A Global TextBook of Radiology II

T h e N IC E R C e n te n n ia l
B ook 1995
A Global
TextBook of
Radiology
The NICER C e n te n n ia l
B ook 1995
A Global
TextBook of
Radiology
Edited b y
Holger Pettersson, MD
Professor o f R adiology
U niversity H ospital
Lund, Sw eden
Educational and Scientific D irector
The N IC ER Institute
II
Chest
Abdomen
Urogenital system
Tropical disease
S e r i e s on D i a g n o s t i c I m a g i n g
From
The NICER Institute
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Editorial Board
Sudarshan K. Aggarwal, India
David J. Allison, United Kingdom
Jose Luis Ramirez Arias, Mexico
Albert L. Baert, Belgium
Xing-Rong Chen, China
Mahmoud R. Elmeligi, Egypt
Philippe Grenier, France
Derek Harwood-Nash, Canada
Charles B. Higgins, USA
Takahiro Kozuka, Japan
Javier Lafuente Martinez, Spain
Peter Peters, Germany
Howard Pollack, USA
Donald Resnick, USA
Leonid S. Rosenstrauch, Russia
Michael Sage, Australia
This book is partly based on a Scandinavian Textbook of Radiology

(Nordisk Larobok i Radiologi, Studentlitteratur, Lund, Sweden, 1993),
and the publisher’s permission to use material from this book is highly
appreciated.
Editors of the Scandinavian Textbook:

Holger Pettersson, Sweden
Niels Egund, Denmark
Baldur Sigfusson, Iceland
Amulf Skjennald, Norway
Carl-Gustaf Standertskjold-Nordenstam, Finland
Contents
VOLUME I
Chapter 1 W.C. Roentgen and the discovery of X-rays............. 1

Peter Peters, Germany
Chapter 2 Radiology in an international perspective................ 13
Carl-Gustaf Standertskjold- Nordenstam, Finland
Chapter 3 Radiophysics................................................................ 17
Aar о Kiuru, Finland
Chapter 4 Modalities and methods............................................... 47
Hans-Jorgen Smith, Norway
Chapter 5 Radiology worldwide - the WHO approach.............. 85
Philip E.S. Palmer, USA
Thure Holm, Sweden
Gerald P. Hanson, Switzerland
Chapter 6 Digital imaging............................................................ 101
Tatsuo Kumazaki, Japan
Hans Ringertz, Sweden
Chapter 7 Contrast media in diagnostic radiology.................... 115
Torsten Almen, Sweden
Peter Aspelin, Sweden
Chapter 8 Interventional radiology.............................................. 143
Christoph Zollikofer, Switzerland
Chapter 9 The brain........ .............................................................. 167
Kjell Bergstrom, Sweden
Giuseppe Scotti, Italy
VII
Chapter 10 The head and neck....................................................... 229
Sven-Goran Larsson, Saudi Arabia
Anthony Mancuso, USA
Chapter 11 Dental radiology.......................................................... 263
Lars Hollender, USA
Karl-Ake Omnell, USA
Chapter 12 The spine.................................................................... 297

Stig Holtas, Sweden
Maximilian F. Reiser, Germany
Axel Stabler, Germany
Chapter 13 Musculoskeletal radiology....................................... 371
Niels Egund, Denmark
Kjell Jonsson, Sweden
Holger Pettersson, Sweden
Donald Resnick, USA
Chapter 14 Pediatric musculoskeletal radiology......................... 459
Andrew K. Poznanski, USA
Chapter 15 Pediatric radiology..................................................... 533
Donald R. Kirks, USA
Sven Laurin, Sweden
Chapter 16 Pediatric neuroradiology.......................................... 611
O lof Flodmark, Sweden
Derek Harwood-Nash, Canada
Chapter 17 Breast imaging........................................................... 627
Ingvar Andersson, Sweden
Baldur F. Sigfusson, Iceland
Index ....................................................................................... XVII
VOLUME II
Chapter 18 The lungs and mediastinum...................................... 669

A lf Kolbenstvedt, Norway
A rnulf Skjennald, Norway
Chapter 19 The heart.................................................................... 773
A rnulf Skjennald, Norway
VIII
Chapter 20 The peripheral vessels............................................... 809
Christoph Zollikofer, Switzerland
Frode Laerum, Norway
Chapter 21 The lymphatic system............................................... 871
Elias Zerhouni, USA
Chapter 22 The gastrointestinal tract.......................................... 891
Richard M. Mendelson, Australia
Chapter 23 The liver, biliary tract, pancreas and spleen........... 1027
Carl-Gustaf Standertskjold-Nordenstam, Finland
Chapter 24 The acute abdomen................................................... 1079
Olle Ekberg, Sweden
Frans-Thomas Fork, Sweden
Chapter 25 The genitourinary system......................................... 1111
Henrik Thomsen, Denmark
Howard Pollack, USA
Chapter 26 Obstetric imaging..................................................... 1217
Con Metreweli, Hong Kong
Chapter 27 Tropical diseases...................................................... 1237
Philip E.S. Palmer, USA
Stanley P. Bohrer, USA
Carlos Bruguera, Argentina
Xing-Rong Chen, China
Mahmoud R. Elmeligi, Egypt
HassenA. Gharbi, Tunisia
S.B. Lagundoye, Nigeria
M. W. Wachira, Kenya
Chapter 28 Radiology in AIDS.................................................... 1309
Marie-France Beilin, France
Philippe Grenier, France
Nadine Martin-Duverneuil, France
Index ..................................................................................... XV
IX
List of Authors
David J. Allison, BSc, MD, Marie-France Beilin, MD

MRCP, FRCR Department of Radiology
Department of Diagnostic Groups Hospitalier,
Radiology Pitie-Salpetriere,
Royal Postgraduate Medical Paris, France
School,
Hammersmith Hospital, Kjell Bergstrom, MD
London, UK Department of Radiology
Academic Hospital,
Torsten Almen, MD University of Uppsala,
Department of Radiology Uppsala, Sweden
Malmo General Hospital,
University of Lund, Stanley P. Bohrer, MD
Malmo, Sweden Department of Radiology
Bowman Gray School of
Ingvar Andersson, MD Medicine of Wake Forest
Department of Radiology University,
Malmo General Hospital, Winston-Salem, NC, USA
University of Lund,
Malmo, Sweden Carlos Bruguera, MD
Marina del Sol,
Peter Aspelin, MD Victoria S. Fernando, Argentina
Department of Radiology
Huddinge Hospital, Xing-Rong Chen, MD
Karolinska Institute, Department of Radiology
Stockholm, Sweden Hua Shan Hospital,
Shanghai Medical University,
Shanghai,China
X
Niels Egund, MD Gerald Hanson, PhD.
Department of Radiology Radiation Medicine
Odense University Hospital, World Health Organization,
Odense, Denmark Geneva, Switzerland
Olle Ekberg, MD Derek Harwood-Nash, MB,

Department of Radiology ChB, FRCP(C)
Malmo General Hospital, Department of Radiology
University of Lund, The Hospital for Sick Children,
Malmo, Sweden University of Toronto,
Toronto, Ontario, Canada
Mahmoud R. Elmeligi, MD
Department of Radiology Charles B. Higgins, MD
University of Cairo, Department of Radiology
Cairo, Egypt UCSF Medical Center,
San Francisco, CA, USA
Olof Flodmark, MD
Department of Radiology Lars Hollender, Odont dr
Karolinska Hospital, Department of Oral Medicine
Stockholm, Sweden University of Washington,
Seattle, WA, USA
Frans-Thomas Fork, MD
Department of Radiology Thure Holm, MD
Malmo General Hospital, Department of Radiology
University of Lund, University Hospital,
Malmo, Sweden Lund, Sweden
Hassen A. Gharbi, MD Stig Holtas, MD

Department of Radiology, Department of Radiology
Clinique Saint Augustin, University of Hospital,
Tunis, Tunisia Lund, Sweden
Philippe Grenier, MD Kjell Jonsson, MD

Department of Radiology Department of Radiology
Groups Hospitalier, University Hospital,
Pitie-Salpetriere, Paris, France Lund, Sweden
XI
Donald R. Kirks, MD Sven Laurin, MD
Children’s Hospital, University Hospital,
Harvard Medical School, Lund, Sweden
Boston, MA, USA
Anthony Mancuso, MD
Aaro Kiuru, PhD Department of Radiology
Department o f Oncology and University of Florida,
Radiotherapy College of Medicine,
Turku University, Gainesville, FL, USA
Central Hospital,
Turku, Finland Nadine Martin-Duverneuil, MD
Alf Kolbenstvedt, MD Groups Hospitalier,
Department o f Radiology Pitie-Salpetriere, Paris, France
Rikshospitalet,
University of Oslo, Norway Richard Mendelson, MB, ChB,
MRCP, FRCA, FRACA
Tatsuo Kumazaki, MD Department of Diagnostic
Department of Radiology Radiology
Nippon Medical School, Royal Perth Hospital,
Tokyo, Japan Perth, Australia
Frode Laerum, MD Con Metreweli, MB, BChir,

Department of Radiology FRCR, FRCP
Rikshospitalet, Department of Radiodiagnosis
University of Oslo, Norway Prince of Wales Hospital,
Chinese University
S.B. Lagundoye, MD o f Hong Kong,
Department of Radiology Hong Kong
University College Hospital,
Ibadan, Nigeria Karl-Ake Omnell, Odont dr
Department of Oral Medicine
Sven-Goran Larsson, MD University of Washington,
Department of Radiology Seattle, WA, USA
King Faisal Specialist Hospital
& Research Center, Philip E.S. Palmer, MD
Riyadh, Saudi Arabia Professor Emeritus,
Davis, СA, USA
XII
Peter Peters, MD Donald Resnick, MD
Westfalische Wilhelms- Veterans Administration
Universitat, Medical Center,
Munster, Germany San Diego, CA, USA
Holger Pettersson, MD Giuseppe Scotti, MD

University Hospital, Istitutio Scientifico,
Lund, Sweden Ospedale S.Raffaele,
Milan, Italy
Howard Pollack, MD
Department of Diagnostic Baldur F. Sigfusson, MD
Radiology Mammographic Department,
The Hospital of the University Icelandic Cancer Society,
of Pennsylvania, Reykjavik, Iceland
Philadelphia, PA, USA
Arnulf Skjennald, MD
Andrew Poznanski, MD Department of Radiology
Department of Radiology Ulleval Hospital,
The Children’s Memorial University of Oslo, Norway
Hospital,
Chicago, IL, USA Hans-Jergen Smith, MD
Maximilian F. Reiser, MD
Rikshospitalet,
University of Oslo, Norway
Klinikum Grosshadem,
University of Munich,
Carl-Gustaf Standertskjold-
Munich, Germany
Nordenstam, MD
Department of Diagnostic
Hans Ringertz, MD
Radiology
Helsinki University,
Karolinska Hopsital,
Central Hospital,
Stockholm, Sweden
Helsinki, Finland
XIII
Axel Stabler, MD Elias A. Zerhouni, MD
Klinikum Grosshadem, The Johns Hopkins Hospital,
University of Munich, Baltimore, MD, USA
Munich, Germany
Christoph Zollikofer, MD
Henrik Thomsen, MD Department of Radiology
Department o f Radiology Kantonspital Winterthur,
Herlev Hospital, Winterthur, Switzerland
University of Copenhagen,
Copenhagen, Denmark
M.W. Wachira, MD
Kenyatta National Hospital,
Nairobi, Kenya
XIV
Chapter 18
The lungs and mediastinum
Alf Kolbenstvedt, Arnulf Skjennald and

Charles B. Higgins
A chest radiograph is the most frequently performed radiological exam

ination. Radiographs of the lungs are often taken, not only in connection
with diseases of the lungs, but also with a large number of diseases in
other organs that indirectly affect the lungs. A chest radiograph is also
often taken routinely before operations.
Radiographs of the lungs can demonstrate both the presence of vari
ous diseases, and also the severity. These radiographs are also used to
monitor the overall state of the patient in the intensive care unit by pro
viding insight into such factors, as fluid balance.
While plain radiographs of the lungs are still the most common ex
amination, the importance of special techniques such as bronchography,
tomography, and angiography is now reduced, largely because of com
puted tomography, a method that is becoming increasingly common for
assessment of pathological conditions in the lungs and hilum/medi-
astinum. The introduction of digital radiography (DR) has also repre
sented a substantial step forward in the radiological diagnosis of pul
monary diseases, primarily in postoperative and intensive care patients.
MODALITIES
Chest radiographs with supplementary methods of

examination
This is the most frequently performed radiographic examination. It can
be performed rapidly, and can give much valuable information when the
indications are correct.
This examination is the first choice in most diseases in the chest where
imaging techniques are used to reach a diagnosis. Using the plain chest
669
THE NICER GLOBAL TEXTBOOK OF RADIOLOGY
r — -------- Figure 1.
Normal chest x-ray
a) PA view
b) Lateral view
radiograph as a starting point, supplementary radiographs using special

projections may be indicated.
A plain chest radiograph consists of frontal and lateral views (Fig. 1 a, b)
in a standing patient when this is possible. Use of two projections makes
it easier both to find and to localize pathological processes. The frontal
670
THE LUNGS AND MEDIASTINUM
view is taken with foil inspiration and posteroanterior (PA) beam di
rection. The heart thus comes closest to the film, and magnification of
the cardiac shadow caused by ray divergence is minimized. In order to
further reduce the effect of ray divergence, the distance from the tube is
at least 1.5 metres. When bedridden patients are examined using a mo
bile apparatus, the film must be placed behind the back of the patient,
and the distance from the tube must be shorter. The relative magnifica
tion of the cardiac shadow in this circumstance must be considered when
comparing standard (posteroanterior) and portable (anteroposterior) ra
diographs.
The most important examinations that can be obtained to supplement
the frontal and lateral radiographs are oblique views, lateral decubitus
views, expiratory frontal views, overpenetrated films, lordotic views, flu
oroscopy, and tomography.
Oblique views with the left and right sides, respectively, turned for
wards towards the film, can provide valuable additional information on
pleural thickening and are also useful when poorly defined opacities are
seen in the frontal view, but not in the lateral view. These may be caused
by summation phenomena, which can be confused with opacities. The
oblique views may clarify the diagnosis.
Lateral decubitus views are usually taken with a horizontal direction
of the x-ray beam, i.e. a frontal view of a patient lying on his side. The
objective is to identify small amounts of pleural fluid which collect and
become visible at the most dependent region of the pleural space.
Expiratory views are used to identify a small pneumothorax. By re
ducing the volume of the pleural space during expiration, a small amount
of "trapped" air in the pleural cavity will be forced to increase in breadth
so that the surface of the lung is pushed further away from the chest wall,
thus becoming visible.
For overpenetrated films, higher energy rays are used. These can pro
vide additional information about conditions in the mediastinum behind
the heart shadow and about the soft tissues along the vertebral column.
Lordotic views can help to clarify uncertain findings in the apex o f the
lungs that are hidden behind the clavicle and first rib in the standard
frontal view. The patient stands with his back to the film cassette and
bends backwards to that his back is in lordosis. The clavicles are pro
jected above the apex of the lung, and in some cases opacities may be
come more visible and possible to localize (Fig. 2 a, b).
671
Figure 2.
Advantages o f a "lordotic view"
a) PA view o f chest shows an
opacity projected over first
right rib (arrow)
b) Lordotic view shows that the
opacity is completely
extrathoracic, and caused by
an osteochondroma arising
from the transverse process
o f the 7th cervical vertebra.
Fluoroscopy is used to localize and adjust special projections in order

to depict uncertain opacities. It may also be useful for assessing the mo
bility of the diaphragm. Paresis of the phrenic nerve causes the dome of
the affected side of the diaphragm to be elevated. When the patient sniffs
deeply through the nose with the mouth closed, fluoroscopy demonstrates
descent of the diaphragm on the normal side. On the affected side, in
creased intra-abdominal pressure causes the relaxed, paretic hemidi-
aphragm to display rapid upward or inverse movement as proof of
phrenic nerve paralysis. Paralysis of the phrenic nerve may be a sign of
tumor invasion of the mediastinum.
672
Tomography involves sectional imaging. In conventional tomography,

the tube and film are moved in a pendular fashion during exposure. This
technique provides a sectional picture where the contours situated in the
plane of the axis of movement are in focus. The localization and demar
cation of opacities are often shown more clearly on tomograms than on
standard radiographs, and the structures in the hilar regions and near the
mediastinum can often be analyzed better. The method has now been re-
Figure 3.
Bronchography
a) PA view, bronchial tree on right side
1. Main bronchus
2. Upper lobe bronchus
3. Stem bronchus
4. Middle lobe bronchus
5. Lower lobe bronchus
b) Lateral view, bronchial tree on right
side
6. Bronchus to superior (apical) segment
o f lower lobe
c) PA view, bronchial tree on left side
1. Main bronchus
2. Upper lobe bronchus
3. Lingula bronchus
4. Lower lobe bronchus
673
placed by computed tomography (CT).

