of an obstructed
tract.
Ultrasound will show the dilated tract as a central fluid-filled
mass.
Failure to identify the uterus should always raise the possibility
that an abnormal mass is in the uterus.
hourglass shape with the cervix forming the waist. The contents
may be anechoic or exhibit a uniform echogenicity. No Doppler
Figure 36.52 Fluid in the endometrial cavity outlines fine flow will be visible in the fluid. It is not possible to distinguish
strands or synechiae crossing the cavity. blood from mucus or pus on ultrasound. MR can distinguish blood
but clinical features are needed to diagnose pus (pyometrium).
Benign conditions
Nabothian cysts
These are retention cysts of the cervix and are a common benign
finding, more so in those who have had children. Originally
described as cysts visible on the ectocervix, the definition has come
to include any retention cyst in the muscle of the cervix. Ultrasoni-
cally, they appear as echo-free cysts of 620mm in size.98 They are
usually multiple and may distort the endocervical canal but they
do not occur in the canal itself (Fig. 36.58). Debris can be occasion-
ally seen in the cyst. It is of no consequence. Nabothian cysts do not Figure 36.59 Prominent endocervical glands are visible (arrows)
resolve. in this transvaginal view of the uterus. Note that they look different
Cystic spaces centrally within the canal are due to dilated to the endometrium.
endocervical glands (Fig. 36.59). These usually give a tubular, mul-
ticystic appearance and are termed cystic endocervical mucus.
This may coexist with nabothian cysts. Both conditions are entirely
innocent and have no predisposition to cancer.
A pitfall to avoid is mistaking a cervix filled with nabothian cysts
for an enlarged ovary. Finding the endocervical canal and showing The benign cervix
the relationship to the uterine body should prevent this error. Nabothian cysts are often multiple.
Nabothian cysts may mimic the appearances of an ovary look
for the relationship with the uterine body.
Cervical polyp Dilation of the endocervical canal with endocervical glands is an
Cervical polyps are relatively common, being found in 5% of innocent phenomenon.
women referred for hysteroscopy,99 although they may be difficult Cervical polyps are common, but often not seen at ultrasound.
to see on ultrasound without saline contrast. Occasionally they Less than 10% of fibroids occur in the cervix.
become large but usually are only a few millimetres in size. Most Cervical length monitoring in pregnancy can help predict those
are echogenic. They may be mistaken for pedunculated endometrial that will become incompetent.
polyps or fibroids. Most cervical polyps are asymptomatic though
some present with bleeding. There is no known malignant
potential.
most are small. Urinary frequency may be caused by large cervical
fibroids pressing on the bladder. Cervical fibroids may also cause
Cervical fibroid obstructed labour. MR imaging is often better in late pregnancy
Less than 10% of fibroids occur in the cervix (Fig. 36.60). They have than ultrasound in defining the relationship and size of a cervical
the same ultrasound features as fibroids elsewhere in the uterus and fibroid.
713
CHAPTER 36 Uterus and vagina
A B
Figure 36.60 A pedunculated fibroid is seen to be prolapsed into the cervix (A); the pedicle is highlighted by colour Doppler, seen here
in monochrome (B).
A B
Figure 36.61 Cervical cancer. Ultrasound (A) of stage IV disease, with invasion of the bladder. MR scan (B) also shows a large
cavitating mass replacing the cervix and invading the bladder.
Cervical cancer
Second most common gynaecological cancer.
New HPV vaccination programme recently instigated.
Usually asymptomatic and found on screening.
Ultrasound has little or no role in early stage disease.
MR scan is the best imaging tool for staging.
Ultrasound may detect complications such as hydronephrosis
and bladder invasion.
Surgery reserved for stage I and IIa disease.
Stage Description
I Invasive carcinoma confined to cervix
II Extends beyond the cervix, but not to either the
pelvic side wall or the lower third of the vagina
IIa No obvious parametrial involvement
IIb Obvious parametrial involvement Figure 36.62 Cervical cancer. Transverse T2-weighted MR scan
III The pelvic side wall or the lower third of the through the cervix: there is an intact stromal ring, shown by the
vagina are involved dark band (arrows) surrounding the greyer central tumour.
IV Spread beyond the pelvis or involvement of the
bladder or rectum
THE VAGINA
Most vaginal pathology is assessed clinically but some anomalies
Transrectal or transvaginal ultrasound-guided biopsies can be will be found incidentally at pelvic ultrasound. Counter-intuitively,
invaluable in confirming recurrent cervical cancer when clinically the transvaginal scan is least effective at identifying pathology as it
directed biopsies have failed to secure the diagnosis.107 is too close to the lesion or the probe may have gone past it before
the operator starts looking. Transabdominal scans with a full
bladder or transperineal scans show the vagina best.
Management
Surgery with or without adjuvant radiotherapy is reserved for stage Foreign bodies
I and stage IIa disease. Stage IIb and worse are generally treated
with radiotherapy. Compromise to the renal tract will require ure- A tampon is clearly seen because of the air it contains. It produces
teric stenting in order to preserve function. a well-defined, reflective linear shape with posterior acoustic
715
CHAPTER 36 Uterus and vagina
shadowing that lies centrally within the vagina. The innermost end haematomas (most often seen after vaginal delivery) may compress
of the tampon may abut and deform the posterior bladder wall.108 the vagina and be mistakenly thought to be intravaginal. Endome-
Retained tampons or other foreign matter may provoke a vaginitis, triotic implants also occur.
and present with a bloody discharge. If they become infected a foul
discharge will result and the toxic shock syndrome may develop. Solid vaginal lesions
A vaginal ring pessary is used in the treatment of prolapse. These
produce a characteristic appearance on ultrasound. Any cross-sec-
Fibroids very rarely occur within the vagina and may mimic pro-
tion of the pessary produces two rounded lesions, each with a dense
lapse.112 Sometimes pedunculated submucosal fibroids can prolapse
acoustic shadow. Typically, the transverse view of the pelvis will
through the cervix into the vagina.113 The fibroids display the same
show these dense echogenicities laterally in the fornices. Tracing
sonographic features as fibroids anywhere else. Neurofibromas
these masses around confirms the ring shape of the pessary.
occur in the vagina in people with neurofibromatosis.
Gas may be present in the vagina, either as a result of instrumen-
Primary vaginal tumours account for only 12% of gynaecologi-
tation or recent sexual intercourse. Vaginal calculi are rare and
cal malignancies, and most are squamous cell carcinomas and occur
may just be calcification of a retained foreign body. Vaginal
in the elderly. Adenocarcinomas and melanomas are much rarer.
septa or urinary reflux into the vagina can predispose to calculus
Tumours present with a vaginal discharge or blood loss. The diag-
formation.
nosis is invariably made clinically and confirmed by biopsy. Ultra-
Teflon injection used around the urethral sphincter in the treat-
sound shows the tumour as a low-echo mass lying within the upper
ment of urinary incontinence shows up as an echogenic amorphous
third of the vagina, if it is visible at all. Spread of tumour is similar
mass adjacent to the vagina.
to cervical cancer and may cause hydronephrosis. The main imaging
modality is MRI, with ultrasound having little if any role to play.
Fluid-filled vaginal lesions Rhabdomyosarcoma is the commonest soft tissue sarcoma of
childhood and 20% will involve the genitourinary tract. In girls,
Cystic lesions of the vagina are relatively common and usually most are vaginal in origin, although spread to or from the uterus
represent benign lesions. A vaginal cyst may be an embryological also occurs. A rapidly enlarging mass which may protrude through
derivative, ectopic tissue or urological abnormality.109 Hydrocolpos the introitus is associated with vaginal bleeding. Staging with MR
arising as a result of an intact hymen or a congenital vaginal septum is the preferred imaging method, although ultrasound initially may
has been discussed earlier in the Haematometrium and other find the mass incidentally (Fig. 36.64).
related conditions section. There can be associated renal malforma-
tions so the kidneys should always be examined as part of the
ultrasound scan. Hydrocolpos should not be confused with a small
amount of free fluid, such as blood during menstruation or urine
from a fistula or ectopic ureter. A history of persistent wetting The vagina
should lead to the latter diagnosis. Standing the patient up and Transabdominal ultrasound often sees the vagina better than a
rescanning can also help. TV scan.
Gartners duct cysts are remnants of the embryological mesone- Tampons and pessaries have characteristic appearances.
phric duct110 and are usually small, often multiple cysts that lie Cystic lesions may be due to an obstructed genital tract or due
within or adjacent to the anterior vaginal wall (Fig. 36.63). Mlle- to embryological remnants.
rian duct cysts are similarly remnants of the embryological para- Reflux of urine into the vagina during voiding may mimic a cystic
mesonephric duct system and are usually small and located lesion.
anterolaterally. Both types of cyst can appear identical on ultra- Solid lesions are uncommon and are usually fibroids or
sound and only histological examination can tell them apart. Occa- neurofibromas.
sionally both types of cyst can be sufficiently large to prolapse Malignant lesions usually occur in the elderly and account for only
through the introitus.111 An MR scan is useful to give an overview 12% of gynaecological malignancies.
of the anatomy. Both types of cyst are associated with renal anoma- Most malignancies are usually squamous cell carcinomas,
lies. There are usually no symptoms and the cysts are soft to palpate. although adenocarcinomas and melanomas do occur. The young
Dilation of paraurethral glands can produce cysts adjacent to the may get rhabdomyosarcoma.
vagina that sometimes compress the vagina. Similarly, paravaginal
A B
Figure 36.63 Gartners duct cyst. An ovoid cyst is seen arising in the anterior vaginal wall adjacent to the cervix (A) and in close-up (B).
716
References
A B
Figure 36.64 Rhabdomyosarcoma. The initial ultrasound (A) was thought to show a linear echogenic foreign body, but the MR (B)
shows that in reality there is a large vaginal tumour with some central necrosis correlating with the echogenic region seen on ultrasound.
The tumour was proven to be a rhabdomyosarcoma.
REFERENCES 18. Wen L, Tseng JY, Wang PH. Vaginal expulsion of a submucosal
myoma during treatment with long-acting gonadotrophin-releasing
1. Donald I. Use of ultrasonics in the diagnosis of abdominal swelling. hormone agonist. Taiwan J Obstet Gynecol 2006;45:173175.
BMJ 1963;2:11541155. 19. Fogata ML, Jain KA. Degenerating cystic uterine fibroid mimics an
2. Kratochwil A. Ein neues vaginales Schnittbildverfahren. Geburtshilfe ovarian cyst in a pregnant patient. J Ultrasound Med
Frauenheilkd 1969;29:379385. 2006;25:671674.
3. Sherer DM, Cheung W, Gorelick C, et al. Sonographic and magnetic 20. Madan R. The bridging vascular sign. Radiology 2006;238:371372.
resonance imaging findings of an isolated vaginal leiomyoma. J 21. Roy C, Bierry G, El Ghali S, et al. Acute torsion of uterine
Ultrasound Med 2007;26:14531456. leiomyoma: CT features. Abdom Imaging 2005;30:120123.
4. Evans P, Brunsell S. Uterine fibroid tumours: diagnosis and 22. Cobellis L, Pecori E, Rigatti F, et al. A rare case of female pelvic mass:
treatment. Am Fam Physician 2007;75:15031508. angioleiomyoma of the broad ligament. Eur J Gynaecol Oncol
5. Baird DD, Dunson DB, Hill MC, et al. Association of physical activity 2007;28:418420.
with development of uterine leiomyoma. Am J Epidemiol 23. Barnacle S, Muir T. Intermittent urinary retention secondary to a
2007;165:157163. uterine leiomyoma. Int Urogynecol J Pelvic Floor Dysfunct
6. Wise LA, Palmer JR, Stewart EA, Rosenberg L. Polycystic ovary 2007;18:12471248.
syndrome and risk of uterine leiomyomata. Fertil Steril 24. Nikolov A, Tiufekchieva E, Raicheva R. [Torsion of a non-gravid
2007;87:11081115. leiomyomatous uterus] Akush Ginekol (Sofiia) 2006;45:4951.
7. Venkatachalam S, Bagratee JS, Moodley J. Medical management of 25. Ferrero S, Abbamonte LH, Giordano M, et al. Uterine myomas,
uterine fibroids with medroxyprogesterone acetate (DepoProvera):a dyspareunia, and sexual function. Fertil Steril 2006;86:15041510.
pilot study. J Obstet Gynaecol 2004;24:798800. 26. Maizlin ZV, Vos PM, Cooperberg PL. Is it a fibroid? Are you sure?
8. Fiscella K, Eisinger SH, Meldrum S, et al. Effect of mifepristone for Sonography with MRI assistance. Ultrasound Q 2007;23:5562.
symptomatic leiomyomata on quality of life and uterine size: a 27. Vitiello D, McCarthy S. Diagnostic imaging of myomas. Obstet
randomised controlled trial. Obstet Gynecol 2006;108:13811387. Gynecol Clin North Am 2006;33:8595.
9. Chia CC, Huang SC, Chen SS, et al. Ultrasonographic evaluation of 28. Tamura-Sadamori R, Emoto M, Naganuma Y, et al. The
the change in uterine fibroids induced by treatment with a GnRH sonohysterographic difference in submucosal uterine fibroids and
analog. Taiwan J Obstet Gynecol 2006;45:124128. endometrial polyps treated by hysteroscopic surgery. J Ultrasound
10. Kaunitz AM. Progestin-releasing intrauterine systems and Med 2007;26:941946.
leiomyoma. Contraception 2007;75(6 Suppl):S130S133. 29. Harmanli OH, Bevilacqua SA, Dandolu V, et al. Adenomyosis
11. Lurie S, Piper I, Woliovitch I, Glezerman M. Age-related prevalence interferes with accurate ultrasonographic detection of uterine
of sonographically confirmed uterine myomas. J Obstet Gynaecol leiomyomas. Arch Gynecol Obstet 2005;273:146149.
2005;25:4244. 30. Aviram R, Ochshorn Y, Markovitch O, et al. Uterine sarcomas versus
12. Neiger R, Sonek JD, Croom CS, Ventolini G. Pregnancy-related leiomyomas: gray-scale and Doppler sonographic findings. J Clin
changes in the size of uterine leiomyomas. J Reprod Med Ultrasound 2005;33:1013.
2006;51:671674. 31. Exacoustos C, Romanini ME, Amadio A, et al. Can gray-scale and
13. Ouyang DW, Economy KE, Norwitz ER. Obstetric complications of color Doppler sonography differentiate between uterine
fibroids. Obstet Gynecol Clin North Am 2006;33:153169. leiomyosarcoma and leiomyoma? J Clin Ultrasound 2007;35:449
14. Vergani P, Locatelli A, Ghidini A, et al. Large uterine leiomyomata 457.
and risk of caesarean delivery. Obstet Gynecol 2007;109:410414. 32. Tropeano G, Amoroso S, Scambia G. Non-surgical management of
15. Nguyen QH, Gruenewald SM. Sonographic appearance of a uterine fibroids. Hum Repro Update 2008;14:259274.
postpartum pyomyoma with gas production. J Clin Ultrasound 33. Cho HH, Kim JH, Kim MR. Transvaginal radiofrequency thermal
2008;36:186188. ablation: a day-care approach to symptomatic uterine myomas. Aust
16. Levens ED, Stegmann BJ, Feinberg EC, Larsen FW. Ultrasonographic N Z J Obstet Gynaecol 2008;48:296301.
characteristics of the endometrium among patients with fibroids 34. Recaldini C, Carrafiello G, Lagana D, et al. Percutaneous
undergoing ART. Fertil Steril 2008;89:10051007. sonographically guided radiofrequency ablation of medium-sized
17. Vimercati A, Scioscia M, Lorusso F, et al. Do uterine fibroids affect fibroids: feasibility study. AJR Am J Roentgenol 2007;189:1303
IVF outcomes? Reprod Biomed Online 2007;15:686691. 1306.
717
CHAPTER 36 Uterus and vagina
35. Hesley GK, Gorny KR, Henrichsen TL, et al. A clinical review of 62. Kanat-Pektas M, Gungor T, Mollamahmutoglu L. The evaluation of
focused ultrasound ablation with magnetic resonance guidance: an endometrial tumors by transvaginal and Doppler ultrasonography.
option for treating fibroids. Ultrasound Q 2008;24:131139. Arch Gynecol Obstet 2007; Nov29 Epub.
36. Peric H, Fraser IS. The symptomatology of adenomyosis. Best Pract 63. Tsikouras P, Liberis V, Galazios G, et al. TV sonographic assessment
Res Clin Obstet Gynaecol 2006;20:547555. in postmenopausal women with bleeding. Eur J Gynaecol Oncol
37. Kepkep K, Tuncay YA, Goynumer G, Tutal E. Transvaginal 2008;29:6771.
sonography in the diagnosis of adenomyosis: which findings are 64. Williams SC, Lopez C, Yoong A, McHugo JM. Developing a robust
most accurate? Ultrasound Obstet Gynecol 2007;30:341345. and efficient pathway for the referral and investigation of women
38. Lee EJ, Joo HJ, Ryu HS. Sonographic findings of uterine polypoid with post-menopausal bleeding using a cut-off of <or= 4mm for
adenomyomas. Ultrasound Q 2004;20:211. normal thickness. Br J Radiol 2007;80:719723.
39. Ors F, Lev-Toaff AS, Bergin D. Echogenic foci mimicking 65. Debby A, Malinger G, Glezeman M, Golan A. Intra-uterine fluid
adenomyosis presumably due to air intravasation into the collection in postmenopausal women with cervical stenosis.
myometrium during sonohysterography. Diagn Interv Radiol Maturitas 2006;55:334337.
2007;13:2629. 66. Takacs P, De Santis T, Nicholas MC, et al. Echogenic fluid collection
40. Levgur M. Diagnosis of adenomyosis: a review. J Reprod Med in postmenopausal women is a significant risk factor for disease. J
2007;52:177193. Ultrasound Med 2005;24:14771481.
41. Dueholm M, Lundorf E. Transvaginal ultrasound or MRI for 67. Takac I. Transvaginal ultrasonography with and without saline
diagnosis of adenomyosis. Curr Opin Obstet Gynecol infusion in assessment of myometrial invasion of endometrial cancer.
2007;19:505512. J Ultrasound Med 2007;26:949955.
42. Levgur M. Therapeutic options for adenomyosis: a review. Arch 68. Takac I. Saline infusion sonohysterography and the risk of malignant
Gynecol Obstet 2007;276:115. extrauterine spread in endometrial cancer. Ultrasound Med Biol
43. Teo SY, Babagbemi KT, Peters HE, Mortele KJ. Primary malignant 2008;34:711.
mixed Mullerian tumor of the uterus: findings on sonography, CT 69. Mansour GM, El-Lamie IK, El-Kady MA, et al. Endometrial volume
and gadolinium-enhanced MRI. AJR Am J Roentgenol as predictor of malignancy in women with postmenopausal bleeding.
2008;191:278283. Int J Gynaecol Obstet 2007;99:206210.
44. Huang MW, Muradali D, Thurston WA, et al. Uterine arteriovenous 70. Yaman C, Habelsberger A, Tews G, et al. The role of three-
malformations: gray-scale and Doppler US features with MR imaging dimensional volume in diagnosing endometrial cancer in patients
correlation. Radiology 1998;206:115123. with postmenopausal bleeding. Gynecol Oncol 2008 Jun 23 Epub.
45. Kwon JH, Kim GS. Obstetric iatrogenic arterial injuries of the uterus: 71. Odeh M, Vainerovsky I, Grinin V, et al. Three-dimensional
diagnosis with US and treatment with transcatheter arterial endometrial volume and 3-dimensional power Doppler analysis in
embolisation. Radiographics 2002;22:3546. predicting endometrial carcinoma and hyperplasia. Gynecol Oncol
46. Jain K, Fogata M. Retained products of conception mimicking a large 2007;106:348353.
endometrial AVM: complete resolution following spontaneous 72. Van den Bosch T, Verguts J, Daemen A, et al. Pain experienced during
abortion. J Clin Ultrasound 2007;35:4247. transvaginal ultrasound, saline contrast sonohysterography,
47. van den Bosch T, Daemen A, Van Schoubroeck D, et al. Occurrence hysteroscopy and office sampling: a comparative study. Ultrasound
and outcome of residual trophoblastic tissue: a prospective study. J Obstet Gynecol 2008;31:346351.
Ultrasound Med 2008;27:357361. 73. Timmermans A, Opmeer BC, Veersema S, Mol BW. Patients
48. Betel C, Atri M, Arenson AM, et al. Sonographic diagnosis of preferences in the evaluation of postmenopausal bleeding. Br J Obstet
gestational trophoblastic disease and comparison with retained Gynaecol 2007;115:11461149.
products of conception. J Ultrasound Med 2006;25:985993. 74. Spencer JA, Messiou C, Swift SE. MR staging of endometrial cancer:
49. Fowler DJ, Lindsay I, Secki MJ, Sebire NJ. Histomorphometric needed or wanted? Cancer Imaging 2008;8:15.
features of hydatidiform moles in early pregnancy: relationship to 75. Welton AJ, Vickers MR, Kim J, et al. Health related quality of life
detectability by ultrasound examination. Ultrasound Obstet Gynecol after combined hormone replacement therapy: randomised controlled
2007;29:7680. trial. BMJ 2008;337:a1190.
50. Allen SD, Lim AK, Secki MJ, et al. Radiology of gestational 76. Barnabei VM, Cochrane BB, Aragaki AK, et al. Menopausal
trophoblastic neoplasia. Clin Radiol 2006;61:301313. symptoms and treatment-related effects of estrogen and progestin
51. Yu D, Wong YM, Cheong Y, et al. Asherman syndrome one century in the Womens Health Initiative. Obstet Gynecol 2005;105:
later. Fertil Steril 2008;89:759779. 10631073.
52. Zimmer EZ, Bardin R, Tamir A, Bronshtein M. Sonographic imaging 77. Vickers MR, MacLennan AH, Lawton B, et al. Main morbidities
or cervical scars after Cesarean section. Ultrasound Obstet Gynecol recorded in the womens international study of long duration
2004;23:594598. oestrogen after menopause (WISDOM): a randomised controlled trial
53. Hamar BD, Saber SB, Cackovic M, et al. Ultrasound evaluation of the of hormone replacement therapy in postmenopausal women. BMJ
uterine scar after caesarean delivery: a randomized controlled trial of 2007;335:239.
one- and two-layer closure. Obstet Gynecol 2007;110:808813. 78. Lethaby A, Suckling J, Barlow D, et al. Hormone replacement
54. Ofili-Yebovi D, Ben-Nagi J, Sawyer E, et al. Deficient lower-segment therapy in post-menopausal women: endometrial hyperplasia and
Cesarean section scars: prevalence and risk factors. Ultrasound irregular bleeding. Cochrane Database Syst Rev 2004;3: CD000402.
Obstet Gynecol 2008;31:7277. 79. Polin SA, Ascher SM. The effect of tamoxifen on the genital tract.
55. Holland MG, Bienstock JL. Recurrent ectopic pregnancy in a Cancer Imaging 2008;8:135145.
caesarean scar. Obstet Gynecol 2008;111:541545. 80. Garuti G, Cellani F, Centinaio G, et al. Prospective endometrial
56. Seffah JD, Adanu RM. Sonographic findings in women with assessment of breast cancer patients treated with third generation
complications after hysterectomy. Int J Gynaecol Obstet aromatase inhibitors. Gynecol Oncol 2006;103:599603.
2008;100:160162. 81. Valenzano Menada M, Costantini S, Moioli M, et al. Evaluation of
57. Brun JL, Descat E, Boubli B, Dallay D. Endometrial hyperplasia: a endometrial thickness in hormone receptor positive early stage breast
review [in French]. J Gynecol Obstet Biol Reprod (Paris) cancer postmenopausal women switching from adjuvant tamoxifen
2006;35:542550. treatment to anastrozole. Breast 2008 Jul 5. Epub ahead of print.
58. Montgomery BE, Daum GS, Dunton CJ. Endometrial hyperplasia: a 82. Ortiz ME, Croxatto HB, Bardin CW. Mechanisms of action of
review. Obstet Gynecol Surv 2004;59:368378. intrauterine devices. Obstet Gynecol Surv 1996;51(12 Suppl):S4251.
59. Marchetti M, Vasile C, Chiarelli S. Endometrial cancer: asymptomatic 83. Peri N, Graham D, Levine D. Imaging of intrauterine contraceptive
endometrial findings. Characteristics of postmenopausal endometrial devices. J Ultrasound Med 2007;26:13891401.
cancer. Eur J Gynaecol Oncol 2005;26:479484. 84. Sviggum O, Skjeldestad FE, Tuveng JM. Ultrasonically guided
60. Opolskiene G, Sladkevicius P, Valentin L. Ultrasound assessment of retrieval of occult IUD in early pregnancy. Acta Obstet Gynecol
endometrial morphology and vascularity to predict endometrial Scand 1991;70:355357.
malignancy in women with postmenopausal bleeding and 85. Keebler C, Chatwani A, Schwartz R. Actinomycosis infection
sonographic endometrial thickness >or= 4.5mm. Ultrasound Obstet associated with intrauterine contraceptive devices. Am J Obstet
Gynecol 2007;30:332340. Gynecol 1983;145:596599.
61. Michail G, Karahaliou A, Skiadopoulos S, et al. Texture analysis of 86. Boardman LA, Peipert JF, Brody JM, et al. Endovaginal sonography
perimenopausal and post-menopausal endometrial tissue in grayscale for the diagnosis of upper genital tract infection. Obstet Gynecol
transvaginal ultrasonography. Br J Radiol 2007;80:609616. 1997;90:5457.
718
References
87. Chang JW, Yang LY, Wang HH, et al. Acute urinary retention as the 100. Lotgering FK. Clinical aspects of cervical insufficiency. BMC
presentation of an imperforate hymen. J Chin Med Assoc Pregnancy Childbirth 2007;7(Suppl 1):S17.
2007;70:559561. 101. Pugatsch R, Elad D, Jaffa AJ, Eytan O. Analysis of cervical dynamics
88. Asha B, Manila K. An unusual presentation of uterus didelphys with by ultrasound imaging. Ann N Y Acad Sci 2007;1101:203214.
obstructed hemivagina with ipsilateral renal agenesis. Fertil Steril 102. Incerti M, Ghidini A, Locatelli A, et al. Cervical length < or = 25 mm
2008 Jul 12 (epub ahead of print). in low-risk women: a case control study of cerclage with rest vs rest
89. Ghirardo V, Cecchetto G, Minucci D, et al. Haematometra in uterus alone. Am J Obstet Gynecol 2007;197:315.e14.
didelphys: a pitfall in teenagers with lower abdominal mass. Report 103. Roman AS, Rebarber A, Pereira L, et al. The efficacy of
of two cases. Paediatr Med Chir 2008;30:4144. sonographically indicated cerclage in multiple gestations. J
90. Anguenot JL, Ibecheole V, Salvat J, Campana A. Hematocolpos Ultrasound Med 2005;24:763768.
secondary to imperforate hymen, contribution of transrectal 104. Rust OA, Atlas RO, Kimmel S, et al. Does the presence of a funnel
echography. Acta Obstet Gynecol Scand 2000;79:614615. increase the risk of adverse perinatal outcome in a patient with a
91. McCausland AM, McCausland VM. Long-term complications of short cervix? Am J Obstet Gynecol 2005;192:10601066.
endometrial ablation: cause, diagnosis, treatment and prevention. J 105. Fischerova D, Cibula D, Stenhova H, et al. Transrectal ultrasound and
Minim Invasive Gynecol 2007;14:399406. magnetic resonance imaging in staging early cervical cancer. Int J
92. Bollapragada SS, Sircar S, Rae DW, Walker E. Unexplained Gynecol Cancer 2008;18:766772.
postmenopausal hematometra. Acta Obstet Gynecol Scand 106. Ghi T, Giunchi S, Kuleva M, et al. Three-dimensional transvaginal
2006;85:121123. sonography in local staging of cervical carcinoma: description of a
93. Sadan O, Golan A, Girtler O, et al. Role of sonography in the novel technique and preliminary results. Ultrasound Obstet Gynecol
diagnosis of retained products of conception. J Ultrasound Med 2007;30:778782.
2004;23:371374. 107. Roy D, Kulkarni A, Kulkarni S, Thakur MH, et al. Transrectal
94. Ustunyurt E, Kaymak O, Iskender C, et al. Role of transvaginal ultrasound-guided biopsy of recurrent cervical carcinoma. Br J Radiol
sonography in the diagnosis of retained products of conception. Arch 2008 Jul 28 epub ahead of print.
Gynecol Obstet 2008;277:151154. 108. Caspi B, Zalel Y, Katz Z, et al. The role of sonography in the
95. Sawyer E, Ofuasia E, Ofili-Yebovi D, et al. Ultrasound Obstet Gynecol detection of vaginal foreign bodies in young girls: the bladder
2007;29:205209. indentation sign. Pediatr Radiol 1995;25(Suppl 1):S6061.
96. Rufener SL, Adusumilli S, Weadock WJ, Caoili E. Sonography of 109. Eilber KS, Raz S. Benign cystic lesions of the vagina: a literature
uterine abnormalities in post partum and postabortion patients: a review. J Urol 2003;170:717722.
potential pitfall of interpretation. J Ultrasound Med 2008;27:343348. 110. Deppisch LM. Cysts of the vagina: classification and clinical
97. Dubinsky TJ, Reed SD, Grieco V, Richardson ML. Intracervical correlations. Obstet Gynecol 1975;45:632637.
sonographic-pathologic correlation: preliminary results. J Ultrasound 111. Kresowik J, Kennedy CM, Wing S, Galask RP. Prolapsing vaginal
Med 2003;22:6167. cyst: a case report. J Reprod Med 2007;52:852854.
98. Fogel SR, Slasky BS. Sonography of nabothian cysts. AJR Am J 112. Leron E, Stanton SL. Vaginal leiomyoma an imitator of prolapse. Int
Roentgenol 1982;138:927930. Urogynecol J Pelvic Floor Dysfunct 2000;11:196198.
99. Bajo J, Moreno-Calvo FJ, Uguet-de-Resayre C, et al. Contribution of 113. McCarthy S, Taylor KJW. Sonography of vaginal masses. AJR Am J
sonography to the evaluation of benign cervical conditions. J Clin Roentgenol 1983;140:10051006.
Ultrasound 1999;27:6164.
719
CHAPTER
Gynaecological intervention
techniques
Michael J. Weston
37
colon, appendix, pancreas and stomach.24 The treatment of these
INTRODUCTION 720 different tumours varies and debulking surgery is contraindicated
OMENTAL BIOPSY 720 in some. Modern histology techniques, including immunohisto-
Rationale 720 chemistry, allow a site-specific diagnosis to be made in over 90% of
Method 720 biopsies taken.
Complications 722 Seeding of tumour along a biopsy track or into the peritoneal
cavity is a potential risk, though not one that has been quantified.