Under ideal working conditions, the radiologist assesses the referral
note and the chest radiograph as soon as the films are developed, and
then makes a decision on whether supplementary films are necessary.
The simplest supplementary examinations are carried out before the pa
tient leaves the department. The patient may often provide additional
clinical information when the referral note is incomplete.
In digital radiography of the chest, the appropriate information appears
in digital electronic form and is displayed on a monitor. Shades of grey
can be adjusted on the monitor before it is transferred to film. Contrast
can be optimized for lung tissue, the mediastinum, or the skeleton. This
technique is particularly useful in bedside postoperative films to ’’save"
an incorrectly exposed film, and to obtain comparable exposures from
day to day.
Bronchography
For this procedure, local anaesthesia is given by inhalator, after which a
soft catheter is passed into the main bronchus on the side to be exam
ined. Fluoroscopy is used for guidance, both at the level of the larynx
and at the level of the carina. The bronchial tree is made visible by ad
ministering an iodized contrast medium in aqueous suspension, which
lines the walls of the bronchial branches (Fig. 3 a-c).
The main indications are the demonstration of bronchiectasis,
bronchial anomalies, and occasionally a fistula communicating with the
pleural cavity.
Because of the use of bronchoscopy and/or high resolution CT, the use
of bronchography has greatly diminished.
Angiography
Pulmonary angiography is used to demonstrate the pulmonary arteries
and veins (Fig. 4). Using fluoroscopic guidance, ECG and pressure mon
itoring, a catheter is passed into the pulmonary artery. After injection of
contrast medium, a series of film sequences are acquired to follow the
passage of the contrast bolus through the pulmonary circulation. The
main indications are suspected pulmonary embolism, vascular anom
alies, or malformations.
The trachea and bronchi receive their nourishment via the bronchial
arteries which originate from the upper part of the descending aorta. In
674
Figure 4.
Pulmonary angiography.
Normal finding. Subtraction
film.
chronic haemoptysis it may be necessary to examine the vessels sup

plying the bronchi using bronchial arteriography. Occlusion of the bleed
ing vessels via the catheter may be carried out.
Computed tomography (CT)

The advantage of CT is that sectional imaging of high quality in the trans
verse plane is made possible, using a method that is simple and without
discomfort. CT has better contrast resolution than conventional tech
niques, and the organ structures in the mediastinum are clearly demar
cated. Measurement of attenuation values sometimes permits character
ization of tissues (fat, clear fluid, etc). It is often necessary to visualize
the vascular structures in the mediastinum. The CT sections are then ex
posed immediately after the injection of a contrast bolus into a vein in
the forearm.
The good contrast resolution increases the possibility of demonstrat
ing small round shadows in the lungs, for example in patients with pre
sumed solitary metastases where thoracotomy is being considered. CT
has to a large extent replaced conventional tomography, for example in
staging lung cancer. By using a special computer program (high resolu
tion CT), a detailed representation of pulmonary infiltrates and diffuse
conditions of the parenchyma can be obtained. CT is also valuable for
demonstrating localised fluid or air-filled cavities, and for defining dis
eases of the thoracic wall.
CT sections are also of great value for assessing the depth of lesions
prior to needle biopsy and for adjustment of external radiotherapy.
675
Figure 5.
Bronchial carcinoma right up
per lobe.
a) Chest x-ray shows a large,
well-defined expansive
process in right apex.
b) T1-weighted MR image
(coronal section) shows
growth into the chest wall
between the ribs, and into the
mediastinum where air chan
nels and vascular structures
appear as signal-free struc
tures.
Magnetic resonance imaging (MRI)

This technique is used in selected cases where conventional chest radio
graph combined with CT has not been sufficient to make a diagnosis.
The advantage of MRI is the possibility o f making sections in the coro
nal and sagittal planes in addition to the transverse plane. MRI provides
excellent definition of the mediastinal structures, as the high signal of
mediastinal fat on T1-weighted images provides good contrast.
Moreover, the low or absent signal of vascular structures and airways
permits discrimination of these structures without the need for contrast
media (Fig. 5 a, b). MRI is of special value if expansive lesions in the
mediastinum and hilar region are suspected, and in the case of occlusion
or aneurysm of mediastinal vessels. MRI is of little value for assessment
of details in lung parenchyma, and calcifications in the pleura, lung, and
hilar regions will generally not be visible.
676
Figure 6.
a) ECG gated spin echo
MR image in the
transcaial plane demon
strates an aneurysm o f
the sinuses o f Valsalva
in a patient with
Marfan's syndrome.
b) ECG gated spin echo
MR image in the coro
nal plane demonstrates
an aneurysm o f the as
cending aorta in a pa
tient with Marfan's syn
drome.
MRI has now been available for more than ten years, but its clinical
role in the thorax is still evolving. Moreover, the indication for prefer
ential use of MRI rather than CT remains controversial. MRI can be con
sidered comparable or preferable to CT for the following indications:
1. Thoracic aortic disease including aortic dissection and aneurysm

(Fig. 6)
2. Thoracic venous disease including superior vena caval syndrome
(Fig. 7), and suspected brachiocephalic venous occlusions
3. Pulmonary arterial diseases such as pulmonary arteriovenous mal
formation
4. Staging of lung cancer for specific questions such as chest wall inva
sion (Fig. 8), superior sulcus tumors (Fig. 9), invasion of the peri
cardium and cardiovascular structures (Fig. 10), differentiation o f re
current tumor vs fibrosis after surgery or radiation therapy
5. Staging and post therapy follow-up of lymphoma
677
Figure 8. ECG gated spin echo images

with T1-weighting (a), T2-weighting (b),
and T1 -weighting after administration o f
gadodiamide injection (Omniscan) (c).
After contrast enhancement the sites o f
chest wall invasion (arrows) are clearly
defined. Chest wall invasion is also evi
с dent on the T2-weighted images because
o f the increased signal intensity o f the
chest wall muscles. Central low intensity
region is tumor necrosis.
Figure 9. ECG gated spin echo image in the

sagittal plane shows extension o f a Pancoast
(superior sulcus) tumor into the neck and en
casement o f subclavian artery and adjacent
brachial plexus.
678
Figure 10.
ECG gated spin echo image in
the coronal plane demonstrates
inoperability o f lung cancer
due to encasement and inva
sion o f the posterior portion o f
the aortic arch.
Figure 11.
a/ ECG gated spin echo image
in the transaxial plane
shows a paracardiac mass
(lymphoma). The mass is
separated from the cardiac
structures by the low
intensity pericardial line,
b/ ECG gated spin echo image
in the transaxial plane
shows a paracardiac mass
invading the right and left
atrial walls.
6. Evaluation of brachial plexopathy

7. Mediastinal masses, especially paracardiac masses (Fig. 11) and pos
terior mediastinal masses with possible intraspinal extension
8. Inconclusive CT scan, which is usually caused by inadequate vascu
lar opacification or contraindications to the use of iodinated contrast
media
A variety of MRI techniques are applicable in the assessment of thoracic

diseases. Most MRI studies of the thorax require the use of prospective
or retrospective electrocardiographic (ECG) gating. ECG gated T l-
weighted spin echo images are used to evaluate both vascular and non-
vascular pathology. MR contrast medium, gadolinium chelates, can be
used to increase the signal of lung and mediastinal lesions. The gradient
echo technique shows bright signal of the blood pool; consequently, this
technique is frequently used to evaluate vascular abnormalities (Fig. 7).
Ultrasound (ultrasonography)
Since ultrasound waves do not penetrate through aerated alveoli, the use
of ultrasound in the diagnosis of disease o f the chest is confined mostly
to assessment of the heart by echocardiography (which is usually per
formed in the cardiology department), pleural effusion and specific parts
of the mediastinum.
Pleural fluid can become loculated. This makes the drainage of fluid
difficult. Demonstration of the loculation(s) using ultrasound facilitates
drainage with a minimum of punctures. Samples of tissue may also be
collected through ultrasonographically guided needle punctures.
Isotope scanning
Radioactive isotope scanning is frequently used for the evaluation of sus
pected pulmonary embolism.
An intravenous injection of radioactive particles is administered for
perfusion scintigraphy. The size of these particles is such that they are
’’trapped" by the pulmonary capillaries. A scan is acquired of the iso
tope-containing lungs using a gamma camera. The areas of perfused
lungs emit radiation. Areas that emit relatively less or no radiation are
considered to be underperfused or nonperfused.
Reduced radioactivity may be due to pulmonary embolism, but also
to other conditions, such as interlobar pleural fluid, emphysematous bul-
680
lae, pneumonia, etc. In order to distinguish embolism from other condi

tions with reduced perfusion, ventilation scintigraphy is also performed.
During this procedure, a radioactive gas, such as xenon-133, is inhaled.
In the presence of embolism (unlike the other conditions entailing re
duced perfusion mentioned above), ventilation of the effected areas will
usually be maintained. A combination of reduced perfusion and normal
ventilation is an indication of the presence of embolism.
NORMAL ANATOMY AND VARIATIONS
Chest wall
The chest wall is made up of the thoracic skeleton and the surrounding
soft tissues. The shape of the thorax varies considerably, from the very
tall, thin individuals, on whom a superficial glance at the frontal view
may lead one to suspect hyperinflation, to short individuals with a large
anteroposterior diameter and an almost barrel-shaped chest in the lateral
view. The clavicles appear symmetrically on either side of the mid-line.
This is an important observation, as asymmetry indicates inadvertent
oblique positioning. In such slightly oblique films, the ascending aorta
and the manubrium stemi may emerge from the medastinal shadow and
give rise to misinterpretations. The medial epiphysis of the clavicle does
not ossify before adulthood, and the epiphysis should not be confused
with a lung opacity. There is a hollow (rhomboid fossa) on the lower side
of the medial end of the clavicle. This can sometimes be so deep and ob
vious that it is confused with a pathological erosion.
681
Figure 13.
Bilateral cervical ribs
(arrows).
It is important to be familiar with the appearance of the ribs, and to be

able to follow the rib from behind - where they are horizontal or slightly
sloping - forwards to where they turn medially and caudally. Medially,
they become cartilaginous and are then not visible on the radiograph un
less calcified. Calcification may be distributed in patches, and be con
fused with calcifications of the kidney or gallbladder by inexperienced
observers. The arrangement and direction of the longest axis of the cal
cifications are usually such that it is normally not necessary to take
oblique pictures to verify (Fig. 12).
Anomalies of the ribs in the form of bridge formation between two ad
jacent ribs or Y-shaped division of a rib in the front (bifid rib) may oc
cur and be confused with a lung opacity. Cervical ribs usually articulate
with the 7th cervical vertebra (Fig. 13). They appear as tap-shaped out
growths, which point caudally over the apex of the lung.
Frontal views of the thorax are exposed with the back of the hand
placed on the iliac crest and the elbows pushed forward in order to lat
erally rotate the shadow of the scapula. With insufficient rotation, the
lower comer of the scapula will be projected over the lateral segments
of the lung, and may be confused with a pleural lesion.
O f the soft tissue structures of the chest wall, breasts produce the most
obvious shadows. Large breast shadows may cause insufficient exposure
of the underlying parenchyma. After unilateral resection of a breast, the
underlying lung area will be more translucent, and this should not be mis
interpreted as a pathological condition. In the absence of one breast
shadow, the ribs and lungs should be scrutinized for metastases.
682
The nipple of the breast may be confused with a round basal shadow
in the lung. This is generally no problem as both nipples are seen sym
metrically on either side of the midline in the frontal view, while no
shadow at the corresponding level is seen in the lateral view. The lateral
border of the shadow of the nipples is often more distinct than the me
dial border. Other soft tissue structures that can be identified in frontal
views are the lower part of the sternocleidomastoid and pectoral mus
cles. Misinterpretations may occur when the pectoral muscles have been
removed operatively or are atrophic (for example after poliomyelitis),
and the underlying lung may be regarded as emphysematous, or it is
thought that the contralateral lung has increased opacity.
Pleura
The parietal pleura lines the inner side of the thoracic cavity and the lat
eral side of the mediastinum without passing into the normal lung fis
sures (Fig. 14). Around the structures in the hilar region, it crosses to
cover the medial surface of the lung and continues as visceral pleura on
the surface of the lobes o f the lung. The pleural cavity is located between
the two layers of the pleura, and normally surrounds the whole lung ex
pect the hilar region. In some cases, a fold of the pleura extends from the
hilar region to the diaphragm, forming a ligament that obstructs direct
continuity medially between the front and back of the pleural space. This
ligament, the pulmonary ligament, may form a small tent-shaped trian
gular opacity extending from the hilum toward the dome of the di
aphragm, which may be confused radiologically with adhesion between
683
Figure 15.
The rounded, smooth bor
dered prominence in the
right tracheobronchial an
gle (v.a) is caused by a di
lated azygos vein. The p a
tient had occlusion o f the
inferior vena cava and col
lateral circulation to the
azygos vein.
the two layers of pleura. Unlike the parietal pleura, the visceral pleura
follows the surface of the lobes of the lungs into the fissures.
The fissure between the upper and lower lobe (major interlobar fis
sure) is found bilaterally. On the right side, an additional fissure, the mi
nor interlobar fissure, between the middle and upper lobes is also pre
sent. This is the only fissure visible in the frontal plane, while the fis
sures between the upper and lower lobes are projected over each other
in lateral views. The CT scan shows the major interlobar fissure on both
sides.
The fissures may be incomplete, and accessory lobes and fissures may
occur. A fissure consists of two layers of pleura with a potential cleft be
tween them.
A special anomaly found in almost 1% of the population is the azy
gos lobe (Figs. 12, 14). This is due to an abnormal course of the azygos
vein. Normally, this vein runs up along the vertebral column and turns
forwards in the mediastinum to open into the anteriorly situated superior
vena cava at the level of the tracheo-bronchial angle (Fig. 15). When the
anomaly is present, the veins run more laterally and curves forwards. It
makes a deep groove in the right apex. On the medial side of the groove,
one gets the impression of an extra lobe of the lung, and its fissure is es
pecially prominent because it consists of four layers of pleura, since the
vein lies outside the pleura throughout its whole course (Fig. 14). At the
transition between the diaphragm and the chest wall, the layers of the
pleura form a very acute angle, the costophrenic angle. Posteriorly, it ex
tends in a caudal direction; this anatomic feature may explain that a metal
684
Figure 16. Lobes and segments o f the lungs.
clip, lost during thoracotomy may appear on a frontal radiograph of the

abdomen just above the upper pole of the kidney.
Lungs
The lungs are divided into lobes, the lobes into segments, which in turn
consist of still smaller units, the so-called secondary lobules. The right
lung has three, and the left two lobes (Fig. 16). The right lower lobe has
five segments, the superior (apical) and four basal (anterior, posterior, me
dial, and lateral) segments. The left lower lobe lacks the medial segment.
Both upper lobes have three segments. The right has posterior, apical,
and anterior segments, while the left has apico-posterior, anterior, and lin
gular segments. The latter extends caudally and anteriorly, corresponding
685
Figure 17.
Visible lines between secondary
lobules in a patient with intersti
tial edema (Kerley's В lines).
to the position of the middle lobe on the right side.

The bronchial tree divides into bronchial branches to the lobes, and
these divide again forming a segmental bronchus to each segment. The
lingular bronchus originates from the left upper lobe bronchus (Fig. 16),
in agreement with the fact that the lingula is a segment of the upper lobe.
Infectious processes, for example lobar pneumonia, respect the anatom
ical boundaries between the lobes of the lung, but there are no corre
spondingly distinct anatomical boundaries between the segments. The
superior segments o f the lower lobes extend in a cranial direction poste
riorly, so that an opacity, which appears level with the manubrium stemi
in a frontal view, is not necessarily located in the upper lobe. Lateral
views are required to localize findings to the individual segments.
Secondary lobules are 1-2.5 cm large, and although their shape may
vary, they often appear to be pyramid-shaped with their base towards the
pleura, in the centre of the pyramid there is a terminal bronchiole that
supplies three to five acini with branches. Branches of the pulmonary
and bronchial arteries run along the bronchioles. The veins run in the in
terlobular septa between the individual lobules together with lymph ves
sels and strands of connective tissue. Neither the secondary lobules nor
the interlobular septa are seen in radiographs of normal patients. In pa
tients with venous congestion or lymphatic obstruction with accompa
nying interstitial edema, the septa become visible as thin, one or two cen
timeter long stripes perpendicular to the pleura, at the base of the lungs.
These are the Kerley В lines (Fig. 17), which may be due to venous con-
686
gestion, lymphatic obstruction, or in some cases of pneumoconiosis.

Normal aerated bronchi are not visible peripheral to the hilar area un
less the x-ray beam is parallel to them. They then sometimes appear as
ring-shaped structures.
The normal lung markings are chiefly due to blood in the arteries and
veins that ramify out towards the lung surface. The lung markings are
therefore pronounced when the vessels are distended. In the upright po
sition, the upper thirds of the lungs are relatively poorly perfused be
cause of low. pressure in the pulmonary arteries. The vessels in the up
per third therefore contain less blood than the vessels in the lower third,
and they seem to be narrower. This will change when lying down or in
the case of failure of the left side of the heart with pulmonary conges
tion. An increase in breadth and opacity of the vessel shadows in the up
per segments of the lungs may therefore be an important observation.
When considering lateral views, it is useful to note that there are nor
mally few soft tissue structures and therefore radiolucency of the film
behind the upper part of the sternum, where the mediastinum may con
sist of a very thin tissue lamella. Increased opacity here may be due to
expansive processes, a wide ascending aorta, or enlargement of the heart.
The soft tissue structures in the axillae and shoulder region make the
upper part of the thoracic column appear to be radiodense in lateral pic
tures. Normally, radiolucency over the thoracic vertebral column in a lat
eral view should gradually increase caudally. An opacity posteriorly in
the lower lobes can often be discovered because the radiolucency over
the lower part of the vertebral column diminishes (the column becomes
lighter).
Mediastinum
The mediastinum is the area lying between the medial parts of the right
and left pleura. The mediastinum is mobile from side to side, and ob
servation of mediastinal displacement and movement provides impor
tant diagnostic information about the nature of the disease process.
Normally, the lower part of the right mediastinal outline is made by the
right atrium. When this is not the case, but rather this outline is made by
the vertebral column, it is a sign of displacement of the heart and lower
part of the mediastinum to the left.
Above the hilar region, the right mediastinal outline is made by the su
perior vena cava and the brachiocephalic vessels (Fig. 18). Above the
687
left hilum, the upper mediastinal ouline is made by the arch of the aorta
and subclavian vessels. A right-sided aortic arch forms a prominence of
the upper right mediastinal outline. This may be misinterpreted as an ex
pansive process unless the absence of a normal aortic arch is recognized.
In patients whose thorax is very deep (and those with emphysema), the
anterior, upper mediastinum consists o f a tissue lamella so narrow that
the lungs almost meet in the mid-line. When this lamella is oriented sag-
itally (parallel to the x-ray beam) it forms a linear opacity in the mid-line
(anterior junction line) on the frontal film. Further posteriorly, the me
diastinum has narrow areas, for example under the arch of the azygos
vein, where the pleural cavity approximates the oesophaus (the azygo-
oesohpageal recess).
In the tracheo-bronchial angle on the right side, a circular shadow rep
resents the arch o f the azygos vein, lying parallel to the x-ray beam (in
the same way as the aortic arch on the left side). In the presence of ve
nous obstruction and collateral circulation through the azygos system,
the diameter of the azygos vein may increase. Close to the azygos arch,
there is an important lymph node, the azygos node. Like the other lymph
nodes in the mediastinum and hilum, this is only visible in standard ra
diographs when it is enlarged. The azygos node is the primary lymph
node in the spread o f lung cancer from the right lung and from the left
lower lobe. The corresponding node for spread from the left upper lobe
lies to the left in the mediastinum, under the arch of the aorta, with the
left pulmonary artery below it. The node lies close to the obliterated duc
tus arteriosus, and is therefore called the ’’ductus node". The area in which
it lies is called the "aortopulmonary window". In this area, relatively large
expansive processes may escape attention in standard chest radiographs,
while they are easily discovered by CT scan. CT scans disclose normal
mediastinal lymph nodes when there is sufficient mediastinal fat so that
the organs do not all coalesce. The mediastinal lymph nodes are divided
into the anterior, middle, and posterior nodes, with a series of subgroups.
If lymph node enlargement is suspected, one should systematically in
spect the fat spaces in front of and lateral to the trachea, in front of the
carina, below the carina (in the angle between the left and right main
bronchi), and in the aortopulmonary window. The normal size of the me
diastinal lymph nodes varies from one region to another, and there is no
set limit where all larger lymph nodes are pathological and all smaller
ones are normal.
688
The posterior part of the mediastinal shadow is made up of the tho