TRANSVAGINAL BIOPSY OR CYST ASPIRATION 722
Rationale 722 Most reports are anecdotal. However, this perceived risk influences
Method 722 practice and routes of access. Consequently, percutaneous biopsies
Complications 723 are not done in suspected malignancy unless there is already evi-
dence of spread from the primary tumour. Computed tomography
PELVIC ABSCESS DRAINAGE 724 or MRI should be performed to stage the tumour before considering
Rationale 724
any biopsy. These scans not only stage the tumour but also allow
Method 724
Complications 727 planning of the biopsy procedure.
Figure 37.1 Three examples of omental tumour. A: The omental cake is seen as an irregular lumpy sheet within a large pool of
ascites. The cake is still seen as a sheet of tissue whether the probe is held in the transverse or longitudinal plane. B: Less ascites is
present but it still outlines a sheet of omental tumour (between the callipers). Note that it has a lumpy outline similar to the disease seen in
A. C: An example of a smaller amount of omental tumour, more adherent to the anterior abdominal wall.
Omental biopsy
Percutaneous omental biopsy is safe.
Imaging-guided biopsy avoids the need for laparoscopic or open
biopsy.
Technique is no different to any other biopsy.
Time spent in preparation is never wasted.
target. The operator needs to ensure that they line up their needle
with the guide so that when they push, the needle is not forced into
a bend. The quick advancement of the needle through the guide
improves visualisation of the tip of the needle. The position of the
needle tip and the mechanism of firing the cutting mechanism will
vary between manufacturers. The operator needs to be familiar
with the needle they are using.
The core retrieved should be inspected to see if it contains the
Figure 37.2 Omental tumour being scanned to plan the route of expected firm white tissue that most malignant deposits exhibit.
biopsy. A colour Doppler box is used to check there are no large The number of needle passes made depends on the quality of the
vessels in the intended target. The needle guide lines are graduated specimen. Two good cores are usually enough to allow histology
with centimetre marks. This helps to judge where to place the and various different immunohistochemistry stains.
biopsy needle and how far the needle will throw on firing. Once the nick in the skin has stopped bleeding and a small dress-
ing has been applied, the woman can sit up. They can leave straight
away if they wish but most people prefer to sit for half an hour with
a soft drink before leaving.
721
CHAPTER 37 Gynaecological intervention techniques
Complications Method
Percutaneous omental biopsy is a very well tolerated and extremely Transvaginal biopsy can be done as an outpatient procedure. No
safe procedure. No significant complications have been recorded in particular preparation is needed although clotting abnormalities
several series. Bowel seems remarkably tolerant to the passage of require correction. The patient lies in the usual position for a trans-
an 18-gauge needle and no descriptions of bowel damage are vaginal scan. Stirrups are not necessary. Some authorities advocate
reported. The occasional haematoma is seen (1 out of 90 patients in vaginal cleansing with povidone-iodine and a course of antibiotics
one series). as the vaginal route of access is only semi-sterile. However, in my
own practice, I have found that the use of an antiseptic cream as
the probe lubricant and no antibiotics has not resulted in any infec-
tive complications in almost one hundred biopsies.
TRANSVAGINAL BIOPSY OR Some authorities prefer to perform transvaginal biopsies under
CYST ASPIRATION conscious sedation.8 If this approach is used then fasting for 6 hours
and adherence to your own institutional guidelines are required.
Sedation is not essential, however, and in my practice I have found
Rationale it is rarely needed. Careful discussion with the woman beforehand
and an appropriate reassuring environment usually allow the
Masses in the pelvis may be inaccessible percutaneously because of biopsy to take place without undue discomfort.
intervening bowel, bladder or vascular structures. The transvaginal A transvaginal transducer with a needle guide attachment is
route of access can allow the probe to be positioned directly adja- essential (Fig. 37.4). It should be possible in most cases to position
cent to the target lesion. The need for a biopsy is usually the same the probe within a few millimetres of the lesion so that there is not
as described in the omental biopsy section above. One potential much more than the vaginal wall for the needle to traverse before
advantage of the transvaginal route is that if there is any seeding hitting the lesion (Figs 37.5 and 37.6). Once the target for biopsy is
of tumour down the biopsy track it is not upstaging the tumour identified with due consideration to any intervening structures and
by spreading disease into a different compartment. However, it is blood vessels then the probe should be pushed gently but firmly.
still best avoided in lesions thought to be confined to the ovary This is to stretch the vaginal wall and make it taut so that the needle
(stage I).6 will puncture it more readily. It is almost impossible to infiltrate
Aspiration of simple cysts is neither advised nor needed.7 It has
been shown that the rate of resolution of simple cysts is the same
whether treated with watchful waiting or with aspiration. Cysts
Transvaginal intervention
often recur after aspiration. Endometriomas in particular have a
high rate of recurrence and are also quite painful to drain. Transvaginal biopsy is well tolerated.
Women who are undergoing palliative treatment for peritoneal Sedation is not normally required.
cancer may develop pelvic symptoms due to the local pressure Draining simple cysts is no better than watchful waiting.
effects of a malignant cyst. It is entirely reasonable to offer palliation Allows access to lesions that cannot be reached percutaneously.
of these symptoms by draining the cyst (Fig. 37.3).
A B
Figure 37.3 Transvaginal drainage of a malignant cyst to palliate pelvic symptoms. A: The large pelvic cyst clearly has tumour
nodules around its margin. The transvaginal probe is pushed against the cyst to indent its margin and stretch the vaginal wall. Note that
the amount of tissue the needle has to pass through to penetrate the cyst is minimal if it travels along the dotted guide line. B: The same
cyst is shown collapsed and empty after successful transvaginal aspiration of its contents.
722
Transvaginal biopsy or cyst aspiration
A B
Figure 37.4 Transvaginal biopsy. A: An endoluminal ultrasound probe with a probe cover and needle guide attachment. A needle has
been passed through the guide to show its route of passage relative to the probe. B: A transvaginal scan with the tip of the probe pushed
into the margin of a cyst to stretch the vaginal wall. A needle has been passed into the cyst. The tip can be seen as a bright echo along
the dotted needle guide line.
local anaesthetic adequately and doing so may cause more discom- Once the biopsy or drainage is done, the woman should be
fort than just passing the biopsy needle. Generally, the least amount warned to expect a little vaginal bleeding not unlike menstrual loss.
of needle manipulation is the most comfortable. A single pass with Most women are fit enough to leave the department after half an
an 18-gauge core-biopsy needle is usually enough to sample a solid hour. It helps if they attend with a companion. Women who have
lesion though most women will allow a second pass if needed. been sedated will need somewhere to recover before they can be
If a cystic lesion is being drained, this can usually be achieved allowed home.
through a 19-gauge sheathed needle. The needle is placed into the
lesion using the same technique as described for a biopsy above. Complications
The metal inner part of the needle is removed and the outer plastic
sheath left in the lesion. An assistant can then drain the lesion using Complication rates are very low. Most of those described in the
a syringe and some connecting tubing to the back of the sheath. literature are related to draining endometriomas.9
723
CHAPTER 37 Gynaecological intervention techniques
A B
Figure 37.6 A: Rounded serosal tumour deposit on a loop of bowel. B: Transvaginal needle biopsy of the mass note the bright white
line from the cavitation artefact caused by firing the needle. A path has been chosen that avoids the bowel lumen.
724
Pelvic abscess drainage
B
B
C C
Figure 37.7 Transrectal aspiration of a small presacral Figure 37.8 Gas makes abscesses hard to see with
abscess. A: Pelvic CT scan showing an abscess in front of the ultrasound. A: CT scan of a pelvic diverticular abscess containing
sacrum. Note that bowel and bladder prevent an anterior mostly air. B: Transrectal ultrasound scan of the abscess. The gas
percutaneous approach to aspiration. A transgluteal approach renders the abscess invisible, leaving a only bright shadowing edge
would be possible but this route can be quite painful. B: Magnified visible. C: CT scan of a postoperative pelvic abscess containing an
view of the presacral abscess on CT. C: A transrectal ultrasound airfluid level. This abscess can be drained percutaneously using
image showing the same presacral abscess with a needle tip in its CT guidance. Alternatively, turning the patient so the gas is out of
centre. Only a short distance has had to be traversed for the the way allows ultrasound to be used for guidance as well.
needle to reach the lesion. The ultrasound probe has to be angled
posteriorly for the lesion to be visualised.
725
CHAPTER 37 Gynaecological intervention techniques
Figure 37.9 Three examples of a guide-wire placed transrectally into an abscess. A: Tumour related abscess. The wire is easily
visible. B: Post-bowel-surgery abscess. The ultrasound probe is in the residual rectal stump. C: Diverticular abscess. The wire can be seen
to be curled within the collection. Note that in all three cases the distance from rectum to the abscess is very small.
Complications the cervix becomes less favourable for passage of a cannula. Most
women will have a standard pelvic ultrasound scan done first, by
Theoretically, septicaemic shock, haematoma, haemorrhage and both transabdominal and transvaginal routes. This is to ensure
damage to adjacent organs are all possible. However, the literature there is not some larger pathology or adnexal mass that might be
does not report any of these events in the absence of blood dyscra- missed by concentrating just on the endometrium.
sias and if antibiotics have been given.1013 A sterile catheter is prepared by attaching a syringe filled with
saline to it and flushing it to expel any air. The saline should have
been drawn up into the syringe in a slow steady fashion so as not
to aerate the saline and render it opaque to ultrasound. Special
SALINE INFUSION HYSTEROGRAPHY hysterosonography catheters are made by several manufacturers;
these come with a balloon that can be inflated to retain the catheter
in the uterus and to prevent leakage of saline out through the cervi-
Rationale cal os (Fig. 37.12). They are relatively expensive. An alternative is
to use a simple 6F infant feeding tube (which costs about 15 pence).
The disadvantage of this is that without a balloon to hold it in place
This is the instillation of sterile saline into the endometrial cavity to
it may dislodge and saline might leak so fast through the os that
act as a negative contrast agent in order to help demonstrate
the cavity is not distended. Women tolerate the simple tube better
endometrial abnormalities. It is a minimally invasive, outpatient
procedure designed to reduce the need for hysteroscopy. It is done
as an adjunct to normal transvaginal ultrasound and in a depart-
ment set up to offer the service, only adds 10 or 15 minutes to the
appointment time for an ordinary scan. Studies on acceptability
have shown that patients prefer saline infusion hysterography over
outpatient flexible hysteroscopy.14,15
Saline infusion hysterography improves detection of focal
endometrial abnormalities, polyps and submucous fibroids (Figs
37.10 and 37.11) and may improve the assessment of depth of inva-
sion in endometrial cancer.
Some centres have advocated ultrasound-directed endometrial
biopsy as a way of improving the detection of focal abnormalities
over a blind pipelle biopsy.16 Specific sampling devices have been
designed for use during saline infusion hysterography.
Method
Saline infusion hysterography is best done after menstruation and
within the first 10 days of the cycle. If done during menstruation, Figure 37.10 Saline infusion hysterography picture of increased
blood clot may mimic the appearances of a polyp. Later in the cycle endometrial thickness.
A B
Figure 37.11 Pathology visible on saline infusion hysterography. A: Saline outlines a submucosal fibroid. Note that most but not all
fibroids appear relatively echo-poor. B: Saline outlines an endometrial polyp. Note that most but not all polyps appear relatively
echo-bright.
727
CHAPTER 37 Gynaecological intervention techniques
than the balloon catheter and it will be successful in 80% of exami- the endometrial cavity whilst transvaginal ultrasound images are
nations. If not, a balloon catheter can then be placed. obtained.
The woman lies supine, usually with her bottom raised on a If a balloon catheter is used, it may be necessary to deflate the
wedge or pillow. A speculum is advanced into the vagina to allow balloon to allow visualisation of the full endometrial cavity. The
visualisation of the cervix. The cervix is cleaned with povidone- balloon can otherwise obscure endometrial pathology.
iodine. If there are symptoms or signs of vulval or vaginal infection The same technique can be used to instil a positive contrast agent
the procedure should not be done. The pre-prepared catheter is to outline the fallopian tubes in women with delayed conception
introduced through the cervix into the endometrial cavity. It may (Fig. 37.13).
be necessary to grip the cervix and pull it down in order to straighten
out the cervical canal and allow passage of the catheter. Occasion-
ally a sound needs to be passed to dilate the cervix prior to catheter Complications
placement. The speculum is withdrawn, leaving the catheter in
place. A standard transvaginal ultrasound probe is inserted in order Ascending infection, intravasation of saline and abdominal cramp-
to visualise the uterus. A few millilitres of saline are injected into ing pain are potential complications.
A B
Figure 37.12 Saline infusion hysterography. A: Longitudinal transvaginal ultrasound view of the uterus. The endometrial cavity is
distended with saline. The balloon of the catheter is visible in the cavity. B: View of the tip of a hysterography catheter with its balloon
inflated.
REFERENCES 10. Alexander AA, Eschelman DJ, Nazarian LN, Bonn J. Transrectal
sonographically guided drainage of deep pelvic abscesses. AJR Am J
1. Spencer JA, Anderson K, Weston M, et al. Image guided biopsy in the Roentgenol 1994;162:12271232.
management of cancer of the ovary. Cancer Imaging 2006;6:144147. 11. Ryan RS, Mcgrath FP, Haslam PJ, et al. Ultrasound-guided
2. Hewitt MJ, Anderson K, Hall GD, et al. Women with peritoneal endocavitary drainage of pelvic abscesses: technique, results and
carcinomatosis of unknown origin: efficacy of image-guided biopsy to complications. Clin Radiol 2003;58:7579.
determine site-specific diagnosis. Br J Obstet Gynaecol 2007;114:4650. 12. Nielsen MB, Torp-Pedersen S. Sonographically guided transrectal or
3. Fischerova D, Cibula D, Dundr P, et al. Ultrasound guided tru-cut transvaginal one-step catheter placement in deep pelvic and perirectal
biopsy in the management of advanced abdomino-pelvic tumours. Int abscesses. AJR Am J Roentgenol 2004;183:10351036.
J Gynecol Cancer 2007 Aug 30, epub. 13. Sudakoff GS, Lundeen SJ, Otterson MF. Transrectal and transvaginal
4. Que Y, Wang X, Liu Y, et al. Ultrasound-guided biopsy of greater sonographic intervention of infected pelvic fluid collections: a
omentum: an effective method to trace the origin of unclear ascites. complete approach. Ultrasound Q 2005;21:175185.
Eur J Radiol 2008 Mar 5, epub. 14. Rogerson L, Bates J, Weston M, Duffy S. A comparison of outpatient
5. OConnell AM, Keeling F, Given M, et al. Fine-needle trucut biopsy hysteroscopy with saline infusion hysterosonography. Br J Obstet
versus fine-needle aspiration cytology with ultrasound guidance in the Gynaecol 2002;109:800804.
abdomen. J Med Imaging Radiat Oncol 2008;52:231236. 15. Van den Bosch T, Verguts J, Daemen A, et al. Pain experienced during
6. Bret PM, Guibaud L, Atri M, Gillet P, et al. Transvaginal US-guided transvaginal ultrasound, saline contrast sonohysterography,
aspiration of ovarian cysts and solid pelvic masses. Radiology hysteroscopy and office sampling: a comparative study. Ultrasound
1992;185:377380. Obstet Gynecol 2008;31:346351.
7. Zanetta G, Lissoni A, Torri V, et al. Role of puncture and aspiration in 16. Gorlero F, Nicoletti L, Lijoi D, et al. Endometrial directed biopsy
expectant management of simple ovarian cysts: a randomised study. during sonohysterography using the NiGo device: prospective study
BMJ 1996;313:11101113. in women with abnormal uterine bleeding. Fertil Steril
8. ONeill MJ, Rafferty EA, Lee SI, et al. Transvaginal interventional 2008;89:984990.
procedures: aspiration, biopsy and catheter drainage. Radiographics
2001;21:657672.
9. Zanetta G, Trio D, Lissoni A, et al. Early and short-term complications
after US-guided puncture of gynecologic lesions: evaluation after 1000
consecutive cases. Radiology 1993;189:161164.
729
CHAPTER
Endometriosis
INTRODUCTION The classical ground glass appearance of endometriotic deposits is
described in detail in Chapter 35 (Fig. 38.3) although it is worth
Specialists in reproductive medicine have come to rely heavily on mentioning that the majority of endometriosis will not be visible
ultrasound imaging, and IVF units incorporate their own dedicated with ultrasound. However, small deposits may exhibit acute peri-
ultrasound machines and ultrasonographers. Vaginal transducers toneal tenderness or lead to quite dense fibrosis. Therefore note
are used almost exclusively in reproductive medicine because should be taken of areas within the pelvis that are tender to the
the close apposition of the reproductive organs to the vaginal vaginal probe or that do not exhibit the usual tissue compliance.
fornices enables probes of high frequency and hence higher resolv- The significance of endometriosis from the reproductive point of
ing power to be used. Serial observations of graafian follicle devel- view is far from simple. Endometriosis is common in women with
opment within the ovary allow functional as well as structural normal fertility, but even more common in women with subfertility.
assessments. Ovarian and uterine images are used as an aid to Extensive deposits can, of course, cause considerable distortion to
diagnosis, as a way of educating and counselling patients, and, the pelvis or block the fallopian tubes completely. Ovarian endome-
characteristically, as a way of determining the functional response triomas are thought to interfere with the process of ovulation and
to treatment. possibly affect the quality of the oocyte5 but in the vast majority of
The management of subfertile couples begins with an assessment cases the association between minimal endometriosis and subfertil-
of the expected chances of natural conception given the ages, ity remains unexplained. In the only randomised double-blind
medical history, and lifestyle of both partners. Many couples retain placebo-controlled study to address the problem,6 laparoscopic
an unrealistic expectation of their chances of conception. destruction of minimal endometriosis was shown to improve fertil-
The most informative way to display chances of conception is ity in subfertile women, but to nowhere near normal levels and to
with the use of cumulative pregnancy rates (Fig. 38.1). No couple much less than could be achieved by IVF. The implication is that
ever has a chance of conception greater than 1 in 3 per month and whatever results in pelvic endometriosis also results in subfertility
in population studies the chance of pregnancy is on average only and that treatment of the endometriosis does not eliminate what
91% in the first year of trying.1 Although there is some evidence caused it to occur in the first place. It is pragmatic, in the light of
that the incidence of infertility is decreasing in the developed current knowledge, to place cases of subfertility with minimal
world,2 there is still a huge unmet need for medical services for endometriosis in the unexplained aetiological category.
subfertile couples.1 The definition of infertility is usually taken to The decision as to whether to surgically remove endometriotic
be lack of conception after one year of unguarded intercourse, deposits as part of a programme of fertility treatment is hence
although such a strict interpretation may not be clinically useful complex and should be taken on an individual patient basis. The
and in this chapter the term subfertility will be used to indicate a ultrasonographer can help by determining the size and exact ana-
reduced chance of conception compared with what might be tomical location of all deposits, and to determine whether these
expected for a couple of given age and lifestyle. correspond to sites of any pelvic pain.
730
Causes of subfertility
1 Months 12
(Figs 38.5A and B). The exact anatomical location of the fibroid, its
Fibroids
size, the extent it protrudes into the cavity and the thickness of the
overlying myometrium are all important when considering whether Up to 70% of women will develop uterine fibroids.
to undertake hysteroscopic myomectomy in order to enhance Submucous fibroids lower the chances of pregnancy from IVF by
fertility.17 70%.
Hysteroscopic myomectomy can improve pregnancy rates.
Osseous metaplasia of the endometrium Fibroid size, position and overlying myometrium thickness
determine whether hysteroscopic myomectomy can be
performed.
Osseous metaplasia of the endometrium is a rare condition, often
Saline infusion is essential for precise imaging of intrauterine
occurring many years after a failed pregnancy, but the ultrasound
pathology.
appearances are characteristic. Small bony deposits within the
uterine cavity create a hyper-reflective endometrium18 with shad-
owing (Fig. 38.6). The cavity is indistensible when saline is injected
A B
Figure 38.5 Submucous fibroid. Longitudinal views of the uterus showing a fundal fibroid (A) before and (B) after the instillation of saline
into the uterine cavity. Saline infusion enables the fibroid to be seen as totally submucous and therefore comparatively easy to remove
hysteroscopically. It is also possible to see the indentation created by the fibroid in the posterior endometrium. First published R-ITI
copyright RCR.
732
Causes of subfertility
and this may result in considerable pain for the patient. Pregnancy Hydrosalpinges
rarely occurs unless the deposits are removed hysteroscopically.
A hydrosalpinx results when the distal end of the fallopian tube
Endometrial polyps becomes occluded by chronic infection. The walls of the fallopian
tube initially thicken and the tube becomes swollen and oedema-
Endometrial polyps are histologically similar to the endometrium tous, but with continued tissue destruction, probably over several
and retain a little of their hormone sensitivity. Their relevance to years, the walls become devoid of muscle and the whole tube
implantation is hence far less than that of a submucous peduncu- expands into a retort-shaped bag of fluid (Fig. 38.8B).
lated fibroid. Nevertheless pregnancy rates in response to treatment Quite apart from their obvious block to natural conception, hyd-
with intrauterine insemination have been shown to increase after rosalpinges lower implantation rates following IVF by 50%.21 The
hysteroscopic polypectomy in a prospective randomised study.19 presumed mechanism is the gradual leakage of small volumes of
As for other intrauterine pathology, saline infusion is helpful for hydrosalpingeal fluid through the uterine end of the fallopian tube
imaging endometrial polyps (Fig. 38.7) and should be utilised if the into the uterine cavity where it is embryotoxic and/or interferes
location and size need to be accurately determined. Polyps adjacent with implantation. Either placing a clip on the fallopian tube adja-
to the ostium of the fallopian tube may have a greater effect on cent to the uterus or removing the tubes completely at laparoscopy
fertility than those situated elsewhere.20 Small polyps may only be restores IVF pregnancy rates to those that would be expected in
apparent during a single ovarian cycle and therefore surgical women without hydrosalpinges.22 An alternative approach is to
removal should only be considered if the polyp persists after aspirate the hydrosalpinx under ultrasound control at the time of
menstruation. oocyte capture.23
Hydrosalpinges are usually easy to identify with ultrasound (Fig.
38.8A). Their fluid content and hence their size may vary through-
out the menstrual cycle and occasionally they may only become
apparent during ovarian stimulation, when serum hormone levels
are particularly high. If the fallopian tube expands into a hydros-
alpinx when contrast is injected during HyCoSy (see below), there
is a high risk of stimulating a recurrence of the pelvic infection and
antibiotics should be prescribed.
A B
Figures 38.8 Hydrosalpinges, how they typically appear (A) ultrasonographically and (B) at operation. First published R-ITI copyright
RCR.
733
CHAPTER 38 Ultrasound assessment of fertility
HyCoSy
There is grade A evidence that HyCoSy is the investigation of Figure 38.12 3D coronal view of uterus with the positive
choice for all otherwise asymptomatic subfertile women. contrast medium Echovist in the uterine cavity. Contrast could be
HyCoSy has the sensitivity to detect virtually all cases of fallopian seen to pass into both fallopian tubes but it is not possible to show
tube occlusion. the main part of the cavity and the origin of both fallopian tubes in
About two-thirds of the fallopian tubes that cannot be shown as the same plane. Hence only the left tube is shown. The balloon of
patent using HyCoSy are truly occluded. the catheter is situated in the cervix.
A learning curve of up to 50 procedures may be necessary for
those who do not have previous experience of vaginal scanning.
If the semen analysis is abnormal tests of fallopian tube patency
are unwarranted as IVF will probably be necessary even if both
tubes are patent.
Fallopian tubes may be diseased even if they are not occluded. inadequate training because the learning curve is shallow and an
experience of up to 50 procedures30 may be required before consist-
ently reliable reports can be obtained from those who do not previ-
ously have experience of vaginal scanning.
Semen analysis should precede any assessment of fallopian tube
Clinical Excellence, NICE, recommends HyCoSy as the first-line
patency because an abnormal ejaculate might necessitate IVF
investigation for tubal patency assessment in otherwise asympto-
regardless of tubal status and hence tubal investigation becomes
matic women.32
irrelevant. It should also be appreciated that just because a fallopian
The procedure may be uncomfortable, particularly if larger
tube is shown to be patent it is not necessarily completely healthy.
volumes (>5mL) or undue pressure is used, but in our unit more
The delicate endosalpinx can be damaged by infection without the
than 1000 procedures were performed over the first 8 years of our
tube becoming blocked.
HyCoSy programme without the need for narcotic analgesia or any
sort of resuscitation (Fig. 38.11). Pain may be reduced by warming
the contrast medium33 although this will reduce the time over
which the medium is stable and effective. Salpingitis following the SCANNING THROUGH AN IVF CYCLE
procedure is rare but the use of prophylactic antibiotics is
recommended.
During an IVF and embryo transfer (ET) cycle ultrasound is used
Fallopian tubes are muscular and can go into spasm for several
to check for downregulation, to follow the response of the ovary to
minutes, effectively occluding the tube to the passage of contrast
superovulation and then to facilitate both oocyte capture and
medium. A positive screen is defined as when a tube cannot be
embryo transfer.
demonstrated as patent over a 5-minute period.30 Some practition-
ers advocate the use of intravenous anti-spasmodics such as hyos-
cine but this is no more effective than merely waiting patiently for Downregulation
any spasm to recede.
Fallopian tubes are mobile and can twist and turn in their anatomi- During an IVF cycle the pituitary gland must be inhibited from
cal path from the uterus to the ovary so the vaginal probe may need delivering an luteinising hormone (LH) surge, which would result
to be angled and rotated in order to follow the contrast medium and in premature luteinisation. This can be achieved by administering
it may not be possible to show more than a short length of tube at either superagonists or antagonists of gonadotrophin-releasing
any one time. Doppler or 3D techniques can be employed but add hormone (GnRH). If superagonists are used the gland is initially
little, if anything, to the diagnostic ability of the procedure, although stimulated for several days in the luteal phase, and a check must
3D recordings have an advantage for retrospective reporting and be made that ovarian activity has ceased before superovulation can
demonstration purposes (Fig. 38.12). Several groups have criticised commence. The first scan in an IVF/ET cycle therefore checks that
HyCoSy, either because of poor results or because of significant pain all the antral follicles within the ovary are small (<9mm) and that
during the procedure. These instances may have been the result of the endometrium is thin (<5mm).
735
CHAPTER 38 Ultrasound assessment of fertility
A record of the antral follicle count at this time can be used to The average number of oocytes harvested during a superovu-
predict the probable number of oocytes which will be obtained lated IVF cycle is about 10 or 11, but especially in younger women
during the cycle34 and help to decide on the initial dose of follicle- or in women with polycystic ovaries many more large antral folli-
stimulating hormone (FSH). Antral follicle counts reflect the number cles may develop and serum oestradiol levels may rise to 20 or 30
of oocytes remaining in the ovaries (the ovarian reserve) and hence times the values seen during a spontaneous ovulatory cycle. It is
the likely response to treatment and the likelihood of an early important to recognise such an over stimulated ovary as early as
menopause.35 possible because when the ovulatory trigger of hCG is given it can
result in ovarian hyperstimulation syndrome (see below). There is,
Follicular development however, no precise definition of when an ovary is over-stimulated
and risks of hyperstimulation syndrome must be carefully assessed
in each case. The ovulatory trigger is withheld and the treatment
Ovarian follicular development during superovulated IVF treat-
cycle abandoned if more than a certain number of follicles develop
ment is stimulated by FSH injections. Once a cohort of follicles has
and the risk of hyperstimulation syndrome becomes too high. An
emerged their growth is usually about 2mm diameter every 24
alternative approach is to coast the ovary by continuing down-
hours. Ultrasound is used to determine the number and size of all
regulation whilst omitting FSH for several days.38 The serum oestra-
follicles. In a superovulated ovary with as many as 10 follicles of
diol may be a slightly better predictor of the risk of hyperstimulation
different sizes crammed together, follicle shape is rarely spherical
syndrome and coasting is usually continued until oestradiol levels
and a standard measure of size is necessary. Although linear meas-
fall below an agreed threshold, usually about 10000pmol/L.
urements can be performed in all three planes or volume measure-
Ultrasound is also used to monitor ovulation induction in treat-
ments determined by 3D imaging, this can be difficult and
ment cycles other than IVF, where the aim is to achieve conception
time-consuming and a reproducible standard is the mean follicle
by means of natural intercourse or intrauterine insemination. In
diameter as determined by the mean of the longest diameter and
these cases there is a risk of a multiple gestation if more than one
the diameter at right angles at the midpoint of the first measure-
pre-ovulatory sized follicle develops and so the assessment of fol-
ment (Fig. 38.13). Serum oestradiol can be measured at intervals but
licle size and number is critical. Follicles greater than 14mm in
is proportional to follicle growth (most precisely to the sum of the
diameter are capable of ovulating viable oocytes leading to preg-
squared diameters because oestradiol must defuse out through the
nancy39 and if several such follicles develop it is necessary to with-
follicle basement membrane and diffusion is dependent on area)
hold the ovulatory trigger and any further treatment, and for the
and hence adds little to the decisions which need to be made about
couple to refrain from intercourse until the follicles regress.
FSH dose and the timing of the ovulatory trigger. A recent Cochrane
review has not shown any improvement in pregnancy rates by
adding routine serum oestradiol monitoring to ultrasound follicle Oocyte capture
monitoring.36
Patients progressing through IVF treatment often find the process Vaginal ultrasound with conscious sedation is by far the most
stressful.37 The ultrasonographer has an opportunity during the common method of harvesting mature oocytes for IVF. Previous
scanning sessions to provide support and counselling. This oppor- ultrasound approaches have been transvesical, perurethral and
tunity should not be missed. The male partner should be present transcutaneous directly into the peritoneal cavity. These approaches
during the scans. An explanation of the images and of the physio- may occasionally be necessary with ovaries congenitally or surgi-
logical processes taking place add to a couples knowledge and cally displaced within the peritoneum. The procedure can also be
understanding. performed under general anaesthesia if necessary.