racic column and the paravertebral soft tissues. In a correctly exposed
frontal view of the thorax, it should be just possible to see the thoracic
vertebrae. A well penetrated view shows them better, and also shows two
accompanying soft tissue shadows along the left side (Fig. 19). The
shadow furthest to the left is the outline of the descending aorta. In older
people this will bulge slightly, with lateral convexity. The paravertebral
soft tissue stripe lies between this and the vertebral column, and repre
sents the medial part of the pleura behind the aorta. This is most often
only seen clearly on the left side, and has a straight course along the ver
tebral column. A number of pathological conditions may lead to a spin
dle-shaped swelling of the paravertebral soft tissue shadow.
The hilar shadows are chiefly made up of the pulmonary arteries and
veins (Fig. 18). The hilar shadow on the left side is a little higher than
on the right. Doubt can sometimes arise as to whether the hilar shadows
are enlarged or not, and in these cases it is useful to study the lateral
views as well.
689
690
Figure 21.
Significance o f good inspiration
when taking chest x-rays
a) Firstfilm. Large heart and basal
opacities?
b) New film after instruction on
inspiration. Normal findings.
Diaphragm a
The diaphragm originates from
the lumbar vertebrae posteri
orly with its two crurae (Fig.
20), from a ligament (arcus
tendinosus) between the verte
bral column and the lowest ribs,
from the ribs at the back and lat
erally, and from the sternum in
front. The fibers course upward
in an even curve towards the
central tendinous part, which
has openings for the esopha
gus, vena cava and aorta.
The level of the right dome of the diaphragm is usually somewhat
higher than the left, while the left has greatest mobility, about five to six
cm. On full inspiration, the upper part of the right dome of the diaphragm
is near the tip of the sixth rib at the front, and between the 10th and 11th
rib at the back.
It is important that the patients understand that they must breathe in
and hold their breath. What appear to be basal opacifites in the lung can
vanish on a repeat film obtained with full inspiration, shown by the po
sition of the domes of the diaphragm (Fig. 21a, b). The outline of the
lower side of the diaphragm is only shown when there is free intraperi-
toneal air providing contrast. The complete outline of the upper side of
the diaphragm is seen against the aerated lung tissue, except in the area
where the heart shadow lies in direct contact.
691
Figure 22.
Normal retrocrural space (R). The
space consists o f the posterior, infe
rior part o f the mediastinum and
contains fat, vessels, nerves, and
lymph nodes. Aorta (A). Diaphragm
(arrows).
The posterior parts of the domes of the diaphragm are only seen in a
lateral view. In lateral films of normal individuals, the outline o f the right
dome of the diaphragm can be followed forward to the chest wall, while
the left is obliterated in front because of contact with the heart shadow
(Fig. 18). The gastric air bubble may also help to identify the left from
the right diaphragmatic dome in the lateral view. A staircase-shaped di
aphragm in the lateral projection may be a normal variant. In such cases
the frontal view may show two outlines at different levels.
The crurae originate from the anterior part of the lumbar column as far
down as L3 on the right side and L2 on the left. In a CT section of the
abdomen, the crurae may be seen as oval prevertebral structures, which
can be confused with enlarged lymph nodes. In a CT section further cra-
nially, the upper parts of the crurae form a bowed structure over the aorta
at the thoracolumbar transition. In such sections, the other abdominal or
gans are seen in front of the diaphragm, and the retrocrural space, which
is the very lowest part of the chest cavity, is seen behind it (Fig. 22). This
space may contain pathologically enlarged lymph nodes that can only be
demonstrated by CT scan (or MRI).
692
Figure 23.
Bulging o f the right mediastinal
outline caused by kyphoscolio
sis. Note the short distance
between the ribs on the left,
large distance on the right side.
PATHOLOGY
Chest wall
Most of the pathological conditions here are due to diseases of the tho
racic cage. With deformities of the thorax such as kyphoscoliosis, the
scoliotic spine may give the impression of a large mediastinal mass (Fig.
23), until a penetrated flm shows the striped translucencies that repre
sent the intervertebral discs. At the same time, the intercostal spaces are
narrowed and ribs vertically oriented on the concave side, with widen
ing intercostal space and diverging ribs on the convex side. Similar
changes can be seen in healed pulmonary tuberculosis with massive
shrinking and volume reduction of the hemithorax on the affected side
with growth retardation. Thoracoplasty performed to eradicate tubercu
lous cavities in the apex of the lung may produce thoracic deformity due
to resection of four to six upper ribs.
A funnel-shaped sternum may be projected deep into the thorax in the
lateral view (Fig. 24), and the heart may be displaced to the left. A bowed,
forward bulging sternum may be seen with congenital heart diseases and
pulmonary emphysema. Aneurysms in the ascending aorta may cause
notching of the sternum.
Fractures are the most common cause of changes in the ribs. A very
recent fracture is often difficult to recognize unless the fragments are dis
located. It is usually unnecessary to verify clinically suspected fracture
693
Figure 24.
Lateral view o f patient with funnel
chest (pectus excavatum). The
sternum is projected over the heart
shadow.
of the ribs by radiography. If an accompanying pneumothorax is sus

pected, a radiograph is necessary. Rib fractures become readily visible
on healing, with callus formation; old healed rib fractures may be mis
interpreted as lung opacities by the inexperienced observer. Rib de
struction may be recognized as indicative of metastases to the thoracic
cage or direct invasion of the chest wall by intrathoracic neoplasms. The
bone structure may have vanished along part of the course of the rib.
Destruction of ribs can easily be overlooked unless each rib is system
atically evaluated from the back to front, comparing the two sides.
Rib notching consists of small depressions of the lower edges of the
ribs. They are usually caused by pressure from dilated pulsating inter
costal arteries in coarctation of the aorta. The narrowed section of the
aorta is located below the origin of the left subclavian artery. In order to
preserve the blood supply to the descending aorta, collateral circulation
develops through branches of the subclavian arteries, the internal mam
mary arteries with blood flowing retrograde through the intercostal ar
teries to the descending aorta. Multiple neurinomas in the intercostal
nerves (neurofibromatosis) can also cause rib notching. Patients with
694
pain in the front of the chest wall, costochondral osteochondritis (Tietze

syndrome), usually have no radiological changes.
After dissection of lymph nodes or other extensive surgery in the neck,
caudal displacement of the lateral clavicle and so-called "hanging shoul
der" may be observed. This is due to a paresis of the trapezius muscle
because of damage to the 11th cranial nerve (accessory nerve).
Diaphragm
The position of the diaphragm varies considerably with the phase of res
piration, and also from one individual to the next. In children and pa
tients who have a deep thorax, or are overweight, the level of the di
aphragm is higher than in tall thin individuals. The diaphragm is also
higher on films taken with the patient supine or in lateral decubitus.
Table 1. Causes o f elevation o f both domes o f the diaphragm

- Incomplete inspiration (Fig. 21)
- Overweight
- Pregnancy
- Ascites
- Meteorism
- Large abdominal tumor
- Hepatosplenomegaly
- Bilateral subphrenic abscesses
- Bilateral reduction in volume of basal parts of the lungs
Table 2. Causes o f elevation o f one dome o f the diaphragam

- Deformity of the thorax with scoliosis
- Volume loss of one lung
- Pulmonary embolism or atelectasis
- Paresis of the phrenic nerve
- Subphrenic abscess
- Subphrenic tumor
Volume loss of the lung produces elevation of the diaphragm, causing a

triangular shape of the dome, as though it had been pulled up by a fibrous
cord. Phrenic paresis is discovered by observation of inverse mobility
during fluoroscopy.
695
Figure 25.
Kyphoscoliosis and hiatus hernia.
a) Wide lower mediastinal shadow
because o f scoliosis. Fluid level
projected over the heart
shadow.
b) Lateral view with contrast in
the esophagus and cardiac part
o f the stomach. The flu id level is
behind the heart, and is caused
by herniation o f the body o f the
stomach (paraoesophageal
hernia).
The diaphragm has several weak points that may give rise to hernias.
The most frequent is hiatal hernia through the oesophageal hiatus (Fig.
25 a, b). Parts of the stomach herniate up into the chest cavity. This con
dition is suspected when a frontal view shows a horizontal line (fluid
level) projected over the cardiac shadow. The diagnosis is confirmed by
finding an air-filled cavity behind the cardiac shadow on the lateral film.
For further confirmation, a barium swallow can be done.
696
Figure 26.
Rounded opacity in the right
cardiodiaphragmatic angle. Air-
filled haustra (arrows) in the
opacity. Morgagni hernia
containing omentum and a loop
o f the colon.
Hernia can also arise between the diaphragmatic fibers that originate
from the sternum and those originating from the ribs. These may contain
omentum, and give rise to a well-defined, upwards convex opacity be
side the heart. The differential diagnosis is between a cardiophrenic fat
pad, which is a normal variant of no pathological significance, and a peri
cardial cyst. An air-bubble indicates herniated intestine in addition to
omentum, and this can be verified by barium enema, or possibly a bar
ium swallow. Anterior hernias of this type are called Morgagni hernias
(Fig. 26).
Posterior hernias (Bochdalek hernias) are seen as a localized, upward
convex, rounded swelling of the diaphragm, paravertebrally. The open
ing is situated between the fibres of the diaphragm that originate from
the tendinous arch over the psoas and quadratus lumborum muscles, and
the fibres originating from the ribs posteriorly. This type of hernia usu
ally contains retroperitoneal fat, but the upper pole of the kidney, the
adrenal gland, and parts of the liver can also herniate. Sometimes it may
be difficult to decide whether there is in fact a hernia, or whether there
is only a localized relaxation of the diaphragm, an eventration. This is a
congenital condition where parts or most of the diaphragm lack muscu
lature and only consist of a thin membranous sheet.
With rupture of the diaphragm, which most often involves the left
dome, the contents of the abdomen, often the stomach, herniate up into
the chest cavity. When the body and antrum of the stomach herniate, the
greater curvature will lie with its convexity upwards, and obstruction
697
with distention may occur, so that the herniated greater curvature is con
fused with the dome of the diaphragm, and the rupture may be over
looked. A barium swallow can confirm the diagnosis because the cardiac
part of the stomach does not usually herniate, and the outline o f the edge
of the hernia can be seen against the stomach. A CT scan may also con
tribute to a correct diagnosis.
Pleural lesions
The pleural membranes produce pleural fluid, which is resorbed through
lymph channels in both layers. Increased production or diminished re
sorption leads to pathological accumulation of fluid in the pleural cavity.
The pleural fluid may consist of clear transudate, serofibrinous exudate,
blood or haemorrhagic effusion, or chylous exudate. With plain chest ra
diographs it is not possible to differentiate between the different types of
pleural fluid. Pleurocentesis can be performed under guidance of imag
ing techniques. Pleural transudate is clear, yellow, and usually bilateral.
The commonest cause of transudate is cardiac failure. Other causes may
be chronic renal failure, hypoproteinaemia, or over-transfusion.
Exudates may be yellow-brown or purulent, and are caused by tuber
culosis or other pulmonary or pleural infections, or by a subphrenic ab
scess. Other causes are lung cancer and systemic connective tissue dis
eases such as lupus erythematosus or rheumatoid arthritis. Blood in the
pleural cavity can be caused by open or closed thoracic trauma, or haem
orrhagic diseases with prolonged bleeding time. Blood-coloured pleural
fluid may be found with pulmonary embolism and lung cancer.
Chylothorax may be seen after thoracic trauma, or with obstruction of
the thoracic duct or the bronchomediastinal lymph trunks because of ma
lignant disease of infective conditions (filariasis).
In the upright position, small amounts of fluid will accumulate in the
costophrenic angle, first posteriorly, then also laterally. The acute angle
between the diaphragm and the chest wall is filled by an opacity, which,
as the volume of fluid increases, gradually stretches up along the inside
of the chest wall like a cloak (Fig. 27).
If one is uncertain whether there is fluid or only the remains of previ
ous pleural pathology with pleural thickening, the diagnosis can be ver
ified by taking a supplementary film. This is acquired with the patient in
lateral decubitus position with the affected side down, and a horizontal
x-ray beam (Fig. 28). Even small amounts of fluid drain by gravity along
698
Sinus not free- Loteral decubitus view with patient lying

pleural fluid on right side shows free pleural fluid
Figure 28. Standing and lateral decubitus views o f the thorax.
the dependent chest wall and collect as a narrow band between the lat
eral chest wall and the lung. The breadth of the band of fluid increases
when the film is exposed with the diaphragm elevated, i.e. on expiration.
Pleural thickening may also give a band-shaped opacity in a lateral de
cubitus film, but the breadth of this opacity will be the same whether the
patient is upright or lying down.
Large volumes of fluid may give massive opacities over the entire
hemithorax, but usually some aerated lung tissue is visible at the apex.
When this condition is unilateral, the mediastinum will be displaced to
wards the normal side, a sign that is useful in differentiating this opac
ity from that seen in total collapse of the lung (atelectasis) (Fig. 29 a, b).
699
A) Greater than normal proportion o f the heart shadow is located to the right o f the
vertebral column. Slight rightward displacement o f the trachea. These findings indi
cate a left-sided expansion, as caused by a large left pleural effusion.
B) The vertebral column is seen more clearly than normal along the right border o f the
mediastinum. The trachea is shifted to the left. This indicates left-sided reduction o f
volume, caused by atelectasis.
With total collapse, the mediastinum will be pulled towards the involved
side. In the presence o f bronchial cancer and simultaneous total collapse
of the lung and large amounts of pleural fluid, the mediastinum may re
main in the midline.
Sometimes pleural fluid may have a subpulmonary localization on up
right films. On the left side this condition is readily recognized because
of the increased distance between air in the stomach and the base of the
lung. On the right side, the condition can be confused with an elevated
diaphragm, as the upper surface of the accumulated fluid is misinter
preted as the diaphragm. Usually, the costophrenic angle will be rather
round laterally and posteriorly and a lateral decubitus film may disclose
large volumes of fluid.
The pleural fluid may also be loculated in closed pockets (loculi),
which are formed by adhesions between the visceral and parietal pleura.
Encapsulated fluid of this kind will not float freely on lateral decubitus
films; consequently the diagnosis of fluid must be verified by CT scan
or ultrasound. Thoracocentesis of loculated fluid can be guided by ul
trasonography. Free pleural fluid flows into the fissures (Fig. 27) as a
wedge-shaped opacity with the pointed end towards the hilum and the
base peripherally. Encapsulated interlobar fluid also occurs. It usually
assumes a biconvex lens shape using a tangential x-ray beam, but it may
also be globular and be confused with a tumor. As the fluid is gradually
700
Figure 30.
Empyema
a) The right sinus is filled by an
opacity that extends upward along
the chest wall, and has an upward
convex border.
b) CT section at the thoracoabdomi
nal transition showing right-sided
empyema with gas bubbles.
resorbed and the appearance returns to normal, this type of interlobar

fluid has been called a "vanishing tumor".
In active infection with production of a large amount of pus, the pleural
fluid not only flows passively up along the chest wall with a medially
concave border, but may also bulge in towards the lung with a medially
convex border (Figs. 27, 30 a, b). This leads one to suspect empyema,
which may develop in connection with pneumonia or pulmonary abscess.
The empyema can break through the visceral pleura to communicate
with aerated lung tissue and the bronchial tree. Communication like this
may also occur when an infection in the lung breaks through the pleura
from the lung side. The radiograph raises the suspicion of the presence
of this type of bronchopleural fistula when air enters a fluid-containing
701
Pleural fluid Adhesion
Figure 31. Development o f pleural adhesions
pleural cavity, giving fluid levels in upright films, and the air is not re
sorbed but increases with time. When the empyema and fistula heal, a
thickened pleura remains with adhesions, which may cause traction upon
the heart and mediastinum. The diaphragm may be tethered upward and
attached to the chest wall, with loss of diaphragmatic motion. Pleural
thickening is often caused by infections and is an accompanying phe
nomenon in pulmonary tuberculosis. The thickening is often seen at the
base, combined with adhesions in the costophrenic angle, which becomes
shallow and right-angled (Fig. 31). The thickening can also be observed
at the inferior extent of the fissures, where it produces linear thickening
of the interlobar fissure. Tent-shaped basal opacities may represent
pleural adhesions after earlier pleurisy. Above the apex of the lung, lo
calized pleural thickening may occur, producing a downwardly concave
half-moon-shaped opacity.
After tuberculous pleurisy, and after bleeding in the chest cavity, large
calcified pleural plaques may be formed. In pneumoconioses such as as-
bestosis, pleural thickening is also a common phenomenon, and thin,
well-defined stripes of calcium in the basal part of the chest wall along
the dome of the diaphragm may also be found. Calcification and pleural
thickening of this kind are best seen in the tangential projection, and ra
diographs of the lung may be supplemented by oblique films with this
type of problem. The optimal method for displaying pleural plaques and
calcification is by CT.
702
Figure 32.
Pneumothorax. A 2-3 cm broad air
cap has developed after fine needle
puncture o f tumor (T). The arrows
show the surface o f the lung.
Extensive nodular pleural thickening is seen with mesothelioma, a ma

lignant pleural tumor which occurs in connection with long-lasting ex
posure to asbestos. Mesothelioma often gives rise to hemorrhagic pleural
fluid, which can mask the pleural tumor. Air in the pleural cavity, pneu
mothorax (Fig. 32), may arise spontaneously, as a result of rupture of
small subpleural emphysematous cysts or larger emphysematous bullae.
Air in the pleural cavity will usually be seen as a narrow, dark zone with
no vascular markings along the chest wall. In check valve pneumotho
rax, pressure in the pleural cavity progressively increases, causing pro
gressive collapse of the lung with contralateral mediastinal shift.
When there are adhesions, the air may be confined to encapsulated lo-
culi, and the adhesions may partly or completely prevent collapse o f the
lung. CT is very useful for localizing small bullae and limited pneu
mothorax. Pneumothorax may also occur as a result of penetration o f the
chest wall, for example during tapping of pleural fluid, or after needle
biopsy of lung tumors. Damage to air-filled organs in the mediastinum,
703
Figure 33.
Stripe along the lateral chest
wall (arrows) resembles pneu
mothorax, but some scanty vas
cular markings are seen periph
eral to the stripe. Repeat x-ray
after change in position showed
normalfindings. The stripe had
been caused by a skin fold.
or damage to the diaphragm combined with rupture of part of the in