An ovulatory trigger in the form of human chorionic gonado- A single or, more usually, double lumen needle is passed through
trophin (hCG) or LH is given when the majority of follicles are a guide attached to the vaginal probe, through the lateral fornix of
thought to be mature, usually when the lead follicle is about 20mm the vagina, through the peritoneum and into the ovary, its path
diameter, so as to finalise the maturation of each oocyte ready for indicated by a computer-generated line on the display (Fig. 38.14).
fertilisation. The antral fluid of each follicle is aspirated and immediately
Ultrasound
Classification features Other features
Mild Ovarian volume Abdominal
<8cm3 bloating
Free fluid in pelvis Mild abdominal
pain
Moderate Ovarian volume Moderate
812cm3 abdominal pain
Fluid in pelvis, Nausea vomiting
elsewhere in
abdomen and
around kidneys
Severe Ovarian volume Clinical ascites
Figure 38.17 Ovarian hyperstimulation syndrome. >12cm3 Pleural effusion
Fluid in pelvis, Oliguria
elsewhere in Haematocrit >45%
IVF abdomen, around Hypoproteinaemia
kidneys and in
Polycystic ovarian morphology predicts an increased risk of pleural cavity
ovarian hyperstimulation. Critical Ovarian volume Tense ascites
Antral follicle counts performed at downregulation correlate well >12cm3 Large pleural
with final number of oocytes obtained. Abundant fluid in effusion
Ultrasound monitoring of follicle growth is not aided by additional pelvis, elsewhere Haematocrit >55%
routine serum oestradiol measurements. in abdomen, White cell count
Routine ultrasonically guided oocyte capture is safe and easily around kidneys >25000/mL
achievable under conscious sedation. and in pleural Oliguria
Routine embryo transfer is not aided by ultrasound control if a cavity Thromboembolism
mock embryo transfer has been performed. Acute respiratory
distress syndrome
738
References
12. Kupesic S, Kurjak A. Role of three-dimensional ultrasound in 31. Schwarzler P, Concin H, Wohlgenannt K. Transvaginal sonographic
diagnosis of uterine anomalies. Ultrasound Rev Obstet Gynecol assessment of the uterine cavity and the Fallopian tubes with
2005;5(3):194200. echo-enhancing agents. Ultraschall Med 1997;18(1):813.
13. Baird DD, Dunson DB, Hill MC, et al. High cumulative incidence of 32. NICE clinical guideline number 11. Fertility: Assessment and
uterine leiomyoma in black and white women: ultrasound evidence. treatment for people with fertility problems. Feb 2004.
Am J Obstet Gynecol 2003;188:100107. 33. Nirmal D, Griffiths AN, Jose G, Evans J. Warming Echovist contrast
14. Somigliani E, Vercellini P, Daguati R, et al. Fibroids and female medium for hysterocontrastsonography and the effect on the incidence
reproduction: a critical analysis of the evidence. Hum Reprod Update of pelvic pain. A randomized controlled study. Hum Reprod
2007;13(5):465476. 2006;21(4):10521054.
15. Pritts EA. Fibroids and infertility: a systemic review of the evidence. 34. Jayaprakasan K, Hilwah N, Kendall NR, et al. Does 3D ultrasound
Obstet Gynecol Surv 2001;56:483491. offer any advantage in the pretreatment assessment of ovarian reserve
16. Botsis D, Papagianni V, Makrakis E, et al. Sonohysterography is and prediction of outcome after assisted reproduction treatment? Hum
superior to transvaginal sonography for the diagnostic approach to Reprod 2007;22(7):19321941.
irregular uterine bleeding in women of reproductive age. J Clin 35. Lutchman Singh K, Davies M, Chatterjee R. Fertility in female cancer
Ultrasound 2006;34:434439. survivors: pathophysiology, preservation and the role of ovarian
17. Sardo ADS, Mazzon I, Bramante S, et al. Hysteroscopic myomectomy: reserve testing. Hum Reprod Update 2005;11(1):6989.
a comprehensive review of surgical techniques. Hum Reprod Update 36. Kwan I, Bhattacharya S, McNeil A, Van Rumste MME. Monitoring of
2008;14(2):101119. stimulated cycles in assisted reproduction (IVF and ICSI). Cochrane
18. Basu M, Mammen C, Owen E. Bony fragments in the uterus: an Database Syst Rev 2008;2:14691493X.
association with secondary subfertility. Ultrasound Obstet Gynecol 37. Verhaak CM, Smeenk JMJ, Evers AWM, et al. Womens emotional
2003;22(4):402406. adjustment to IVF: a systematic review of 25 years of research. Hum
19. Perez-Medina T, Bajo-Arenas J, Salazar F, et al. Endometrial polyps Reprod Update 2007;13(1):2736.
and their implication in the pregnancy rates of patients undergoing 38. Aboulghar MA, Mansour RT. Ovarian hyperstimulation syndrome:
intrauterine insemination: a prospective, randomized study. Hum classifications and critical analysis of preventive measures. Hum
Reprod 2005;20(6):16321635. Reprod Update 2003;9(3):275289.
20. Yanaihara A, Yorimitsu T, Motoyame H, et al. Location of endometrial 39. Farhi J, West C, Patel A, Jacobs HS. Treatment of anovulatory
polyp and pregnancy rate in infertility patients. Fertil Steril infertility: The problem of multiple pregnancy. Hum Reprod
2008;90(1):180182. 1996;11(2):429434.
21. Zeyneloglu HB, Arici A, Olive DL. Adverse effects of hydrosalpinx on 40. Bhal PS, Pugh ND, Chui DK, et al. The use of transvaginal power
pregnancy rates after in vitro fertilization-embryo transfer. Fertil Steril Doppler ultrasonography to evaluate the relationship between
1998;7(3):492499. perifollicular vascularity and outcome in in-vitro fertilization
22. Kontoravdis A, Makrakis E, Pantos K, et al. Proximal tubal occlusion treatment cycles. Hum Reprod 1999;14(4):939945.
and salpingectomy result in similar improvement in in vitro 41. Bodri D, Guillen JJ, Polo A, et al. Complications related to ovarian
fertilization outcome in patients with hydrosalpinx. Fertil Steril stimulation and oocyte retrieval in 4052 oocyte donor cycles. Reprod
2006;86(6):16421649. BioMed Online 2008;17(2):237243.
23. Hammadieh N, Coomarasamy A, Ola B, et al. Ultrasound-guided 42. Lesny P, Killick SR. The uterine junctional zone and its contractions. Br
hydrosalpinx aspiration during oocyte collection improves pregnancy J Obstet Gynaecol 2004;111(11):11821189.
outcome in IVF: a randomized controlled trial. Hum Reprod 43. Lesny P, Killick SR, Robinson J, Maguiness S. Transcervical embryo
2008;23(5):11131117. transfer as a risk factor for ectopic pregnancy. Fertil Steril
24. Fauser BCJM, et al. (The Rotterdam ESHRE/ASRM-sponsored PCOS 1999;72:305309.
consensus workshop group). Revised 2003 consensus on diagnostic 44. Fanchin R, Righini C, Olivennes F, et al. Uterine contractions as
criteria and long-term health risks related to polycystic ovary visualised by ultrasound alter pregnancy rates in IVF and embryo
syndrome. Hum Reprod 2004;19(1):4147. transfer. Hum Reprod 1998;13:19681974.
25. Hassan MA, Killick SR. Ultrasound diagnosis of polycystic ovaries in 45. Drakeley AJ, Jorgensen A, Sklavounos J, et al. A randomised control
women who have no symptoms of polycystic ovary syndrome is not trial of 2295 ultrasound-guided embryo transfers. Hum Reprod
associated with subfecundity or subfertility. Fertil Steril 2003;80(4): 2008;23(5):11011106.
966975. 46. Biervliet FP, Lesny P, Maguiness SD, et al. Transmyometrial embryo
26. Balen AH, Laven JSE, Tan SL, Dewailly D. Ultrasound assessment of transfer and junctional zone contractions. Hum Reprod 2002;17(2):
the polycystic ovary: international consensus definitions. Hum Reprod 347350.
Update 2003;9:505514. 47. Ng EHY, Chan CCW, Tang OS, et al. The role of endometrial and
27. Fulghesu AM, Ciampelli M, Belosi C, et al. A new ultrasound criterion subendometrial vascularity measured by three-dimensional power
for the diagnosis of polycystic ovary syndrome: the ovarian Doppler ultrasound in the prediction of pregnancy during frozen
stroma:total area ratio. Fertil Steril 2001;76:326331. thawed embryo transfer cycles. Hum Reprod 2006;21(6):16121617.
28. Adams J, Polson DW, Abdulwahid N, et al. Multifollicular ovaries: 48. Killick SR. Ultrasound and the receptivity of the endometrium. Reprod
clinical and endocrine features and response to pulsatile BioMed Online 2007;15(1):6367.
gonadotrophin releasing hormone. Lancet 1985;ii:13751379. 49. Cluroe AD, Synek BJ. A fatal case of ovarian hyperstimulation
29. Kyei-Mensah A, Tan SL, Zaidi J, Jacobs HS. Relationship of ovarian syndrome with cerebral infarction. Pathology 1995;27(4):344346.
stromal volume to serum androgen concentration in patients with 50. Royal College of Obstetricians and Gynaecologists. Green-top
polycystic ovary syndrome. Hum Reprod 1998;13:14371441. guideline number 5. September 2006.
30. Killick SR. Hysterosalpingo contrast sonography as a screening 51. DAngelo A, Amso N. Embryo freezing for preventing ovarian
test for tubal patency in infertile women. J R Soc Med 1999;92: hyperstimulation syndrome. Cochrane Database Syst Rev
628631. 2007;3:14691493.
739
CHAPTER
Ultrasound in the first trimester of pregnancy has come a long way 1. Properly trained, accredited and dedicated staff, following a
from the first reports of Cacciatore etal.1 to the present day. Not training programme that is recognised and regulated.
only does transvaginal ultrasound have the central role in diagnosis Training must be continuous and must be audited.
of first trimester problems but it is now involved in: 2. High quality equipment that is properly maintained and
1. providing patients with choice in terms of therapy, frequently replaced.
safely facilitating a wait and see policy 3. Properly constructed departmental guidelines and protocols,
2. providing prognostic information on the likely outcome of a which should reassure and inspire confidence in both service
pregnancy providers and patients.
3. monitoring of methotrexate therapy in cervical, caesarean scar The use of transvaginal ultrasound has resulted in some unex-
and interstitial ectopic pregnancies. pected side effects:
It is universally acknowledged that ultrasound has transformed 1. Loss of reassurance. A transvaginal scan can often detect a
the first trimester, providing knowledge and insight for physicians heartbeat in an embryo when it measures only 2mm in size.
and parents alike into the embryology and physiology of a preg- However, the natural loss rate of very early embryos means
nancy. Some cautions must be sounded. The demands from doctors that detecting a heartbeat so early is not as reassuring as
and parents have led to a rapidly expanding service; however, the expected.
quality of this service must not be compromised and must comprise 2. An entirely new diagnostic concept: the pregnancy of
the following: unknown location (PUL). This is proving costly financially
740
The normal first trimester
and is increasing workload. As a consequence this is sonographic embryology (Table 39.1). Without knowledge of the
producing increased stress and anxiety for staff and parents normal sequence of events and biological variation, the diagnosis
alike. of first trimester pathology is not possible.
The best scan is the scan performed to a high standard to answer
a specific clinical question by properly trained ultrasound person-
nel. Whilst some uncertainty will always exist, this should not be
Thickening of the endometrium
uncertainty generated by poor technique, substandard knowledge The first, quite non-specific, sign of early pregnancy is thickening
or poor understanding of natural processes. With such a wonderful of the endometrium to approximately 17mm in true anteroposte-
technique available to us, opening insights on a very remarkable rior sagittal dimension (Fig. 39.1). The differential diagnosis for this
process, we must first do no harm. The greatest concern relating to finding includes:
ultrasound safety comes not from the physical ultrasound process 1. late luteal phase of a normal cycle
but from the use of the technique in unsafe hands. 2. very early ectopic gestation.
The intra-decidual sign has been reported within the homo
geneously thickened endometrium. This is a highly reflective area
TRANSVAGINAL SCANNING IN EARLY within the thickened endometrium which is thought to represent
PREGNANCY the early implantation site.6 This is very difficult to demonstrate and
is therefore an unreliable finding.
The first trimester of pregnancy is the time interval between the last
menstrual period and the end of the twelfth completed week of Appearance of the gestation sac
gestation.
It was Sir Ian McDonald who described the first 12 weeks of The gestation sac is first seen as a tiny hypoechoic chorionic fluid
pregnancy as the most crucial period of existence.2 It is not only a collection within the thickened endometrium. The earliest a tiny
very dynamic phase of development but also an emotionally gestation sac can be seen is approximately 4 weeks 4 days gesta-
charged time with a high complication and loss rate. tional age when it is only 23mm in size (Fig. 39.2).7
The advent of high-resolution transvaginal ultrasound has The size of the gestation sac is quantified by the mean gestational
enabled the anatomy and physiology of the human fetus and the sac diameter (MGSD). In the very early stages when the sac is
adnexae to be visualised from as early as the third week post round, a single chorionic margin to chorionic margin measurement
implantation.3 As transvaginal scanning produces accurate images will suffice. Once the sac is ovoid the measurement must be the
of the early gestational sac and its contents, it has provided clues mean of the three orthogonal measurements, each one taken from
to the epidemiology and pathophysiology of early pregnancy chorionic margin to chorionic margin of the gestational sac with the
failure. Ultrasound has changed the medical approach to early transverse measurement only taken from the transverse plane (Fig.
pregnancy failure. 39.3).8 The MGSD is an adequate estimation of gestational age in a
normally developing pregnancy. The normal gestational sac grows
at 1.1mm per day.
At first, the gestation sac simply looks like a fluid collection
THE NORMAL FIRST TRIMESTER within the endometrium. This is a non-specific sign of which there
are other causes (Table 39.2; Figs. 39.4, 39.5). Recognition of the true
gestation sac at this stage is dependent on subtle features of the sac
Normal sonographic pregnancy itself (Table 39.3; Figs 39.6, 39.7). The appearance of the yolk sac and
development then the embryo confirms the intrauterine collection as a true sac.
The central endometrial cavity echo is formed by opposing
The primary objective of transvaginal scanning in early pregnancy margins of the endometrial lining. The true sac implants within the
must be to be accurate. Characterisation of normality is of funda- endometrium on one or other side of the central endometrial cavity
mental importance. Knowledge of the typical ultrasound appear-
ances of normal early pregnancy and a good understanding of
the pitfalls is essential for the diagnosis and management of early
pregnancy failure.
It is fortunate that the development of a normal pregnancy occurs
in a very predictable manner.4 Every stage of development may be
characterised by threshold and discriminatory levels.5 These levels,
in association with beta human chorionic gonadotrophin (-hCG)
levels, predict what should or should not be seen on ultrasound
scan. The threshold level is the earliest age at which we would
expect to see a pregnancy reach a certain sonographic milestone.
The discriminatory level is that age at which failure to detect a
certain biological landmark on ultrasound is not consistent with
normal development and is therefore evidence of pregnancy failure.
It is important to recognise and understand the sequence of
Figure 39.2 A tiny 4 week gestation sac (white arrow) only 2 to Figure 39.4 Pseudo sac of an ectopic pregnancy (arrow)
3mm in size accentuated by a large sub chorionic haematoma which is simply fluid within the central endometrial cavity.
(black arrow).
echo.9 A positive double decidual sac sign confirms a normal Figure 39.10 A low normal sac implantation within the uterine
intrauterine pregnancy (Fig. 39.8).10 The absence of this sign does isthmus, the arrow at the level of the internal os.
not rule out an intrauterine gestation but suggests the existence of
an abnormality.
There are important pitfalls and normal variations to the classic
sonographic diagnostic criteria of the true gestation sac, not only in
terms of shape but also in its location. An over-distended bladder
will distort the sac when visualised on the transabdominal approach
and fibroids can produce pronounced misshaping of the sac (Fig.
39.9). There is a normal lower uterine body implantation called a
lower isthmus implantation, where the sac is low, unchanging and
well established in the lower uterine cavity but not within a caesar-
ean section scar (Fig. 39.10).
Figure 39.13 The maximum size of the yolk sac is never more
than 6mm in transverse section at 10 weeks. Defining features of the true gestation sac
The early gestation sac is simply a tiny hypoechoic fluid
collection.
The eccentric location and the double decidual sac sign suggest
Table 39.4 Size of the gestation sac on transvaginal (TV) a true intrauterine sac.
scanning with respect to yolk sac appearance and The appearance of the yolk sac confirms the intrauterine
visualisation collection as a true sac.
A MGSD 13mm (6.4 weeks) is the discriminatory level for yolk
1. When on TV the MGSD is 6mm (5.5 weeks) the yolk sac sac visualisation.
is usually seen. This is the threshold level for yolk sac
A MGSD of 1518mm (6.4 weeks) is the discriminatory level for
visualisation
embryo visualisation.
2. When on TV the MGSD is 8mm (5.7 weeks) the yolk sac
is always seen
3. When on TV the MGSD is 13mm (6.4 weeks) the yolk
sac must be seen. This is the discriminatory level for yolk The appearance of the embryo
sac visualisation
The embryo is first seen as a disc adjacent to but distinct from the
yolk sac, developing along the chorionic margin of the yolk sac (Fig.
39.14). It is approximately 2mm in length at 5 weeks. Prior to this
into the primitive foregut. The main initial sonographic importance the beat of the developing embryonic heart can often be seen
of the yolk sac is that it confirms that the fluid collection within without the embryo itself.14 Once it is larger than 2mm it is discoid
the endometrium is indeed a true intrauterine sac. It is therefore with a proportional width relative to its length. The normal embry-
important to be aware of the timing of the appearance of the onic growth rate is initially 1.2mm/day. Once it measures 5mm
yolk sac within the gestation sac, i.e. to be aware of the threshold in a sac of 1518mm size (a gestational age of approximately 6.5
and discriminatory levels of sac size and yolk sac visualisation weeks), it will be seen consistently as a discrete structure and it will
(Table 39.4).13 always have cardiac pulsations, if it is living (Fig. 39.15).15
744
The normal first trimester
Figure 39.18 The amnion (arrow) slowly moving away from the
developing embryo by accumulating amniotic fluid.
The crownrump length (CRL) is used to measure the embryo
within the first trimester (Fig. 39.16). The term CRL is initially a
misnomer as before 7 weeks there is no crownrump differentiation
to the embryo. The assumption is that the longest dimension of the
embryo is the most accurate, which is true, provided other struc-
Appearance of the membranes:
tures such as the yolk sac are not included in the measurement. the amnion and chorion
As with the yolk sac, it is extremely important to be aware of the The chorionic cavity is the first cavity seen. The fluid is faintly
timing of the appearance of the embryo within the gestation sac, i.e. echogenic (Fig. 39.17). The chorion contains the secondary yolk sac
to be aware of the threshold and discriminatory levels of sac size and the chorionic margin always leads to the placental margin. The
and embryo visualisation (Table 39.5). chorion is gradually obliterated by expansion of the amnion and
complete fusion is usually complete by 12 weeks.
The amnion appears at the same time as the yolk sac, i.e. when
The embryonic heartbeat the MGSD is 6mm (55.5 weeks). The amnion and the yolk sac
Embryonic heart pulsation is the earliest proof that the embryo is produce an initial double bleb not seen sonographically. The
alive. Cardiac pulsation has been documented in utero by trans- amnion goes through a period of sonographic invisibility due to the
vaginal scanning as early as 36 days menstrual age, the time when fact that this is a very thin structure very close to the embryo. With
the heart tube starts to beat. Theoretically cardiac activity should newer ultrasound systems sonographic invisibility is less common.
always be evident when the embryo is over 2mm in size. In around It is reliably seen once again at about week 7 when the accumulating
510% of embryos between 2 and 4mm it cannot be demonstrated, amniotic fluid pushes it away from the embryo (Fig. 39.18). Visuali-
although the pregnancies will have a normal outcome.14 From 5 to sation of an amnion without an embryo is impossible in a normal
9 weeks of gestation, there is a rapid increase in the mean heart rate gestation and the empty amnion sign is universally predictive of
from 110 to 175bpm.16 pregnancy failure.17
745
CHAPTER 39 The first trimester, gynaecological aspects
Figure 39.25 A single large yolk sac (thin arrow) in the chorionic
cavity with 2 embryos, one showing abnormal development (block
arrow) within a single amnion consistent with a MCMA pregnancy
complicated by Twin Reversed Arterial Perfusion (TRAP) sequence. Figure 39.27 Conjoined twins; the type of union in this case is
omphalophagus-xiphophagus.
Twinning
Twinning occurs in 1% of all pregnancies.
Two-thirds of twins will be dizygotic and one-third will be
monozygotic.
Dizygotic twins will always have a dichorionic placentation.
The lambda (twin peak) sign occurs in a dichorionic gestation
when both placentas have formed adjacent to each other.
The lambda or twin peak sign is most reliable between 10 and
14 weeks.
Absence of the lambda sign at 20 weeks gestation does not
exclude a dichorionic gestation nor does it imply a monochorionic
gestation.
The perinatal mortality associated with twinning is six times that
for singletons.
The perinatal mortality of a monochorionic (MC) gestation is three
to four times that of a dichorionic (DC) gestation.
A B
A B
Figure 39.35 Acute echogenic and heterogenous Figure 39.37 A moderate subchorionic haematoma.
haemorrhage (thin arrow) adjacent to a gestation sac containing a
dead embryo (block arrow).
3. chorioamniotic
4. intra-amniotic.
Subchorionic haemorrhage
This type of intrauterine haemorrhage (IUH) is the commonest site
of bleeding within the early gestation sac and is a crescent-shaped
echo-free area between the chorionic membrane and the myo-
metrium. The appearance of the blood depends on the age of the
haematoma. Acute bleeding will be echogenic and particulate (Fig.
39.35). As the haemorrhage evolves it becomes less echogenic (Fig.
39.36). Understanding of the resolution of these haematomas and
the prognostic relevance of this ultrasound finding is limited.40
The size of a subchorionic haematoma is graded according to the
percentage of the chorionic cavity elevated by the haematoma:
n small: < 1 3
n moderate: 1 3 2 3 (Fig. 39.37)
n large: > 2 3 (Fig. 39.38). Figure 39.38 A haematoma (black arrow) that is so large that the
The overall loss rate with a subchorionic haematoma is 9.3% gestation sac (white arrow) appears to have no attachment to the
(7.79.5% with a small to moderate haematoma and 18.8% with a endometrium.
752
Early pregnancy complications
Table 39.9 Adverse outcome related to maternal age Table 39.10 Location of ectopic gestations
and gestational age at presentation
95% of all ectopics are tubal in location:
Maternal age <35 years: loss rate 7% 70% will be ampullary
Maternal age >35 years: loss rate 14% 2% will be in the isthmus of the fallopian tube
5% of ectopics will be non-tubal in location:
Gestational age <8 weeks: loss rate 14% 25% will be cornual or interstitial in location
Gestational age >8 weeks: loss rate 6% 0.51% of all ectopics will be ovarian
0.1% of all ectopics will be cervical
Table 39.11 The endometrial appearances in ectopic The adnexal findings in ectopic pregnancy
gestation
The appearances of the adnexal region (Table 39.12) will depend on
1. Homogeneously thickened and echogenic: secretory
the gestational age at which the patient is being examined.
endometrium seen in 22% of cases
2. Thin
3. Trilaminar in appearances: early proliferative endometrium Normal adnexal regions
seen in 12% of cases (Fig. 39.39)
4. Demonstrate a pseudo-gestation sac Adnexal abnormalities are not always observed in ectopic gesta-
5. Non-specific thickening often quite heterogeneous: decidual tions, particularly in patients undergoing IVF due to the very early
reaction seen in 42% of cases (Fig. 39.40) timing of the scan. In 1535% of women there will not be an identifi-
able adnexal lesion. Even in the presence of normal adnexa, there
is still a risk of about 5% for the presence of an unruptured ectopic
findings (Figs 39.6, 39.7 and 39.8). A recent study suggests that pregnancy.53 Any adnexal finding assumes greater importance if the
74% of ectopic pregnancies can be visualised at first ultrasound pregnancy test is positive and there is no evidence of an intrauterine
examination.49 pregnancy, particularly if the risk of ectopic gestation based on the
history is high. The negative predictive value of normal adnexa in
this situation will be much lower.54
Endometrial appearances
Failure to diagnose an intrauterine pregnancy means that the Tubal ring with yolk sac/tubal ring with embryo
assessment of the endometrium itself is of major importance. There
are a number of possible endometrial appearances that can occur The presence of an adnexal mass with a yolk sac or an embryo is
in an ectopic pregnancy (Table 39.11; Figs 39.39 and 39.40).50 It found in 1632% of all ectopics (Fig. 39.43). Higher rates are a
754
Early pregnancy complications
A B
Complex mass
A complex mass within the adnexa is the most frequent sonographic
finding seen in 1520% of ectopics (Fig. 39.48).58 This complex mass
is either a tubal miscarriage or tubal rupture. Transvaginal scanning
is expanding its role from simple diagnosis to determining progno-
sis, with an increasing role in selecting patients who can be managed Figure 39.45 An unruptured ectopic bagel sign (thin arrow)
conservatively or medically rather than surgically.59 ipsilateral to the corpus luteum (thick arrow).
755
CHAPTER 39 The first trimester, gynaecological aspects
Intraperitoneal fluid
The role of Doppler ultrasound in
Intraperitoneal fluid is found in 1030% of all ectopics and fluid will
be seen in 20% of normal pregnancies due to exudation from the
the diagnosis of ectopic pregnancy
normal corpus luteum. There is no quantitative amount of fluid that
is diagnostic but the greater the volume the greater the likelihood There are three areas in the pelvis that can be evaluated with colour
of an ectopic gestation (Fig. 39.51). The possibility of finding a rup- Doppler as an adjunct to simple greyscale ultrasound assessment
tured ectopic is extremely low if there is no free intraperitoneal when attempting to diagnose an ectopic pregnancy:61
fluid. The nature of the fluid can be useful as echogenic fluid will 1. An adnexal mass, if it is due to ectopic trophoblastic tissue,
be found in 2536% of patients with an ectopic gestation.60 will demonstrate peritrophoblastic flow, i.e. intense
756
Early pregnancy complications
Figure 39.56 A sac can be seen within the cervix (thin arrow) Figure 39.57 In the cervical stage of a miscarriage the
but this uterus is enlarged and globular and the endometrium is endometrium (block arrow) will be heterogenous and ill defined
heterogenous (block arrow). and the internal os (thin arrow) is open.
Table 39.17 Ultrasound features that facilitate a Table 39.18 Falling -hCG level
diagnosis of caesarean scar pregnancy
A falling -hCG level is most likely consistent with a failed
1. The uterus is empty pregnancy, which may simply be an:
2. The endometrium is clearly demonstrated and not distorted 1. Arrested intrauterine pregnancy (Fig. 39.62) previously
by blood or fluid called an anembryonic gestation
3. The cervical canal is empty and not ballooned 2. Tubal miscarriage
4. The gestational sac shows a double ring sign in the 3. Spontaneously resolving ectopic pregnancy
anterior part of the isthmic portion of the uterus
5. The gestational sac is embedded and surrounded by a
diminished myometrial layer
6. A discontinuity in the anterior wall of the uterus
7. The gestation sac is separated from the endometrial cavity
8. Evidence of functional trophoblastic/placental circulation on
Doppler examination
9. Negative sliding organs sign, which is defined as the
inability to displace the gestational sac from its position at
the level of the internal os using gentle pressure applied by
the transvaginal probe
Negative ultrasound
Patients are being scanned increasingly early in their pregnancies
and some patients may fail to demonstrate either an intrauterine
pregnancy or an adnexal abnormality when initially scanned. Some
may never demonstrate an abnormality at all. It is essential to
acknowledge and understand that ultrasound, no matter how good,
must never be used in isolation when evaluating a patient. The
clinical presentation and findings as well as the serum -hCG level
are very important.
Figure 39.62 A crenellated pseudo gestation sac filled with
The role of a discriminatory serum debris consistent with an ectopic gestation.
-hCG level
A viable intrauterine pregnancy will show a 66% rise in -hCG
every 48 hours in the first 40 days of pregnancy.69 Only 13% of
ectopic pregnancies will show such a rise in levels. A -hCG rise of
<50% in 48 hours is almost always associated with a non-viable Pregnancy of unknown location
pregnancy of either intra- or extrauterine origin. Pregnancy of unknown location (PUL) means that the location of
An ectopic pregnancy is considered very likely in the absence the pregnancy is not determined at the initial visit.
of an intrauterine pregnancy on transvaginal scanning when the The incidence of PUL depends upon gestational age at
serum -hCG level is greater than a certain discriminatory level. presentation and operator experience.
There is controversy about the discriminatory level of -hCG above Only a minority of PUL will have an ectopic pregnancy (814%).
which a viable intrauterine pregnancy should be seen on the scan Most pregnancies of unknown location may be safely managed
(15002000IU/L).70 The problem with discriminatory levels for bio- expectantly.
chemical parameters is that there is no known discriminatory level
for twin gestations and there is a very great variability in expertise
amongst sonographers.71
Table 39.19 Range of possible outcomes with an initial Table 39.20 The risk of demise related to the heart rate
diagnosis of PUL in embryos less than 5mm
1. 4550% pregnancies resolve spontaneously and the initial A heart rate of less than 80bpm was universally associated
true origin will never be identified with subsequent embryonic demise
2. 814% are due to ectopic gestations A heart rate of 8090bpm was associated with a 64% risk of
3. 2747% evolve into normal intrauterine pregnancies demise
A heart rate of 9099bpm was associated with a 32% risk
A heart rate of 100bpm or more was associated with an
11% risk
THE ROLE OF ULTRASOUND IN
PREDICTING AN ABNORMAL
PREGNANCY OUTCOME
Figure 39.68 This rather suspicious looking mass was Figure 39.69 A large pedunculated fibroid which became
removed at 16 weeks and was histologically confirmed as a extremely painful at 16 weeks and underwent necrotic cystic
decidualised endometriotic cyst. change (thin arrow).
Fibroids
Approximately one-third of women experience fibroid growth in
the first trimester; the remaining women have stable or reduced
fibroid size during pregnancy.82 Changes in the uterine blood
supply may render a fibroid ischaemic and produce painful acute Figure 39.70 A retro placental fibroid (arrow). The echotexture
necrosis and cystic degeneration (Fig. 39.69). Calcification with is hypoechoic relative to the normal myometrium.
acoustic shadowing may be either central in nature or peripheral in
location, which is more common after fibroid embolisation. Of great
importance is the sonographic differentiation between a fibroid and
a myometrial contraction. The echotexture of a fibroid may be
hypoechoic, hyperechoic or isoechoic relative to the normal myo-
metrium. A contraction will be of the same echogenicity as the rest
of the myometrium and it will resolve/change over the course of
the scan.
Fibroids may produce problems in all three trimesters:
1. Spontaneous miscarriage in the first trimester is more
common due to abnormal placentation.
2. There is an increased risk of placental abruption, antepartum
haemorrhage, retained placenta, postpartum haemorrhage
and premature rupture of the membranes. The risk of
abruption appears to be related to the size and location of the
myoma; it is substantially increased if the myoma is large, e.g.
6cm) or subjacent to the placental site (Fig. 39.70)
3. In the third trimester there may be fetal compression
deformities and malpresentation, particularly with cervical
fibroids (Fig. 39.71). Figure 39.71 A cervical fibroid which may produce dystocia.