testinal tract may also give rise to pneumothorax.
A very large emphysema bulla, which takes up most of the chest cav
ity, may be confused with a pneumothorax. Puncture of this type of bulla
in order to drain it may give the patient a true pneumothorax. A small
rim of air around the lung may be difficult to discover, especially in over
exposed (dark) film. Expiratory films are taken routinely when pneu
mothorax is suspected.
In bedridden patients, who have lost weight in connection with their
disease, skin folds that run parallel to the chest wall may easily be con
fused with pneumothorax (Fig. 33). By examining the film in bright light,
it is possible to trace vascular patterns peripherally to the line caused by
the skin fold, or to see that the skin fold extends outside the thorax. When
in doubt, a repeat film should be performed as the lines formed by the
skin folds are not reproduced after the patient has changed position.
Most cases of pneumothorax show spontaneous regression, but the pa
tients must be checked clinically and radiologically so that a thoracic
tube with suction can be introduced if the condition progresses because
of a check valve mechanism, or if spontaneous improvement does not
occur. In pneumothorax in a patient with pleural fluid, upright films will
show a horizontal fluid level, as a sign of hydropneumothorax. When the
lung is adherent to the chest wall laterally, a fluid level may be the sign
that discloses the presence of pneumothorax (Fig. 34).
704
Figure 34.
Horizontal fluid level in the
right thoracic cavity (open
arrow) shows that both pleural
fluid and pneumothorax
(hydropneumothorax) must be
present. The mediastinum is
pulled to the right because o f
atelectasis o f the lower lobe.
Pericardial calcification
(closed arrow) after
pericarditis.
Figure 35.
A mass anteriorly and cranially in the
mediastinum caused by calcified ret
rosternal goiter (s).
Mediastinal lesions
A lateral view can be used to localize to the anterior, superior or middle
mediastinum a mass observed on the frontal view. The anterior medi
astinum consists of the retrosternal space and the heart, the middle con
sists of the structures along the trachea, esophagus, and between the hi
lar shadows, while the posterior includes the areas on both sides of the
thoracic column.
Anterior mediastinal masses may be caused by retrosternal goitre (Fig.
35), tumor/cyst in the thymus (Fig. 36 a - c), dermoid cyst, and other
705
Figure 36.
Thymoma (T) in the anterior mediastinum.
a) PA view
b) Lateral view
c) The CT section shows the thymoma with
peripheral calcification. It is close to
the ascending aorta (A). Pulmonary
artery (P). Vertebral column (C).
Figure 37.
Malignant thyroid tumor with pulmonary
metastases. Compression o f the trachea
from the left (arrows). Bilateral pulmonary
metastases.
Figure 38.
Mass (T) in the middle, lower part o f the
mediastinum, behind the heart shadow.
Picture after oral contrast medium
showed oesohageal cancer.
germinal tunors. Goitre usually causes deviation and compression of the

trachea (Fig. 37). The thymus is examined in patients with myasthenia
gravis. Other possible masses are lymphoma, aneurysm of the ascend
ing aorta, and tumors arising from the sternum and underlying soft tis
sues. Near the diaphragm, anterior mediastinal masses are usually peri
cardial fat pad, pericardial cyst or anterior diaphragmatic (Morgagni)
hernia (Fig. 25). Masses in the right cardiophrenic angle are common,
but are seldom of clinical significance.
Masses localized to the middle mediastinum (Fig. 38) are most fre
quently aneurysms of the aortic arch, bronchogenic cysts, lesions of the
oesophagus and enlarged lymph nodes. Contrast medium in the oesoph
agus may contribute to the correct diagnosis.
Posterior mediastinal masses are frequently neurogenic tumors, which
may extend into or originate from the spinal canal. Spindle-shaped en
largement of the paravertebral soft tissue shadow may be due to spondyli
tis and hematomas subsequent to fractures of the vertebral column.
Metastases to the vertebral column with bone destruction may also lead
to swelling of the soft tissue shadow, which may also be caused by en
largement of paravertebral lymph nodes. Expansive processes in the
lungs and pleura may be adjacent to the paravertebral soft tissues and re
semble mediastinal masses.
707
Figure 39.
Pneumomediastinum. Stripes o f
air (arrows) along the outlines o f
the heart and mediastinum and
up on the right side o f the neck.
Tracheal tube and feeding tube.
Thorax drain on right side.
CT scans can precisely define the location o f mediastinal masses and

their effect on normal structures; consequently, CT scans are usually
done for the evaluation of mediastinal masses. Likewise, MRI can pro
vide the same information and in some cases, better characterize the na
ture of the mass. MRI is favored in the evaluation of mediastinal masses
in some circumstances, especially when a vascular mass is suspected
(Fig. 6). MRI is also favored for the evaluation of paracardiac masses
(Fig. 11) and posterior mediastinal masses.
Damage of aerated organs in the neck or in the medastinum may give
rise to mediastinal emphysema, with striped air loculi in the mediastinum
(Fig. 39), which often spreads into the soft tissues of the neck and the
chest wall.
Mediastinitis may arise after perforation of the esophagus or thoraco
tomy and may also cause an increase in width of the mediastinum, or be
localized as a mediastinal abscess. It is generally accompanied by bilat
eral pleural fluid. After radiotherapy of the mediastinum, fibrosis caused
by the radiation in the lung adjacent to the mediastinum may lead to a
straight lateral border, corresponding to the limit of the field (Fig. 40).
Mediastinal fibrosis may give rise to shrinking and narrowing of the me
diastinal vessels and the development of venous collaterals. MRI or mag
netic resonance angiography is now usually employed for the definitive
diagnosis of obstruction, occlusion or thrombosis of the brachiocephalic
veins and superior vena cava (Fig. 7).
708
Figure 40.
Linear border o f the right medi
astinal outline and fan-shaped
opacity in the right apex caused
by radiation fibrosis after radio
therapy fo r breast cancer.
Hilar enlargement
The hilar shadows are made up of the pulmonary vessels. When these
are enlarged, it is necessary to decide whether the enlargement is due to
dilated vessels, or enlarged lymph nodes or other masses. Bilateral en
larged hilar shadows, which seem to ramify, suggest dilated pulmonary
vessels. Conditions that give rise to this include pulmonary hyperten
sion, chronic embolism, excessive pulmonary blood flow such as with
left-to-right shunts, anemia, and pregnancy, or post-stenotic dilatation
associated with pulmonary arterial stenosis.
Enlargement of the hilar shadows without branching suggests a non-
vascular nature. A polycyclic border (Fig. 41 a, b) is characteristic of en
larged hilar lymph nodes. With bilateral enlargement of hilar nodes, the
most important differential diagnoses are sarcoidosis and lymphoma.
With unilateral enlargement, the most important differential diagnoses
are metastases from lung cancer, malignant lymphoma, and infections
such as tuberculosis or histoplasmosis. The radiological finding in lung
carcinoma may be the same as that in unilateral hilar expansion.
709
Figure 41.
Hilar gland enlargement in sar
coidosis.
a) PA view. Lobulated border o f
left-sided hilar enlargement (ar
rows).
b) Lateral view shows the changes
more clearly (arrows)
Respiratory diseases and emphysema
Asthma
In bronchial asthma, radiographs of the lungs are often completely nor
mal. There are no specific radiological findings, and the object of radi
ography is partly to exclude other causes of breathing difficulties such
as pulmonary edema or tracheal obstruction, and partly to detect com
plications such as pneumothorax or atelectasis caused by mucus plugs.
710
Chronic bronchitis
Like asthma, chronic bronchitis is defined on the basis of the clinical pic
ture. Half the patients with chronic bronchitis have a normal radiograph,
and the changes that occur are caused by secondary conditions such as
pneumonia or emphysema. Striped or mottled opacities may be due to
scars after previous infections, possibly combined with fluid-filled
bronchiectatic cavities. Bronchography shows irregularities in the walls
and dilated openings from the mucous glands, and the bronchial tree has
fewer and coarser branches than normal.
Emphysema
Unlike asthma and chronic bronchitis, emphysema is defined in strict
morphological terms as a condition of the lung characterized by abnor
mal permanent enlargement of air spaces distal to bronchioles, accom
panied by destruction of their walls without obvious fibrosis. The defin
ition does not include any functional impairment or airway obstruction.
Thus, abnormal function tests or airway obstruction are not invariably
present in emphysema. Emphysema is a general pathological mechanism
with a multitude of causes and appearances. Imaging features correlate
well with microscopy using serial sections, less well with various func
tional parameters.
Classification
Emphysema may be pan-acinar with involvement of the whole acinus,
or it may be localized only in the central or only in the peripheral parts
of the acini (centrilobular and paraseptal emphysema).
Table 3. Classification o f emphysema
Type Clinical association

Panlobular a l antitrypsin deficiency
Centrilobular Smoking
Paraseptal Spontaneous pneumothorax
Irregular Paracicatrical, old adjacent scar, rarely symptomatic
711
Figure 42.
Emphysema
a) PA view
b) Lateral view
Scanty peripheral vascular shadows,

specially basally. Low level o f
diaphragm domes and increased
amount o f retrosternal aerated lung
tissue. Small heart shadow.
The chest film diagnosis of emphysema (Fig. 42) is based on:

1. Signs of hyperinflation (flat diaphragm, increased retrosternal space,
bullae, large chest cage), and
2. Vascular criteria (decreased peripheral vessels, narrowed midline ves
sels, local avascular areas, large pulmonary arteries)
The overall diagnostic accuracy is 65-80% depending on the clinical

material studied. The false negative rates are significant. The sensitivity
increases with increasing severity of emphysema in the population stud
ied. Specificity is relatively good with few false positives. These are due
712
Figure 43.
Child, suspected o f having aspirated
a foreign body. A foreign body
occludes the middle lobe bronchus,
causing atelectasis o f the middle
lobe. In addition there is a valvular
mechanism in the main bronchus
with hyperinflation o f the right lower
and upper lobes.
to misinterpretation of normal variation of vascularity, abnormalities of

the thoracic cage, asymmetry of thoracic soft tissues (mastectomy, mus
cular atrophy), or overexposed radiographs.
Emphysematous conditions may be associated with obstruction of air
ways (air trapping), e.g. in chronic bronchitis, foreign body (Fig. 43), or
congenital lobar emphysema. Emphysema without obstruction occurs
with pure destruction of lung tissue (for example centrilobular emphy
sema) or with compensatory emphysema, when, for example, a lobe of
the lung expands into the available space in the chest cavity after a lobec
tomy. Hyperinflation is a better term for air space expansions without
tissue destruction.
In about a third of the patients with extensive emphysema, aerated thin-
walled cavities or bullae are found. These may vary from less than one
to several centimetres in diameter, and sometimes expand to the extent
that one or a few bullae can occupy most of the chest cavity and com
press the remaining, healthy lung tissue (Fig. 44).
The cause of unilateral emphysema (MacLeod’s syndrome) is not
known. It is postulated that the condition is caused by an infective con
dition in childhood with involvement of small bronchi and bronchioles,
resulting in obstruction and dilatation of the peripheral air spaces. The
effected lung has a small artery, and both the arteries and bronchial tree
have fewer branches than normal. The lung is more radiolucent than the
contralateral lung and retains its volume during expiration.
713
Figure 44.
CT picture ofpatient with emphy
sema. Large, air-filled bullae. Note
that only the narrow "anterior
junction line" separates the two
lungs at the front.
Another cause o f unilateral emphysema is unilateral lung transplanta

tion in the treatment of emphysema. The remaining emphysematous lung
will push the mediastinum towards the transplanted lung.
With obstruction of a lobar bronchus in the newborn period, congen
ital lobar emphysema may occur that only involves one lobe. It is im
portant not to confuse this type of condition with compensatory emphy
sema due to atelectatis of the adjacent lobe of the lung.
Computed tomography (particularly high resolution CT) has proved
useful in the diagnosis of emphysema. The grading of emphysema is
done by:
- quantitative analysis, or
- visual grading
Quantitative analysis is based on density measurements with a variety
of density or pixel indices. With visual grading, emphasis is on non-pe-
ripheral, unmarginated low attenuation areas.
CT is superior to conventional radiography in detection, grading, and
characterization of emphysema and the inter-observer agreement is also
better. CT is useful in the detection of bullae and in the evaluation of in
dications for bullectomy.
Bronchiectasis
In healthy individuals, the bronchial tree has smooth walls and the cali
bre of the branches gradually decreases towards the periphery. In
bronchiectasis, an irreversible dilatation o f the bronchial branches oc
curs. This may be due to congenital or acquired weakness of the wall due
to infection with shrinking and pulling on the wall, or to chronic ob-
714
Figure 45.
Different types o f bronchiectasis.
1. normal bronchial tree;
2. cystic bronchiectasis
3. cylindrical bronchiectasis;
4. multiple successive dilatations
("varicose" bronchiectasis)
Figure 46.
Annular opacities at the base o f the
upper and lower lobes due to
bronchiectasis.
struction. There is often a combination of causes. Cylindrical bronchiec

tasis is present when a bronchial branch retains its calibre without nar
rowing peripherally. Other types include cystic bronchiectasis, which
has an appearance mimicking bunches of grapes, or there may be mul
tiple successive dilatations of a bronchial branch (Fig. 45).
Standard radiographs may be normal. In some individuals, the dilated
areas are displayed as round translucencies (Fig. 46). When these con
tain some dependent fluid, the diagnosis is easier as the fluid assumes a
crescent shape with upward concavity. When the dilated bronchi are full
of fluid or pus, they appear as oblong opacities, most often in a lobe with
a reduced volume.
715
Figure 47.
CT section o f patient with p ro
nounced bilateral bronchiectasis.
Bronchography has been a common supplementary examination when

bronchiectasis is suspected, and also to clarify the extent of disease be
fore possible lobectomy. High resolution CT can demonstrate bronchiec
tasis (Fig. 47), and the need for bronchography is therefore diminishing.
Atelectasis
This is a term that is used to describe volume-reduced, collapsed non
aerated lung tissue. Atelectasis is a condition that can be congenital or
acquired, and the atelectatic areas may be limited to small parts o f a seg
ment, or there may be collapse of a whole lobe or lung.
Atelectasis may be caused by obstruction of a bronchus, or external
compression of the lung tissue.
Table 4. Causes o f bronchial obstruction

- foreign body
- bronchial cancer
- benign intrabronchial tumor
- mucus plug
- incorrectly placed bronchial tube
- stenosis after infection
- compression of a bronchus from the outside (tumor, lymph node)
716
Atelactasis of right upper lobe Atelectasis of left lower lobe
column; obliterated left

diaphragm posteriorly
Figure 48. Drawing o f changes due to atelectasis o f upper and lower lobes.
Table 5. Causes o f compression o f lung tissue

- fluid in the pleural cavity
- air in the pleural cavity
- elevated diaphragm
- deformity of the chest wall
- deliberate compression by surgery (thoracoplasty, oil in the chest
cavity)
Table 6. Radiological findings with lobar or segmental collapse

- the collapsed segment of the lung appears itself as an opacity
- the outlines of the mediastinum, heart or diaphragm, are obliterated
because of absence of adjacent aerated lung tissue
- change in position o f neighbouring structures such as the medi
astinum, diaphragm, or lobe of lung in order to compensate for the
volume reduction
When there is collapse of the upper lobes, the lateral films will show the
posterior limit of the collapsed lobe distinctly. In the frontal picture, the
superior mediastinal outline will be obliterated (Fig. 48). On the left side,
parts of the cardiac margin will also be obliterated because the lingular
lobe is part of the left upper lobe. The lateral outline of the collapsed right
upper lobe is normally distinct, because the x-ray beam is tangential to
the superiorly displaced border to the middle lobe. The lateral border of
717
Figure 49.
Atelectasis o f the right lower lobe in
patient with metastases from rectal
carcinoma.
a) The PA view shows atelectasis o f
the lower lobe (A), as a sharply
defined triangular opacity. A large
metastasis is seen below the right
hilum, and several small meta
stases (arrows).
b) Lateral view. No sharply defined
opacity, but increased density over
basal parts o f the thoracic column,
which normally becomes darker
caudally. Obliterated posterior
part o f the left dome o f the
diaphragm (arrows).
a collapsed left upper lobe is

usually indistinct, and the opac
ity has a completely gradual
transition to normal aerated
tissue in the hyperinflated left
lower lobe.
Collapsed lower lobes will
generally have a distinct border
in the frontal film. The collapsed
left lobe may be hidden behind
the heart shadow, and only ob
served as a retrocardiac triangu
lar opacity on well penetrated
films. In the lateral projection,
the collapsed lower lobes do not
have a distinct anterior border, but they are discovered because the tho
racic column, which appears progressively darker towards the di
aphragm, appears lighter because of the adjacent collapsed lobe (Fig. 49
a + b, 50 a + b). The dome of the diaphragm is obliterated where there
is absence of normal aerated adjacent lung tissue (Fig. 48).
An atelectatic middle lobe is seen distinctly in the lateral film as a nar
row triangular opacity with the tip towards the hilum. In the frontal film,
the right heart outline is obliterated. Rapid treatment of the middle lobe
718
Figure 50.
Atelectasis o f the lower lobe.
a) PA view. Indistinct opacity be
hind the heart shadow (arrows),
with obliteration o f medial part o f
left diaphragmatic outline.
Clearly visible thoracic column
because the heart and medi
astinum are pulled across to the
left.
b) Lateral view. No sharply defined
opacity, but gradually increasing
opacity caudally down the verte
bral column, and obliteration o f
the left diaphragmatic outline.
atelectasis with adequate

physiotherapy is important be
cause re-expansion may be
difficult. Deficient re-expan
sion may lead to middle lobe
fibrosis.
In total collapse, the volume
of the lower lobe may be so
small that it may be difficult to
recognize. There will be con
siderable compensatory hy
perinflation of the upper lobe,
which can be misinterpreted
as a unilateral emphysematous
lung. Careful inspection will
usually reveal an area of obliterated diaphragmatic outline, and the col
lapsed lobe can easily be demonstrated by CT scan.
Deficient re-expansion of lung tissue after pneumonia or embolism
with bleeding may lead to persistent linear opacities, which often occur
in the base of the lungs as 3-5 cm long bands, and represent platelike
atelectasis.
In the presence of pleural fluid, the tongue of lung tissue that normally
projects into the posterior costophrenic angle may float upward and be
719
folded behind the lung. Adhesion may occur between the folded up part
and the posterior surface of the lung. When the fluid is resorbed, the
folded part may not re-expand because o f the adhesions. It then lies as a
round opacity towards the posterior pleura, while the other parts of the
lower lobe expand into the costophrenic angle. This type o f opacity has
a characteristic appearance and is called round atelectasis.
Neoplasms
Lung cancer is one of the commonest types of cancer in men. Smoking
and air pollution are important causes. The most common histological
types are:
- squamous cell carcinoma
- adenocarcinoma (including alveolar cell tumors)
- small cell carcinoma
- large cell carcinoma
The histological classification is of significance because small cell car

cinoma is treated differently from the other types; therefore, lung carci
noma is classified as small cell or non-small cell. The histology cannot
be deducted with certainty from chest films, although the different types
of tumor may have certain characteristics.
Squamous cell carcinoma often starts centrally, while adenocarcinoma
starts as a peripheral tumor. The border o f peripheral tumors is often ir
regular, with lobulation and outgrowing strands. Cavities are common,
while calcification is unusual. Alveolar cell tumors may start as solitary
round shadows. The cells tend to line the alveolar walls and fill the alve
oli instead of destroying them. They may therefore look like multiple
opacities with indistinct borders, sometimes confluent, and may be con
fused with bronchopneumonia.
In small cell carcinoma, there is often visible mediastinal widening
when the diagnosis is first made (Fig. 51). Unlike squamous cell carci
noma, there is no necrosis in small cell tumors.
The first finding in a central tumor is often a pneumonic opacity, as
stagnation of secretion peripheral to an endobronchial tumor disposes to
infection. The picture may become normal again with adequate treat
ment of the pneumonia, since the tumor itself is not large enough to be
visible, or is hidden by the mediastinal shadow. Recurrent pneumonia or
atelectasis of the same lobe must result in cancer being suspected and
720
Figure 51.
CT section o f the thorax in a
patient with small cell pulmonary
carcinoma. Spreading to the medi
astinum at the time o f diagnosis.
Descending aorta (A), pulmonary
artery (P), tumor (T). Small right
sided pleural effusion.
lead to bronchoscopy.
It is important to obtain tissue for biopsy, and this is done either using
bronchoscopy or by needle puncture through the chest wall under the
guidance of fluoroscopy. When the diagnosis of cancer is established, an
attempt is made to classify the tumor by assessing the size and possible
growth into the adjacent organs. A search for lymph node metastases,
and distant metastases is also performed.
On the chest radiograph, the presence of the following should be as
sessed systematically:
- Central or peripheral tumor
- Invasion of the hilum or mediastinum
CT scan has become a routine method of assessing invasion of the

medastinum. The layers of fat in front of the trachea and carina, the sub-
carinal area, and the aortopulmonary ’’window” (between the aortic arch
above and the pulmonary artery below) are all inspected. MRI has been
found to be particularly effective for demonstrating invasion of central
cardiovascular structures (Fig. 10).
- Pleural fluid
Malignant cells in pleural fluid are a poor prognostic sign.

- Invasion of the chest wall (Fig. 5) with destruction of ribs.
- A special type of carcinoma (Pancoast or superior sulcus tumor) is
squamous cell carcinoma in the apex of the lung, destruction of the
721
upper ribs and involvement of the brachial plexus. These patients may
have shoulder pain as the first symptom and be referred for radio
therapy of the shoulder. The extent o f these tumors is now optimally
evaluated by MRI using sagittal and/or coronal planes to determine
penetration of tumor through the apical fat pad with possible in
volvement of the brachial plexus, chest wall, or neck (Figs. 8, 9).
- Elevated diaphragm
If fluoroscopy shows paradoxical motion, this indicates invasion of the

mediastinum with involvement of the phrenic nerve and paralysis of
the ipsilateral dome of the diaphragm.
- Metastases to the contralateral lung or ribs
Such findings in the chest film may save the patient from further di
agnostic examinations and thoracotomy.
Metastases
Pulmonary metastases may be solitary or multiple (Figs. 37, 49). They
are often globular with a smooth surface. When multiple, the sizes dif
fer from one lesion to another. Most metastases are near the surface of
the individual lobe of the lung (including those that lie close to the in
terlobar fissure). Preoperative CT scan is necessary in patients with pre
sumably solitary metastases. It will then be possible to detect additional
metastases located near the mediastinum or in the sinus posteriorly.
Lymphangitic carcinoma
When cancer cells spread to the mediastinal lymph nodes, obstruction to
the flow of lymph from the lung towards the hilum may occur, and can
cer cells may grow along the lymph vessels peripherally. On thoracic ra
diographs, this phenomenom will appear as radiating strands from the
hilar region, and the strands will be accompanied by thickening of the
peripheral interstitial septa. This condition often develops gradually, un
like interstitial edema caused by heart failure where the symptoms often
develop more rapidly.
Pulmonary embolism, pulmonary infarction

Pulmonary embolism usually originating from thrombus in the veins of
the pelvis or lower extremities is very common, especially in bedridden
patients who have undergone major surgery. In most patients, the flow
722
of blood through the bronchial circulation is sufficient to prevent the oc

currence of tissue necrosis and infarction. In patients with heart failure
and reduced oxygenation, the bronchial circulation may not be sufficient,
so that pulmonary infarction occurs.
The findings on a standard chest radiograph will depend on whether
infarction or bleeding is present, and may be described as follows:
Chest radiograph in pulmonary embolism

1) Embolism without infarction
a) Without bleeding
No pathological changes
Elevation and reduced mobility of ipsilateral dome of diaphragm
Narrowing of vessel shadows peripheral to the embolus
Blunting of the costophrenic angle by pleural fluid (confirmed by lat
eral decubitus view)
b) With bleeding
Diffuse, indistinct opacity which is rapidly absorbed
2) Embolism with infarction
Basal pyramidal or hemispherical opacity with the base towards the
pleura and the tip pointing to the hilum (Hampton's hump)
Healed infarct or bleeding may be seen as residual linear opacities, of

ten combined with pleural involvement such as a blunted costophrenic
angle and pleural thickening.
The findings on standard chest radiographs are not specific and iso
tope scanning or angiography is needed to confirm the diagnosis.
Ultrasonography or phlebography should be used to identify deep ve
nous thrombosis of the lower extremities.
Isotope scanning, perfusion and ventilation scintigraphy are useful, as
areas with reduced perfusion and normal ventilation are typical of pul
monary embolism (Fig. 52 a + b) (see Modalities). If there is uncertainty,
pulmonary angiography can be done. This is the most accurate method
for identifying clot in the individual pulmonary arteries (see Modalities).
Lung infections
Lung infection (pneumonia) may be bacterial, viral or fungal. Various
kinds of protozoa can also cause lung infection. In pneumonia, opacities
develop in the affected segments of the lung. The opacities may vary
723
Figure 52. Scintigraphy findings in pulmonary embolism.

a) Perfusion scintigraphy with distinct areas without perfusion
b) Ventilation scintigraphy
ties.
b) Lobar pneumonia, right upper lobe (lateral projection) - uni-focal opacity, distinct
borders. Basally, the opacity is close to the interlobar pleura on the right lower
lobe, but does not affect the lower lobe.
considerably in appearance and distribution. In some types of pneumo

nia, the opacities consolidate as the disease progresses. The appearance
of this type of consolidation may vary considerably, both in a macro
scopic lung preparation and in a radiograph, depending on the etiology
and distribution. Alveolar consolidation is the most common, and may
be segmental or lobar. The appearance varies considerably depending on
724
bronchial branches are seen in the opacity.
whether only single segments, or whole lobes of the lung are affected.
The opacities in pneumonia are often bilateral and are often accompa
nied by collections of fluid in the pleural cavity.
Earlier, it was common to differentiate between the terms lobar pneu
monia (Fig. 53 a, b) and bronchopneumonia (Fig. 54). Lobar pneumo
nia is usually unifocal and concentrated to a single lobe where the opac
ity will be homogenous with sharp outlines which follow the borders of
the affected lobe. The volume of the affected area is not reduced, the
bronchial branches may be aerated, and a so-called air bronchogram -
visible bronchial branches in an opacity - is common. In bronchopneu
monia, the opacities are more scattered and are often seen in several lobes
at the same time. Atelectasis (volume reduction) is common. The opac
ities in bronchopneumonia are thus much less homogenous than in lobar
pneumonia, and seem less consolidated. The air bronchogram is not nor
mally seen.
It is no longer usual to maintain the differentiation between lobar pneu
monia and bronchopneumonia as the radiological picture may vary con
siderably.
725
Figure 55.
Pneumococcal pneumonia
- massive opacity left lung
with air bronchogram.
Bacterial infections
Bacterial pneumonia may occur in normal ’’healthy" individuals, but in
today’s modem society, bacterial pneumonia often occurs in patients with
reduced resistance to infection. Special risk groups will be patients with
advanced cancer, nutritional disturbances, or immunodeficiency caused
either by immunological disease or various drugs.
Gram positive infections

Pneumococcal pneumonia (Fig. 55)
Streptococci pneumoniae are the bacteria that most often cause lung in
fections (80-90%). Pneumococci are part of the normal bacterial flora
in the respiratory tract, and can be isolated from larynx swabs in up to
60% of all normal invididuals.
Pneumococcal pneumonia is most frequently seen in older, frail pa
tients, alcoholics, and patients with chronic obstructive lung disease. The
typical radiological finding is a homogenous, non-segmental, circum
scribed consolidation of lung tissue. The opacities are situated anywhere
in the lungs, although they are located most often in the basal segments,
and are unifocal or multifocal. An air bronchogram is often seen and is
considered to be characteristic of pneumococcal pneumonia. The af
fected segments of the lung are not reduced in volume. Pleural involve
ment as pleural effusion is not usual.
Small amounts o f fluid that can only be diagnosed in lateral decubitus
views can, however, be seen in up to 15% of the cases. Empyema is un
usual, as is necrosis of the infected lung tissue with abscess formation.
726
Figure 56.
a) Staphylococcal pneumonia
with mottled multifocal bilat
eral pulmonary opacities.
b) Staphylococcal pneumonia -
late stage. The opacities coa
lesce and become homoge
nous in character.
c) Staphylococcal pneumonia -
late stage with consolidated
pulmonary opacities. Bilateral
pneumothorax has developed.
Staphylococcal pneumonia (Fig. 56 1 - c)

Staphylococcus aureus is normally present in the nose and throat of 20%
of healthy adults. Staphylococcal pneumonia is most often seen in
children, frail old people, and in patients who have aspirated stomach
contents into the respiratory tract. As staphylococcus aureus produces
727
Figure 57.
Staphylococcal pneumonia, right up
p er lobe. Volume reduction o f the
upper lobe is seen as the horizontal
fissure has been pulled cranially.
toxins, the infection frequently spreads to large parts of the lungs.

Complications such as lung abscess, empyema, and bronchopleural fis-
tulae are frequently seen.
The radiological appearance is that of typical bronchopneumonia with
segmental and mottled opacities, which are usually multifocal and bi
lateral. In the later stages of the disease, the opacities may coalesce and
become homogenous. The volume of the affected lung segment is usu
ally reduced (Fig. 57). An air bronchogram is seldom seen.
Gram negative infections (Fig. 58)

The most common Gram negative infections are caused by Klebsiella
pneumoniae, Escherichia coli, Pseudomonas aeruginosa, Haemophilus
influenzae, and Proteus. The radiological picture is almost identical, and
it is not possible to differentiate between the different bacteria. Gram
negative lung infections are most often seen in chronically ill patients
who are weakened by other diseases such as alcoholism, chronic lung
diseases, diabetes, or different types of cancer. Aspiration to the respi
ratory tract is the commonest single cause of Gram negative pneumonia.
Opacities caused by Gram negative bacteria are usually localized in
the basal lung segments. It is not possible to differentiate these opacities
from those caused by staphylococcus aureus. Complications such as
empyema and lung abscess are frequently seen (Fig. 59 a, b). The mor-
728
Figure 58.
Homogenous consolidated in
filtrate right lower lobe.
Klebsiella pneumonia.
Figure 59.
a) Gram negative pneumonia
with abscess formation.
Considerable volume
reduction o f the affected
lobe. Compensatory
emphysema left lung.
b) CT thorax. Gram negative
pneumonia. Opacity with
abscess formation in right
lower lobe. Pleural fluid
right side.
tality in Gram negative pneumonia is relatively high in spite of adequate

treatment with antibiotics.
Anaerobic infections
The most common anaerobic infection, tuberculosis, is caused by my
cobacterium tuberculosis. Tuberculosis is most often seen as limited epi
demics in densely populated areas. The primary infection is almost al
ways due to inhalation of mycobacterium tubeculosis, usually to the mid
dle or basal segments of the lung. After this, spread of bacteria occurs
internally in the lung, possibly also via lymph channels, to lymph nodes
in the mediastinum. The immunity reaction tends to encapsulate the ac
tual tubercle bacillus, which then enters an inactive "dormant” stage. The
tubercle bacilli are most often implanted in areas of the lung with a high
oxygen tension, usually in the apical segments (Fig. 60). At this stage,
the tuberculous opacity looks like a segmental or lobar opacity with con-
730
Figure 61.
Reactivated old tuberculosis with
cavitation andfluid levels in the left
upper lobe.
Figure 62.
Reactivated old tuberculosis with f i
brous, striped opacities and less ex
tensive infiltrates in right upper
lobe.
solidated lung tissue. Accompanying enlargement of lymph nodes in the

hilus is usual. Sometimes pleural effusion occurs. These changes often
disappear spontaneously, sometimes after chemotherapy. The consoli
dated lung tissue shrinks so that the remaining lesion is a pulmonary nod
ule, which may become calcified at a later stage. The same process takes
place in the lymph nodes in the hilum. The combination of peripheral
pulmonary calcification and calcification o f the hilar lymph nodes is
called a primary complex, and is a typical finding in primary tuberculo
sis. It can be seen in about 50% of infected patients.
Reactivation of old tuberculosis infection (Fig. 61) may occur many
years after the primary infection, and is most frequently localized to the
731
apical and posterior segments of the upper lobes and to the superior seg
ments of the lower lobes. It is seen as a mottled, poorly defined alveolar
infiltrate, often with the formation of cavities. In most cases, only one
lung is involved, but bilateral changes are seen in the more advanced cases.
At this stage, the lung changes are very variable with cavities, single or
multiple nodular opacities, pleural fluid, large consolidating infiltrates
(both lobar an diffusely scattered), or pneumothorax (Fig. 62). The great
variability in the radiological picture at this stage makes it difficult to
make a diagnosis on the basis of the radiological picture alone. Infectious
diseases and lung cancer may be relevant differential diagnoses.
Tuberculosis occurs infrequently outside the lungs. Tuberculous lym-
phadenopathy is common, as is involvement of the visceral and parietal
pleura, the pericardium, and the peritoneum. The tuberculous infection
may be disseminated and involve both lungs (miliary tuberculosis). In
these cases characteristic changes are seen with small miliary opacities
diffusely scattered over both lungs.
Tuberculomas in the lungs are seen both in the primary and the later
phases of the disease. A tuberculoma represents a limited, localized con
dition of the parenchyma which heals and later shrinks. Finally, a sharply
limited node-like opacity, usually 1-5 cm in diameter, is seen. This is
usually localized in the upper segment o f the lung. Tuberculomas are
usually solitary, but may be multiple and often calcify. Formation of cav
ities is rare. The differential diagnosis between tuberculoma and a pri
mary lung tumor, or possibly a metastasis may be difficult.
The lung changes in tuberculosis will improve after adequate treat
ment, but often leave considerable changes with fibrosis, infiltrates,
calcification, shrinking, and pleural thickening and pleural adhesions
(Fig. 63). Response to treatment is indicated by shrinking of infiltrates,
reduced wall thickness of the cavities, and fibrosis.
However, any residual tuberculous process may become reactivated
at any time in the later stages of the disease. Reactivation often occurs
many years after the initial primary tuberculous infection.
Before chemotherapy of tuberculosis became usual, pulmonary
tuberculosis was often treated surgically. One of the most common types
of operation was thoracoplasty, where the upper ribs were removed in
order to collapse the upper segments of the lung, where the disease was
most frequently located (Fig 64). Other forms of treatment not
infrequently used were induction of pneumothorax and injection of
732
Figure 63.
Old tuberculosis, predominantly
right-sided, with fibrous infiltrates,
calcification, pleural thickening
with adhesions, and shrinking.
Figure 64.
Left-sided thoracoplasty with resec
tion o f cranial ribs.
sclerosing substances into the pleural cavity.
Viral and viral-like infections

Viral pneumonia and pneumonia with viral-like aetiology are common
in children and young people, but are less frequent in adults. In children,
pneumonia is most often caused by the respiratory syncytial virus and
parainfluenza virus. In older children and adults, non-bacterial pneumo
nia is most often caused by mycoplasma pneumoniae, less often by the
733
Figure 65.
Varicella pneumonia; alveolar
opacities symmetrical distrib
uted in both lungs.
adenovirus and parainfluenza virus.
Influenza virus
There are a series of different viruses of this type (influenza A, B, and
C), with several variants within each group- The antingen component
may thus vary considerably, and immunological resistance to the influ
enza virus is therefore infrequent. In uncomplicated influenza, the chest
radiograph is normal. In complicated lung infections caused by the in
fluenza virus, signs of bilateral pneumonia with pronounced consolida
tion of the lung parenchyma are usually seen. Bacterial pneumonia is
often seen in connection with influenza. Radiologically, it is not possi
ble to differentiate between pneumonia caused by the influenza virus
and bacterial pneumonia.
In rare cases, a number of other types of virus such as parainfluenza,
respiratory syncytial-, adeno-, rhino-, and herpes viruses may cause
pneumonia. None of these types have special radiological characteris
tics, and it is not possible to differentiate these infections from bacterial
pneumonia.
Varicella virus (Fig. 65)

Varicella and herpes zoster are caused by the same virus (varicella-zoster
virus), and occur mainly in children (varicella) and in older patients (her
pes zoster). The lung picture shows mottled alveolar opacities, which can
vary in size from node-like opacities to extensive changes which may in
volve most of the lungs. The opacities are usually from 5-10 mm in dia-
734
Figure 66.
Mycoplasma pneumonia -
pneumonic opacities in
both lower lobes, most
pronounced on the right
side.
meter, and normally disappear within a week. In a few patients, the opac
ities may persist for several months. In about 2 % of the patients, the opac
ities may resemble small nodules which calcify causing permanent
changes.
M ycoplasma pneum onia

Mycoplasma pneumonia is most often seen in children and young peo
ple. Up to 15% of all cases of pneumonia in patients younger than 40
years are caused by mycoplasma pneumoniae. Most mycoplasma infec
tions are manifested clinically as bronchitis and/or pharyngits.
Pneumonia develops in between 3 and 10% of the patients.
The radiological picture is extremely variable, but one or both lower
lobes are usually involved. The opacities usually start as partly mottled,
partly node-like peribronchial opacities, which may gradually develop
to involve whole segments or lobes. Consolidation is frequently seen
(Fig. 66). This typical progression is often seen in mycoplasma pneu
monia, and the diagnosis may therefore sometimes be made on the radi
ological picture alone. The upper lobes are seldom affected. A volume
reduction of the affeted segments or lobes of up to 10% is usual. Pleural
effusion and abscess formation are seldom seen. The opacities that de
velop with mycoplasma pneumonia usually take far longer to disappear
than opacities caused by bacteria or viruses.
735
Figure 67.
Actinomycosis - pneumonic
opacity, right upper lobe, with
volume reduction o f the upper
lobe.
Fungal pneumonia, protozoal pneumonia

The commonest of this type of lung infection is caused by Histoplasma
capsulatum, and is most frequently seen in USA. The radiological
changes in the lungs caused by this bacteria have no typical characteris
tics, but have many features in common with tuberculosis both in the
early active and in the late stages.
The opacities are non-specific, and in most cases they heal with fibro
sis and calcification. In late stages with extensive calcification, the
changes may be difficult to differentiate from the calcification which may
occur after varicella pneumonia.
Other fungal infections such as cryptococcosis, nocardiosis, blasto
mycosis, and actinomycosis (Fig. 67) are very seldom seen.
Aspergillus infections are encountered a little more frequently, and
most often as secondary changes in lung cavities.
The most important protozoal infections are caused by pneumocystis
carinii (see lung diseases with immunosuppresion), toxoplasma gondii
and entamoeba histolytica. There are also a number of metazoan infec
tions caused by different organisms, o f which the most usual are
echinococci (Fig. 68 a, b).
Diffuse generalized pulmonary disease

The radiological changes seen in diffuse generalized pulmonary disease
can be divided into two main groups - alveolar and interstitial opacities.
Alveolar pulmonary opacities affect the aerated segments of the lungs
- the trachea, bronchi and alveoli. These changes may be found only in
the alveolar area, but larger parts of the aerated bronchial tree including
736
Figure 68 a + b.
PA and lateral views - echinococcal
cyst right lower lobe. Sharply defined
homogenous opacity. Minimal
amounts ofpleural fluid.
the alveoli will usually be involved.