763
CHAPTER 39 The first trimester, gynaecological aspects
A B
Figure 39.75 A and B The presence of localized placental molar change (block arrows) and an embryo (thin arrow) consistent with
the diagnosis of partial molar change.
CHM PHM
THE ULTRASOUND DIAGNOSIS OF
Chromosomal Diploid Partial moles are RETAINED PRODUCTS OF CONCEPTION
complement chromosomal almost always
complement triploid
Scan requests for retained products of conception pose a very sig-
Origin of Paternal genome Diandric due to two nificant time and financial burden on ultrasound departments. The
chromosomes as a result of sets of management of this problem is compounded by the fact that there
fertilisation of an chromosomes of is no consensus agreement as to the appearance of the endometrium
oocyte by a paternal origin ( 2 3
that is consistent with retained products of conception, either in
diploid of all triploidies)
terms of actual endometrial thickness or abnormal morphology
spermatozoon Digynic origin due such as an echogenic mass (Fig. 39.77). As a consequence reliance
to a double on the use of sonography to diagnose retained products of concep-
maternal tion is associated with an unacceptably high false positive rate.
contribution Various studies have suggested endometrial measurements
Chorionic villi Marked oedema Marked oedema varying from 15 to 25mm but studies have shown that many of
and enlargement and enlargement these levels are neither sensitive nor specific enough to be of
Villous blood Disappearance of benefit.88 Other studies have considered the morphological appear-
vessels the villous blood ances of the postpartum endometrium (the presence of an echo-
vessels genic mass) (Fig. 39.79) and yet others have factored the use of
Trophoblast Proliferation of the Focal trophoblastic Doppler into algorithms for diagnosis (Fig. 39.78).89 Even if a con-
lining trophoblast hyperplasia sensus could be reached in terms of definition of terms there would
Fetal tissue Absence of fetal Presence of fetal still be problems with rigid application of limits to ultrasound
tissue tissue measurements of endometrial thickness. It has been shown that
even in women with endometrial thickness <10mm on preopera-
tive ultrasound scan, chorionic villi have been detected on histo
logy. This group of women would not have fulfilled any of the
sonographic definitions for diagnosis. Conversely, many women
have quite thickened endometria but do not consider the blood
Table 39.23 Structural defects associated with triploidy loss they are experiencing to be significant in terms of amount or
duration.
1. Central nervous system: agenesis of the corpus callosum, More importantly, women with incomplete miscarriages who
DandyWalker malformation, holoprosencephaly, spina
present for the first time with a relatively thin endometrium on
bifida
ultrasound scan are likely to be classified as having pregnancies of
2. Facial: cleft lip, micrognathia, hypertelorism
3. Cardiovascular: ventricular septal defect, atrial septal defect unknown location.90 These women are often perceived as being at
4. Genitourinary: renal agenesis, multicystic kidneys, and risk of having ectopic pregnancy and they are routinely followed
hypospadias by serial blood tests to measure the dynamic of hCG levels.
5. Intrauterine growth retardation, cystic hygroma, The diagnosis of retained products is a very pertinent example
omphalocele, club foot, syndactyly, sandal gap of the necessity to perform a scan only for a good clinical reason.
What is likely to be more important is what the endometrium looks
765
CHAPTER 39 The first trimester, gynaecological aspects
twin chorionic peak sign in dichorionic pregnancies. Obstet Gynecol tubal ring of ectopic pregnancy with the corpus luteum. J Ultrasound
1997;89:439441. Med 2004;23:5762.
29. Selpulveda W. Chorionicity determination in twin pregnancies: double 56. Frates MC, Visweswaran A, Laing FC. Comparison of tubal ring and
trouble? Editorial. Ultrasound Obstet Gynecol 2002;10:7981. corpus luteum echogenicities: a useful differentiating characteristic.
30. Bora SA, Papageorghiou AT, Bottomly C, et al. Reliability of J Ultrasound Med 2001;20:2731.
transvaginal ultrasonography at 79 weeks gestation in the 57. Bhatt S, Ghazale H, Dogra V. Sonographic evaluation of ectopic
determination of chorionicity and amnionicity in twin pregnancies. pregnancy. Radiol Clin North Am 2007;45(3):549560.
Ultrasound Obstet Gynecol 2008;32(5):618621. 58. Barnhart K, Esposito M, Coutifaris C. An update on the medical
31. Robinson HP, Fleming JE. A critical evaluation of sonar crown rump treatment of ectopic pregnancy. Obstet Gynecol Clin North Am
length measurements. Br J Obstet Gynaecol 1975;82:702710. 2000;27(3):653667.
32. Harville EW, Wilcox AJ, Bird DD, Weinberg CR. Vaginal bleeding in 59. Job-Spira N, Fernandez H. Ruptured tubal ectopic pregnancy: risk
very early pregnancy. Obstet Gynecol Surv 2004;59(3):172173. factors and reproductive outcome: results of a population based study
33. Silver RM, Ware Branch D. Sporadic and recurrent pregnancy loss. In: in France. Am J Obstet Gynecol 1999;180:938944.
Reece AE, Hobbins JC, Gant NF, editors. Handbook of clinical 60. Wachsberg RH, Levine CD. Echogenic peritoneal fluid as an isolated
obstetrics: the fetus and mother. Oxford: Blackwell Publishing; sonographic finding; significance in patients at risk of ectopic
2007. pregnancy. Clin Radiol 1998;53(7):520522.
34. Farquharson RG, Jauniaux E, Exalto N. Updated and revised 61. Dubinsky TJ, Pravey HR, Maklad N. Endometrial color flow/image
nomenclature for description of early pregnancy events. Hum Reprod directed Doppler imaging: negative predictive value for excluding
2005;20(11):30083011. ectopic pregnancy. J Clin Ultrasound 1997;25(3):103109.
35. Robinson HP. Detection of fetal heart movement in the first trimester 62. Agarwal SK, Wisot AL, Garzo G, Meldrum DR. Cornual pregnancies
of pregnancy using pulsed ultrasound. BMJ 1972;4:466468. in patients with prior salpingectomy undergoing in vitro fertilization
36. Schouwink MH, Fong BF, Mol BWJ, van der Veen F. Ultrasonographic and embryo transfer. Fertil Steril 1996;65:659660.
criteria for non-viability of first trimester intra-uterine pregnancy. 63. Ackerman TE, Levi CS, Dashefsky SM, et al. Interstitial line:
Early Pregnancy 2000;4(3):203213. sonographic finding in interstitial (cornual) ectopic pregnancy.
37. RCR/RCOG Committee. Guidance on ultrasound procedures in early Radiology 1993;189:8387.
pregnancy. 1995 reissued without change 2006. Royal College of 64. Ushakov FB, Elchalal U, Aceman PJ, Schenker JG. Cervical pregnancy:
Radiologists. The Royal College of Obstetricians and Gynaecologists. past and future. Obstet Gynecol Surv 1997;52:45.
38. Exalto N, Christiansen OB, Farquharson RG, Jauniaux E. Early 65. Gun M, Mavrogiorgis M. Cervical ectopic pregnancy: a case report
pregnancy failure: a review. Eur Clin Obstet Gynaecol and literature review. Ultrasound Obstet Gynecol 2002;19:297301.
2006;2(4):171179. 66. Comstock CH. Antenatal diagnosis of placenta accreta: a review.
39. McKenna KM, Feldstein VA, Goldstein RB, Filly RA. The empty Ultrasound Obstet Gynecol 2005;26:8996.
amnion sign: a sign of early pregnancy failure. J Ultrasound Med 67. Chang FW, Chen CH, Liu JY. Early diagnosis of ovarian pregnancy by
1995;14(2):117121. ultrasound. Int J Obstet Gynecol 2004;85:186187.
40. Maso G, DOttavio G, De Seta F, et al. First trimester intra uterine 68. Comstock CH, Huston K, Lee W. The ultrasonic appearances of
hematoma and outcome of pregnancy. Obstet Gynecol ovarian ectopic pregnancies. Obstet Gynecol 2005;105:4245.
2005;105:339344. 69. Tay JI, Moore J, Walker JJ. Ectopic pregnancy. BMJ 2000;320:916.
41. Weiss J, Malone F, Vidaver J, et al. Threatened abortion: a risk factor 70. Seeber BE, Banhart KT. Suspected ectopic pregnancy. Obstet Gynecol
for poor pregnancy outcome, a population based screening study. Am 2006;107(2 Pt 1):399413.
J Obstet Gynecol 2004;190:745750. 71. Kadar N, DeVore G, Romero R. Discriminatory hCG zone: its use in
42. Johns J, Hyett J, Jauniaux E. Obstetric outcome after threatened the sonographic evaluation for ectopic pregnancy. Obstet Gynecol
miscarriage with or without a haematoma on ultrasound. Am J Obstet 1981;58:156.
Gynecol; 2003;102:483487. 72. Bottomley C, Van Belle V, Mukri F, et al. Ability to make a diagnosis at
43. Bromley B, Harlow BL, Laboda LA, Benacerraf BR. Small sac size in first early pregnancy ultrasound assessment according to gestational
the first trimester: a predictor of poor fetal outcome. Radiology age. Ultrasound Obstet Gynecol 2007;30(4):388.
1991;178:375377. 73. Banerjee S, Aslam N, Zosmer N, et al. The expectant management of
44. Zane SB, Kieke BA, Kendrick JS, Bruce C. Surveillance in a time of women with early pregnancy of unknown location. Ultrasound Obstet
changing health care practices: estimating ectopic pregnancy incidence Gynecol 1999;14:231236.
in the United States. Matern Child Health J 2002;6:227. 74. Condous G, Okaro E, Bourne T. Pregnancies of unknown location:
45. Lewis G, editor. The Confidential Enquiry into Maternal and Child diagnostic dilemmas and management. Curr Opin Obstet Gynecol
Health. (CEMACH). Saving mothers lives: reviewing maternal deaths 2005;17:568573.
to make motherhood safer 20032005. The Seventh Report on 75. Jauniaux E, Gavriil P, Nicolaides KH. Ultrasonographic assessment of
Confidential Enquiries into Maternal Deaths in the United Kingdom. early pregnancy complications. In: Jurkovic D, Jauniaux E, editors.
London: CEMACH; 2007. Ultrasound and early pregnancy. Carnforth, UK: Parthenon
46. Kamwendo F, Forslin L, Bodin L, Danielsson D. Epidemiology of Publishing; 1996. p. 53.
ectopic pregnancy during a 28 year period and the role of pelvic 76. Sawyer E, Jurkovic D. Ultrasonography in the diagnosis and
inflammatory disease. Sex Transm Infect 2000;76:28. management of abnormal early pregnancy: first trimester pregnancy
47. Ankum WM, Mol BWJ, Van Der Veen F, et al. Risk factors for ectopic complications. Clin Obstet Gynecol 2007;50(1):3154.
pregnancy: a meta analysis. Fertil Steril 1996;65:1093. 77. Chama CM, Marupa JY, Obed JY. The value of the secondary yolk
48. Filly RA. Ectopic pregnancy [Figure 32.2, p 642]. In: Callen PW, editor. sac in predicting pregnancy outcome. J Obstet Gynecol 2005;25(3):
Ultrasonography in obstetrics and gynecology. Philadelphia: Saunders; 245247.
1994. p. 641659. 78. Jauniaux E, Jurkovic D, Henriet Y, et al. Development of the secondary
49. Kirk E, Papageorghiou AT, Condous G, et al. The diagnostic human yolk sac: correlation of sonographic and anatomic features.
effectiveness of an initial transvaginal scan in detecting ectopic Human Reprod 1991;6:11601166.
pregnancy. Hum Reprod 2007;22:17441750. 79. Mara E, Foster GS. Spontaneous regression of a yolk sac associated
50. Lazarus E. Whats new in first trimester ultrasound. Radiol Clin North with embryonic death. J Ultrasound Med 2000;19:655656.
Am 2003;41(4):663679. 80. Filly RA: Ovarian masses what to look for what to do. In: Callen
51. Mehta TS, Levine D, McArdle CR. Lack of sensitivity of endometrial PW, editor. Ultrasonography in obstetrics and gynecology.
thickness in predicting the presence of an ectopic pregnancy. Philadelphia: Saunders; 1994. p. 625639.
J Ultrasound Med 1999;18:117122. 81. Giuntoli RL, Vang RS, Bristow RE. Evaluation and management of
52. Wachsberg RH, Karimi S. Sonographic endometrial three layer pattern adnexal masses during pregnancy. The adnexal mass. Clin Obstet
in symptomatic first trimester pregnancy: not diagnostic of ectopic Gynecol 2006;49(30):506516.
pregnancy. J Clin Ultrasound 1998;26:199201. 82. Salvador E, Penstock J, Blakemore KJ, Pressman E. Leiomyomata uteri,
53. Jurkovic D, Mavrelos D. Editorial. Catch me if you scan: ultrasound genetic amniocentesis, and the risk of second-trimester spontaneous
diagnosis of ectopic pregnancy. Ultrasound Obstet Gynecol abortion. Am J Obstet Gynecol 2002;186:913.
2007;30:17. 83. Callen PW. Ultrasound evaluation of gestational trophoblastic
54. Condous G. The management of early pregnancy complications. Best neoplasia. In: Callen PW, editor. Ultrasonography in obstetrics and
Pract Res Clin Obstet Gynaecol 2004;18(1):3757. gynecology. Philadelphia: Saunders; 1994. p. 625639.
55. Stein MW, Ricci ZJ, Novak L, et al. Sonographic comparisons of the 84. Benson CB, Genest DR, Bernstein MR, et al. Sonographic appearance
768
References
of first trimester complete hydatidiform moles. Ultrasound Obstet miscarriage: an evaluation of transvaginal ultrasound criteria for
Gynecol 2000;16:188191. diagnosing an empty uterus. Am J Obstet Gynecol 2004;191:11331137.
85. Betel C, Atri M, Arensen AM, et al. Sonographic diagnosis of 90. Luise C, Jermy K, Collins WP, Bourne TH. Expectant management of
gestational trophoblastic disease and comparison with retained incomplete, spontaneous first trimester miscarriage: outcome
products of conception. J Ultrasound Med 2006;25:985993. according to initial ultrasound criteria and value of follow-up visits.
86. Fowler DJ, Lindsay I, Seckl MJ, Sebire NJ. Routine pre-evacuation Ultrasound Obstet Gynecol 2002;19:580582.
diagnosis of hydatiform mole: experience of more than 1000 cases 91. Elson J, Tailor A, Salim R, et al. Expectant management of miscarriage-
from a regional referral centre. Ultrasound Obstet Gynecol prediction of outcome using ultrasound and novel biochemical
2006;27:5660. markers. Hum Reprod 2005;20(8):23302333.
87. Jauniaux E, Nicolaides KH. Early ultrasound diagnosis and follow-up 92. Kirk E, Condous G, Bourne T. The non-surgical management of
of molar pregnancies. Ultrasound Obstet Gynecol 1997;9:1721. ectopic pregnancy. Ultrasound Obstet Gynecol 2006;27:91100.
88. Sawyer E, Ofuasia E, Ofili-Yebovi D, et al. The value of measuring 93. Jongeward KL, Kutella ET, Fleischer AC, et al. Sonographic features of
endometrial thickness and volume on transvaginal ultrasound scan for ectopic pregnancies following systemic methotrexate therapy: a case
the diagnosis of incomplete miscarriage. Ultrasound Obstet Gynecol series. Ultrasound Obstet Gynecol 2008;32(3):OP12.08:349350.
2007;29:205209.
89. Leung SW, Pang MW, Chung TKH. Retained products of gestation in
769
INDEX
Note: Page numbers followed by b indicate Abdominal trauma, 828846 postoperative, 805, 805f806f
boxes, f indicate figures and t indicate tables. bladder trauma, 841 types of, 801t, 806b
bowel trauma, 841, 842f infections, 799800, 801f
computed tomography lipoma, 805, 806f
A versus contrast-enhanced ultrasound, liposarcoma, 806
832833, 833f masses, 805807, 806b
Abdomen versus full potential ultrasound, musculo-cutaneous flaps, 800
interventional techniques, 847864 832833, 841b nerve entrapment, 807
(see also specific techniques) contrast-enhanced ultrasound, 832f pathological conditions affecting, 798801
muscles, 1076 versus computed tomography, sarcoma, 806
trauma see Abdominal trauma 832833, 833f trauma, 801
wall see Abdominal wall diaphragm trauma, 841 ultrasound technique, 798
Abdominal aorta FAST, 828829, 829b, 829f830f varices, 805806
anatomy, 773, 774f versus full potential ultrasound, Abductor digiti minimi, accessory, 1160
aneurysms see Abdominal aortic 831832 Abductor pollicis longus (APL), 1055
aneurysms follow-up, 844845, 844f845f Ablation
atherosclerosis, 787, 788f free peritoneal fluid, 833835, 834f, 835b endovenous, 12461248
diameter, 774, 774t full potential ultrasound, 829831, 831b, tumour see Tumour ablation
dissection, 789, 789f 831f see also specific techniques
occlusion, 788789 versus computed tomography, 832 Abscesses
stenosis, 788f versus FAST, 831832 abdominal, 1401
Abdominal aortic aneurysms gallbladder trauma, 841 abdominal wall, 799800
aortic diameter and, 774, 774t liver trauma, 835837 adrenal gland, 1464
background, 774775 classification, 835836, 835t appendiceal, 391, 392f, 1397, 1397f
causes of, 774775 general considerations, 835 aspiration/drainage, 1192, 1193f
diagnosis, 1198 mechanisms of injury, 835836 breast, 989
dissecting, 775 ultrasound findings, 836837, intra-abdominal, 815
duplex scanning, 777781 836f837f liver, 124, 125f
abnormal appearance, 777779, pancreas trauma, 841 pelvic see Pelvic abscess drainage
778f780f penetrating, 843 breast, 989, 989f
distance between renal arteries and pitfalls, 841842, 842f cervical, in children, 1304
aneurysm sac, 780 renal trauma, 838841 chest wall, 1352f1353f
limitations and pitfalls, 781 classification, 839840, 839t Crohns disease, 374375, 375f
measurement of aneurysm size, 780, general considerations, 838841 dental, 906, 906f
781f mechanisms of injury, 839840 epididymal, 615, 615f
normal appearance, 777, 778f ultrasound findings, 840841, fallopian tubes, 682, 683f
objectives, 777, 777f 840f841f intra-abdominal, 813815, 814f815f, 815b
patient preparation, 777, 778f scanning methodology, 828833, 829b liver, 124127, 145146, 146f147f
variability of measurement between spleen trauma, 837838 amoebic, 126127, 127f128f,
ultrasound and CT, 779 classification, 837838, 838t 13641365
false, 775 general considerations, 837 bacterial, 123f126f, 124126, 145146
mycotic, 775, 779 mechanisms of injury, 837838, 838f brucellar, 126
risk factors, 775, 775b ultrasound findings, 838, 839f in children, 13641365, 1364f
saccular, 775 unstable patient, 843, 843f lungs, 1015, 1015f, 1340, 1342f
shapes and types, 775, 776f Abdominal wall, 798807 muscle, 1156
size, 775 abscess, 799800 neonatal cerebral, 1273, 1275f
surveillance programmes, 775776, 777b, anatomy, 798, 799f800f, 799t ovarian, 682, 683f
777t, 782787 cysts, 805807, 806b pancreatic, 299, 300f
symptoms, 775 desmoid tumours, 806, 807f parotid gland, 903, 904f
treatment, 781782 divarication of the rectus muscles, 800 pericholecystic, 244245, 245f246f
endovascular repair, 781787, endometriomas, 806, 806f perirenal, 462
783f787f, 783t784t, fibromatosis, 806 post-liver transplantation, 212, 215, 215f
784b hernias, 801805, 1081 (see also specific post-renal transplantation, 535
open repair, 781 types) prostatitis, 582584, 582f, 583t, 591
psoas muscle, 821, 823, 823f pancreatic, 306309, 307f310f, 309b gallbladder, 1375
renal, 462, 462f, 496497, 496f497f, small bowel, 380, 381f Mllerian duct, 1473
1452f vaginal, 716 pancreas, 1378
retroperitoneal, 821, 823, 823f824f Adenoid cystic carcinoma renal, 1418, 1419f
spleen, 338340, 339f340f parotid gland, 902 AIDS see Acquired immunodeficiency
testicular, 604, 605f submandibular gland, 897 syndrome (AIDS)
thyroid, 1310, 1310f Adenolymphoma, parotid gland, 901, 901f AIDS-related parotid cysts, 905
tubo-ovarian, 682, 683f Adenomas AIUM/NEMA Output Display Standards
ultrasound appearances, 1116 adrenal, 636, 636f (ODS), 51
Absorption, 11 bile duct, 261 Alagilles syndrome, 216, 13711372, 1374f
Acalculous cholecystitis, 1375 gallbladder, 249, 249f Albumin-coated microbubbles, 80
Accessory muscles, 11411143, 1146t1147t, hepatic, 1363 Alcohol
1160 liver, 143145, 145f fatty liver, 105
hand/wrist, 10661067 metanephric, 508 hepatitis, 121122, 122f
Acetabulum, labral abnormalities, 10701071, papillary, 508 pancreatitis risk, 294, 301
1072f parathyroid, 886887, 886f887f tumour ablation, 859860
Achalasia, oesophageal, 359360 parotid gland, 899f Alcoholic liver disease, 216
Achilles bursa injection, 1188, 1188f pleomorphic, 899f, 900, 901f Aliasing, 28, 41, 41f, 7475
Achilles tendon, 10931095, 1094f1095f renal, 508, 508f -Fetoprotein (AFP)
injection, 11881189, 1188f1189f salivary gland, 1308, 1309f cirrhosis screening, 115116
paratenon, 10931094 submandibular gland, 897 hepatoblastoma, 13601361
injection, 1189, 1189f thyroid, 13101312, 1312f hepatocellular carcinoma screening, 154
tears, 1102, 1102f Adenomatoid tumour, epididymis, 610, 610f 5-Alpha reductase agents, 581
tendinopathy, 11011102, 1101f1102f Adenomyomatosis, 247, 248f Amaurosis fugax, 941942, 965
xanthomas, 1117, 1118f Adenomyosis, 694695, 694b Amenorrhoea, 14811482, 1481t, 1482b
Acinic cell carcinoma, parotid gland, 902 diagnosis, 694695, 694f695f American Association for the Surgery of
Acoustic cavitation, 5, 87 symptoms, 694 Trauma (AAST)
definition, 5455 Adnexal torsion, 14881489 liver injury scale, 835836, 835t
experimental work associated with, 55 Adolescents, ovarian cysts, 1484, 1485f renal trauma, 839, 839t
factors affecting incidence of, 5556 Adrenal glands, 632642 spleen trauma, 837838, 838t
hazards from, 55 abscess, 1464 American Joint Committee on Cancer (AJCC)
high risk situations, 56 adenoma, 636, 636f classification, 921
in-vivo animal and human effects, 55 agenesis, 634 Amnion, 745, 745f, 750, 750f
modelling, 55 anatomy, 632633 Amoebic colitis, 391392, 400, 400f
reducing the risk of, 56b calcification, 635 Amoebic liver abscess, 126127, 127f128f,
safety, 5456 in children, 14641466, 1464f 145146, 13641365
and tissue, 55b computed tomography role, 642 Amoebomas, 400
Acoustic energy absorption, 52b congenital anomalies, 634, 634f Amplitude, 3, 4f
Acoustic impedance, 9 congenital hyperplasia, 1464 Amplitude modulation/power modulation
Acoustic output regulation, 51 cortical carcinoma, 637, 639f (PM/AM), 82, 82f
Acoustic shadowing see Shadowing cysts, 634635, 634f, 1464, 1465f Ampullary carcinoma, 263
Acquired cystic disease of the kidney discoid, 634, 634f Amyloid
(ACDK), 453454, 454f, 498, embryology, 1464 liver, 117
498b, 499f enlargement, 14751476, 1479f renal, 452, 452f
Acquired immunodeficiency syndrome haemorrhage, 635, 635f, 1464, 1464f Amyloidosis, 1134
(AIDS) post-liver transplantation, 213, 213f Anal canal, 405409
and liver disease, 131132 hyperplasia, 634635, 634f anatomy, 406407, 406f
renal infections in, 465 imaging anatomy, 1464 anorectal tumours, 407408, 407f
spleen in, 343 magnetic resonance imaging role, 642 sepsis, 408, 408f
Acromioclavicular joint, 10391040 metastases, 640641, 640f641f sphincters see Anal sphincters
cyst, 10391040, 1040f myelolipoma, 636637, 637f trauma, 408, 408f
injection, 1040, 1173, 1175f neuroblastoma, 637640, 640f, 1459t, ultrasound technique, 405406
osteoarthritis, 10391040 14641466, 1465f, 1465t Anal sphincters, 406407, 406f
Actin, 1138 normal appearances, 633, 633b, 633f abnormalities, 409, 409b
Actinomycosis, intrauterine devices, 708 phaeochromocytoma, 637, 638f639f solitary rectal ulcer syndrome, 409
Acute tubular necrosis (ATN), 449, 451, 484, scanning techniques, 632633 traumatic injury, 408
532, 542 staging, 1465t Anaplastic carcinomas, thyroid, 879880,
in children, 1443 tumours, 635641 880b, 880f
Adductor brevis, 1075 Adrenal rest cells, 603, 603f Anastrozole, 706
Adductor longus, 10721073, 1075, 1076f Adrenarche, 1470 Anconeus epitrochlearis, 11411143
1077f, 1081, 1082f isolated premature, 1481 Androblastoma, ovarian, 678
Adductor magnus, 1075 Adrenocorticotrophic hormone (ACTH), 635 Anencephaly, 746747
Adductor muscles, 1081 testicular adrenal rest tumours, 603 Aneurysm Detection and Management
Adductor origin injection, 1180, 1181f Adult polycystic liver disease (APLD), 9798, (ADAM) Veterans Affairs
Adenocarcinomas 98f Cooperative Study Group, 775
appendiceal, 393 Advanced Trauma Life Support (ATLS), 843 Aneurysms
bladder, 561562 Agenesis aortic see Abdominal aortic aneurysms;
colonic, 402 adrenal glands, 634 Aorta, aneurysms
in children, 1401, 1401f Bakers cyst, 1089, 1090b, 1090f, 1115 dilatation, 254255, 254f256f, 1372
gallbladder in, 242243, 242f, 811, 812f paediatric, 1510, 1510f post-liver transplantation, 211, 220, 221f
loculated, 811, 811f Bandwidth, 18 ultrasound signs, 254, 255f
malignant, 812, 812f814f Barbotage, 1037, 1038f without jaundice, 255
in ovarian tumours, 678 of calcific supraspinatus tendinopathy, gallbladder distension, 256258, 257f
subtle, 810811, 811f 1172, 1172b, 1172f gas in, 259, 260f
Ashermans syndrome, 697, 709 Barcelona Clinic Liver Cancer (BCLC) hypoplasia, 216
Asphyxia, perinatal, 1265 classification, 172 injury, intraoperative ultrasound, 279
Aspiration, 1169 Barlow test, 14971498, 1498f jaundice see Jaundice
abscess, 1192, 1193f Barretts oesophagus, 356, 358f measuring, 189, 234236, 235f
cystic lesions, 11921193 Bartonella hensellae, 133134 neoplasms, 261263, 261f265f, 13721375
diagnostic, versus drainage, 853 Basilar artery, 1259t normal anatomical variants, 227228,
ganglion cysts, 1178, 1179f anatomy, 976 234f236f
hip, 11811184, 1184b, 1184f transcranial Doppler ultrasound, 976 obstruction, 1372
knee, 11851186, 1186f1187f Basilic vein, 1043 pancreatitis complications, 299
tibiofibular joint, 1187 bypass grafts, 12071208 without dilatation, 255
see also Drainage techniques Basivertebral veins, 13201322 oriental cholangiohepatitis, 265266
Asplenia, 330, 331f, 1356 Baums bumps, 940, 941f pathology, 253267
Asteroid hyalosis, 949, 949f Beak sign, simple renal cysts, 487, 487f sclerosing cholangitis, 267, 267f
Astrocytomas, neonatal, 1333 Beam edge artefacts, 1126, 1127f spontaneous perforation, 1370, 1373f
Asymptomatic Carotid Artery Surgery Trial, Beam former, 21, 23b stones see Choledocholithiasis
965966 Beams, 6, 17 strictures, 212f
Atelectasis, 10101011, 1011f electronic focusing, 21, 21f Biliary ascariasis, 266, 266f
in children, 13391340 steering, 19f, 20, 42, 43f Biliary atresia
Atheroma, carotid arteries, 966 width of, 17 congenital extrahepatic, 216
Atherosclerosis Beam width artefacts, 7274, 72f73f, 73b extrahepatic, 13681369, 1369f1370f
abdominal aorta, 787, 788f Behets syndrome, 379t Biliary atresia-splenic malformation
grading, 788 Benign lymphoepithelial lesions (BLELs), syndrome, 13681369, 1370f
imaging, 788 904905, 906b Biliary cirrhosis, 115, 116f, 154
peripheral arterial disease, 1198 Benign prostate hyperplasia/hypertrophy post-liver transplantation, 216
signs, 788 (BPH), 579581, 580t, 581f582f, Biliary epithelial dysplasia of the intrahepatic
upper limb, 1214 583t bile ducts, 150
waveform appearance, 788, 788f Benign sternomastoid tumour of infancy, Biliary sludge, 240241, 241f242f, 1375, 1375f
Athletic groin pain, 10811082 1302, 1303f Biliary system
adductor muscles, 1081, 1082f Berardinelli-Seip syndrome, 116 cystadenocarcinoma, 161