Alveolar opacities, opacities with air bronchogram, and atelectasis are
thus all variants within the same group, i.e. involvement of the aerated
parts of the lung.
Interstitial opacities can be divided into four main types - reticular,
nodular, reticulonodular, and linear. These are changes seen in the lung
tissue itself - i.e. the lung tissue located between the alveoli (in the in-
terstitium). Reticular opacities resemble a network, and are often graded
from fine reticular to coarse reticular. Fine reticular changes can be com
pared with the network seen in nylon stockings, while coarse reticular
opacities are characterized by larger, almost cyst-like cavities of 1 cm or
more in diameter, with a rough, thickened periphery surrounding the cav
737
ities. Nodular opacities are seen when more node-like lesions arise in the
interstitium. These opacities are homogenous, well-defined, and many
vary considerably in size.
Reticulonodular opacities may be seen when several nodular opacities
coalesce forming network-like opacities. Linear, striped opacities may
represent thickening of interalveolar clefts or interlobular septa (Kerley's
A and В lines). In interstitial opacities, a combination of these four main
types is often seen.
Pulmonary congestion/pulmonary edema

The capillary bed in the lungs has a surface of between 70 and 140 m2.
The endothelial cells in the pulmonary capillaries are permeable to wa
ter, but impermeable to proteins and other large- molecule fluids. The
alveolar epithelium on the other hand is almost impermeable to water as
well.
In normal lungs, a continuous stream o f fluid flows from the capillary
bed to the alveolar interstitium. In the interstitium there are a number of
lymph vessels which remove superfluous fluid.
Pulmonary congestion and pulmonary edema arise when the amount
of extravascular fluid in the lungs increases.The major causes o f this are
shown in the following table.
Causes of extravascular fluid in the lungs

Increased hydrostatic pressure
Increased capillary permeability
Over-hydration
Pulmonary infiltration
Pulmonary vein occlusion
Pulmonary embolism
Reduced osmotic pressure
Transfusion reaction
Reduced production of plasma proteins
ARDS (Adult Respiratory Distress Syndrome)
These changes are usually symmetrical, but asymmetrical pulmonary

congestion/pulmonary edema may also occur. The most frequent causes
of asymmetrical distribution are shown in the following Table.
738
Causes of asymmetrical congestion/edema

Gravitational (lying preferentially on one side)
Emphysema (unilateral)
Unilateral venous occlusion
Occlusion of a pulmonary artery
Bronchial occlusion
Thrombosis/embolism
Lymphatic obstruction
After removal of pneumothorax or pleural effusion
Pulmonary congestion and edema develop in two stages. Initially, in

terstitial edema occurs with collection of fluid in the interalveolar septa
and Kerley В lines appear. Kerley В lines are seen as 3-6 mm long hor
izontal lines in the lateral basal segments of the lung, near the chest wall
(on the frontal film). They develop when the pressure in the interstitium
exceeds about 18-20 mm Hg. At this stage, the patient usually becomes
dyspnoeic with tachypnoea, but with minimal changes in the arterial
blood gases.
Further progression of congestion and edema produces fluid in the
alveoli. This reduces the alveolar surface for the exchange of gases. At
this stage, the chest film shows a combination of alveolar and interstitial
opacities.
Cardiogenic congestion/edema
The first radiological sign of interstitial edema is blurred outlines o f the
pulmonary arteries. The blurring is observed first and most readily in the
hilar regions. In addition, the basal segments of the lung often seem rather
blurred. At the same time, a redistribution o f flow occurs with equiva
lent or larger diameter of the arteries of the upper lobe compared to lower
lobe vessels (antler sign). When fluid collects in the interlobular and in
teralveolar septa, the so called A and В lines (Kerley A/Kerley B) are
formed. When the congestive changes progress, alveolar edema with
fluid in the alveoli develops. This produces diffuse lung opacities with
out air bronchogram. The edema fluid usually develops symmetrically
and collects mainly in the lowest parts of the lungs (Fig. 69). However,
asymmetrical distribution of edema is not unusual, and is most often re
lated to the patient’s position in bed (lying on right or left side). The fact
that the opacities in edema tend to be most pronounced in the lowest lung
739
Figure 69.
Enlarged heart with congestive
changes in both lungs. Bilateral
pleural fluid.
Figure 70.
Pulmonary congestion/edema
with congestive changes chiefly
in the hilar regions. Relatively
sharply defined opacities (Bat-
wing).
segments, and are symmetrical, may be used in the differential diagno

sis between congestion/edema and pneumonia.
In some cases the congestive changes/edema are limited to the hilar
regions (Fig. 70). The peripheral borders of these opacities may be
sharply defined (Bat-wing). These opacities were previously regarded
as characteristic of uremia, but may equally often be seen in heart
failure.
In most cases of pulmonary congestion/edema, the heart will be en
larged (Fig. 71), but with acute pump failure of the left ventricle (for
example as a result of acute myocardial infarct or rupture of papillary
740
Figure 71.
Heart failure with consider
ably enlarged heart (cor bov-
inum) with congestive changes
in both lungs.
Figure 72.
Near drowning-pronounced
pulmonary congestion (edema
with extensive alveolar
opacities caused by large
collections o f fluid in the
alveoli).
muscles), there may be pronounced congestive changes without simul

taneous heart enlargement.
Non-cardiogenic congestion/edema
Drowning
Congestion/edema changes are seen in patients who have almost
drowned (Fig. 72). Diffuse alveolar opacities caused by edema fluid can
be seen on the chest radiograph, tn addition, there is usually aspiration
of water and stomach contents. Increased capillary permeability also
leads to interalveolar collection of edema fluid that is rich in protein,
741
Figure 73.
Pulmonary congestion in a p a
tient with reticular opacities in
both lungs.
which may in turn lead to formation of hyaline membranes.
Inhalation o f gases
The most common gases are nitrogen, phosporus, sulphur dioxide, am
monia, chlorine, and ordinary smoke (in connection with fires).
Congestion/edema usually occurs as a result of a direct effect of the gases
on the endothelial cells in the alveoli. The accompanying edema is usu
ally fairly pronounced with diffuse blurring of the affected lung segment.
The size of the heart is always normal.
R enal failure
Pulmonary congestion/edema is frequently seen in patients with both
acute and chronic renal failure, and is a common cause of death in pa
tients with acute nephritis (Fig. 73). However, the most frequent cause
of the development of pulmonary congestion/edema in these patients is
failure of the left side o f the heart.
Sepsis
Pulmonary congestion/edema is frequently seen in patients with sepsis.
The primary cause is probably the release of vasoactive substances that
affect the permeability of the capillaries/alveoli. It is not possible to make
a radiological differentiation between this type of pulmonary congestion
and that seen in heart failure. However, the size of the heart will be nor
mal unless there is a simultaneous involvement of the heart.
742
A R D S (Adult R espiratory Distress Syndrom e)

Pulmonary congestion is always seen in patients with ARDS (see this
section).
Diffuse pulmonary fibrosis

Pulmonary fibrosis is seen in the course of a number of lung diseases as
shown in the following table:
Causes of diffuse pulmonary fibrosis

Tuberculosis
Fibrosing alveolitis
Pneumonoconioses
Chronic pulmonary disease
Asbestosis
Organic/inorganic disease
Silicosis
Chronic infections
Sarcoidosis
Diseases such as asbestosis, silicosis, and sarcoidosis all lead to the

development of pulmonary fibrosis.
Fibrosing alveolitis
This is a group of diseases characterized by an inflammatory reaction in
the endothelial cells in the alveoli with an alveolar exudate. As the dis
ease progresses, there is destruction of the alveolar architecture. The dis
ease is also called Hamman-Rich disease. Fibrosing alveolitis may be
seen at the same time in systemic diseases such as rheumatoid arthritis,
disseminated lupus erythematosus, ulcerous colitis, and chronic hepati
tis. The disease is characterized by rapid progression, with only mild
non-specific blurring of the affected lung segment in the early stages,
followed by an increasingly diffuse outline of the pulmonary arteries,
and gradual development of fine reticulonodular opacities in the basal
lung segments (Fig. 74). Gradually, as the fibrosis develops rapidly, there
is reduced volume of the affected lung segment. The reticular opacities
become steadily coarser and gradually appear as annular shadows with
diameters from 5 to 10 mm. The annular shadows represent cystic cavities
in the lungs, giving these a typical honeycomb appearance. This is best
743
Figure 74.
Fibrosing alveolitis with retic
ular opacities in both lungs.
seen in lateral views of the lungs, most often basally and posteriorly.
Pneumoconioses
The common characteristic of this group o f diseases - of which asbestosis
and silicosis are the most important - is that they are caused by organic
dust particles that are small enough to reach the alveoli where a type III
Arthus tissue reaction takes place. Four to six hours after exposure, hy
persensitivity pneumonia develops. Initially, the chest radiograph is nor
mal. Later, diffuse blurring of the basal lung segments develop. The in
volved parts of the lungs have reduced circulation because of oblitera
tion of small pulmonary vessels. After temporary exposure to dust
particles, the condition returns to normal, both clinically and radiologi-
cally. However, residual changes may be seen as reticulonodular opac
ities 1-3 mm in diameter.
With continuing exposure to dust, pulmonary fibrosis gradually
develops, characterized by coarse linear striped opacities, specially in
the middle and upper part of the lungs. Considerable volume loss is seen
at a late stage in the development of fibrosis. In pulmonary fibrosis caused
by pneumoconiosis, small round shadows, 5-8 mm in diameter with a
central translucency are seen, giving a honeycomb appearance. This
special fibrosis is most typically seen in the upper lobes, unlike fibrosing
alveolitis where the fibrosis is most pronounced in the basal lung
segments.
Asbestosis
The first visible radiological changes in asbestosis are small irregular
opacities, mainly in the basal parts of the lungs. The middle and upper
744
Figure 75.
Asbestosis - irregular striped
opacities, most pronounced in
the basal lung segments.
parts are involved at a later stage. In the earliest stages, the opacities are
thread-like and are often confused with vascular shadows that branch
into fine thread-like structures (Fig. 75). As the disease progresses, the
linear opacities become coarser and broader, and may obscure the pul
monary arteries that branch out to the involved area. In severe cases,
there are diffuse coarse reticulonodular opacities, which gradually be
come honeycomb-like. These opacities may be so large that they com
pletely obscure the outline of arteries in the area, and also obliterate the
outline of adjacent parts of the diaphragm and heart.
Typical changes in asbestosis are pleural involvement as plateau-
chaped pleural thickening. This is typically seen in the parietal pleura,
while the visceral pleura is not involved. Pleural changes are seldom ob
served unless the disease has lasted for at least ten years. In the frontal
view, the pleural thickening is observed where the pleura is in contact
with the ribs, most often in the middle third of the chest wall. The typi
cal disk-shaped thickening of the pleura is usually called a pleural plaque.
The upper and basal parts of the pleura are not affected until the more
advanced stages of the disease. A pleural plaque is best shown on chest
films taken tangentially.
The standard examination when asbestosis is suspected includes
oblique views of the lungs with the patient rotated 45 degrees (Fig. 76).
In the late stages of the disease (usually after more than twenty years),
there is fairly extensive calcification in the pleural plaques. The disease
is gradually dominated by extensive fibrosis with marked shrinking and
considerable pleural thickening containing calcification. Calcification is
745
Figure 77.
Asbestosis - linear opacities in
the basal lung segments, which
obliterate the outline o f the p u l
monary arteries peripherally.
most often observed in the parietal pleural on the domes of the diaphragm
(Fig. 77).
Pleural fluid is unusual in asbestosis. If pleural fluid is seen, it is a
strong indication of the development of malignant mesothelioma. In such
cases, the pleural fluid contains blood. A chest radiograph is usually not
sufficient to clarify the degree of spread of the malignant mesothelioma.
This evaluation is best done by CT scan, which shows the extent of the
pleural changes. By examining in the supine and prone positions, possi
bly also in lateral decubitus, it is easy to differentiate between pleural
746
Figure 78.
Acute silicosis, alveolar infil
trate right upper lobe with air
bronchogram.
fluid and pleural thickening. Invasion into and destruction of ribs is com
mon with advanced mesothelioma, as are metastases to the lungs and
mediastinum. Distant metastases are also frequently seen.
A needle biopsy of the pleural thickening or tumor mass, under guid
ance of CT, gives the diagnosis, as does cytological examination o f the
hemorrhagic pleural fluid. In addition to the risk of developing malig
nant mesothelioma, patients with asbestosis also show a higher incidence
of lung cancer.
Silicosis
Silicosis was previously a common disease in miners, and is due to in
halation of silicate crystals (silicon dioxide) into the alveoli. Inhaled sil
icate crystals develop small nodes of collagenous hyaline material. These
nodes are visible on the frontal film. The lymph nodes in the hilum o f
the lung are usually enlarged. Eggshell-like calcification in the periph
ery of these lymph nodes is typical of silicosis. Although corresponding
calcification may be seen in sarcoidosis, histoplasmosis, scleroderma and
amyloidosis, it is rarer than in silicosis.
Infiltration of plasma cells and lymphocytes is seen in the alveolar
walls. The typical picture in acute silicosis is thus dominated by an alve
olar infiltrate with air bronchogram (Fig. 78). The alveolar infiltrate may
appear as small nodules. If chronic changes develop, these typical nod
ules disappear and the involved areas appear more like consolidated in
filtrates with fibrosis (Fig. 79).
Patients with silicosis have an increased incidence of pulmonary tu
berculosis.
747
Figure 79.
Silicosis, consolidated infil
trates with development o f fi
brosis in both lungs, most p ro
nounced in right upper lobe.
Sarcoidosis
Sarcoidosis is a disease of unknown etiology, characterized by diffuse,
non-caseating granulomas. Granulomas are typical of sarcoidosis, but
may also be seen in other diseases such as tuberculosis, diverse fungal
infections, and in patients with carcinoma and lymphoma. The develop
ment of sarcoidosis is probably determined immunologically by an in
teraction between an unidentified antigen and the organism. Sarcoidosis
is sometimes associated with erythema nodosum. Although sarcoidosis
is most frequent in the lung and mediastinum, the disease is also en
countered in other organs such as skin, peripheral lymph nodes, spleen
and the central nervous system. The diagnosis is usually made defini
tively by a lymph node biopsy.
The radiological picture is characterized by:

1. lymphadenopathy, and
2. parenchymal opacities
Lymphadenopathy is the most common, and is always seen in the early

stages. A typical finding consists of enlarged lymph nodes in both hilar
regions (Fig. 80 a, b). The lymph node enlargement is usually symmet
rical and may be considerable. Lymph nodes in the mediastinum are also
frequently affected, so that the radiological picture is dominated by ’’me
diastinal tumor" and bilateral hilar lymph node enlargement (Fig. 81).
748
Figure 80.
Sarcoidosis
a) Frontal view shows enlarged lymph
nodes in both hilar regions
b) Lateral view shows enlarged lymph
nodes in hilar regions.
Figure 81.
Sarcoidosis - mediastinal tumor and
bilateral hilar gland enlargement.
Figure 82.
Sarcoidosis - small nodular
opacities in both lungs.
Bilateral hilar lymphadenopa-
thy.
Although changes in the lung parenchyma are seen histologically in

all patients, lung changes visible on a chest radiograph only develop in
about 2/3 of the patients. The earliest parenchymal changes appear as
small, round, irregular nodes from 1-3 mm in diameter. These are usu
ally symmetrical and evenly distributed from the base of the apex of the
lung (Fig. 82). If the disease progresses, homogenous, diffusely limited
opacities appear in both lungs. Air bronchogram is frequently seen in
these opacities. The opacities often appear to be consolidated infiltrates,
but may also be so irregular that they appear to be nodular. In rare cases,
larger almost tumor-like opacities from 1—4 cm in diameter may be seen.
These have poorly defined outines, are multiple and bilateral. The poorly
defined outline generally makes it simple to distinguish these opacities
from metastases, which usually have clearly defined outlines.
In 2/3 of all patients with sarcoidosis, the radiological changes im
prove with adequate treatment with steroids. If the disease progresses,
extensive pulmonary fibrosis with marked volume reduction (shrinking)
occurs. A fairly typical frontal film shows considerable upward retrac
tion of the hilar outlines bilaterally. At the same time as the fibrosis, large
emphysematous areas develop.
It is not possible to differentiate the fibrosis that develops in connec
tion with sarcoidosis from other types of pulmonary fibrosis. Pleural
thickening with pleural fluid may be seen in sarcoidosis, but is not usual.
Collagen vascular diseases

Collagen diseases are a heterogeneous group of chronic diseases that may
also affect the lung and pleura. The diseases are caused by immunolog-
750
ical factors. The radiological changes are non-specific, and normally it

is not possible to differentiate the various collagenous vascular diseases
from each other. Nor is it possible, on the basis of a chest radiograph, ei
ther to make the diagnosis of collagenous vascular disease, or to distin
guish these from ordinary infections and edematous conditions. A list of
collagenous vascular diseases is given in Table 7.
Table 7. Collagen vascular diseases

Disseminated lupus erythematosus
Systemic vasculitis
Rheumatoid disease
Polyarteritis nodosa
Systemic adenosis
Wegener’s granulomatosis
Ankylosing spondylitis
Sjogren’s syndrome
Dermatomyositis
Disseminated lupus erythematosus is the most common of the col

lagenous diseases, and effects in the pulmonary vessels and inter-stitium.
The most usual changes are pleural fluid, small areas of atelectasis in the
basal segments of the lungs, pneumonia-like opacities, pulmonary con
gestion/edema, small collections of fluid in the pericardium, and in the
later stages, development of a diffuse interstitial fibrosis. Secondary in
fections are frequent. Systemic disseminated lupus erythematosus often
involves the kidneys and heart as well. Simultaneously, diminishing
function of these organs alters the typical radiographic appearance, mak
ing the differential diagnosis from other diseases extremely difficult.
The most frequently seen types of systemic vasculitis are polyarteri
tis nodosa and Wegener’s granulomatosis. The typical angiographic
changes in the liver and kidneys observed with polyarteritis nodosa are
very rarely seen in the pulmonary arteries. The radiological changes are
completely non-specific (Fig. 83).
In Wegener’s granulomatosis, necrotizing granulomas are present,
usually as multiple, well-defined opacities that may vary in size from one
to several cm in diameter (Fig. 84). There is often central necrosis in the
opacities. The differential diagnosis from metastases may be difficult,
but metastases will generally be more sharply defined than granulomas.
751
Figure 83.
Collagenous vascular disesae
- non-specific changes with
diffuse interstitial fibrosis,
mainly on right side.
Consolidated infiltrate cra-
nially, lateral to right hilum.
Figure 84.
Wegener's granulomatosis - necro
tizing granuloma with flu id level
(arrow) in right upper lobe.
Central necrosis is also rare in metastases.

In Sjogren’s syndrome, there is pleural fluid and diffuse bilateral retic-
ulonodular opacities on the basis of a fibrosing alveolitis. The radiolog
ical findings are non-specific.
752
Figure 85.
Pneumocystis carinii pneumo
nia in HIV/AIDS patient.
a) Indistinctly marginated infil
trate o f mixed alveolar/in
terstitial type, chiefly in left
lower lobe
b) Bilateral infiltrates, most
pronounced on right side.
The infiltrate has indistinct
borders. An obvious air
bronchogram is seen in the
infiltrate on the right side.
c) Lateral view o f b) above.
Middle lobe is also seen to
be involved.
Lung diseases connected with immunosuppression

Lung changes in immunosuppressed patients have become common in
recent years, because of both increased use o f advanced treatment with
cytotoxic agents, and increased occurrence of HIV/AIDS. The radio
logical changes in the lungs in immunosuppressed patients are non-spe
cific, but vary depending upon the type of the opportunistic infection.
The lung opacities are either localized, and then unilateral, or they may
be diffuse and then usually bilateral.
The localized unilateral opacity is chiefly caused by bacterial pneu
monia, but may also be seen in fungal infections. The most common bac
teria are pseudomonas and klebsiella. If the radiological changes are dif
fuse and bilateral, the most likely organism is pneumocystis carinii (Fig.
85 a, b, c). The opacities in the lungs with these infections appear as in
filtrates, most often bilateral. The infiltrates have indistinct borders, and
are of mixed alveolar and interstitial type. Progression in the course of
days is often seen, causing involvement of most areas of both lungs. The
radiological appearance is often identical with that seen with conges
tion/edema. However, air bronchogram is frequently seen.
Medically-induced pulmonary disease

Lung opacities are not infrequently caused by reaction to drugs. In prin
ciple, most of the lung changes caused by drugs and visible on a chest
radiograph resemble the changes encountered with pneumonia. A review
of some of the drugs that may cause lung changes is shown in Table 8.
Table 8. Drugs that may cause lung changes
Pulmonary con
gestion/edema Fibrosis Alveolar opacities Hilar lymphadenopathy
Salicylates Furadantin Salicylates Methotrexate
Phenylbutazone Oxygen Anticoagulants Antiepileptics
Heroin Bleom ycin Bleomycin
Methadone Methotrexate
Trauma
Thorax injuries vary considerably from simple, uncomplicated rib frac
tures to large complicated injuries effecting the chest, combined with in
juries in the head, abdomen and extremities. The cause of injury is most
754
often a deceleration trauma, with blunt violence to the chest. In such cases,
there is often a combination of injuries to the chest wall, pleura, lungs,
and mediastinum.
When a patient with multiple injuries is examined, a lateral view of
the cervical column, a frontal chest radiograph, and a frontal view o f the
pelvis is usually obtained. The frontal radiograph of the lungs must be
obtained sitting if the patient’s condition permits, otherwise lying. At this
stage the primary concern is to detect life-threatening conditions such as
tension pneumothorax, haemothorax, mediastinal bleeding, and rupture
of the diaphragm. In recent years, it has become increasingly frequent to
use CT scans early in the examintaion of severely multitraumatized pa
tients. Thus, one and the same examination provides more complete de
tails of injuries in different organs, together with the possibility of mak
ing a more precise diagnosis of the extent o f the chest injury. For exam
ple, a small anterior pneumothorax is far easier to diagnose by CT scan
than by a frontal view of the lungs. This also applies to bleeding in the
lung and pleural cavity, and, above all, to mediastinal injuries, the most
important of which is aortic rupture.
Chest wall injuries

Fractured ribs are the most common
finding in trauma of the thorax.
Fractures of the 5th - 9th ribs are most
often seen. Fractures of the 1st, and to
some extent the 2nd rib, do not usually
occur as isolated findings, but are seen
in combination with other injuries to the
thorax, for example fracture of the clav
icle. Fractures of the 1st and 2nd ribs
necessitate considerable blunt vio
lence, and are usually accompanied by
injuries to vessels and nerves, together
with mediastinal injuries such as rup-
Figure 86.
Fracture o f sternum through the upper part o f
the body o f the sternum with forward and cra
nial dislocation o f the distal fragment
(arrows).
755
Figure 87.
Fracture o f sternum with large
retrosternal haematoma.
Considerable widening o f the
mediastinum in PA chest x-ray.
Figure 88.
Fracture o f sternum with large
retrosternal haematoma —CT
scan.
ture of vessels and the trachea. Fractures o f the lowest ribs are often ac
companied by simultaneous injuries of the liver and spleen (rupture).
Fractured ribs may be seen together with pneumothorax, indicating a
penetrating pleural injury. Multiple fractured ribs may cause pulmonary
collapse involving larger or smaller parts o f a lung, and accompanied by
unstable respiration (flail chest).
Fracture of the sternum is frequently seen with severe injuries to the
thorax (Fig. 86), usually with dislocation of the different fragments in
relation to each other. A retrosternal hematoma of varying size often de
velops. This will be visible as a widening of the mediastinum (Fig. 87).
A CT scan is necessary (Fig. 88) in order to assess the extent of the
hematoma and to verify the diagnosis, making certain that it is not caused
756
Figure 89.
Traffic injury with penetrating
left-sided thorax trauma.
Pneumo-thorax with total col
lapse o f the left lung (arrows).
by another simultaneous large mediastinal injury such as rupture o f the

aorta. Cardiac injury, such as myocardial contusion or traumatic ventric
ular septal defect, should be considered in patients with sternal fracture.
Pleural injuries
Pleural injuries are due to complications arising from rib fractures and
other penetrating injuries. The most common complications are pneu
mothorax (Fig. 89), and hemothorax. A chest radiograph aimed at diag
nosing pneumothorax should be taken in the expiratory phase.
Tension pneumothorax may arise after penetrating injuries. Positive
pressure arises in the punctured pleural cavity, with displacement of the
heart and mediastinal structures over towards the contralateral side. This
may compromise venous return to the heart and reduce filling pressure
in the right ventricle. This is a life-threatening condition needing imme
diate relief, e.g. drainage of the affected pleural cavity.
Bleeding into the pleural cavity is usually caused by severance of veins,
and is most often seen at the same time as pneumothorax (hemopneu-
mothorax). If fat is present in the pleural fluid, it is a sign of chylotho-
rax and is due to rupture of lymph vessels. Rupture of the thoracic duct
may occur with blunt trauma.
Lung injuries
Lung injuries, usually contusion of lung tissue, may be accompanied by
injuries of the ribs and pleura (Fig. 90), but are seen just as often with
out simultaneous rib fractures (Fig. 91). With a compression injury of
the lungs, extravasation of blood into the alveoli occurs followed by de-
757
Figure 90.
Traffic injury with fracture o f
the 2nd, 3rd, 4th, 5th and 6th
right ribs. Contusion o f lung
tissue in both upper lobes. No
pneumothorax.
Figure 91.
Extensive contusion changes in
both lungs. Thoracic drainage
tubes inserted bilaterally, to
gether with endotracheal tube.
velopment of a secondary transudate. Contusion injuries may cause hy

poxia. Bleeding into the lung parenchyma is often seen with contusions.
The localization of the bleeding may be both interstitial and intra-alve-
olar. The radiological changes after contusion resolve rapidly, and after
pulmonary contusion the lungs usually return to normal in the course of
5-10 days. However, it may take months before the opacities caused by
a haematoma disappear. After a severe lung injury, ARDS (adult respi
ratory distress syndrome) frequently occurs.
758
Figure 92.
a) PA chest x-ray immediately
after admission to the ward
after head-on collision in a
car. Opacities in left upper
lobe. Large left-sided ex-
trathoracic hematoma.
b) After 2 hours, considerable
widening o f the mediastinum
has occurred as a sign o f
rupture o f the aorta.
Mediastinal injuries
The most frequent injuries
of the mediastinum are
a
aortic rupture, esophageal
rupture, tracheal/bronchial
rupture, pneumomediast
inum, pneumopericardium,
and diffuse mediastinal
bleeding.
Aortic rupture is one of
the most important causes
of death after traffic acci
dents with thorax injuries.
b
The sites of predilection in
the aorta are the ascending aorta immediately before the origin of the in
nominate artery, and the descending thoracic aorta immediately after the
origin of the left subclavian artery (70%). If the rupture is situated in the
ascending part of the aorta, it is frequently accompanied by cardiac tam
ponade. Most of these patients die before hospitalization. Of the patients
who survive the initial injury, 30% die in the course of the first four hours.
Chest radiography sitting in bed is an important examination in pa
tients with thorax injuries. If the width of the mediastinum is increased
in a sitting chest radiograph, or increase in width occurs during the course
of the first hours after admission to hospital, aortic rupture is strongly in
dicated, and angiography should be done emergently (Fig. 92 a, b). A
collection of blood over the apex of the left lung (pleural cap) also points
strongly towards aortic rupture. It is extremely important to rapidly es-
759
Figure 93.
a) Aortography, right posterior
oblique (left side elevated) - aortic
rupture (arrow)
b) Aortography, lateral - aortic rup
ture
tablish this diagnosis, and up to

90% normal findings are accep
ted on aortography in order to
disclose 10% of patients with
aortic rupture. However, widen
ing of the mediastinum may also
occur with diffuse mediastinal
bleeding caused by severance of
veins. Aortography should al
ways be performed by puncture
o f the femoral artery, with ad
vancement of a catheter into the
ascending aorta immediately
above the aortic valves. A right
posterior oblique serial radiog
raphy is the best projection for
making a diagnosis of aortic rup
ture, although frontal and lateral
views may sometimes be neces
sary in order to demonstrate ex
travasation of contrast from the
aortic lumen (Fig. 93 a, b).
Computed tomography may
also provide the diagnosis. The
examination shows that a rup
ture exists, but the site of the rupture may be difficult to demonstrate with
CT, which makes angiography a better choice as the first examination
with suspected aortic rupture.
760
Figure 94.
Rupture o f the esophagus - PA
chest x-ray. A collection o f air
is seen in the mediastinum
with stripes o f air round the
arch o f the aorta and
bronchial tree (black arrows).
Rupture of the esophagus, trachea and/or bronchial tree may be seen

with severe injuries of the thorax, but may be obscured by other, more
dramatic injuries. Injuries of this type usually give changes on the chest
film in the course of the first 24 hours. The most common findings are
pneumomediastinum (Fig. 94), pneumothorax, subcutaneous emphy
sema and pleural fluid. The diagnosis is made by having the patient
swallow water-soluble contrast, thus demonstrating the leakage from
the esophagus. If rupture is suspected, contrast media containing bar
ium sulphate must be avoided. One of the two main bronchi usually
rupture when there is tracheal/bronchial rupture. The diagnosis is most
easily made by bronchoscopy, thus determining localization and extent
of the injury.
Diaphragm injuries
Rupture of the diaphragm is encountered usually as a complication of
blunt trauma to the thorax. The left diaphragm ruptures more often than
the right (Fig. 95). The injury to the diaphragm will often be obscured
by the accompanying chest injuries, and not infrequently remains undi
agnosed in the period immediately after the injury. If it continues to be
undiagnosed and untreated, hernias develop through which parts of the
abdominal organs enter the thoracic cavity. If intestine herniates into the
chest cavity, strangulation may occur. As injuries to the diaphragm are
often accompanied by an elevated diaphragm, rupture of the diaphragm
may be difficult to detect, especially in the initial phase when the pa
tient's condition makes it difficult to obtain a frontal film in the standing
761
Figure 95.
PA chest x-ray - left-sided rup
ture o f diaphragm with exten
sive changes in the basal 2/5 o f
the left lung. Two thoracic
drainage tubes have been in
serted into the pleural cavity
on the left side.
Figure 96.
Rupture o f left dome o f di
aphragm with herniation o f the
fundus o f the stomach (v) up
into the thoracic cavity. The
fundus o f the stomach is filled
with contrast. Atelectatic lung
tissue is seen lateral and poste
rior to the fundus.
position. Computed tomography of the thorax will usually provide the

diagnosis (Fig. 96).
The postoperative intensive care patient

A chest radiograph is frequently taken in the postoperative phase, and in
patients in surgical or medical intensive care units. These examinations
are generally carried out in the postoperative intensive care unit, reduc
ing the possibility o f obtaining optimal films, compared with those taken
in the radiological department with permanently installed equipment.
Radiological examination of these patients is more difficult to carry
out than a corresponding examination of other groups of patients, as they
are less mobile and in poor condition, weakened by the underlying dis-
762
Figure 97.
Right-sided pneumonectomy -
empty right hemithorax. Drain
inserted into chest cavity.
ease or the operative trauma. They often have difficulty in sitting up in

bed, and the films must be taken with the patient more or less lying down.
The newly operated patient also has difficulty with deep inspiration, so
that the air content is often reduced in the basal segments of the lungs.
Use of digital radiography has, however, considerably improved the
quality of these examinations.
It is important to take lateral decubitus views with a horizontal beam
in these patients. In this way, collections of fluid in the pleural cavity can
be evaluated on the dependent side, while possible pneumothorax can be
evaluated in the non-dependent hemithorax. Ultrasound is frequently
used in this group of patients to assess collections of fluid in the pleural
cavity, and to drain these under the guidance of ultrasound. CT scans of
these patients is also becoming increasingly more common, and is often
carried out in patients in a respirator.
Thoracic surgery
Pneumonectomy
Immediately after removal of a lung, the chest radiograph shows an
empty hemithorax (Fig. 97). A thoracic drain connected to suction lies
in the empty chest cavity in order to create negative pressure so that the
mediastinum remains in the mid-line, and the opposite lung remains ex
panded. The mediastinum and trachea will remain in the mid-line with
uncomplicated postoperative progress.
763
Figure 98.
a) Chest x-ray 3 weeks after
right-sided pneumonectomy.
Most o f the thoracic cavity
is filled with flu id (PA view)
b) Chest x-ray 3 weeks after
right-sided pneumonectomy
- most o f the thoracic cavity
is filled with flu id (lateral
view).
In the course o f a few

days, the empty pleural
cavity will gradually fill
with fluid. In the course of
weeks, most of the thoracic
cavity will be filled with
fluid, giving a homoge
nous opacity, possibly
with a small residual air-
cap apically, which may
take a long time to resorb
completely (Fig. 98 a, b).
A mediastinum shifted
towards the non-operated
side indicates increased
pressure on the operated side, which may be an indication of complica
tions such as empyema, hemothorax, or chylothorax. A bronchopleural
fistula may also be a cause of a shifted mediastinum.
Lobectomy
After removal of a lobe of the lung, the remaining lobes on the operated
side will increase in volume. Since the amount of tissue in these is con
stant, the remaining lobes, which are to fill the chest cavity, become hy
perinflated and seem to be emphysematous (compensatory emphysema).
If these lobes do not succeed in filling the chest cavity completely, the
remaining space will be filled with fluid or air. Small collections of fluid
764
Figure 99.
Postoperative total atelecta
sis o f the right upper lobe.
The upper lobe is seen as a
widening o f the mediastinum
cranially on the right side.
may remain in the chest cavity for several weeks, but are gradually ab
sorbed. The patient is treated in the postoperative phase with a thoracic
drain to maintain negative presssure in the pleural cavity and thus ex
pand the remaining lobes of the lung. Complications such as bron
chopleural cysts and empyema may be seen in this phase. Protracted col
lections of air in the chest cavity postoperatively should raise concern
for the development of a bronchopleural fistula. In such cases, bron
chography will be able to demonstrate the site of leakage.
Heart surgery
Heart surgery is usually performed through a median sternotomy.
Insertion of an aortocoronary by-pass is the most common type o f oper
ation.
In the early postoperative phase, knowledge of the exact position of
the inserted catheters/tubes is important (see separate section). On chest
radiographs, which will nearly always be frontal views, it is important
to assess the aeration of the lungs, and to ascertain whether there is post
operative atelectasis (Fig. 99), collection of fluid in the pleural cavity
(Fig. 100), pulmonary congestion indicating either heart failure, over
hydration, or widened mediastinum. A widened mediastinum may indi
cate postoperative bleeding. If the heart shadow increases in size, this
may be a sign of bleeding into the pericardial cavity, which may induce
cardiac tamponade.
Most patients operated by insertion of an aortocoronary by-pass have
atelectatic changes in the left lower lobe during the first postoperative
765
Figure 100.
Large amounts o f right-sided
pleural fluid with basal right
sided opacity. Complete
obliteration o f outline o f
right dome o f the diaphragm.
Figure 101.
Postoperative atelectatic
changes in the left lower lobe
with opacities in the lower
lobe and drawing up o f the
left dome o f the diaphragm.
Considerably dilated gastric
fundus - the fluid level in the
fundus is seen below the
dome o f the diaphragm.
days (Fig. 101). Diagnosis of this type of atelectasis and assessment o f

possible progress/regression is important for the evaluation of the type
of physiotherapy to be given to these patients postoperatively.
Postoperative monitoring
Central venous catheters are inserted after all types of lung and heart
surgery, partly to monitor the central venous pressure, and partly for par
enteral nourishment. Access is usually obtained by percutaneous punc
ture of the subclavian vein. Chest radiography after insertion of the cen-
766
Figure 102.
Frontal film shows proper in
sertion o f left-sided thoracic
drainage tube, tip o f the tube is
located apically and posteri
orly (same patient as in Fig.
101).
Figure 103.
Swan-Ganz catheter inserted
via the right jugular vein and
superior caval vein (black ar
row) through the right atrium
and right ventricle to a lower
lobe artery on the right side
(white arrow). Aortic balloon
pump (open arrow) in the
proximal descending aorta. It
is located near but below the
origin o f the left subclavian
artery.
tral venous catheter is therefore carried out to diagnose possible com

plications such as pneumothorax (Fig. 102) and to visualize the position
of the inserted catheter. Very often, the position of the catheter has to be
adjusted after examining the chest radiographs. This is important in or
der to avoid inserting the tip of the catheter into the right atrium or right
ventricle, as this may cause arrhytmias. At the same time, the catheter
must be placed centrally in order to avoid damage when parenteral nour
ishment is infused via a peripheral vein (perforation, thrombosis).
Swan-Ganz catheters (Fig. 103) are inserted to measure the pressure
in the pulmolnary arteries, and the capillary wedge pressure. Perforations
may occur and give venous bleeding, which seldom leads to any conse
quences for the patient because of the low venous pressure. Catheter per
foration of the right atrium and right ventricle may lead to cardiac tam
ponade, but this complication is extremely rare.
767
In connection with heart surgery in ill heart patients (left ventricular

failure), an aortic balloon pump is sometimes inserted via one of the
femoral arteries. A chest radiograph is necessary to check the position
of the aortic balloon pump, as the tip o f the pump must lie close to the
arch of the aorta, but not extend into the actual curve of the arch or arch
branches (Fig. 103).
Transvenous pacemaker electrodes are usually inserted via the exter
nal jugular vein under guidance of fluoroscopy to the anterior basal parts
of the right ventricle. In these cases, frontal and lateral chest radiographs
are always taken in order to check for possible loops or kinks, which may
lead to disruption of electrodes. Perforation of the myocardium by the
catheter has been seen, but does not usually lead to cardiac tamponade,
even when the tip of the electrode is drawn back through the perforated
myocardium.
An endotracheal tube is used postoperatively in most patients who have
undergone lung or heart surgery. The tip of the endotracheal tube should
lie about 6 cm above the carina (Fig. 103). The correct position o f an en
dotracheal tube should always be checked. This is especially important
in small children, where the distance between the carina and the larynx
is short, often only a few centimetres. Patients with a prolonged postop
erative course, who require respirator support, will usually require tra
cheostomy. A chest radiograph should always be performed after tra
cheostomy to check the correct position of the tracheal cannula, and to
diagnose possible bleeding in the mediastinum, indicated by mediasti
nal widening.
Postoperative pathological conditions
Atelectasis
Atelectasis is frequently seen in the postoperative phase, and may be
caused either by hypoventilation, retained secretion in the bronchial tree,
or aspiration. In a frontal chest radiograph it is important to identify the
horizontal fissure on the right side in order to assess possible loss o f vol
ume of the different lobes of the lungs. Volume-reduced lung segments
or lung lobes usually appear as homogenous opacities. Rapid changes,
both progression and regression, are typical features of postoperative at
electasis.
768
Aspiration pneum onia