anatomy, 1081, 1081f -human chorionic gonadotropin (-hCG), cystadenoma, intrahepatic, 149150
clinical overview, 1081 758 hypoplasia, 13711372
normal ultrasound appearances, 1081 Bezoars, 1387, 1387f rhabdomyosarcoma, 1374f
role of ultrasound, 1082 Biceps femoris, 1075, 1091, 1091f Biliary tree
symphysis pubis, 1081, 1081f Biceps tendon anatomy, 228f
ultrasound-guided intervention, 1082 anatomy, 1043, 1044f endoscopic ultrasound, 236, 236f
Attenuation, 11, 11t, 13b dislocation, 1039, 1039f1040f intraoperative ultrasound, 279280, 280f
Attenuation coefficients, 52, 52t injury, 1048, 1048f1049f laparoscopic ultrasound, 236, 273
Atypical ductal hyperplasia (ADH), breast, long head of liver transplantation complications,
991 anatomy, 1030 211212, 220221, 221f
Autoimmune pancreatopathy, 305306, 305f fatty atrophy, 1039, 1039f normal anatomy, 227
Autonephrectomy, 463464, 465f normal, 1032f ultrasound technique and appearance,
Autosomal dominant polycystic kidney pathology, 10371039, 1039f 228236
disease (ADPKD), 9798 Bicipital groove, 10301031, 1032f Bilirubin, 1367
in children, 14361437, 1437f1438f Bicipitoradial bursitis, 1050, 1050f Biometry
and pancreatic cysts, 1378 Bifid median nerve, 1159, 1160f eye, 958, 958f
Autosomal recessive polycystic kidney Bile first trimester, 748749
disease (ARPKD) echogenic, 240241, 241f242f Biomicroscope, ultrasound
in children, 1436, 1436f leaks, post-liver transplantation, 212, eye, 942
Axial resolution, 15 221 Biopsies, 1169
Axillary artery, 1213 milk of calcium (limy), 240 bone lesions, 11911193, 1192f
Axillary vein, 1241 volume increase, 256 breast, 10001002, 1001t, 1002f
Axilla staging in breast cancer, 997999, Bile ducts, 9495 cervical lymph nodes, 934935, 935b
998f999f anastomosis, strictures, 211, 212f coaxial technique, 850
Axons, 1158 anatomy, 227, 229f, 234f core see Core biopsy
Azathioprine, 529530 ascariasis, 266, 266f fine-needle aspiration see Fine-needle
biliary epithelial dysplasia of, 150 aspiration (FNA)
Carolis disease, 264265, 266f general principles, 847853
B in children, 13561375 hepatocellular carcinoma, 154
cholangiocarcinoma, 156160 large-bore vacuum-assisted, 10011002,
Backscatter, 14 choledochal cysts, 263264, 265f266f 1001t
Bacteroides spp., 124 choledocholithiasis see Choledocholithiasis liver, 167170
Bagel sign, 754755, 755f diameter changes, rapid, 255258 complications, 170, 170b
image-guided approach, 167168, 168f fistulae to the, 566, 567t, 568 dynamic range, 36, 36f37f
indications, 169, 169b, 169f flowmetry, 554555, 555f focus, 36, 38f
patient management, 170, 170b flow patterns, 555556, 555b frequency, 36
percussion-palpation approach, 167 foreign bodies, 556558, 558f559f gain, 34, 35f
quality of specimen, 168169 gross anatomy, 550 harmonics, 37, 38f
technique, 167169, 168t harmonic imaging, 551552 spatial and frequency compounding,
type of needle, 168 infection, 568, 568b 3738, 39f
lungs, 10171018 inflammation, 568 time gain control/depth gain control,
needle guides, 852, 852f leiomyosarcoma, 562 35, 35f
needle tip visualisation, 850852, 851b, lower urinary tract symptoms, 553, 553b zoom, 3637, 38f
851f852f lumen, 556559 penis, 623624
omental, 720722, 721b, 721f lymphoma, 562 Peyronies disease, 628
complications, 722 masses, 561566 priapism, 627
method, 720721 megacystis, 1425 principles, 1718
rationale, 720 metastases, 562 pulse-echo cycle, 17f
pancreas, 290, 318319, 318f, 319b microscopic anatomy, 550551 scanners, 32, 39b
complications, 318319 neck, cysts, 581 Bochdalek hernias, 13481349, 1350f
indications, 318 neurogenic, 1425, 1430f Bone-at-focus thermal index (TIB), 54
results, 318 normal sonographic appearance, 576 Bone(s), 1029
techniques, 318 outflow obstruction, 560, 562b, 562f erosions see Erosions
patient selection/preparation, 847848 pelvi-ureteric dilatation, 436438 implications of heating, 53
post-procedural care, 853 partial resections, 568 lesions, biopsy, 11911193, 1192f
pre-procedural assessment, 848 pathology outside the bladder, 566568 Bosniak renal cyst classification system, 488,
procedural planning and ergonomics, 852, postoperative conditions, 568 488t, 489f, 492
852f pregnancy-related pathology, 568 Bowel
prostate, 587591, 589b procedures, 569 large see Colon
abscess/cyst drainage, 591 rhabdomyosarcoma, 562 small see Small bowel
post-prostatectomy bed, 590591, 591f squamous cell cancer, 561562 Boxers knuckle, 10601062
principles, 587590, 590f stones, 556, 557f Brachial artery, 1043, 1213, 1216f
seminal vesicles/ejaculatory ducts suprapubic catheterisation, 569 Brachialis muscle, 1043
injection, 591 transabdominal imaging, 551, 552f Brachial neuritis, 1037
renal, 455458 transitional cell carcinoma, 431 Brachial plexus, 911912, 912f
complications, 456457, 457f trauma, 569, 569b, 841 Brachytherapy
contraindications, 455456 tumours, 561566 ocular melanoma, 952953
indications, 455456 ultrasound technique, 1409, 1413f1414f tumour ablation, 860, 860f
renal transplant, 457458 urachus, 559, 561f Brain
technique, 456, 456f ureteroceles, 558559, 560f561f neonatal see Neonatal brain
safety/complications, 853 urothelium, 551 see also specific anatomical areas
small bowel, 385, 386f volume, 553556 Brain death evaluation, 983, 1290, 1290f
soft tissue masses, 11911192, 1191b, 1192f assessment, 1413f Branchial cleft cyst, 908, 908b, 909f910f
specimen handling, 852853, 853f estimation, 554f Branchial cysts, 905, 12961297, 1297f1298f
spleen, 345 accuracy of, at different volumes BRCA1-related tumours, 996
track seeding, 853 and in bladder shapes, 554 Breast, 9871004
Tru-cut, 318 calculating, 554b abscess, 989, 989f
Birth-related brain injury, 1285, 1289f technology comparisons, 554 benign pathology, 987993, 989b
Birth weight, epidemiological studies, 56 wall, 560 cystic lesions, 987989, 988f989f
Bladder, 550571 thickness, 1414f solid lesions, 989993, 990f992f
adenocarcinoma, 561562 Blakes pouch cyst, 12791280 cancer see Breast, malignant pathology
anatomy, 550551 Blood clot complex sclerosing lesions, 992993
cancer, 561, 562t pelvi-ureteric dilatation, 434 core biopsy, 1001, 1002f
invasion from adjacent tumours, see also Thrombosis equipment, 987
565566, 566f Blood flow see specific organs; specific vessels fat necrosis, 988, 988f
staging, 563564, 563b, 564f565f Blood supply fibroadenoma, 990991, 990f
tumour detection, 562563, 563f ovaries, 648 fine-needle aspiration, 1001
tumour follow-up, 564565, 565f prostate, 574 galactoceles, 988, 988f
catheter balloon puncture, 569 seminal vesicles, 574 hamartoma, 991
in children, 1409, 1413f1414f, 14221428 small bowel, 371 implants, 1000, 1000f
colour duplex imaging: ureteric jets, 551, uterus, 649 infection, 989
553f see also specific organs; specific vessels large-bore vacuum-assisted biopsy,
conduits, 568 B-mode imaging, 17f, 18b 10011002
contrast imaging, 85, 552553 aortic dissection, 789 lipoma, 991, 991f
development, 14071409, 1408f artefacts in, 6176 malignant pathology, 9931000, 993b, 994f
diverticula, 566, 567t, 1425, 1429f hypoxic ischaemic encephalopathy, 1266 angiosarcoma, 997
ears, 1425, 1429f image processing, 23, 23f, 25b assessment of response after
emptying (residue), 553556 instrumentation, 25b chemotherapy, 999
endocavity ultrasound, 551 parameters, 32, 3440, 39b axilla, 997999, 998f999f
endometriosis, 568 adaptive processing, 3840 BRCA1-related tumours, 996
extrinsic masses, 567568, 567f depth, 36, 37f classification, 993996
Coats disease, 955, 955f Colour Doppler imaging, 2829, 29f30f post-processing, 4244
Coccygeus, 647 abdominal aorta atherosclerosis, 788 power, 40
Coded excitation, 84 abdominal trauma, 830 priority, 4244, 44f
Coeliac artery, 789, 790f acute appendicitis, 389390, 391f scale/pulse repetition frequency, 4041,
stenosis, 789791, 791f adenomyosis, 694695 40f41f
Coeliac disease, 385 adrenal glands, 637 space/time, 4244, 45f
Cogwheel sign, pelvic inflammatory disease, aortic dissection, 789 penis see Penis, stimulated colour Doppler
682 appendix, 1396 ultrasound
Colic veins, 388 artefacts, 88 peripheral veins, 12291232, 1230f1232f
Colitis before aspiration, 1192 Peyronies disease, 628
amoebic, 391392, 400, 400f biliary tree, 279280 portal veins, 179, 180f
in children, 1399, 1400f carotid arteries, 967, 969 stenosis, 209210
differential diagnosis, 399t cerebral arteries, 977 priapism, 627
granulomatous, 1399 cervical lymphatic malformations, proliferative haemangiomas, 1300
infective, 399401, 401b, 401f 12951296 prostate, 576
inflammatory see Crohns disease; cervical node vascularity, 932 retained products of conception, 711
Ulcerative colitis chronic venous insufficiency, 1244 in rheumatological ultrasound, 1132
ischaemic, 399t, 401, 402f colitis, 1399 scanners, 32, 44b
neutropenic, 1399, 1400f colour blooming, 88 soft tissue masses, 1113
pseudomembranous, 399t, 400401, 1399, Crohns disease, 1392 spleen
1400f deep vein thrombosis, 1232, 1232t, abscess, 338339
tuberculous, 399400, 399f, 399t 12351236 infarction, 340342
typhlitis, 399t, 401, 401f endoleaks, 785, 787f tendinopathy, 1025
ulcerative see Ulcerative colitis eye, 942, 942f testicular torsion, 617
Yersinia enterocolitis, 399t, 401 gastro-oesophageal reflux, 1384 thoracic disease, 1018
Collateral ligaments gestational trophoblastic disease, 696697 thyroid nodules, 872
elbow, 10451046, 1046f, 1051, 1051f hepatic artery pseudo-aneurysm, 208209 transcranial, 85, 979
fingers, 1064b hepatic veins venous reflux, 1245
knee occlusion, 195 Colour fluid sign, 1018
lateral, 1084, 1091 stenosis, 210211 Column of Bertin, 505, 506f
medial, 1084, 1085f, 1090 hepatocellular carcinoma, 155156 hypertrophied, 1417f
wrist, 10631064 image processing, 30b Comedocarcinoma, prostate gland, 589t
Collateral veins, 1235 instrumentation, 30b Comet-tail artefacts, 68, 69f, 1008, 1008f
Collateral vessel formation, 206207, intussusception, 1390 thyroid nodules, 872, 872f
206f kidneys Common extensor origin injection, 1053,
Collecting duct carcinoma, 517 arteriovenous fistula, 481 11731174, 1176f
Colloid cysts, 1309, 1310f renal cell carcinoma, 513517 Common extensor tendon, 1046, 1046f
Colon, 394405 renal vein thrombosis, 448 Common flexor tendon, 1045, 1046f
adenocarcinoma, 402 simple renal cysts, 487 Common hepatic duct, 95, 103, 103f
anatomy, 394395, 395f transplantation, 530533, 531f Common peroneal nerve, 1100
ascending, 394395 trauma, 840841 Communicating arteries
in children, 13991401, 1399b knee joint effusion, 1088 anterior
colitis, 1399 limitations of, 2930 anatomy, 976
imperforate or ectopic anus, 1399 liver transcranial Doppler ultrasound,
necrotising enterocolitis, 1400, adenoma, 145 976978
1401f angiomyolipoma, 149f posterior, 1259t
neoplasms, 14001401 fibronodular hyperplasia, 142 anatomy, 976
normal anatomy, 1399 haemangiomas, 140 aneurysm, 982f
colitis see Colitis transplantation, 199 transcranial Doppler ultrasound,
congenital abnormalities, 395396, 395f lung cancer, 1017 976977, 979f, 981f
descending, 394395 ocular melanoma, 951952 Communicating cavernous ectasia of the
diverticular disease, 395f396f, 396397 ovaries intrahepatic ducts see Carolis
right-sided, 397, 397f lesions, 670 disease
duplication cyst, 395396, 395f torsion, 668, 1489 Compartment syndromes, 11551156
endometriosis, 402, 404f pancreas, 288290, 290f acute, 1155
epiploic appendagitis, 402405, 405f transplantation, 320 chronic exertional, 11551156
haustrations, 395, 395f tumours, 309 Complete portal tracts (CPTs), 168
intussusception, 402, 405f parameters, 32, 4044, 44b Compression stockings, venous
lipoma, 402, 404f beam steering in linear arrays, 42, 43f incompetence, 1246
lymphoma, 402, 404f box/area size, 42, 42f Compression technique, appendix
pseudo-kidney appearance, 402, 403f filter, 4244 assessment, 388
scanning technique, 394395, 395f flow settings - combination controls, Computed tomography (CT)
sigmoid, 394395 44, 45f abdominal aorta, 773
transverse, 394395 focus, 42, 43f aneurysm, 779
trauma, 841, 842f frequency/patient type, 41, 42f adrenal glands, 632, 636, 640, 642
tumours, 402, 403f404f gain, 40, 40f bladder cancer, 562, 564
Colorectal cancer, 275276 invert, 41, 41f cervical cancer, 714
Colour blooming, 88 persistence, 4244 cholangiocarcinoma, 158160
contrast-enhanced see Contrast-enhanced Connective tissue disorders, kidney hepatic artery thrombosis, 206207
computed tomography (CECT) involvement, 453 hepatocellular carcinoma, 155156,
elbow loose bodies, 1047 Conns syndrome, 636 157f159f, 200201
endometrial cancer, 705 Consolidated lungs, 13391340, 1341f liver
epithelioid haemangioendothelioma, Continuous ambulatory peritoneal dialysis abscess, 124, 125f
160161 (CAPD), 454455 lymphoma, 160
erosions, 1129 in children, 1444 radio-frequency ablation, 172, 173f
versus full potential ultrasound in Continuous wave (CW) Doppler, 15, 26, 27f trauma, 837
abdominal trauma, 832 peripheral arterial disease, 11991200, neuroendocrine tumours, 314
inguinofemoral hernia, 1077 1203b pancreas, 288, 291f
kidneys transducers, 8 tumours, 306309
abscess, 496 Contrast agents, 7789 portal venous thrombosis, 201
renal cell carcinoma, 513517, 523 bladder, 552553 renal trauma, 840841
trauma, 840841, 1458 breast cancer diagnosis, 993 spleen, 326327
kidneys, ureter and bladder, 428 British Medical Ultrasound Society abscess, 338339
liver (BMUS) guidelines, 58 infarction, 341f
focal lesions, 138 cavernous haemangioma, 141142 metastases, 334
metastases, 151153 clinical applications of, 8486 trauma, 838
radio-frequency ablation, 172 diffuse parenchymal liver disease, 104 tumours, 334337
lung biopsy, 10171018 European Federation of Societies of in tumour ablation, 863
oesophageal cancer, 354 Ultrasound in Medicine and Contrast resolution, 15
ovarian cancer, 669 Biology (EFSUMB) guidelines, 58 Conus medullaris, 1319
paediatric chest, 1337 fallopian tube patency, 734735 Copper intrauterine devices, 706707
pancreas, 285 generations, 79 Coracoacromial ligament, 1030, 1032f
biopsy, 318 history and development, 77 Coracohumeral ligament, 1030, 1032f
pancreatitis imaging artefacts, 88 Core biopsy, 318
acute, 295296 kidneys, 467, 470f breast, 1001, 1001t
chronic, 301302 acute tubular necrosis, 484 cervical lymph nodes, 935, 935b, 936f
tumours, 306 renal cell carcinoma, 513 versus fine-needle aspiration, 848
peripheral nerves, 1158 liver, 84, 85f, 138139, 139t lungs, 1017
small bowel diffuse parenchymal liver disease, 104 needle types, 849850, 849f, 849t
ischaemia, 379 metastases, 151153 fully automated sheathed, 850
obstruction, 384 microbubbles see Gas bubbles manual sheathed, 849
thymus, 1339 optimisation, 139140 Menghini technique, 849
thyroid, 867 scanning strategy, 139140 semi-automated sheathed, 849, 850f
transitional cell carcinoma, 518520, 521f types of, 7881, 79t, 81b Cornea, 938
in tumour ablation, 863 World Federation for Ultrasound in Coronary artery bypass, vein mapping,
unstable trauma patient, 843 Medicine and Biology (WFUMB), 12481249
uterus, 687 5859 Coronary ligaments, liver, 93
Computed tomography (CT) angiography see also Contrast-enhanced computed Coronary vein varices, 183, 184f
peripheral arterial disease, 1197, tomography (CECT); Contrast- Coronoid fossa, 1043
12001201 enhanced intraoperative Corpora amylacea, 576
pulmonary embolus, 1015 ultrasound (CE-IOUS); Contrast- Corpora cavernosa, 621, 622f
renal artery stenosis, 474, 474t475t enhanced ultrasound (CEUS) air in, 623624, 623f
Computed tomography during arterial Contrast-enhanced computed tomography Corpus callosum, 1257
portography (CTAP), 277 (CECT) dysgenesis of the, 1279, 1281f
Congenital anomalies hepatic artery Corpus luteum, 662663, 663f
liver, 97 pseudo-aneurysm, 208209 cysts, 663, 762763, 762f
prostatic, 579 stenosis, 208 Corpus spongiosum, 621, 622f
see also specific anomalies thrombosis, 205207 Cortical necrosis
Congenital cystic adenomatoid malformation hepatocellular carcinoma, 200201 acute, 452, 452f
(CCAM), 1341, 1343, 1344f portal venous thrombosis, 201 in children, 1444
Congenital extrahepatic biliary atresia, 216 post-transplant lymphoproliferative Couinaud classification, 93, 9596, 179, 180f,
Congenital generalised lipodystrophy (CGL), disease, 213 193
116 Contrast-enhanced intraoperative ultrasound Courvoisiers law, 256
Congenital malformations, neonatal brain, (CE-IOUS), 273 Cranial bone thermal index (TIC), 54
12791283 liver metastases, 152153, 277278, Cranial sutures, 1254
Dandy-Walker complex, 12791280, 277f278f Cremasteric artery, 594595
1281f Contrast-enhanced ultrasound (CEUS) Crescent in doughnut sign, 384, 385f
destructive lesions, 1283, 1283f abdominal trauma, 829830, 832833, Cribriform carcinoma, breast, 995
disorders of sulcation and migration, 832f833f Cricoid cartilage, 914
12801282, 1282f bladder, 553 Crohns disease, 371376, 372b
dysgenesis of the corpus callosum, 1279, cholangiocarcinoma, 158160 abscess, 374375, 375f
1281f versus computed tomography in activity, 375376
holoprosencephaly, 1280, 1282f abdominal trauma, 832833, 833f appendiceal, 394, 394f
tuberous sclerosis, 1282, 1283f epithelioid haemangioendothelioma, in children, 13921393, 1393f
Conjoined twins, 748, 748f 160161 clinical features, 372
Connatal cysts, 12571258 gallbladder polyps, 249 colonic, 397, 397b, 398f
paralysis and paresis, 1350, 1351f main renal trunks, 471472, 471f473f, Ductal carcinoma in situ (DCIS)
rupture, 1007 477 breast, 991, 996, 996f, 1002
trauma, 841 normal pattern, 469470 vacuum-assisted biopsy, 1002
Diastematomyelia, 1325, 1326f parenchymal disease, 483484, 484b Duct ectasia, 583584, 583t, 584f
Dicrocoelium dendriticum, 251 renal artery occlusion, 478f Ductus deferens, artery to the, 594595
Diffraction, 56, 6f renal artery stenosis, 448, 467, Ductus epididymis, 594
Digastric muscles, 891 474t475t, 475477 Duodenum, 365, 366f
Dilated pelvicalyceal system, 493, 494f, 518 renal infarcts, 478, 479f atresia, 1388, 1389f
Dimples, spinal, 13281330 renal vein thrombosis, 479480 duplication, 1394, 1394f
Disciform lesions, retina, 948, 948f small vessel disease, 484 haematoma, 1394, 1394f
Disease-modifying anti-rheumatic drugs spectral (pulsed wave) arterial pattern, Duplex scanning
(DMARDs), 1132 469470, 470f abdominal aortic aneurysms, 777781
Distal augmentation, peripheral veins, 1231, technique, 470472 abnormal appearance, 777779,
1231f, 12341235, 1236f transplantation, 467468, 530533 778f780f
Distal intersection syndrome, 1059 tubulo-interstitial disease, 484 distance between renal arteries and
Distortion, non-linear, 12 vasculitis, 484 aneurysm sac, 780
Diverticular disease muscle injury, 1137 limitations and pitfalls, 781
bladder, 566, 567t, 1425, 1429f ocular melanoma, 952953 measurement of aneurysm size, 780,
calyceal, 493, 494f, 1442f ovaries 781f
colonic, 396397, 396f endometriosis, 681 normal appearance, 777, 778f
right-sided, 397, 397f haemodynamics, 655 objectives, 777, 777f
renal pelvic, 493, 494f lesions, 670 patient preparation, 777, 778f
Doppler imaging, 1314, 13f14f, 14b, 2630 pancreatic tumours, 309 variability of measurement between
abdominal trauma, 829 pelvi-ureteric dilatation, 441 ultrasound and CT, 779
aliasing, 28 portal hypertension, 181 bladder, 551, 553f
aortic dissection, 789 power see Power Doppler peripheral arterial disease, 12001207,
artefacts, 88 pulsed wave see Pulsed wave Doppler 1203b, 1203f1204f
arteriovenous fistula, 481 pyelonephritis, 460 aorto-iliac and femoropopliteal
autocorrelator, 29 resolution, 15 segments, 1206
axillary lymph nodes, 998 in rheumatological ultrasound, 1126, below-knee segments, 12061207, 1207f
breast cancer 1132 reporting, 1207, 1208f
diagnosis, 993 shift frequency estimation, 29 scanning technique, 12051206,
response to chemotherapy, 999 transcranial, 85 1205f1206f
carotid arteries, 969971, 970t, 971f, transducers, 8 peripheral artery bypass grafts, 1209
976983 transjugular intrahepatic portosystemic transcranial, 85
carpal tunnel syndrome, 10641065 shunt, 187188, 188b Duplication cysts, 816, 1347b, 1348
cervical lymph nodes, 932, 933f uterus haemodynamics, 655 duodenal, 1394, 1394f
colour flow see Colour Doppler imaging Dorsal dermal sinuses, 13261327, neonatal, 1483
continuous wave see Continuous wave 1327f1328f pancreas, 1378
(CW) Doppler Dorsalis pedis artery, 1207, 1207f Dupuytrens contracture, 1122
in ectopic pregnancy, 756757 Double-bleb sign, 750, 750f Dynamic range, 2324, 24f
endoleaks, 787 Double-bubble sign, 1388 Dynamic scanning
eye, 941942, 942f Double decidual sign, 751 carpal tunnel syndrome, 10641065
frequency estimation and display, 28, Double wall sign, 1483 muscle injury, 1137
29f Doughnut sign, 384, 385f, 1390 Dysfunctional uterine bleeding (DUB),
hepatic artery, 189192 Drainage techniques, 853857 688689
stenosis, 208 abscesses, 1192, 1193f Dysgerminoma, ovarian, 676
thrombosis, 205207 breast, 989 Dyslexia, 5657
hepatocellular carcinoma, 155156 intra-abdominal, 815 Dysmenorrhoea, 688
high pass filtering, 28, 28f liver, 124, 125f Dyspareunia, 688, 691
hypoxic ischaemic encephalopathy, 1266, pelvic see Pelvic abscess drainage
1269 cyst ablation, 856857
inferior vena cava thrombosis, 792 diagnostic aspiration versus, 853 E
instrumentation, 28b drain fixation, 856, 856b, 857f
kidneys, 467, 469470, 1409, 1412f drain placement, 854856, 856f857f Eagle-Barrett syndrome, 14271428
abnormalities in hypertension, 475476, drain types, 854, 856f, 856t Echinococcal cyst, 129130, 130f131f, 170
478f locking drains, 813 see also Hydatid disease
acute glomerulonephritis, 484 nature of the collection, 854, 854t, Echinococcosis see Hydatid disease
acute tubular necrosis, 484 855f Echinococcus granulosus, 129, 339340
arteriovenous fistula, 481 post-procedural care, 856 Echinococcus multilocularis, 130
arteriovenous malformations, 482 pre-procedural assessment, 854 Echo-endoscopes, 351352, 352f
in children, 14561457 Seldinger technique, 804f, 816 Echoes
chronic renal failure, 484 side holes, 813815 B-mode imaging, 17
colour flow map, 469, 469f sump drains, 813 definition, 16
disease, 447 Trocar technique, 815816 dynamic range, 2324, 24f
haematoma, 495 Dromedary hump, renal, 505, 506f liver, 104105, 106f
hepatorenal syndrome, 484 Drug delivery, contrast microbubbles, 87 multiple, 6568, 67f
intrarenal vessels, 470471, 477 Drusen (hyaline bodies), 948, 948f scattered, 6162
Echogenic bile, 240241, 241f242f pulled, 1051, 1052f diagnosis, 702705, 702f705f
Echogenic fluid, 6465, 65f synovial osteochondromatosis, 10471048, management, 705
Echogenic swirling sign, 1009 1048f other investigations, 705
Echovist, 79, 734, 735f synovitis, 1047, 1047f screening, 705
Ectopia lentis, 943, 944f technique, 10431046, 1046b staging, 704705, 706f, 706t
Ectopic pregnancy, 753b tendon injury, 10481050, 1048f1049f symptoms, 702
adnexal findings, 754756, 755f, 755t Elderly patients, acute appendicitis, 389 cyst, 742f
bagel sign, 755f Electronic focusing, 21, 21f in ectopic pregnancy, 754, 754f, 754t
-hCG level, 760, 760t Elevation focusing, 21, 22f endometriosis see Endometriosis
caesarean scar, 758, 759f, 760t Emboli endometritis see Endometritis
cervical, 757758, 758f759f, 758t counting, 979980, 980f haematometrium and related conditions,
complex mass, 755756, 756f757f pulmonary, 10151016, 1016b, 1016f 709711, 711f712f
Doppler ultrasound, 756757 Embryo hormone replacement therapy and,
endometrial appearances, 754f, 754t appearance in the first trimester, 744745, 705706
heterotopic gestation, 753 744f745f, 745t hyperplasia, 700, 700b, 700f, 700t, 706
incidence, 753 heartbeat, 745, 761, 761t hysteroscopy, 688
interstitial, 757, 757f758f, 757t transfer, 737, 737f intrauterine devices, 706708, 707f709f,
intraperitoneal fluid, 756, 757f Embryology 708b
locations, 753t adrenal glands, 1464 intrauterine synechiae, 709
methotrexate, 757, 767, 767t implications of heating, 53 medications and, 705706
negative ultrasound, 760 ovaries, 14681470 normal, 699f, 700
non-surgical management, 766767 parathyroid, 884 oral contraceptive pill and, 705
normal adnexal regions, 754 prostate, 572 osseous metaplasia, 732733, 732f
ovarian, 758 renal tract, 14071409 polyps, 693, 700702, 701f, 702b, 733, 733f
pregnancy of unknown location, 760, spine, 1322 postpartum uterus, 711712, 712f
760b, 760f, 761t testis, 593594 retained products of conception, 696,
pseudo-gestation sac, 754, 755f thyroid, 868869 711712
risk factors, 753 uterus, 14681470 tamoxifen and, 706, 707f
tubal miscarriage, 756, 757f Embryonal cell carcinoma, testicular, 599600, thickening in early pregnancy, 741, 741f
tubal ring with yolk sac/embryo, 754755, 600f Endomysium, 1138
755f756f Emphysema, congenital lobar, 13431344 Endoneurium, 1158
tubal rupture, 756, 756f, 756t Emphysematous pyelitis, 460 Endoscopic retrograde
unusual gestations, 757758, 757f Empty amnion sign, 745, 750, 750f cholangiopancreatography
uterine findings, 753754, 754f, 754t Empyema, 1009, 1009f (ERCP)
Egyptian eye, 12441245, 1244f in children, 1346f bile duct calculi, 236
Ejaculation, retrograde, 580t Encephalopathy, hypoxic ischaemic, choledocholithiasis, 280
Ejaculatory ducts, 574 12641269, 1266b, 1267t, pancreatitis, chronic, 302
cysts, 583t, 584f 1268f1270f Endoscopic ultrasound (EUS)
injection of contrast, 591 Endarterectomy, 966 biliary system, 236, 236f
normal sonographic appearances, 576579 Endoanal ultrasonography, 406 equipment, 351352, 352f
obstruction, 584, 585f Endocardial border definition (EBD), 79, general principles, 351b
Elastofibroma, 1122 8586 islet cell tumours, 279
Elastography, 1213 Endocavity ultrasound neuroendocrine tumours, 314315
breast cancer diagnosis, 993 bladder, 551 pancreas, 285, 288291, 291f292f
pancreas, 288 transducers, 19f biopsy, 318
soft tissue masses, 1113 Endocrine development, female, 1470 pancreatitis
thyroid nodules, 872 Endodermal sinus tumours see Yolk sac acute, 296
Elbow, 10431054 tumours chronic, 302304
anatomy, 10431046, 1046b Endoleaks, 782, 783t, 784b, 784f, 786f787f, tumours, 309, 310f
anterior compartment, 10431044, 1044f 787 upper gastrointestinal tract, 353f
bursitis, 1050, 1050f1051f Endoluminal ultrasound, bladder cancer, 564 appearance, 352353
effusion, 1047, 1047f Endometrioid tumours, 673, 673f cancer staging, 353354, 355t, 356f
injection, 1053 Endometriomas, 402 357f, 360
interventional techniques, 11731175 abdominal wall, 806, 806f clinical indications, 353
joint aspiration, 1053 extraperitoneal, 1117 equipment, 351352
joint injection, 1175, 1177f ovarian, 680681, 681b, 681f, 730 oesophagus, 354360
lateral compartment, 1046, 1046f Endometriosis, 402, 404f present and future, 366
lateral epicondylitis (tennis elbow), 1049, bladder, 568 stomach, 360365
1050f as a cause of subfertility, 730 Endotension, 783t
ligament injury, 1051, 1051f ovarian, 680681, 681b, 681f Endovaginal ultrasound, bladder, 551
loose bodies, 10471048, 1047f1048f Endometritis, 709, 709b, 710f Endovascular aneurysm repair (EVAR),
medial compartment, 1045, 1046f pelvic inflammatory disease, 682, 682f abdominal aortic aneurysm,
medial epicondylitis (golfers elbow), Endometrium, 700712 781787, 783f787f, 783t784t,
1050 ablation, 697 784b
nerve entrapment, 10521053, 1052b, anastrozole and, 706 Endovascular Aneurysm Repair Trial 1
1052f1053f Ashermans syndrome, 709 (EVAR1), 782
paediatric bony injury, 1051, 1051b, 1052f cancer, 702705, 705b Endovenous ablation, 12461248
posterior compartment, 1045, 1045f aetiology, 702 Enhancement, 64, 64f
Entamoeba histolytica, 126, 400, 13641365 Extensor carpi radialis longus (ECRL), 1055, rhegmatogenous, 944
Entheseal disease, 1131, 1131b, 1132f 1056f, 1058f traction, 946947, 947f
Enthesitis, 1131, 1132f Extensor carpi ulnaris (ECU), 1055, 1056f, vitreoretinal traction, 944945,
Enthesopathy, ankle, 11021103, 1103f 1062 944f945f
Enuresis, 1462 Extensor digiti minimi (EDM), 1055, 1056f disciform lesions, 948, 948f
Ependymomas, 1333 Extensor digitorum brevis (EDB), 1098 drusen (hyaline bodies), 948, 948f
Epicondylar groove, 1052 Extensor digitorum communis (EDC), 1055, haemorrhage, 952
Epicondylitis 1056f tear, 944945, 945f
diagnosis, 1053 Extensor digitorum longus (EDL), 10971099 sclera, 938, 940f
lateral, 1049, 1050f Extensor hallucis longus (EHL), 10971098 trauma, 956958, 956f958f, 957b
medial, 1050 Extensor indicis proprius (EIP), 1055, 1056f tumours, 951955
Epidemiology, safety of ultrasound, 5657 Extensor pollicis brevis (EPB), 1055, 1056f ultrasound features, 938941
Epidermal inclusion cysts, 1116 Extensor pollicis longus (EPL), 1055, 1056f, vitreous, 949950
Epidermoid cyst, 893894, 894f 1058, 1058f asteroid hyalosis, 949, 949f
testicular, 602, 603f Extensor tendons, 1055, 1056f haemorrhage, 952, 956, 956f
Epididymis tears, 1057, 1058f persistent hyperplastic primary, 949,
abscess, 615, 615f External oblique muscle, 1076 949f, 955
adenomatoid tumour, 610, 610f Extra-corporeal shock-wave lithotripsy posterior detachment, 949950,
anatomy, 594 (ESWL), 55 949f950f
appendage torsion, 617, 618f Extradural haematoma, 1285 incomplete, 950, 951f
cysts, 608, 609f Extrahepatic biliary atresia (EHBA), 1368 synchysis scintillans, 949
inflammatory disease, 614615 1369, 1369f1370f see also Orbit
leiomyoma, 610 Extrahepatic duct, 95
normal ultrasound appearance, 595598, Extramedullary haematopoiesis, 507
597f Extrarenal pelvis, 1412, 1417f F
tubular ectasia, 608 Eye, 938958
vasectomy, 608, 609f anatomy, 938941, 939f941f Falciform ligament, liver, 93, 205, 205f
Epididymitis, 614615, 614f biometry, 958, 958f Fallopian tubes
chronic, 615 British Medical Ultrasound Society abscess, 682, 683f
tuberculous, 615, 615f (BMUS) guidelines, 58 hysterosalpingo-contrast sonography for
Epididymo-orchitis, 612615, 615b choroid, 940 patency of, 734735, 735f
paediatric, 1492, 1493f detachment, 946 normal development, 1469f
Epigastric hernia, 804, 804f haemangioma, 954, 954f patency of, 734735, 735f
Epiglottis, 913, 913f melanoma, 951953, 951f953f pelvic inflammatory disease, 682,
Epimysium, 1138 metastases, 953, 954f 682f683f
Epineurium, 1158 naevus, 954 rupture in ectopic pregnancy, 756, 756t
Epiphyses, elbow, 1043 osteoma, 954, 954f spasm, 735
Epiploic appendagitis, 402405, 405f ciliary body, 940 torsion, 14881489
Epithelial cell tumours, ovarian, 1487 melanoma, 951953, 953f Fascia bulbi, 938
Epithelioid haemangioendothelioma, cornea, 938 Fasciculi, 1138
160161 examination technique, 941943 Fasciola hepatica, 131, 251
Erectile dysfunction, 621623 A-scan, 941, 942f Fascioliasis
arteriogenic, 624 Doppler, 941942, 942f acute, 131
background, 621623 2D scanning, 941 gallbladder, 251
physiology of the erectile process, 623 3D scanning, 943, 943b FAST see Focused assessment with
priapism, 627, 627b, 627f ultrasound biomicroscope, 942, 942f sonography in trauma (FAST)
veno-occlusive, 624625, 626f eyeball, 938, 959 Fat atrophy, muscle, 1154, 1154f
Erosions, ultrasound features of, 1129, 1129b, foreign bodies, 957958, 958f Fat necrosis, 1115, 1115f
1130f indications, 943, 943b breast, 988, 988f
Escherichia coli iris, 940 Fatty infiltration
epididymo-orchitis/epididymitis, 614 lens, 943 infraspinatus, 1035, 1035f
liver abscess, 124 cataract, 943, 943f liver see Fatty liver
renal abscess, 496 ectopia lentis, 943, 944f Fatty liver, 105111, 146148
urinary tract infection, 1448 intraocular implant, 943, 943f causes of, 105
Ethanol ablation, parathyroid lesions, 887 trauma, 956, 956f in children, 13591360, 1359f1360f
European Carotid Surgery Trial (ECST), 965 muscles, 959960 conditions associated with, 107t
European Federation of Societies of refracting media, 940941, 941b diffuse, 105106, 108f
Ultrasound in Medicine and retina, 940, 941f, 943948 focal fatty change, 107, 109f, 110b, 147
Biology (EFSUMB), 58 acquired retinoschisis, 947948, 948f focal fatty sparing, 108110, 109f110f,
contrast agents guidelines, 139 detachment, 943947, 944f 110b, 147, 148f
contrast-enhanced ultrasound for liver choroidal detachment, 946, 947f histology, 105, 106f
metastases, 153 conditions mimicking, 947b multifocal steatosis, 147148
European Society of Hysteroscopy fibroid exudative, 946 non-alcoholic fatty liver disease, 105,
classification, 691 non-rhegmatogenous, 946 110111, 111f
Ewings sarcoma, 1110f posterior vitreous detachment, non-alcoholic steatohepatitis, 110111, 111f
Extended field-of-view (EFOV) imaging, 1137 944945, 945f temporal changes, 105, 107f
Extensor carpi radialis brevis (ECRB), 1055, proliferative vitreoretinopathy, Female pseudohermaphrodites, 14751476
1056f 945946, 946f Female sexual cycle, 649, 650f
Femoral artery, 12291230 congenital generalised, 13021303 Flexor hallucis brevis, 1096
occlusion, 1205f deep, 1122 Flexor hallucis longus, 1096, 1104, 11061107
stenosis, 1204f1206f, 1206 infantile (desmoid-type), 1303 Flexor pollicis longus (FPL), 1055, 1056f,
Femoral canal, 10791080 palmar, 1122 1059f
Femoral hernias, 803804, 804f, 10791080, plantar, 1122 Flexor retinaculum, 1057
1080f plantar fascia, 1106 Flexor tendons, 1055, 1056f
Femoral neck fracture, 1070 superficial, 1122, 1122f tears, 10581059, 1059f
Femoral veins, 12281230 Fibromatosis colli, 1302, 1303f, 1511, 1511f Flowmetry, 554555, 555f
duplication, 1234 Fibronodular hyperplasia (FNH), 142143, Fluid bronchogram, 1014
spontaneous flow, 12301231 144f145f Fluid collections
Femoroacetabular impingement, 10701071 Fibrosarcoma, 1123 aspiration/drainage, 11921193
Fertility Fibrosis liver transplantation, 212213
assessment of, 730739 hepatic, 111, 111f nature of, in drainage, 801t, 803f, 807809
and fibroids, 691 penile, 628 peritoneum, 815816, 816f
hysterosalpingo-contrast sonography for Fibrotic haemangioma, liver, 141142, 143f retroperitoneum, 821823, 822t,
tubal patency, 734735, 734f Field, 6 823f825f
735f, 735b FIGO staging Fluid colour sign, 1008, 1009f
infertility see Infertility cervical cancer, 715t Focal nodular hyperplasia (FNH), 1364f
scanning through an IVF cycle, 735738 endometrial cancer, 706t in children, 1363
downregulation, 735736 Filum terminale, 1318 Focused assessment with sonography in
embryo transfer, 737, 737f lipoma, 1324, 1324f trauma (FAST), 829f
follicular development, 736, 736f tight filum terminale syndrome, 1324 abdominal aortic aneurysm, 775
oocyte capture, 736737, 736f 1325, 1325f abdominal trauma, 828829, 829b,
ovarian hyperstimulation syndrome, Fine-needle aspiration (FNA) 829f830f, 831832, 843
738, 738f, 738t breast, 1001, 1001t bladder, 569
subfertility see Subfertility cervical lymph nodes, 934935, 935b, 935f versus full potential ultrasound, 831832
Fetal anomalies, first trimester, 746747, versus core biopsy, 848 unstable trauma patient, 843
746f general principles, 847853 Focused ultrasound, tumour ablation, 859
Fetal heart monitoring, British Medical lungs, 1017 Focusing
Ultrasound Society (BMUS) needle guides, 852, 852f electronic, 21
guidelines, 58 needle tip visualisation, 850852, 851b, elevation, 21
Fibroadenoma, breast, 990991, 990f 851f852f Foley balloon catheter, 556, 558f, 569
Fibro-adipose septa, 1026 needle types, 848849, 848b, 849f, 849t Follicle(s)
Fibrohistiocytoma, retroperitoneal, 819820 oesophageal cancer, 354 development, 736
Fibroids, 668, 689694, 693b pancreas, 290 rupture, 730
bridging vascular sign, 691 biopsy, 318 Follicle-stimulating hormone (FSH), 649, 661
calcification, 691692, 692f patient selection/preparation, 847848 in in-vitro fertilisation, 736
as a cause of subfertility, 731732, 732b, post-procedural care, 853 menarche, 14721473
732f pre-procedural assessment, 848 Follicular neoplasm, thyroid, 876878, 877b,
cervical, 713, 714f procedural planning and ergonomics, 852, 877f878f
in early pregnancy, 763, 763f 852f Fontanelles, 1254, 1254f1255f
fertility and, 691 safety/complications, 853 Food and Drug Administration (FDA), 51, 57,
malignant change, 693 specimen handling, 852853, 853f 57t
necrosis, 692, 693f spleen, 345 Foot
nomenclature of site of, 691 thyroid nodules, 882 anatomy, 1098, 1100b
pregnancy and, 690, 690f track seeding, 853 disease processes, 11061107, 1107b
pyomyoma, 690 Fistulae interventional techniques, 11871190
risk factors, 689 aortocaval, 795 mass lesions, 1107
size and age, 690 arteriovenous see Arteriovenous fistula pain, 11061107
subserosal, 691 to the bladder, 566, 567t, 568 plantar aspect, 11001101, 1100f1101f
symptoms, 691 Crohns disease, 375, 376f short muscles, 1101
torted pedunculated, 691 dialysis, 455, 455f technique, 1098, 1098f, 1101b
treatment, 693694 haemodialysis access, 1215, 1220t1221t, Footballers ankle, 1105
ultrasound appearances, 691693, 1223, 1224f Foramen of Winslow, 93
691f692f inferior vena cava, 795, 795f Forearm muscles, 1140t, 1141, 1142f
vaginal, 716 trans-sphincteric, 408 Forefoot injections, 11891190
vascularity, 693 Flash artefact, 1126, 1127f Foregut
venetian blind pattern, 691692, 692f Flash contrast imaging, 8284, 83f duplication cysts, 1347b, 1348
Fibrolamellar hepatocellular carcinoma Flash frames, 8283, 83f malformations, congenital, 1299
(FLHCC), 160, 201, 216 Flexor carpi radialis (FCR), 10551056, 1056f, Foreign bodies
Fibrolipoma, filum terminale, 1324 10591060, 1060f bladder lumen, 556558, 558f559f
Fibrolipomatous hamartoma, 1166 Flexor carpi ulnaris (FCU), 10551056, eye, 957958, 958f
Fibromas 10591060, 1061f granulomas, 1117
medullary, 512 Flexor digitorum longus, 1096, 1104 localisation, 11901191
ovarian, 678, 679f Flexor digitorum profundus (FDP), 1055, paediatric, 15071508, 1508f
plantar fascia, 1106 1056f vaginal, 715716, 1490
Fibromatosis, 1122 Flexor digitorum superficialis (FDS), 1055, Fourier components, 7, 7f8f
in children, 13021303 1056f Fourniers gangrene, 618, 618f
Hashimotos thyroiditis, 869, 880, 883f alcoholic, 121122, 122f lumbar, 804
in children, 1310 in children, 1358t Morgagni, 13481349
Head masses in children, 12941314 viral, 120121, 121t, 122f muscle, 1113, 1114f
Heart in children, 1357, 1358t myofascial, 11541155, 1155f
anatomy, 77 chronic, 122123, 123f para-umbilical, 804
contrast imaging, 8586, 86f in children, 1357 parts of, 801, 802f
disease, hepatic venous waveforms in, gallbladder wall thickening in, 243, 244f postoperative, 805, 805f806f
195197, 197f granulomatous, 132133 Spigelian, 804, 1081, 1081f
thrombus, contrast imaging, 86, 86f see also Hepatitis B; Hepatitis C sportsmans, 804805
Heart block, complete, 197 Hepatitis B types of, 802b
Heating hepatocellular carcinoma risk, 153 umbilical, 804, 1081
due to tissue absorption, 5253 post-liver transplantation, 215216 Herniography, 10761077
experimental investigation of, 5253 Hepatitis C Herpes simplex, 1273, 1274f
implications of, 5354, 54b hepatocellular carcinoma risk, 153 Heterotaxy syndrome, 330, 331f
mechanisms, 52, 52t and non-Hodgkins lymphoma, 160 Heterotopic gestation, 753
transducer, 53 post-liver transplantation, 215216 High pass filtering, 28, 28f
Helicobacter pylori, 360 Hepatoblastomas Hill-Sachs deformity, 1041, 1041f
Hemidiaphragm, 1007f1008f, 1008 in children, 13601361, 1361f Hindfoot injections, 1188, 1188f
Henoch-Schnlein purpura, 379t, 1443, 1444f liver transplantation complications, 221 Hip
in children, 13931394, 1393f1394f Hepatocellular carcinoma (HCC), 153156, anatomy, 1498, 1498f
scrotal involvement, 1494 157f159f, 201f anterior capsular distance, 1503, 1504t
Hepatic alveolar echinococcosis (HAE), 130 arterial neo-angiogenesis, 155156 arthroplasty, 10711072, 1072f
Hepatic arteries, 189192 basket pattern, 155156 aspiration, 10691070, 11811184, 1184b,
anatomy, 94, 94f, 102, 189, 232f in children, 222, 1361 1184f
aneurysms, 192, 192f and cirrhosis, 153156, 155f156f blind aspiration or injection, 10691070
flow changes in portal hypertension, 182 differentiation from adenomas, 145 capsular thickening, 1070t
hereditary haemorrhagic telangiectasia, diffuse, 155 clinical examination, 1498
192, 193f dysplastic nodules and, 154156, 156f developmental dysplasia of the, 1497,
liver transplantation complications, 205, fibrolamellar, 160, 201, 216 1498t
209b incidence, 153 direct needle visualisation, 1070
normal anatomical variants, 228, 232f233f intraoperative ultrasound, 278279, 278f femoroacetabular impingement,
normal findings, 189192 massive, 155 10701071
pre-liver transplantation assessment, nodular, 155 Graf technique see Graf technique, hip
202203, 203f percutaneous ethanol injection, 174t examination
pseudo-aneurysm, post-transplantation, poorly differentiated, 158f Harcke technique, 15011503, 1502f1503f
208209, 209f post-liver transplantation, 216, 222 injection, 10691070, 1071f, 11811182
scanning techniques, 189 pre-liver transplantation ultrasound, interventional techniques, 11811185,
stenosis, post-transplantation, 207208, 200201 1182f1183f
208f, 220 presentation, 155156 irritable, 15031505, 1504f
thrombosis, post-transplantation, 205207, pseudo-capsule, 155 joint effusion, 10691070, 1070f1071f,
206f207f, 219220, 219f radio-frequency ablation, 174175, 1070t
Hepatic ducts, 227 174t175t labral abnormalities, 10701071, 1072f
anatomy, 95, 228f regenerating nodules and, 154156, 155f paediatric, 14971505, 1505b
normal anatomical variants, 227228 screening and surveillance, 153154 Terjesen technique, 1503
Hepatic pedicle, 93 well-differentiated, 155, 156f, 159f transducer choice, 1069
Hepatic veins, 192197 Hepatogastric ligament, 93 transient synovitis, 15031504, 1504f
anatomy, 9496, 94f95f, 102103, Hepatomegaly, 101 ultrasound examination, 14981503
102f103f, 192193, 194f Hepatorenal fossa, 413, 808 ultrasound-guided aspiration,
liver transplant complications, 210211, Hepatorenal syndrome, 453, 484 10691070
220 Hereditary haemorrhagic telangiectasia Histiocytic necrotising lymphadenitis, 934
normal anatomical variations, 193194 (HHT), 192, 193f Histiocytomas
occlusion, post-transplantation, 210211 Hereditary neuropathy with liability to extra-testicular, 611
outflow obstruction, 194195, 196f pressure palsies (HNPP), malignant fibrous, 1123
peliosis hepatis, 197, 197f 11611162 Histocompatibility testing, 529
pre-liver transplantation assessment, 202, Herlyn-Werner-Wunderlich syndrome, 710 HIV see Human immunodeficiency virus
202f Hermaphrodites, 14761477 (HIV)
scanning technique, 192193 Hernias, 10761081, 1080b Hodgkins disease, 263, 263f, 1348f
stenosis, post-transplantation, 210211, abdominal wall, 801805, 1081 in children, 1307
211f Bochdalek, 13481349, 1350f liver metastases, 160
thrombosis, 194195, 196f (see also diaphragmatic, 13481350, 1350f spleen in, 331333
Budd-Chiari syndrome) epigastric, 804, 804f thyroid, 880
transit times, 197 femoral, 803804, 804f, 10791080, 1080f Hoffas ganglia, 1186, 1187f
veno-occlusive disease, 195, 196f incisional, 804, 1081 Holoprosencephaly, 1280, 1282f
waveforms, 194, 194f195f inguinal, 612, 802803, 802f Hormone replacement therapy (HRT),
in cardiac and pulmonary disease, direct, 802803, 804f 705706
195197, 197f indirect, 802, 803f Horseshoe kidneys, 424425, 425f, 14191420,
Hepatitis, 120123, 121f inguinal-scrotal, 1491 1421f
acute, 120122, 121t inguinofemoral, 10761079 Housemaids knee, 1089
Human chorionic gonadotrophin (hCG), 667 Hypoxic ischaemic encephalopathy, 1264 renal, 477478, 478f479f
in in-vitro fertilisation, 736 1269, 1266b, 1267t, 1268f1270f splenic, 340342, 341f, 342t, 838
ovarian hyperstimulation syndrome, 738 Hysterectomy, 697700 testicular, 603, 604f, 614615, 614f
Human immunodeficiency virus (HIV)- fibroids, 693694 Infections
associated nephropathy, 465 subtotal, 697700 abdominal aortic aneurysms, 775
cervical lymph nodes in, 934 Hystero-contrast-sonography (HyCoSy), abdominal wall, 799800, 801f
and liver disease, 131132 653654, 688, 688f, 734735, 735f bladder, 568, 568b
salivary gland disease in, 1308, 1308f Hysterography, saline infusion see Saline breast, 989
Human papilloma virus (HPV), 714 infusion hysterography colitis, 1399
Humero-radial articulation, 1043 Hysterosalpingogram (HSG), 656657, 658f, joint, 11341135, 1135b
Humero-ulnar articulation, 1043 688, 688f muscle, 1156, 1156f
Humerus, supracondylar process, 1160 Hysteroscopy, 688 neonatal brain, 12731274
Hrthle cell neoplasms, 878 postnatal causes, 12731274,
Hyaline bodies, 948, 948f 1275f1276f
HyCoSy see Hystero-contrast-sonography I prenatal causes, 1273, 1274f
(HyCoSy) pancreatic, 299301, 300f
Hydatid disease, 129130, 130f131f, 170 Ileitis, 377, 377f parotid gland, 903
in children, 13631364 Ileocaecitis, infectious, 377, 377f pelvi-ureteric dilatation, 434
hepatic alveolar, 130 Ileocolic veins, 388 post-liver transplantation, 215, 215f
presentation, 487 Iliac arteries, 773 renal cysts, 490491, 490f
renal, 464, 490491 aneurysm, 779, 780f spleen, 338340, 340f
renal involvement, 14531454 in renal transplantation, 532 splenomegaly, 332t
soft tissue involvement, 1117 stenosis, 1201, 1203f, 1206 see also specific infections
spleen, 339340, 341f Iliac fossae, 369370, 370f Inferior epigastric vessels, 1077
Hydranencephaly, 1283, 1283f Iliacus, 647 Inferior mesenteric artery (IMA), 773, 789,
Hydroceles, 611612, 613f Iliac veins, 792, 1228 790f
abdominal wall, 805806 assessment, 12331234 Inferior oblique muscle, 959960
paediatric, 1491, 1491f in renal transplantation, 532 Inferior vena cava (IVC), 792795
Hydrocephalus, 12741279, 1277f1280f spontaneous flow, 12301231 abnormal findings, 792794
Hydrocolpos, 716, 1473, 1476f Ilioinguinal nerve, 1081 anatomy and flow patterns, 792, 792f, 792t
Hydrometrocolpos, 1473, 1476f Iliopsoas bursal injection, 1185, 1186f assessment, 12331234
Hydromyelia, 1325, 1328 Iliopsoas muscle, 10721073, 1073f1074f caval filters, 794, 794f
Hydronephrosis, 421, 422f, 1433 Iliotibial band, 1084, 1085f, 1091 fistulae, 795, 795f
in the newborn, 1433 Images, 1617, 16f liver, 9495, 94f95f
physiological, of pregnancy, 421, 422f B-mode imaging, 1718 liver transplantation, 220, 794, 794f
postnatal evaluation of antenatally formats, 1820, 19f membranous obstruction, 195
detected, 14331434 frame averaging, 26, 26f objectives of the scan, 792
renal, 493, 494f memory, 25 portacaval anastomosis, 795f
in renal transplantation, 542 processing, 2326 renal cell cancer propagation into, 480,
Hydrops, gallbladder, 251, 253f colour Doppler imaging, 30b 480f
Hydrosalpinx demodulation, 25, 25f scanning technique, 792, 793f
as a cause of subfertility, 733, 733f dynamic range, 2324, 24f thrombosis, 792, 793f
pelvic inflammatory disease, 682, field of view, 2526 tumour obstruction, 793794, 793f
682f harmonic imaging, 2425, 24f Infertility
Hymen, imperforate, 1473, 1476f image memory, 25 male
Hyoglossus muscle, 891895 post, 26, 26f evaluation of, 584
Hyoid bone, 893, 913 pulse coding, 25, 25f obstructive, 580t
Hyperbilirubinaemia time gain compensation, 23 see also Fertility; Subfertility
conjugated, 1368 zoom, 2526 Inflammatory arthritis, 1130
unconjugated, 1367 quality of, 31 Inflammatory masses
Hypercalciuria, idiopathic, 1445 Image speckle, 67, 7f in children, 13031307
Hypereosinophilic syndrome, 134 Imagify, 79t, 81 liver, 13641365
Hyperoxaluria, 1445 Imavist, 79t, 80 Inflammatory pseudo-tumour (IPT), liver,
Hyperparathyroidism, 884, 887 Immunosuppression, renal transplantation, 131, 150
in children, 1445 529530 Inflammatory soft tissue masses, 11161117
Hyperplastic cholecystoses, 247, 248f Imperforate anus, 1399, 1399f Infrapatellar bursa, 1089
Hyperreactio luteinalis, 667668 Impingement syndrome, shoulder, 10321033, Infrapatellar fat pad impingement, 1186
Hypertension 1033f, 1036b Infraspinatus, 1030, 1031f
in children, 14551457 Inborn errors of metabolism, 1284, 13571358 fatty infiltration, 1035, 1035f
kidney disease, 449 Incidentalomas, thyroid, 881882 Infundibular stricture, 434
renal artery stenosis, 448 Incisional hernias, 804, 1081 Inguinal canal evaluation, 1077
renovascular see Renal arteries, stenosis; Indifferent gonads, 1468 examination technique, 1077
Renovascular hypertension Inertial (transient) cavitation, 78, 87 normal anatomy, 1077
Hypertrophic pyloric stenosis (HPS), Infarcts normal ultrasound appearances, 1077,
13851386, 1385f neonatal brain, 12691272, 1270f, 1272f 1078f1079f
Hypoalbuminaemia, 242243, 243f omental, 14011402, 1402f Inguinal hernia, 612, 802803, 802f
Hypoglycaemia, 12831284, 1284f prostate, 589t direct, 802803, 804f
Hypotension, 843 pulmonary, 1018 indirect, 802, 803f
Inguinofemoral hernias, 10761079 laparoscopic see Laparoscopic ultrasound cysts, 1134, 1134f
bulging, 1079, 1080f techniques, 273275, 275f effusion see Joint effusion
differing imaging modalities, 10761077 Intraperitoneal fluid, ectopic pregnancy, 756, infection, 11341135, 1135b
inguinal canal evaluation, 1077 757f interventional techniques, 1135
examination technique, 1077 Intrarenal vessels, 470471, 477 masses, 11331134
normal anatomy, 1077 Intrauterine devices (IUDs), 706708, rheumatological ultrasound, 1126
normal ultrasound appearances, 1077, 707f709f ultrasound-guided techniques, 1135
1078f1079f Intravenous urography (IVU), transitional cell Jugular varix, 1301, 1302f
overview, 10761077 carcinoma, 518 Jugular veins, 908
postoperative evaluation, 1079, 1080f Intraventricular haemorrhage, neonatal, thrombosis, 908909, 910f911f, 1304
pre-hernia complex, 1079 12601263, 1262f1265f, 1262t in thyroid carcinoma, 873
ultrasound appearance of, 10771078, Intussusception Jugulodigastric node, 908, 925, 925f
1078f1079f in children, 13901391, 1392f Jumpers knee, 10841086, 1086f
In-plane resolution, 15 colonic, 402, 405f Juvenile nephronophthisis, 1438
Inspissated bile syndrome, 1370, 1372f small bowel, 384, 1391 Juvenile recurrent parotitis, 905, 905f
Insulinomas, 279, 313314, 316f In-vitro fertilisation (IVF), 667 Juxtarenal process, 1448, 1451f
Intensity, 5, 5f scanning through a cycle, 735738, 738b Juxtaventricular cysts, 12571258
Intensity spatial average, 15 downregulation, 735736
Intensity spatial peak, 15 embryo transfer, 737, 737f
Intensity spatial peak pulse average, 15 follicular development, 736, 736f K
Intensity spatial peak temporal average, 15 oocyte capture, 736737, 736f
Intercostal artery, 1012, 1012f ovarian hyperstimulation syndrome, Kagers fat pad, 10931094
bleeding, 1013, 1013f 738, 738f, 738t Kaposis sarcoma, 1121
Interference, 56, 6f, 8b IPMN (intraductal papillary mucinous Kasabach-Merritt syndrome, 140, 334, 1301
Intermenstrual bleeding, 688 neoplasm), 312, 313f Kasai procedure, 216, 1369
Intermittent claudication, 1198 Iris, 940 Kidneys, 413427
Internal oblique muscle, 1076 Ischaemia abscesses, 462, 462f, 496497, 496f497f,
Interosseous ligaments, 1101 acute, peripheral arterial disease, 1211 1452f
Interstitial ectopic gestation, 757, 757f758f, liver, 206207, 207f access sites, 415, 415f
757t lower limb, 1198, 1211 acute tubular necrosis, 484
Interstitial laser photocoagulation (ILP), small bowel, 379, 379t adenomas, 508, 508f
859 symptoms, 965966 metanephric, 508
Interstitial nephritis, acute, 451, 452f Ischaemic colitis, 399t, 401, 402f papillary, 508
Interventional techniques Ischaemic stroke, 982983 anatomical relations, 413, 414f
abdomen, 847864 Islet cell tumours anatomy, 413414, 414f
joints, 1135 endoscopic ultrasound, 279 aneurysms, 495496, 496f
musculoskeletal procedures, 11681193 intraoperative ultrasound, 279 angiomyolipoma, 509512, 509f511f
elbow, 11731175 arteriolar resistance, 469
foot and ankle, 11871190 arteriovenous fistula, 481, 481b, 481f
foreign body localisation, 11901191 J arteriovenous malformations, 481482,
hip, 11811185 482f483f, 495496, 507
knee, 11851187 Jaundice, 253254 atrophy, 425, 426f
masses, 11911193 causes of, 253 autonephrectomy, 463464, 465f
pelvis, 11801181 diagnosis, 253254 bifid renal pelvis, 1420, 1422f
risks of, 1169b gallbladder distension in, 256258 biopsy, 455458
shoulder, 11701173 medical, 253 complications, 456457, 457f
wrist and hand, 11751180 neonatal, 13671372, 1371b contraindications, 455456
see also specific techniques prolonged, 1368 indications, 455456
Intestines surgical causes of, 13681372 renal transplant, 457458
large see Colon obstructive, 253255, 254f technique, 456, 456f
small see Small bowel in older children, 13721375, 1374b blood flow
Intracranial pressure, transcranial Doppler surgical, 253254 changes in pelvi-ureteric dilatation,
ultrasound, 980 Jejuno-ileal atresia, 13881389 440441
Intraductal papillary mucinous neoplasm Jersey finger, 1058 damped waveform, 476
(IPMN), 312, 313f Joint effusion disturbance (turbulence), 476
Intradural lipoma, 1324 ankle, 1104, 1106 increased velocity, 475476, 476t, 478f
Intrahepatic biliary cystadenoma, 149150 elbow, 1047, 1047f calcification, 451, 451b, 451f, 463464, 465f
Intraocular lens implant, 943, 943f glenohumeral joint, 1040, 1040f candidiasis, 1453, 1455f
Intraoperative ultrasound (IOUS), 273281 hip, 10691070, 1070f1071f, 1070t, 1503, in children, 1409, 1411b
clinical applications, 275280 1504f abnormalities, 14181420, 1418f
biliary tree, 279280, 280f knee, 1088, 1088f1089f, 1089b cystic disease, 1435b, 1435t
liver, 275279, 275f279f monitoring, 1132 duplex anomalies, 14201422, 1423f
pancreas, 279, 279f, 291293, 293f ultrasound features of, 1129, 1129b, end-stage failure, 14441445
urology, 280, 280f 1129f fetal lobulation, 1412
contrast-enhanced see Contrast-enhanced Joint(s), 1029, 1029f infectious diseases of, 14531454
intraoperative ultrasound aspiration malignancy, 14581462
(CE-IOUS) elbow, 1053 normal appearances, 14091412, 1416f,
equipment, 273275, 274f hip, 10691070, 1071f 1416t
normal sonographic values, 14121418 glomerulonephritis, 449 mixed epithelial and stromal tumour, 492,
transplantation, 14441445 hepatorenal syndrome, 453 497498
trauma, 1458f medical, in children, 14421444 multilocular cystic nephroma, 497498,
collecting duct carcinoma, 517 medullary changes, 446447 497f
collecting system, 413, 421422, 422f medullary sponge kidney, 450, 450f nephropathy, HIV-associated, 465
duplex, 423, 423f nephrocalcinosis, 451, 451f nephroptosis, 418, 419f, 1419
column of Bertin, 505, 506f renal papillary necrosis, 449450, 450f normal ultrasound appearances, 418422,
congenital solitary, 425426 renal size, 445 14091412, 1410f1411f, 1416f
congenital variants, 423426, 426b sickle cell disease, 453 number abnormalities, 1418
contrast imaging, 8485, 85f, 467, 470f ultrasound features, 445447 obstruction, 300
cortex vascular disorders, 447449, 449f oncocytoma, 508509, 509b
calcification, 446 diverticula, 493, 494f pancake, 424, 425f
changes in disea25, 446447 Doppler imaging see Doppler imaging, papillary necrosis, 493, 493f
necrosis, 1444 kidneys parasitic infections, 464465, 465b
normal ultrasound appearance, dromedary hump, 505, 506f parenchyma
418419, 419f420f duplex, 435436, 437f438f disease
thickness, 415417, 416f anomalies, 14201422 Doppler studies, 484b
crossed fused ectopia, 1420, 1421f collecting system, 423, 423f vascular aspects, 483484
cystic dysplasia, 14371438, 1439f dysplasia, 14371438, 1439f infection, 460
cysts, 453454, 454f, 486504, 502b ectopic, 418, 418f, 423424, 424f425f, 1419, normal ultrasound appearance,
acquired, 498, 498b, 499f 1419f 418421, 419f
calcified, 491492, 491f examination techniques, 415418, 415b thickness, 415417, 416f
in children, 14341440 extramedullary haematopoiesis, 507 partial duplication, 1420
classification, 488t, 489f extrarenal pelvis, 1412, 1417f pelvic, 1419f
complicated, 488492 failure perirenal structures, 417
contrast imaging, 85f acute, 446f persistent fetal lobulation, 505
differential diagnosis, 493498, in children, 14421443 position abnormalities, 14191420
493f497f, 498b in children, 14421443 positioning for examination, 415
haemorrhagic, 489f490f, 490 chronic post-obstructive cystic dysplasia, 499, 499f
hereditary, 1439 in children, 14421443 pre-renal failure, 484
infected, 462, 490491, 490f Doppler imaging, 484 pseudo-tumours, 505507, 506b
localised, 498 end-stage, 14441445 pyelonephritis
lymphatic, 493495, 495f fetal lobulation, 414, 420, 420b, 1416f acute bacterial, 460, 461f
malignant, 492, 492f, 493b fungal infections, 464, 465b chronic, 462, 464f
medullary, 502 glomerulonephritis, acute, 484 xanthogranulomatous, 463, 465f
milk of calcium, 492 granulomatous pseud-tumours, 507 pyonephrosis, 462, 463f
multicystic dysplastic kidney, 498499, haemangioma, 512 pyramids, 493, 493f
499f, 502b haematoma, 495, 496f renal cell carcinoma see Renal cell
multiple simple, 488, 488f hepatorenal syndrome, 484 carcinoma
polycystic kidney disease see Polycystic hereditary tumours/syndromes, 522 renal sinus, 413, 420b, 421422, 421f
kidney disease hilum, 413 reninoma, 512
septations, 488 horseshoe, 424425, 425f, 14191420, 1421f rotational abnormalities, 1419
simple, 486488, 487f488f, 488b hydatid disease, 464 sarcoma, 521
simple cyst, 1439 hydronephrosis, 493, 494f scarring, 462, 464f, 505, 506f, 1452f
syndromal, 1439 hypertension see Renovascular schistosomiasis, 464465
tuberous sclerosis, 502, 502b, 502f503f hypertension septa of Bertin, 420421, 420b, 421f
Von Hippel-Lindau disease, 500502, and hypertensive disease, 449 size, 415, 416f, 416t, 445, 475, 475t
501f, 502b hypoplasia, 425, 426f small, 475, 475t
development, 1407, 1407f1408f infarction, 477478, 478f479f small vessels, 467, 484
diffusely echogenic, 14401442, 1440t, infectious diseases of, 460466 splenic humps, 420, 420b, 420f
1442t, 1443f intraoperative ultrasound, 280, 280f splenorenal fusion, 505507
dilated pelvicalyceal system, 493, 494f, 518 intrarenal vessels, 470471, 477 stones, 430, 430b, 430f431f
discoid, 1419f junctional parenchymal defect, 414, 414f supernumerary, 1418
disease, 445459 (see also specific diseases) leiomyoma, 512 thoracic, 1419, 1420f
acquired cystic, 453454, 454f leiomyosarcoma, 521, 523f transitional cell carcinoma, 517521
acute cortical necrosis, 452, 452f leukaemia, 521 transplantation see Renal transplantation
acute interstitial nephritis, 451, 452f liver transplantation complications, 214 trauma, 838841, 845, 845f
acute tubular necrosis, 449 lobar nephronia, 460462, 461f in children, 14571458, 1457f1458f
amyloid, 452, 452f lymphatic cysts, 493495, 495f classification, 839840, 839t
autosomal dominant polycystic, 9798, lymphoma, 521, 521b, 522f general considerations, 838841
98f main renal trunks, 471472, 471f473f mechanisms of injury, 839840
connective tissue disorders, 453, 453f malacoplakia, 463 ultrasound findings, 840841, 840f841f
cortical changes, 446 medulla, 418419, 420f tuberculosis, 463464, 465b, 465f,
corticomedullary differentiation, carcinoma, 517 14531454
446447 changes in disease, 446447 tuberous sclerosis, 1441f
diabetes mellitus, 452453 fibromas, 512 tubulo-interstitial disease, 484
dialysis patients, 454455, 455f necrosis, 1444 tumours, 478
end-stage, 454f metastases, 521 ultrasound technique, 1409
unilateral agenesis, 1418, 1419f Lateral humeral condyle fracture, 1051 spinal, 13221324, 1323f
vascular anatomy, 468469, 468f Lateral ligamentous complex, ankle, 1099 subcutaneous, 1117
vascular disorders of, 467485 Lateral meniscus, 1091 submandibular region, 898, 899f
in children, 14541455 Lateral rectus muscle, 959960 uterine, 695
vascular response to disease, 483484 Latero-conal ligaments, 816 variants, 1119
vasculitis, 484, 1443 Left ventricle, apical thrombus, 86, 86f Lipomyelomeningocele, 1323
vessels, 417418, 417f, 421422, 421f, 423f Left ventricular opacification (LVO), 79, 8586 Lipomyeloschisis, 1323, 1323f
viral infections, 465b Leg see Lower limb Liposarcomas, 1119
Kikuchi disease, 934 Legg-Calv-Perthes disease, 1504, 1505f abdominal wall, 806
Kimura disease, 934 Leiomyomas, 1121 retroperitoneal, 819820, 821f
Klatskin tumours, 156157, 261f epididymis, 610 spermatic cord, 611
Klebsiella pneumoniae renal, 512 Lippes loop, 707, 708f
liver abscess, 124 Leiomyosarcomas Lissencephaly, 12811282
renal abscess, 496 bladder, 562 Lister tubercle, 1055, 1056f
Klippel-Trnaunay syndrome, 334, 336f extra-testicular, 611 Liver
Knee, 10841092 malignant, 1121 abscess, 124127, 145146, 146f147f
anatomy, 1084, 1085f1086f renal, 521, 523f amoebic, 126127, 127f128f, 13641365
anterior, 10841089 retroperitoneal, 819 bacterial, 123f126f, 124126, 145146
Bakers cyst, 1089, 1090b, 1090f uterine, 693, 693f brucellar, 126
biceps femoris, 1091, 1091f Lemierres syndrome, 1304 in children, 13641365, 1364f
cruciate ligaments, 1090 Lens, 943 acute failure, 199200, 217
iliotibial band, 1091 cataract, 943, 943f acute fascioliasis, 131
interventional techniques, 11851187 ectopia lentis, 943, 944f adenoma, 143145, 145f, 1363
joint aspiration, 11851186, 1186f1187f intraocular implant, 943, 943f alcoholic disease, 216
joint effusion, 1088, 1088f1089f, 1089b trauma, 956, 956f amyloid, 117
lateral, 1091 Lenses, 1011, 11f anatomical variants, 13561357
lateral collateral ligament, 1091 Lenticulostriate vasculopathy, 1272, 1273f anatomy, 93, 1356
lateral meniscus, 1091 Lesser omentum, 93, 808 segmental, 9596, 96b, 179, 180f
medial, 10901091 Leukaemia variations, 9698, 96f98f
medial collateral ligament, 1090 in children, 1307, 1461 angiomyolipoma, 149
medial meniscus, 10901091, 1090f1091f prostate gland, 589t attenuation, diffuse parenchymal liver
Osgood-Schlatter disease, 1088 renal involvement, 521, 1461 disease, 104, 105f
other bursae, 1089, 1089f testicular involvement, 602, 602f, 1494 biliary architecture, 9495
patellar tendinosis, 10841087, Leukocoria, 949, 955 biliary cystadenocarcinoma, 161
1086f1087f Leukodystrophy, metachromatic, 13751376 biliary epithelial dysplasia of the
pes anserinus bursa, 1091 Levator ani muscles, 576, 647 intrahepatic bile ducts, 150
popliteus tendon, 1091 Levator fascia, 573 biopsy, 167170
posterior, 10891090 Levator palpebrae, 960 complications, 170, 170b
proximal tibiofibular joint, 1091 Levonorgestrel, 689 image-guided approach, 167168, 168f
quadriceps and patellar tendons tears, Levovist, 81, 140 indications, 169, 169b, 169f
10871088, 1087f1088f, 1088b Leydig cell tumour, testicular, 601, 601f, 1494 patient management, 170, 170b
synovial biopsy, 11851186 Lidocaine, 11691170 percussion-palpation approach, 167
ultrasound examination, 1084 Ligaments, 1028, 1028f quality of specimen, 168169
Krukenberg tumour, 678, 680f Ligamentum teres, 93, 98 technique, 167169, 168t
Kupffer cells, deficiency/dysfunction, 139 Ligamentum venosum, 93 type of needle, 168
Kuttner tumour, 897, 897f Lighthouse phenomenon, 10061007 blind area, 99, 99f
Limy bile, 240 blunt trauma, 148
Lipid-stabilised contrast microbubbles, 7980 calcification, 134, 134t, 135f
L Lipohaemarthrosis, knee joint, 1088, 1089f cat scratch fever, 133134
Lipoleiomyoma, uterine, 695 caudate lobe, 96, 97f
Labral cyst, 1037, 1038f Lipomas, 1117, 1119f measurement, 101, 101f
Lambda sign, 747748 abdominal wall, 805, 806f in children, 13561375, 1357f
Laparoscopic ultrasound breast, 991, 991f abscesses, 13641365
biliary tree, 236, 273, 279 chest wall, 10051006 anatomical variants, 13561357
equipment, 274, 274f in children, 1352 anatomy, 1356
islet cell tumours, 279 colonic, 402, 404f diffuse parenchymal disease, 13571360
liver, 273 filum terminale, 1324 focal lesions, 13601364
pancreas, 291293, 293f gastric, 362, 363f inflammatory masses, 13641365
radio-frequency ablation, 278279, 278f hand, 1066 jaundice in older children, 13721375
technique, 275 inter-/intramuscular, 1117 neonatal jaundice, 13671372
urology, 280 intradural, 1324 portal hypertension, 13651367
Large-bore vacuum-assisted biopsy, 1001 liver, 149 technique, 1356
1002, 1001t oesophageal, 358, 359f vascular disorders, 13651367
Large bowel see Colon paediatric, 15111512, 1511f1512f cholangiocarcinoma, 156160
Laryngocele, 917 retroperitoneal, 819820 chronic disease, 200201, 216217
Larynx, 913, 914b size and shape, 1110, 1111f chronic granulomatous disease, 133
tumours, 917 small bowel, 381 cirrhosis see Cirrhosis
Lateral epicondylitis, 1049, 1050f spermatic cord, 609, 610f classic lobule, 95
morphological types, 1139, 1140f masses in children, 12941314 holoprosencephaly, 1280, 1282f
multipennate, 10251026 parotid and buccal region, 898907 tuberous sclerosis, 1282, 1283f
normal sonographic appearance, 1139, normal ultrasound anatomy, 898900, germinal matrix, 12601263, 1262f1265f,
1139f 899f900f 1262t
oblique orientation, 1139 pathology, 900907 hydrocephalus, 12741279, 1277f1280f
parallel, 1139 technique, 898900 hypoxic ischaemic encephalopathy,
pennate, 1139 posterior triangle, 912913 12641269, 1266b, 1267t,
triangular, 1139 normal ultrasound anatomy, 912913, 1268f1270f
tumours, 1121 912f infection, 12731274
unipennate, 10251026 pathology, 913 postnatal causes, 12731274,
upper limb, 11391141, 1140t, 1141f1142f technique, 912913 1275f1276f
Muscularis propria, 352 pulsatile masses, 966, 974, 974b, 975f prenatal causes, 1273, 1274f
Musculo-cutaneous flaps, 800 submandibular region, 894898 intraventricular haemorrhage, 12601263,
Musculoskeletal ultrasound, 10251029 normal ultrasound anatomy, 894895, 1262f1265f, 1262t
paediatric, 14971513 895f896f lenticulostriate vasculopathy, 1272, 1273f
see also Bone(s); Muscle(s) pathology, 895898 metabolic disorders, 12831284
Mycetoma, 464 technique, 894895 hypoglycaemia, 12831284, 1284f
Mycobacterial lymphadenitis, 13051306 submental region, 890894 inborn errors of metabolism, 1284
Mycobacterium avium complex, 131132 normal ultrasound anatomy, 890893, periventricular leukomalacia, 12631264,
Mycobacterium tuberculosis infection 891f893f 1266f1267f
in HIV/AIDS, 131132 pathology, 893894 space-occupying lesions, 1284
splenic involvement, 339, 340f technique, 890893, 891f cysts, 1284
Mycophenolate, 529530 supraclavicular fossa, 911912 neoplasms, 1284, 1285f1287f
Mycotic aneurysms, 775, 779 normal ultrasound anatomy, 911912, vascular malformations, 1284, 1288f
Myeloceles, 1322 912f technique, 12531254, 1254f
Myelolipomas, adrenal, 636637, 637f pathology, 912 trauma, 12851287
Myelomeningoceles, 1322 technique, 911912 accidental injury, 1285
Mylohyoid muscle, 890891, 892f, 894895 Necrosis birth-related injury, 1285, 1289f
boutonnire, 897, 898f cervical lymph nodes, 930931, 931f non-accidental injury, 12851287,
Myocardial perfusion, 79, 86 coagulative, 930, 931f 1289f1290f
Myofascial hernia, 11541155, 1155f cortical, 1444 variation with gestational age, 1258, 1258f
Myofibrils, 1138 cystic, 930 vascular anatomy, 12581260, 1259f1261f,
Myomectomy, fibroids, 693694 lung, 1340, 1342f 1259t
Myometrium, 689700 medullary, 1444 venous thrombosis and infarction, 1255,
adenomyosis see Adenomyosis Necrotising enterocolitis, 1400, 1401f 12701272, 1272f
arteriovenous malformation, 695696, Necrotising fasciitis, 618 ventricular system, 1255, 1255t
696f Needle guides, 852, 852f Neonatal hepatitis syndrome (NHS), 1368
cysts, 694695 Needle placement technique, 1170 Neonates
fibroids see Fibroids Needles adrenal glands, 633
gestational trophoblastic disease, 696697, core biopsy, 849850, 849f, 849t brain see Neonatal brain
696f697f fully automated sheathed, 850 British Medical Ultrasound Society
lipoma, 695 manual sheathed, 849 (BMUS) scanning guidelines, 58
lymphoma, 695 Menghini technique, 849 hydronephrosis, 1433
malignant mixed Mllerian tumours, 695 semi-automated sheathed, 849, 850f ovarian cysts, 1483, 1483f
metastases, 695 fine-needle aspiration, 848849, 848b, 849f, pelvic masses, 1483, 1484f
sarcoma, 695 849t Neopharynx, postoperative, 917, 918f
Myosin, 1138 liver biopsy, 168 Nephrectomy, 517, 522523
Myositis, 960 visualisation, 1170, 1170b Nephroblastomatosis, 1461, 1461f
infective, 1156, 1156f Needle track seeding, 853 Nephrocalcinosis, 446447, 447f, 451, 451f
Myositis ossificans, 1115, 1115f, 1154, 1154f Neisseria gonorrhoeae in children, 1446, 1446t, 1449f
paediatric, 1508 endometritis, 709 Nephrogenic systemic fibrosis (NSF),
Myxoma, 1121 epididymo-orchitis/epididymitis, 614 552553
pelvic inflammatory disease, 682 Nephromas
N Neonatal brain, 12531293 congenital mesoblastic, 1461
anatomy, 12551260, 1255f1257f, 1255t multilocular cystic, 497498, 497f
Nabothian cysts, 713, 713f arterial infarction, 12691270, 1270f1272f Nephropathy, HIV-associated, 465
Naevus, choroid, 954 brain death evaluation, 1290, 1290f Nephroptosis, 418, 419f, 1419
Nasopharyngeal infection in children, 1304 cerebrovascular complications, 12601272 Nephrotic syndrome, 446f
Neck, 890919 premature infants, 12601264 Nephroureterectomy, 520521
anterior (infrahyoid), 913917 term infants, 12641272 Nerve entrapment, 1163f1164f
normal ultrasound anatomy, 913914 congenital malformations, 12791283 abdominal wall, 807
pathology, 914917 Dandy-Walker complex, 12791280, definition, 11611162
technique, 913914 1281f frequently affected nerves, 1166b
jugulodigastric region and deep cervical destructive lesions, 1283, 1283f radiography and computed tomography
chain, 908911 disorders of sulcation and migration, in, 1158
normal ultrasound anatomy, 908 12801282, 1282f ultrasound nerve changes in, 1163b
pathology, 908911 dysgenesis of the corpus callosum, Nerve fascicles, 1158
technique, 908 1279, 1281f Nerve fibres, 1158
Nerves, 1028, 1029f European Federation of Societies of indications for ultrasound, 959b
Nerve sheath, 1158 Ultrasound in Medicine and inflammatory disease (pseudo-tumour),
tumours, 901902, 911, 1120 Biology (EFSUMB) guidelines, 58 960, 961f
Nerve tumours, 11191120 see also Pregnancy lymphoproliferative disorders, 962, 962f
Neurenteric cysts, 1348 Obstructive uropathy, 429, 429b, 441443 metastases, 962
Neurilemmoma see Schwannomas Obturator internus, 647 muscles, 959960
Neuroblastomas Occipital lymph nodes, 927 optic nerve tumours, 962963, 963f
adrenal, 637640, 640f, 1459t, 14641466, Ocular muscles, 959 rhabdomyosarcoma, 962
1465f, 1465t Oedema thyroid ophthalmology, 960, 960f
in children, 1312, 1362f abdominal wall, 799 tumours, 961962
mediastinal, 1347b, 1348, 1349f orbital, 960, 961f ultrasound features, 959960
neonatal, 1333 scrotal wall, 618, 618f varices, 960
Neuroendocrine tumours (NETs) Oesophagus, 914, 916f vascular disease, 941942
imaging, 314 achalasia, 359360 Orchitis, 604, 605f, 615
pancreatic, 313315, 314b, 315f317f anatomical structure, 352, 353f complicated, 615f
ultrasound, 314315 Barretts, 356, 358f see also Epididymo-orchitis
Neurofibromas, 1066, 1120, 1120f, 11641165, benign posterior mediastinal masses, Organ donors
1165f 358359, 359f assessment of living related, 203
cervical, 911 cancer supply, 529
focal, 1120 endoscopic ultrasound, 354356 Oriental cholangiohepatitis, 265266
neonatal, 1333 lymph nodes, 354, 356f357f, 356t Orthotopic liver transplantation (OLT), 204,
optic nerve, 962963 management, 354 204f
parotid gland, 901902 staging, 353354, 357f Ortolani test, 14971498, 1498f
plexiform, 1120, 1312, 1313f in children, 1384b Osgood-Schlatter disease, 1088, 1506
Neurolemmoma, 1119 cysts, 358359, 359f Osseous choristoma, 954, 954f
Neuroma, tibial nerve, 1105 dysmotility disorders, 359360 Osseous lesions in children, 13531354
Neurovascular bundles, prostate, 572 endoscopic ultrasound, 352360 Osseous tumours, extraskeletal, 1124
Neutropenic colitis, 1399, 1400f lipoma, 358, 359f Ossification, 1115
Neutropenic enterocolitis see Typhlitis submucosal (subepithelial) lesions, 358, Osteoarthritis
Nodular fasciitis, 1122, 1303 358f359f acromioclavicular joint, 10391040
Nodular regenerative hyperplasia (NRH), varices, 183, 359, 359f360f ankle, 11041105
116, 117f Oestrogen degenerative, 10591060
Noise, 61, 61b deficiency, 700, 705 glenohumeral joint, 10401041
gain-related, 62f and uterine fibroids, 689 ultrasound features of, 1130
random, 61 Oil cysts, breast, 988 Osteochondritis dissecans, 1047, 1048f
structured, 61, 62f Olecranon bursitis, 1050, 1051f, 1134, 1134f Osteochondroma, 13531354, 1354f
Non-accidental head injury, 12851287, Olecranon fossa, 1045, 1045f Osteochondromatosis, synovial, 1123, 1123f
1289f1290f Omentum Osteoma, choroidal, 954, 954f
Non-accidental injury, 1506 biopsy, 720722, 721b, 721f Osteomyelitis, 1352, 1353f
Non-alcoholic fatty liver disease (NAFLD), complications, 722 paediatric, 15081509, 1509f
105, 110111, 111f method, 720721 Osteophytes, ankle, 1105
Non-alcoholic steatohepatitis (NASH), rationale, 720 Out-of-plane resolution, 15
110111, 111f cysts, 1483 Output, 5, 34
Non-Hodgkins lymphoma infarction, 14011402, 1402f Output Display Standards (ODS), 51
adrenal involvement, 640641 Omohyoid muscle, 908, 925, 926f Ovarian artery, 648649, 655
in children, 1307, 1347 Oncocytic thyroid neoplasms, 878 Ovarian hyperstimulation syndrome,
gastric, 360 Oncocytomas, 509b 667668, 667f
and hepatitis C, 160 parotid gland, 901 Ovarian hyperstimulation syndrome (OHSS),
liver metastases, 160 renal, 508509 738, 738f, 738t
spleen in, 331333, 333f334f On-table cholangiography (OTC), 279 in in-vitro fertilisation, 736
thyroid, 880 Oocytes capture in in-vitro fertilisation, Ovarian remnant syndrome, 666, 666f
Non-involuting congenital haemangioma 736737, 736f Ovarian veins, 648
(NICH), 1301 Ophthalmic artery, 942, 977978 Ovaries, 660685
Norman-Roberts syndrome, 12811282 Opisthorchis felineus, 251 abscess, 682, 683f
North American Symptomatic Carotid Opisthorchis viverrini, 251 adnexal masses, 668670, 669f
Endarterectomy Trial (NASCET), Optic axis, 938 age-related differences in, 655t
965 Optic nerve, 959 anatomy, 647648
tumours, 962963, 963f benign versus malignant lesions, 670, 670b
Optison, 79t, 80, 87 blood supply, 648
O Oral contraceptive pill Brenner (transitional cell) tumours, 674, 674f
abnormal vaginal bleeding, 689 cancer, 670680
Oarsmans forearm, 1059 adenomas and, 143 classification, 671, 671t
Obesity, 689 and the endometrium, 705 epithelial neoplasms, 671674, 673b
Oblique orientation muscle fibres, 1139 Orbit, 959963 germ cell tumours, 674676
Obstetric examination anatomy, 959960, 959f960f metastatic tumours, 678679, 680f
British Medical Ultrasound Society arteriovenous fistula, 960961 omental biopsy, 720
(BMUS) guidelines, contents, 959 risk factors, 670
5758 haemangioma, 961, 961f screening, 678679
sex cord stromal tumours, 677678 teratomas, 14871488 haemangiomas, 12991301, 1299f1300f
symptoms, 671 immature, 676 haematoma, 1507, 1507f
treatment, 669, 669f mature (dermoid), 674676, 674f677f, head and neck masses, 12941314
tumour markers, 676b 676b Henoch-Schnlein purpura, 13931394,
in children, 14681490 thecomas, 678, 679f 1393f1394f
clear cell tumours, 674, 674f torsion, 668, 668f669f, 14881489, 1490f hepatocellular carcinoma, 222
cyclical variations, 655b, 661663, 663f transvaginal scanning technique, 654, 654f hip, 14971505, 1505b
cysts, 663668 ultrasound anatomy, 654, 654f aspiration, 11831184, 1184b, 1184f
adolescent, 1484, 1485f ultrasound technique, 1471 hypertension, 14551457
as a cause of subfertility, 733734, 734b, volume, 660, 661t, 1471, 1472t inflammatory masses, 13031307
734f yolk sac tumours, 676 intussusception, 13901391, 1392f
corpus luteal, 663 Overuse injuries, paediatric, 1506 kidneys, 1409, 1411b
follicular, 663, 663f Overuse tendinopathies abnormalities, 14181420, 1418f
haemorrhagic, 663664, 664f665f, 681, pelvic area, 1072 cystic disease, 14341440, 1435b, 1435t
1485, 1486f wrist, 10591063, 1060f duplex anomalies, 14201422, 1423f
neonatal, 1483, 1483f1485f end-stage failure, 14441445
ovarian hyperstimulation syndrome, malignancy, 14581462
667668, 667f P normal appearances, 14091412, 1416f,
ovarian remnant syndrome, 666, 666f 1416t
paraovarian, 664, 665f Paediatric patients normal sonographic values, 14121418
peritoneal inclusion, 664666, 666f acute appendicitis, 389 renovascular disease, 14541455
polycystic ovaries, 14821483, 1482f adrenal glands, 14641466, 1464f transplantation, 14441445, 1445f
polycystic ovary syndrome (PCOS), appendix, 13951398, 1397f trauma, 14571458, 1457f1458f
666667, 667f, 1482, 1482f abscess, 1397, 1397f leg lengthening, 1509
postmenopausal, 666, 666f appendicitis, 1395, 1396f1397f, leukaemia, 1307, 1461
prepubertal, 14831484 13971398, 1399b lipomas, 1352, 15111512, 1511f1512f
theca lutein, 667 retrocaecal, 1398, 1398f liver, 13561375, 1357f
dysgerminomas, 676 atypical renal infection, 14531454 abscesses, 13641365
echotexture, 14711472 Bakers cyst, 1510, 1510f anatomical variants, 13561357
ectopic gestation, 758 bile ducts, 13561375 anatomy, 1356
embryology, 14681470 bladder, 1409, 1413f1414f, 14221428 diffuse parenchymal disease, 13571360
endometrioid tumours, 673, 673f bony elbow injury, 1051, 1051b focal lesions, 13601364
endometriosis, 680681, 681b, 681f branchial cysts, 12961297, 1297f1298f inflammatory masses, 13641365
epithelial cell tumours, 1487 cancer, 56 jaundice in older children, 13721375
fibromas, 678, 679f cartilaginous lesions, 13531354 neonatal jaundice, 13671372
follicles, 661 cellulitis, 1352, 1352f portal hypertension, 13651367
development, 1473 cervical lymphadenopathy, 13031304, technique, 1356
normal appearance, 14711472 1304f transplantation, 216222, 220b,
germ cell tumours, 1485, 1486f1487f, cervical lymphatic malformations, 13761377, 1376f1377f, 1377b
14871488 12951296, 1296f clinical indications, 216217
granulosa cell tumours, 677, 678f chest, 13371355 complications, 219221, 219f
growth, 1473 chest wall, 13501354 recurrent disease, 221222
haemodynamics by Doppler imaging, 655 colon, 13991401, 1399b surgical techniques, 217, 218f
inguinal, 1476, 1479f colitis, 1399 ultrasound patient evaluation,
ligaments, 660, 661f imperforate or ectopic anus, 1399 217219
lymphoma, 680 necrotising enterocolitis, 1400, 1401f vascular disorders, 13651367
masses in first trimester, 762763, neoplasms, 14001401 lungs and pleura, 13381347, 1339f
762f763f normal anatomy, 1399 lymphangiomas, 1352f
mucinous tumours, 672, 672f673f congenital cystic lesions, 12941299, 1299b lymphatic malformations, 13511352, 1352f
mural nodules, 664 congenital foregut malformations, 1299 lymphoma, 13941395, 1461, 1462f
neoplasms, paediatric, 14851488, 1486f Crohns disease, 13921393, 1393f mastoid infection, 1304, 1306f
non-visualisation, 1471 cysts, 1510 mediastinum, 13471348
normal appearances, 660663, 662f, 1472f dermoid cysts, 1298, 1298f1299f mesenteric adenitis, 1395, 1395f1396f
of developing, 14711473 diaphragm, 1339, 1339f, 13481350, 1349b muscle injury, 15061507, 1507f
normal development, 14681469, 1469f enuresis, 1462 myositis ossificans, 1508
outline, 1471 fibromatosis, 13021303 nephrocalcinosis, 1446, 1446t, 1449f
pelvic inflammatory disease, 682, 682b, foreign bodies, 15071508, 1508f neuroblastoma, 637, 640f, 1312
682f683f gallbladder, 1356, 13751376 non-accidental injury, 1506
polycystic, 14821483, 1482f gallstones, 1375, 1375f obstructive uropathy, 14281433
position, 660, 661f662f, 1471 ganglion cysts, 1510, 1510f oesophagus, 1384b
pseudomyxoma peritonei, 672673, 673f ganglioneuroblastoma, 1466 osseous lesions, 13531354
round ligament of, 660 ganglioneuroma, 1466 osteomyelitis, 15081509, 1509f
septa, 664, 665f gastro-oesophageal junction, 13831384, ovaries, 14681490
serous tumours, 671672, 671f672f 1384f neoplasms, 14851488, 1486f
Sertoli-Leydig cell tumours gastro-oesophageal reflux, 13831384, overuse injuries, 1506
(androblastoma), 678 1384f pancreas, 13771381, 1380b
sex cord stromal tumours, 1487, 1487f technique and normal anatomy, 1383 cysts, 1378
size, 660661 goitre, 1310 pancreatitis, 13781380, 1379f
calculi, 904, 904f musculoskeletal soft tissue masses, 1082 Periductal mastitis, 989
carcinoma ex-pleomorphic adenoma, neonatal masses, 1483, 1484f Peri-epiglottic fat space, 913
902903 pain Perimysium, 1138
in children, 1307, 1307f in children, 14881490 Perineurium, 1158
cystic hygroma, 905, 906f gynaecological causes of, 1488 Peripheral arterial disease, 11971226
cystic lesions, 905, 905f non-gynaecological causes of, 1490 acute ischaemia, 1211
enlargement, 1308 tendon injury, 10721075 aneurysms, 1211, 1212f
haemangioma, 901, 902f Pelvi-ureteric dilatation, 428444 angioplasty, 1210
infection, 903 causes of, 428438 ankle brachial pressure index, 1199
inflammation, 903905 pathological, 429438 in the arm, 12121214
lymph nodes, 900, 924, 924f physiological, 428429, 429f occlusive arterial disease, 1214
lymphoma, 903 congenital causes, 435436 Raynauds disease, 1214, 1219f
metastases, 903 diagnosis, 438439 Takayasus arteritis, 1214, 1218f
mucoepidermoid carcinoma, 902 Doppler technique, 441, 441f442f thoracic outlet syndrome, 12131214
nerve sheath tumours, 901902 functional evidence using Doppler, ultrasound investigation, 12121214,
neurofibroma, 901902 440441 1216f
normal appearances, 898907, 899f iatrogenic, 438 arteriovenous fistula, 1212, 1216f
oncocytoma, 901 idiopathic, 436 bypass grafts see Peripheral artery bypass
pathology, 900 management of obstructive uropathy, grafts
pleomorphic adenoma, 899f, 900, 901f 441443, 442f clinical problem, 11971198
sarcoidosis, 904 trauma, 438 continuous wave Doppler ultrasound,
schwannoma, 901902 ultrasound appearances, 439440, 440f 11991200, 1203b
technique, 898907 Penile arteries, 621 dissection, 1212, 1216f
tumours, 897, 900903, 903f Penis, 621631 duplex ultrasound, 12001207, 1203b,
Parotitis anatomy, 621, 621b, 622f 1203f1204f
acute, 903, 903f appearances, 621, 622f aorto-iliac and femoropopliteal
in children, 13071308, 1308f arterial supply, 621, 622f segments, 1206
recurrent, 13071308, 1308f erectile dysfunction, 621623 below-knee segments, 12061207, 1207f
chronic, in children, 1308 arteriogenic, 624 reporting, 1207, 1208f
juvenile recurrent, 905, 905f background, 621623 scanning technique, 12051206,
Parsonage-Turner syndrome, 1037 physiology of the erectile process, 623 1205f1206f
Parvus tardus waveform see Damped veno-occlusive, 624625, 626f equipment, 11981199
waveform fibrosis, 628 continuous wave ultrasound, 1198,
Patella, 1085f masses, 628629, 628f629f 1198f
Patellar tendinosis, 10841087, 1086f1087f metastases, 628629 ultrasound scanners, 11981199
Patellar tendon, 1084, 1085b, 1085f Peyronies disease, 627628, 628b, 628f haemodialysis access see Haemodialysis,
tears, 10871088, 1087f1088f, 1088b priapism, 627, 627b access
Patent foramen ovale (PFO), 77, 78f ischaemic, 627, 627b, 627f injuries, 1212
Patient monitoring, transcranial Doppler non-ischaemic, 627, 627b popliteal entrapment, 1211
ultrasound, 980 prostheses, 629f pseudo-aneurysms, 1212, 1213f1215f
Peak systolic velocity (PSV), 1202, 1204f squamous cell cancer, 628629 stenosis criteria, 12011202
Peliosis hepatis, 197, 197f stimulated colour Doppler ultrasound, stents, 1210
Peliosis hepatitis, 150 623626 velocity waveform analysis, 11991200,
Peliosis of the spleen, 340 arteriogenic erectile dysfunction, 624, 1200f1202f, 1202t
Pelvic abscess drainage, 724727, 725f726f, 625f Peripheral artery bypass grafts, 12071210
726b false venous leak, 626, 626f failure, 1207, 1207t, 1209
complications, 727 further imaging, 625626 postoperative scanning, 12091210,
method, 724726 haemodynamic parameters, 626b 1209f1211f, 1210b
rationale, 724 normal response, 624, 624f625f preoperative scanning, 12071208, 1209f
Pelvicalyceal system, dilated, 433434, 433f, pharmacological agents, 623 stenoses in, 12091210, 1209f
435f436f, 493, 494f, 518 technique, 623, 623f Peripheral nerves, 11581167
see also Pelvi-ureteric dilatation veno-occlusive erectile dysfunction, anatomical variations, 11591160, 1159b,
Pelvic brim, 646 624625, 626f 1160f1161f
Pelvic floor, 647, 647f trauma, 629, 629f compression, 11621163, 1166f
Pelvic inflammatory disease (PID), 682, 682b, urethral ultrasound, 629 entrapment neuropathies see Nerve
682f683f venous leak, 623625 entrapment
Pelvis false, 626, 626f examination technique, 11581159
female Pennate muscles, 1139 miscellaneous disorders, 1166
anatomy, 646649 Peptic ulcer disease, 365 normal anatomy, 1158, 1159f
in children, 14701471 Percutaneous aspiration injection and tears, 1161
muscles, 647, 647f648f re-aspiration (PAIR), 130 trauma, 11611163, 1162f1164f, 1163b
skeleton, 646, 646f Percutaneous ethanol injection (PEI), 174, tumours and masses, 11641166,
ultrasound anatomy, 652654 174t 1165f1166f
ultrasound scanning technique, Percutaneous nephrostomy, 442443, 442f ultrasound anatomy, 1158, 1159f
645646, 649654, 14701471 Perforating veins, 1245, 1245f Peripheral veins, 12271250
viscera, 647649, 648f Periareolar infection, 989 anatomical variants, 1234, 1235f
interventional techniques, 11801181 Pericardial cysts, 1348, 1349f clinical applications for ultrasound,
muscle injury, 10721075 Pericholecystic varices, 183 12351240
post rotator cuff repair, 10351036 tuberculosis, 377, 377f378f angle correction errors, 49, 50f
suprascapular nerve palsy, 1037, 1038f tumours, 380381, 384b beam/flow angle, 4546, 46f
technique, 10301032 ultrasound-guided biopsy, 385, 386f gain, 46, 47f
Sialectasis, juvenile, 1308, 1308f vasculitis, 379380, 379t, 380f high pulse repetition frequency, 4648,
Sialoadenitis, 897, 897f, 904, 905b wall 48f
Sialolithiasis, 895897, 1308 layers, 371373 invert, 46, 47f
Sialosis, 906 thickness, 371372 power, 46
Sickle cell disease, 453 Soft tissue infections, paediatric, 1508, 1509b sample volume/gate size, 48, 48f
Side holes, 813815 Soft tissue masses, 11091125 scale, 4648, 48f
Sigmoid colon, 394395 benign, in children, 13501352 sweep, 49, 49f
Sildenafil, 622623 biopsy, 11911192, 1191b, 1192f velocity, 49, 50f
Silicone breast implants, 1000 bursae, 11151116 wall filter, 49, 49f
Silicone granulomas, 1000, 1000f calcification, 11111113, 1113b, 1113f peripheral veins, 1229, 1230f
Sinuses, spinal, 13281330 cysts, 11151116, 1116f (see also Cysts) portal vein, 179, 201
Sinus tarsi syndrome, 1105 echo pattern, 1111 priapism, 627
Sipples syndrome, 929 ganglion, 1116, 1116f (see also Ganglion renal cell carcinoma, 513
Sirolimus, 529530 cysts) renal transplantation, 530532
Sister Josephs nodule, 806 inflammatory, 11161117, 1117f scanners, 32, 50b
Sjgrens syndrome, 904, 904f location, 1110, 1111b Specular interfaces, 6163, 62f, 64b
Skeletal muscle see Muscle(s) malignant, in children, 1353 Speed of ultrasound, 4, 4t
Skiers thumb, 10631064 margin, 1111, 1111b, 1112f Spermatic cord, 594595, 596f
Skin tags, spinal, 13281330, 1330f paediatric, 15091512, 1512f haemangioma, 610, 611f
Slice thickness, 21, 22f pseudo-masses, 11131114, 1114f lipoma, 609, 610f
Slipped femoral capital epiphysis, 15041505, size and shape, 1110, 1111f liposarcoma, 611
1505f tissue density/compressibility, 1113, 1113f rhabdomyosarcoma, 611
Small bowel, 369387 of traumatic origin, 11141115, 1115f spontaneous de-torsion, 617
abnormal ultrasound appearance, 371, tumour-like, 11131117 torsion, 612614, 616617, 617b, 617f,
371b tumours, 11171124 14921493
adenocarcinoma, 380, 381f extraskeletal osseous, 1124 Spermatoceles, 608, 609f
altered blood flow, 371 fibrous and fibrohistiocytic, 11211123 Sperm granuloma, 608609, 610f
anisakiasis, 379 lipomatous, 11171119 Spigelian hernias, 804, 1081, 1081f
blood supply, 371 muscle, 1121 Spina bifida aperta, 1322
carcinoid tumours, 381, 382f nerve tumours and tumour-like lesions, Spina bifida cystica, 1322
in children, 13881395 11191120 Spinal arteries, 1320
masses, 13941395, 1395b synovial, 11231124 Spine
normal anatomy, 1388 vascular, 11201121 infant, 13151336
obstruction, 13881391, 1388f, 1391b ultrasound technique, 1109b1110b, anatomy, 13161322
wall thickening, 13921394, 1393b 11101113, 1110f1111f cervical region, 1320
coeliac disease, 385 vascular, 1117, 1118f coccygeal region, 1318
Crohns disease see Crohns disease vascularity, 1113, 1114f conus, 13191320
duplication cysts, 816 see also specific masses extraspinal, 1316, 1316f
extramural changes, 371 Soft tissue thermal index (TIS), 54 intraspinal, 13181320, 1318b
gastrointestinal stromal tumours, 381, 383f Soleus muscle, 1093 lumbar region, 1318, 1318f1319f
haemorrhage, 1393 accessory, 1143 sacral region, 1318
ileocaecitis, 377, 377f Solid pseudopapillary neoplasm, 312 spinal, 13161318, 1316f1318f
infections, 376379 Solitary fibrous tumour, prostate gland, 589t thoracic region, 13191320,
intussusception, 384, 385f Sonavist, 140 1319f1321f
ischaemia, 379, 379t Sonazoid, 79t, 80 vascular structures, 13201322,
layers, 370 Sonication, 77 1321f
lipoma, 381 Sonoporation, 87 contraindications for ultrasound, 1316
liver transplantation complications, 221 SonoVue, 79, 79t, 80f, 288, 291f embryology, 1322
lumen, 371 Space-occupying lesions, neonatal, 1284 indications for ultrasound, 1316, 1316b
lymph nodes, 371 cysts, 1284 lipoma, 13221324, 1323f
lymphoma, 381, 382f383f, 13941395, neoplasms, 1284, 1285f1287f spinal dysraphism, 13221330
1395f vascular malformations, 1284, 1288f closed, 13221330, 1322b
malrotation, 13891390, 1391f Specimen handling, 852853, 853f open, 1322, 1322b
mesenchymal tumours, 381 Speckle, 67, 7f, 75 technique, 13151316
mesenteric lymphadenopathy, 371 Spectral broadening, 476 trauma, 13301332, 1331f
metastases, 381, 384f Spectral (duplex) Doppler tumours, 13321334, 1333f1334f
mobility, 371 abdominal aorta atherosclerosis, 788 ultrasound versus magnetic resonance
normal ultrasound appearance, 370371, aortic dissection, 789 imaging, 1316
370b, 370f arteriovenous fistula, 481 vascular anomalies, 1332, 1332f1333f
obstruction, 384, 386f, 13881391, 1388f, carotid arteries, 967968 Splanchnic arteries, 789792, 790f791f
1391b hepatic vein occlusion, 195 aneurysm, 791792, 791f
peristalsis, 371 main renal artery trunks, 471472 stenosis, 789791, 791f
plasticity, 371 ovarian lesions, 670 Spleen, 324347
secondary malignancies, 381, 384f parameters, 32, 4449, 50b abscess, 338340, 339f340f
technique, 369370, 370b, 370f angle correction, 4546, 46f accessory, 328329, 328f329f
Suprascapular nerve palsy, 1037, 1038f mature ovarian, 674676, 674f677f, 676b two-tone, 597, 597f
Supraspinatus, 1030, 1031f1032f mediastinal, 1347, 1347b ultrasound examination technique, 593,
barbotage of calcific tendinopathy, 1172, mesenteric, 14021403 594f, 1490
1172b, 1172f ovarian, 674676, 674f677f, 676b, vascular anatomy, 594595, 595f
rupture, 1035, 1035f 14871488 venous infarction, 614615, 614f
Sural nerve, 1095 retroperitoneal, 819820 yolk sac tumour, 600, 600f
Suspensory ligament, 941 sacrococcygeal, 1333, 1334f Tethered cord syndrome, 13241325, 1325b,
Sutures, cranial see Cranial sutures testicular, 599600, 601f 1325f
Symphysis pubis, 10811082, 1081f Teres minor, 1030 Thalamus, 1257
injection, 1082, 11801181 Terjesen technique, 1503 Theca lutein cysts, 667, 764, 764f
Synchysis scintillans, 949 Terminal ileum, 369370 Thecoma, ovarian, 678, 679f
Synchysis senilis, 944945 acute, 1393 Thelarche, 1470
Synechiae, intrauterine, 709, 711f in children, 1393 isolated premature, 1481, 1481f
Synovial cysts, 1115 Tersons syndrome, 950 Thermal effects of ultrasound, 5254
Synovial osteochondromatosis, 10471048, Testicular artery, 594595, 597f experimental investigation of heating,
1048f, 1123, 1123f Testicular veins, 594595 5253
Synovial sarcoma, 1124 Testis heating mechanisms, 52, 52t
Synovial tumours, 11231124 abscess, 604, 605f implications of heating, 5354
Synovitis adrenal rest cells, 603, 603f World Federation for Ultrasound in
ankle, 1104, 1104f, 1107 anatomy, 593595, 594f, 595b, 14901491 Medicine and Biology (WFUMB),
elbow, 1047, 1047f appendage torsion, 617, 618f, 1493, 1493f 58
localised pigmented villonodular, 1066, artefacts, 595598 Thermal index (TI), 34, 5254, 54b
1067f atrophy, 607, 607f bone-at-focus, 54
ultrasound features of, 11271128, 1128b, carcinoma, 598599 British Medical Ultrasound Society
1128f choriocarcinoma, 600 (BMUS) guidelines, 5758
Syringomyelia, 1328, 1329f congenital anomalies, 14911492 cranial bone, 54
Systemic lupus erythematosus, 379t, 453, 453f cystic dysplasia, 607, 1492 hazard indication, 54
Systolic acceleration time (SAT), 207208 cysts, 605606, 606f soft tissue, 54
embryology, 593594 use of during ultrasound examination,
embryonal cell carcinoma, 600 54
T epidermoid cyst, 602, 603f Thermography, 1227
focal lesions Thigh muscles, 1141, 1143t, 1144f
Tacrolimus, 529530, 536, 539 neoplastic, 598602, 599t Thoracic outlet syndrome, 12131214
Takayasus arteritis, 1214, 1218f non-neoplastic, 602607 Thoracic ultrasound, 10051021
Tamm-Horsfall proteinuria, 1443, 1443f germ cell tumours, 599600, 600f601f, see also specific anatomical areas
Tamoxifen, 706, 707f 1494 Thoracoscopy, 10131014
Tampons, retained, 715716 gonadal stromal tumours, 600601 Three-dimensional scanning
Tapeworm, 129 haematoma, 604605, 605f artefacts, 75
Tardus parvus waveform, hepatic artery, inguinal, 1491, 1491f bladder cancer, 562563
206208 intra-testicular abnormalities, 598608 cervical cancer, 714
Targeted contrast microbubbles, 8687 leukaemia, 602, 602f, 1494 endometrial cancer, 704
Tarsal tunnel syndrome, 1105 Leydig cell tumour, 601, 601f, 1494 eye, 943
Tear, 944945 lymphoma, 601602, 602f, 1494 Thrombin injection
Technique, 12531254 macrocalcification, 607608, 608f oesophageal varices, 359, 360f
Temporal resolution, 15 metastases, 602, 602f pseudoaneurysms, 301
Tendinitis microlithiasis, 607608, 608b, 608f, 1492, Thrombolysis, 980982
biceps, 1039 1492f Thrombolysis in Brain Ischaemia (TIBI)
calcific, 1037, 1037f1038f normal ultrasound appearance, 595598 classification, 980
Tendinopathy, 1025, 1026f normal variants, 595598 Thrombosis
calcific, 1172, 1172b, 1172f orchitis, 604, 605f calf vein, 1233, 1233f
Tendinosis, 1025, 1026f paediatric, 14901494, 1494b haemodialysis access, 1222
ankle, 1107b post-biopsy, 605 hepatic artery, 205207, 206f207f, 219220,
triceps, 10481049, 1049f postoperative, 605 219f
Tendons, 10271028, 1027f1028f, 1028b prosthesis, 607, 607f hepatic veins, 194195, 196f (see also
disease, ultrasound features of, 11301131, rhabdomyosarcoma, 1494 Budd-Chiari syndrome)
1131b, 1131f sarcoidosis, 604, 604f inferior vena cava, 792, 793f
neovascularity, 1025, 1025b segmental infarction, 603, 604f internal jugular vein, 1304
Tendon sheath injection, 11751176, 1177b, Sertoli cell tumour, 601 jugular veins, 908909, 910f911f
1178f size, 595, 596f neonatal brain, 12701272, 1272f
Tennis elbow, 1049, 1050f spleno-gonadal fusion, 603, 603f portal vein, 188189, 188b, 188f191f, 201,
Tennis leg, 1089, 1151, 1151f, 1153, 1153f spontaneous de-torsion, 617 220, 220f, 13651366, 1366f
Tenons capsule, 938 teratocarcinoma, 600, 601f renal artery, 533534, 534f, 1455, 1457f
Tenosynovitis, 1130, 1131f teratoma, 600, 601f in renal cell carcinoma, 513517
Tensor fascia lata, 10721074, 1074f torsion, 616617, 617b, 617f, 14921493, renal vein, 447448, 534535, 535f, 535t,
Teratocarcinoma, testicular, 600, 601f 1493f 14541455, 1456f
Teratomas congenital, 14911492 sagittal sinus, 982983
gastric, 1387 trauma, 615616, 616f, 1493, 1494f splenic vein, 342, 343f
immature ovarian, 676 tumours, 1494, 1494f Thymic cysts, 12981299
Thymus, 884, 914, 916f Tibialis posterior, 1096, 1096f, 11031104, square, 22, 22f
anatomy, 1338, 1338f 1103f1104f steered, 20, 20f
in children, 13381339, 1338f, 1340f Tibial nerve stepped, 20, 20f
ectopic, 1340f neuroma, 1105 B-mode imaging, 17
Thyroglossal duct cysts, 893, 914917, 917f posterior, 1096 construction, 18, 18b, 18f
in children, 12941295, 1295f schwannoma, 1105 elevation focusing, 21, 22f
Thyroid gland, 867884 Tibial veins, 1232 endo-cavity, 19f
abscess, 1310, 1310f Tibiofibular joint endoscopic ultrasound, 351
adenoma, 13101312, 1312f aspiration and injection, 1187 focusing, 21, 21f22f
anatomy, 867, 868f proximal, 1091 heating, 53
carcinoma, 1312 Tibiofibular ligaments, 1099, 1099f intraoperative ultrasound, 273274, 274f
in children, 13091312 Tibionavicular ligament, 1097 mechanical, 2223
cysts, 1309, 1310f Tibiotalar joint injection, 1187 paediatric chest, 1337
diffuse disease, 1310 Tibiotalar ligament, 1097 pelvic region, 1069
diffuse parenchymal diseases, Tight filum terminale syndrome, 13241325, 3/4D, 2122, 22f
882884 1325f Transient ischaemic attacks (TIAs), 965
ectopic, 1309 Time gain compensation (TGC), 23 Transient synovitis, hip, 15031504, 1504f
ectopic tissue, 894, 894f Time sampling artefacts, 7475, 74b Transitional cell carcinoma (TCC)
embryology, 868869 Tinel sign, 1119 bladder, 431, 517, 561562
focal lesions, 13101312 Tip of the iceberg sign, mature teratomas, ovarian, 674, 674f
goitre see Goitre 674675, 675f pelvi-ureteric dilatation, 433434,
malignant tumours, 873882 Tissue absorption, heating due to, 5253 433f434f
anaplastic carcinoma, 879880, 880b, Tissue characterisation, 1213, 12f renal, 517521, 519b
880f TNM staging aetiology, 517518
follicular neoplasm, 876878, 877b, bladder cancer, 563, 563b other tests, 519520
877f878f upper gastrointestinal tract cancer, patterns of spread, 520
incidentalomas, 881882 353354, 355t staging, 520t
lymphoma, 880881, 880b, 880f Tongue, 893f survival, 520t
medullary carcinoma, 878879, 879b, Topical anaesthesia, paediatric hip aspiration, symptoms, 518
879f, 929 1183 treatment, 520521
metastases, 881, 881b, 881f Toxocara canis, 129 ultrasound findings, 518519, 519f521f
papillary carcinoma, 873876, 874f Toxocara catis, 129 Transjugular intrahepatic portosystemic
877f, 875b, 928, 929f, 933 Toxocariasis, 129, 955 shunt (TIPS)
nodular disease, 869872 Toxoplasmosis, 1273, 1274f assessment of function, 186187
colour and power Doppler, 872 Trachea, 914 complications, 186
comet tail sign, 872, 872f Trachelectomy, 697700 occlusion, 188
echogenicity, 870 Traction retinal detachment, 946947, 947f portal hypertension, 186188, 186f
elastography, 872 Tranexamic acid, 689 pre-liver transplantation assessment,
generic ultrasound features of nodules, Transabdominal ultrasound 203
869 bladder, 551, 552f, 562 stenosis, 187188
interval growth of nodule, 872 cancer, 563 Trans-mediastinal artery, 595, 597f
investigative strategies for, 881882 female pelvis, 645646, 646b, 649651, Transperineal scanning, anal canal, 405406
margins, 870871 650f651f Transrectal ultrasound (TRUS)
multiple, 882, 882b neuroendocrine tumours, 314 benign prostate hyperplasia/hypertrophy,
nodule size, 869 pancreas, 286288, 287f291f 581, 582f
patterns of calcification, 870, 871f uterus, 686687 bladder, 551
shape: tall versus wide, 871872 Transcranial Doppler ultrasound cervical cancer, 714
solid/cystic nodules, 870, 870f anatomy, 976977 -guided intervention, 587591
solitary versus multiple nodules, aneurysms, 982 haematospermia, 584585
869870, 869f applications, 979983 male infertility evaluation, 584
ophthalmology, 960963, 960f arteriovenous malformations, 982 prostate, 574576, 575f, 576b, 577f, 578b
sarcoma, 879 carotid arteries, 976983 biopsy see Prostate, biopsy
scanning technique, 867 examination technique, 977978 cancer, 566, 585, 586f, 588t
thyroiditis see Thyroiditis pulsed, 978, 978f indications for, 576b
ultrasound features of adjacent structures suboccipital window, 977 TRUS-guided intervention, 587591
suggestive of thyroid carcinoma, transorbital window, 977978 unusual abnormalities, 587, 589f, 589t
872873, 873f transtemporal window, 977, 977f978f Transurethral resection of the prostate
Thyroiditis, 882884 Transcranial imaging (TURP), 581, 582f
acute suppurative, 884, 1310, 1310f British Medical Ultrasound Society Transurethral ultrasound, 563564
classification, 882, 883t (BMUS) guidelines, 58 Transvaginal biopsy, 722723, 722b, 723f724f
de Quervains, 883884, 884f contrast agents, 85 complications, 723
general ultrasound appearance, 883 see also Transcranial Doppler ultrasound method, 722723
Hashimotos, 880, 883, 883f Transducers, 8, 16, 3233, 33f rationale, 722
Riedels, 884 aperture control, 21, 21f Transvaginal scanning (TV)
Tibial artery array, 19f, 23b anal canal, 405406
calcification, 1207f curved, 19f, 20 bladder, 551, 566
stenosis, 1205f, 12061207 curvilinear, 22, 22f in early pregnancy, 741
Tibialis anterior, 10971098, 1098f linear, 19f20f, 20, 42, 43f endometrial cancer, 704, 705f
female pelvis, 646, 646b, 651652, Tubo-ovarian complex, 682, 683f Ureteroceles, 436, 499, 558559, 560f561f
651f652f Tubular necrosis, acute, 449, 451, 532, 542 in children, 1422, 1424f
ovarian cancer, 680 Tubulo-interstitial disease, 484 complications, 1422
transducer heating, 53 Tumour ablation, 816824 ectopic, 559, 1422
uterus, 686687 ablative energy, 816818 orthoptic, 1422
Transverse colon, 394395 brachytherapy, 806f prolapsed, 1425f
Transverse tibiofibular ligament, 1099 cryoablation, 803f, 821 sonographic features, 1422
Transversus abdominis, 1076 focused ultrasound, 823824 Ureteropelvic junction obstruction, 14281430,
Transvesical ultrasound, 566 peri-procedural monitoring, 806f807f 1432f
Trauma post-procedural imaging, 807f Ureters, 551
abdominal see Abdominal trauma procedural targeting, 806f calculi, 430
abdominal wall, 801 interstitial laser photocoagulation in children, 1409, 1413f, 14221428
anal, 408, 408f microwave, 821823 development, 1407
bladder, 569, 569b radio-frequency, 804f, 819821 duplex, 423, 559
carotid arteries, 966 techniques, 818819 megaureter, 1422, 1426f
eye, 956958, 956f958f, 957b tumour pathophysiology and its obstruction, 14301433, 1433f
foot, 1107 modification, 808f acute, 484
neonatal brain, 12851287 Tumours in renal transplantation, 535
accidental injury, 1285 ablation see Tumour ablation stenosis, post-renal transplantation, 537
birth-related injury, 1285, 1289f inferior vena cava obstruction, 793794, ultrasound technique, 1409, 1413f
non-accidental injury, 12851287, 793f Urethra
1289f1290f pathophysiology and its modification, cancer, 565566
paediatric, 15051508, 1506b 861862 in children, 14221428
pelvi-ureteric dilatation, 438 pelvi-ureteric dilatation, 431434 development, 14071409, 1408f
penile, 629, 629f see also specific anatomical areas normal sonographic appearance, 576
peripheral nerves, 11611163, 1162f1164f, Tunica albuginea, 594, 621, 661 posterior urethral valve, 14221425,
1163b calcification, 611612, 611f 1427f1428f
renal, 838841, 845, 845f cyst, 606 sphincters, 574, 576
in children, 14571458, 1457f Tunica vaginalis, 594 ultrasound, 629
classification, 839840, 839t calcification, 611612, 611f Urethrography, 629
general considerations, 838841 cyst, 606 Urinary continence, male, 574
mechanisms of injury, 839840 Turners syndrome, 14771478, 1480f Urinary leak, renal transplantation, 535
ultrasound findings, 840841, 840f841f Twinning, 747748, 747f748f, 747t, 748b Urinary tract dilatation, 14331434, 1434f
soft tissue masses, 11141115 Twin peak sign, 747748 Urinary tract infection (UTI), 568
spinal, 13301332, 1331f Two-tone testis, 597, 597f in children, 1446b, 14481453, 1453f
testicular, 615616, 616f, 1493, 1494f Typhlitis, 399t, 401, 401f imaging protocols, 1453
Triangle sign, 945946, 946f lower, 14491453, 1453f
Triangular fibrocartilage complex (TFC), 1057, U lower, 14491453, 1453f
1063 post-renal transplantation, 536, 540, 543f
Triangular ligaments, liver, 93 UK Collaborative Trial of Ovarian Cancer in pregnancy, 568
Triceps tendon, 1045 Screening (UKCTOCS), 680 upper, 14481449
rupture, 1049, 1049f Ulcerative colitis, 397, 399f, 1399 Urine
tendinosis, 10481049, 1049f versus Crohns disease, 397b echogenicity, 556, 557f
Tricuspid regurgitation, 195, 197f differential diagnosis, 399t flow
Triggered imaging, 8284 Ulnar artery, 1043, 1213 high, 555
Trigger finger, 1060 Ulnar collateral ligament, 1045, 1046f, intermittent, 556
Triploidy, 764, 765t 10631064 low, 555556
Trocar drainage technique, 815816 injury, 1051, 1051f patterns, 555556
Trochanteric bursal injection, 1184, 1185f Ulnar nerve, 1045, 1045f, 1057 rates, 555b
Troisiers sign, 926 compression, 11411143 flowmetry, 554555, 555f
Trousseaus syndrome, 909 division, 1045 Urinomas, 815816, 823
Tubal ring, ectopic pregnancy, 754755, entrapment, 1052, 1052f post-hysterectomy, 697698
755f756f Umbilical hernias, 804, 1081 post-renal transplantation, 535
Tuberculosis Umbilical vein varices, 183, 184f185f Urogenital sinus, 14751476, 1479f
intestinal, 399400, 399f, 399t Uncinate process, 285286 Urolithiasis, 14451446, 1446b, 1446f1448f
liver involvement, 132133, 133f134f United Kingdom Small Aneurysm Trial Urology, intraoperative ultrasound, 280, 280f
lymphadenitis, 13051306 Participants (UKSAT), 775 Uropathy, obstructive, 14281433
Mantoux test, 1306 Upper limb Urothelial cancer see Transitional cell
peritonitis, 812, 813f muscles, 11391141, 1140t, 1141f1142f carcinoma (TCC)
prostate gland, 589t vascular anatomy, 1240, 1240f Uterine artery, 649, 655, 656f
pulmonary, 1015 venous imaging, 12401241 embolisation, 693694
renal, 463464, 465b, 465f, 14531454 Urachus Uterine bleeding, abnormal see Vaginal
small intestine, 377, 377f378f abnormalities, 14251427, 1431f bleeding, abnormal
Tuberculous lymph nodes, 929 bladder, 559, 561f Uterine tubes, 649, 653654
Tuberous sclerosis, 502, 502b, 502f503f, 509f cyst, 807 Uterine vein, 649
neonatal brain, 1282, 1283f Ureteric jets, 441, 442f, 551, 553f Uterovesical pouch, 808809
renal manifestations, 1441f Ureteric JJ stent, 556, 559f Uterus, 687f
Tubo-ovarian abscess, 682, 683f Ureteritis, 14491453 anatomy, 648649