Aspiration is frequently seen postoperatively. Since the patient is intu
bated during and immediately after operation, this will in itself effec
tively prevent aspiration of stomach content to the lungs during this
phase. However, it is not uncommon for aspiration to occur when the pa
tient awakens after deep sedation or anesthesia. The radiological changes
occur rapidly after aspiration of stomach content because of the low pH
of the aspirate.
The radiological changes vary considerably, depending on the content
of the aspirate, the amount, and to which segment of the lung the aspi
ration has occurred. Most of the infiltrates after aspiration resolve in the
course of a week. The infiltrates are mottled and have diffuse borders.
They are usually bilateral, but are generally most pronounced on the right
side because of the anatomical structure of the bronchial tree.
Pulmonary congestion/edem a
Postoperative pulmonary congestion/edema is due either to heart failure
or overhydration, possibly to fluid retention. Sepsis and conditions of
shock may also cause pulmonary edema as a consequence of increased
capillary permeability. The radiological changes in the postoperative pa
tient may be more difficult to assess than in other groups of patients, as
other lung changes such as atelectasis and aspiration may be seen at the
same time. The lungs are usually also considerably less aerated than nor
mal. The radiological picture is otherwise similar to congestive condi
tions with other etiologies.
Pulmonary em bolism
Pulmonary embolism is frequently seen in the postoperative patient. A
prolonged confinement to bed with development of peripheral thrombi
may also increase the frequency of emboli to the pulmonary arteries.
The radiological picture is non-specific and may include atelectasis,
irregularly defined opacities, and pleural fluid. Perfusion scintigraphy is
usually of limited value, as many other postoperative conditions can also
give areas of the lung with reduced perfusion. A combination of perfu
sion and ventilation scintigraphy improves the likelihood of diagnosing
pulmonary embolism, but pulmonary angiography is often necessary.
769
Figure 104.
ARDS - bilateral interstitial
edema - early stage.
Pneumonia
Pneumonia is often seen as a postoperative complication. Pneumonia is
seen particularly often during the development of aspiration or atelecta
sis. The radiological picture may be typical with opacities in ordinary
pneumonia, but the picture is often complicated by the simultaneous pres
ence of other pathological conditions.
A dult respiratory distress syndrome (ARDS)

This syndrome is also often called a shock lung. The aetiology is not
clear, but the syndrome is seen most frequently after major surgery with
complications such as infection, aspiration, contusion, fat embolism, and
DIC (disseminated intravascular coagulation). Severe pancreatitis may
also lead to the development of ARDS.
In the first phase of the syndrome, the lung picture is normal.The first
radiological sign of ARDS is a mild interstitial edema (Fig. 104), which
may relatively rapidly progress to extensive pulmonary edema.
Extensive pulmonary opacities may be formed as the disease develops.
These can vary considerably in appearance from purely congestive con
ditions to almost fibrosis-like changes in a chest radiograph (Fig. 105).
Consolidation of lung tissue is usual in advanced cases of ARDS. The
changes are nearly always bilateral, usually diffusely scattered, and may
be both central and peripheral in the lungs. If the cause is aspiration, the
opacities tend to initially be found in the basal segments of the lungs.
770
Figure 105.
ARDS - massive bilateral pul
monary opacities.
Figure 106.
Lateral decubitus view with hor
izontal beam. The patient is ly
ing on the right side.
Considerable amounts o f right
sided pleural fluid is demon
strated.
Pleural flu id
Pleural fluid is frequently seen after chest surgery, and, in sitting or semi
supine picture taken in bed, it will appear as diffuse blurring of the basal
lung segments, which obliterates the outline of the costophrenic angle
and diaphragm. A radiograph with the patient in lateral decubitus view
with a horizontal beam usually confirms the diagnosis (Fig. 106). In sit
ting or lying pictures, even considerable amounts of fluid may remain
undetected. Ultrasound in sitting patients easily discloses collections of
fluid in the posterior costophrenic angle.
INTERVENTIONAL PROCEDURES
The most common procedure is needle biopsy of pulmonary or medias-
tial nodules or masses. Under the guidance of fluoroscopy, the tip of a
771
needle is introduced into the lesion in question, and a sample o f tissue is

removed for cytological or histological examination. A CT scan per
formed in advance facilitates assessment of the site of puncture and the
depth. Pneumothorax and haemoptysis may occur after such procedures,
most often with spontaneous regression.
Free pleural fluid is evacuated without use of imaging techniques. If
the fluid is encapsulated, evacuation under guidance of ultrasound is ad
vised.
Intravascular interventional procedures in the thorax, for example em
bolization, are carried out in both the pulmonary and bronchial circula
tions. In the pulmonary circulation there may be arterio-venous malfor
mations which shunt non-oxygenated blood in the pulmonary arteries di
rectly into the pulmonary veins. On chest radiographs, these vascular
malformations are seen as rounded opacities with afferent and efferent
linear, vessel-like structures. Pulmonary angiography verifies the diag
nosis. With the guide-wire, small, occluding metal coils can be pushed
out through the catheter to the supplying arteries. The size of the spiral
must be such that it does not slip through to the pulmonary veins, and
thus into the systemic circulation, with a risk of cerebral embolism.
Severe hemoptysis can be mapped and treated by bronchial arterio
graphy and embolization. This is especially useful in patients with cys
tic fibrosis.
The risk associated with this type of embolization is that a spinal artery
may arise from the bronchial artery, and thus become occluded at the
same time. This type of procedure should only be carried out by radiol
ogists with long experience.
772
Chapter 19
The heart
Arnulf Skjennald and Charles B. Higgins
Radiological evaluation of cardiac disease has undergone considerable

development during the last two decades. Cine angiography provided the
capability of depicting not only intracardiac morphology but in addition,
assessment of cardiac contraction and valvular function. This diagnos
tic modality revolutionized cardiovascular diagnosis and provided a ba
sis for new surgical treatment of heart disease. In conjunction with the
development of echocardiography and isotope scanning, this has resulted
in a much better understanding of the various diseases and the patho
physiological changes involved. With the development of modem inter
ventional radiology, which is now also used extensively in heart disease
(especially in angina pectoris), radiology has established an important
role in the treatment, as well as diagnosis o f heart disease.
MODALITIES
Conventional radiology
The cardiac radiographic study consists of one frontal and one lateral
film (Fig. 1 a, b). In addition, two oblique projections are taken in spe
cial cases, but these usually give little additional information beyond that
obtained from frontal and lateral views.
The frontal film is exposed in full inspiration. The distance between
the film and the x-ray tube should be standardized in order to permit mea
surement of cardiac dimensions. The normal focal-film distance is 1.80
metres. In the frontal view, the heart appears as a white shadow, where
it is only possible to assess changes in shape and size.
The lateral view is often taken with contrast medium in the esophagus
to facilitate assessment of the position of the posterior outline (left
atrium). It is not possible on the lateral view to evaluate internal struc-
773
Figure 1.
a) PA view o f heart o f normal size. The
right atrium makes the right, and the
left ventricle makes the left outline.
Cranially, the superior vena cava is
seen on the right and the arch o f the
aorta on the left side.
b) Lateral view o f a heart o f normal size
with contrast in the esophagus. In
front, the right ventricle is next to the
sternum, and the left atrium form s the
upper part o f the posterior heart out
line and is next to the esophagus. The
posterior border o f the left ventricle
makes the lower part o f the heart's
posterior outline.
tures of the heart but rather the heart size and contour are evaluated.
However, intracardiac and pericardial calcification can be readily as
sessed in a lateral view.
Fluoroscopy is used to localize intracardiac calcifications. This
modality permits evaluation of motion of the calcification during the car
diac cycle. Fluoroscopy may also be useful to identify paradoxical move
ment of the left ventricle (with aneurysms of the left ventricle), and to
examine the relationship between the heart and mediastinal structures.

Computed tomography (Fig. 2 a, b) is not used routinely in the radio
logical evaluation of the heart,but CT programs have been constructed
774
THE HEART
Figure 2.
a) Computed tomography; section
through the heart at the level o f
the ventricles. The picture shows
the right and left ventricle and
the course o f the ventricular
septum.
b) Cross section through the upper
part o f the heart; intravenous
contrast medium. The left atrium
is seen at the back, and the right
atrium to the right as a tapering
cleft-like space. The outlets o f the
right and left ventricles, respec
tively, are seen in the middle
anteriorly.
that can follow a contrast bo

lus through the heart from the
right side through the pul
monary circulation to the left
side. Special CT equipment
(ultra fast CT, or cine CT-scan
ner) has also been constructed for dynamic CT studies of the heart. Cine
CT has been shown to be very effective for demonstrating patency of
coronary artery bypasses; quantifying ventricular volumes and function;
evaluating pericardial diseases and complications of myocardial infarc
tions; and defining the morphology of congenital heart disease. Recently,
some enthusiasm has been revived for using cine CT as a highly sensi
tive method for demonstrating coronary arterial calcification and using
this to propose the relative risk of obstructive coronary arterial disease in
specific populations.
Magnetic resonance imaging (MRI)

Magnetic resonance imaging (MRI) (Fig. 3) is used for the diagnosis of
a few specific types of cardiac disease, and will be of great importance
in the future, especially with the continued development of fast MR imag
ing techniques. The initial MRI technique, ECG gated spin echo imag
ing, provides striking depiction of cardiac morphology. Subsequently,
775
Figure 3.
Transverse section through the
heart (MRI). Large dilated left ven
tricle in a child. A small triangular
right ventricle is seen at the fro n t
with the right atrium behind it. The
left atrium is seen in fro n t o f the
vertebral column, with the opening
o f one o f the pulmonary veins on the
left.
Figure 4.
ECG gated spin echo (a) and cine
MR (b) in the transaxial plane
display a dissection o f the descend
ing aorta. The intimalflap (arrow)
separates the true (T) and false (F)
channels. On the spin echo image,
the signal in the false channel is
caused by slow velocity o f blood
flow.
a
cine MRI was introduced,
which provides images corre
sponding to multiple phases of
the cardiac cycle. This en
abled evaluation of cardiac
contraction and valvular mo
tion. It is now possible to ob
tain a cine MRI acquisition
b during a breath hold period of
14 to 16 seconds. MR images
can also be obtained at a rate of one per second or slightly longer in or
der to monitor contrast media distribution in the cardiac chambers and
myocardium. Monitoring of the first pass dynamics of MR contrast me
dia constitutes a new method for evaluating mycardial perfusion. Finally,
nearly real time MR imaging of the heart is possible with echoplanar MRI.
The role of MRI of the heart is still evolving and consensus is not es
tablished regarding all the proposed uses of it for cardiovascular diag
nosis. MRI can be considered for the evaluation of the following clini
cal situations:
776
THE HEART
Figure 5.
ECG gated spin echo images in the
transaxial (a) and coronal (b) planes
in two patients with constrictive
pericarditis. The thick pericardium
is demonstrated in both patients.
Figure 6.
ECG gated spin echo image in the
transaxial plane demonstrates
hemorrhagic (H) and nonhemor-
rhagic (E) pericardial collections.
1. Thoracic aortic disease, including dissections and aneurysms (Fig. 4)

2. Some forms of pericardial disease, especially for the definitive diag
nosis of constrictive pericarditis (Fig. 5); loculated pericardial effu
sions (Fig. 6) and pericardial hematoma (Fig. 6).
3. Intracardiac (Figs. 7, 8) and paracardiac masses (Fig. 9)
4. Complications of acute myocardial infarction such as true and false
ventricular aneurysms and mural thrombus (Fig. 10).
5. Right ventricular dysplasia and outflow tachycardia
777
Figure 7.
ECG gated spin echo images in
the transaxial (a) and coronal (b)
planes demonstrate a large left
atrial myxoma (M) nearly filling
the left atrium. E = pericardial ef
fusion;
P = pulmonary arteries; T = tra
chea; arrow = left upper pul
monary vein.
Figure 8. ECG gated spin echo images be

fo re (a) and after (b) the administration o f MR contrast medium (gadolinium chelate)
demonstrates a left atrial (LA) tumor (arrow) which markedly enhances with this con
trast medium.
778
THE HEART
Figure 9.
ECG gated spin echo image shows a
large tumor (T) o f the lung invading
the left atrium (LA).
RA = right atrium; arrow = peri
cardial effusion
Figure 10.
ECG gated spin echo image in the
coronal plane demonstrates an
aneurysm (arrow) o f the diaphrag
matic segment o f the left ventricle
(LV) after prior myocardial infarc
tion.
A = aortic sinus; P = pulmonary
artery; RA = right atrium
6. Several types of congenital heart disease such as coarctation (Fig. 11);

arch anomalies; pulmonary arterial and venous abnormalities; and
postoperative congenital heart disease.
The cine MRI technique can be used to evaluate dimensions and func
tion of both ventricles. Cine MRI is also used to identify pathological
(high velocity turbulent) flow caused by valvular regurgitation and steno
sis (Fig. 12,13). The velocity encoded cine MRI technique provides mea
surement of blood flow and velocity in the heart and great vessels. It has
been used for quantifying the volume of valvular regurgitation and the
gradient across valvular stenosis. It can also be used to measure the vol
ume of left to right shunts and differential flow in the right and left pul
monary arteries.
779
Figure 11. ECG gated spin echo images in the transaxial (a) and sagittal (b) planes in
a patient with a severe juxtaductal coarctation (arrow) o f the aorta. Large paraverte
bral collateral arteries are demonstrated (arrows).
Figure 12.
Coronal cine MR images in a patient
with aortic regurgitation. Images in the
upper panels are during systole and
those in lower panels are in diastole.
The signal void emanating from the aor
tic valve in diastole represents the je t o f
aortic regurgitation.
Figure 13.
Cine MR image in a patient with aortic
stenosis. Systolic phase. The signal void
emanating from the aortic valve into the
ascending aorta is caused by aortic
stenosis.
780
THE HEART
Angiocardiography/coronary angiography
Angiography (Fig. 14 a-d) is used to examine the heart chambers and the
coronary arteries. Under the guidance of fluoroscopy, a catheter is in
serted, usually via the femoral artery, to the left ventricle, where contrast
is injected. This permits measurement of the volume of the left ventricle
and parameters o f left ventricular function. The movement and compe
tency of the cardiac valves can also be evaluated. The catheter is then
routinely withdrawn to immediately above the aortic valves so that this
portion of the ascending aorta and the aortic valves can be examined. In
addition, selective catheterization of the left and right coronary arteries
is carried out, and films are acquired in several projections to assess
pathological changes such as stenosis or occlusion.
When the right side of the heart is examined (cardiac catheterization),
the catheter is inserted from either the femoral vein, or an antecubital
vein, to selected sites in the right half of the heart or superior vena cava,
depending on the problem under investigation. At the same time, pres
sure is registered, and the oxygen content of the blood is measured. Since
injection of contrast agents into the heart itself necessitates large vol
umes injected very rapidly (45 ml injection volume, 15 to 25 ml per sec
ond with injection into the left ventricle), an automatic high pressure sy
ringe is needed for these injections. Injection into the coronary arteries
is usually carried out by manual injection of from 5 to 8 ml of contrast
medium per injection.
The films in angiocardiography and coronary angiography are usually
recorded on cine film (35 mm film). In order to obtain continuous, sharply
defined images of the movements of the heart, a minimum of 24 frames
per second is often used during these examinations, which can also be
carried out using digital format instead of ordinary cine film.
Echocardiography
Ultrasound scanning of the heart can either be performed as M-mode or
two-dimensional (2-D) echocardiography (Fig. 15 a, b).
M-mode echocardiography gives a one-dimensional image of the struc
tures of the heart. Since the different parts of the heart move synchronously
in relation to each other during the cardiac cycle, the echo from these struc
tures will move coordinate with each other in relation to the ultrasonic
transducer on the chest wall. These echoes are recorded on an oscillograph
or on videotape as a continuous one-dimensional representation.
781
Figure 14.
a) Angiocardiography - catheter from the fem oral artery down into the left ventricle.
b) Thoracic aortography with injection o f contrast medium into the thoracic ascending
aorta immediately above the aortic orifice. Normal right and left coronary arteries
are visible.
c) Selective injection o f contrast medium into the left coronary artery with normal ar
teries to the anterior and posterior walls o f the heart.
d) Selective injection o f contrast medium into a normal right coronary artery.
In two-dimensional echocardiography, the sonic waves travel in one

plane through the heart, and the ehcoes received by the transducer are
shown on a monitor in real time. This provides a tomographic image of
the plane under examination. Most of the heart can be visualized in this
way. The major limiting factors for attaining an acoustic window for
recording are interposition of bony structures of the chest wall or lung.
It has recently become customary to use Doppler echocardiography
when examining the heart. The direction and velocity of blood flow can
be determined using Doppler echocardiography. The Doppler technique
782
THE HEART
Figure 15.
a) Echocardiography (two-dimensional) showing the 4 chambers o f the heart, and the
ventricular septum (many echoes) between the right (RV) and left (LV) ventricles.
b) Two-dimensional echocardiography at the level o f the atria, showing the right and
left atria and an atrial septum defect (ASD).
Figure 16.
a) Cardiac scintigraphy showing both ventricles and the ventricular septum (arrows).
Left ventricle in systole.
b) As 16 a - left ventricle in maximal systole. The ventricular septum is shown by a
black arrow.
is very well suited for detecting pathological changes in the flow of blood,
which may occur with atrial septal defect, ventricular septal defect, and
pathological changes in the heart waves (pulmonary, mitral and aortic
orifices).
783
Isotope scanning
Isotope scanning of the heart (Fig. 16 a, b) is a noninvasive examination
which provides not only pure pictorial information, but also details of-
physiological conditions. This examination can provide information on
function of the left ventricle; myocardial perfusion; presence of my
ocardial infarcts; and presence and volume of intracardiac shunts.
784
THE HEART
Several radioactive isotopes are used in cardiac scintigraphic diagno

sis. The most frequently used are technetium 99m ("m Tc), thallium
201TI, and 99mTc sestamibi.
NORMAL ANATOMY
In a frontal view of the heart and lungs, the right atrium constitutes the
outline of the heart on the right side. Cranially, the right atrium contin
ues into the superior vena cava. The opening of the superior vena cava
into the right atrium is situated in the posterior part of the atrium. The
atrial septum forms the posterior medial wall of the right atrium. In front
of the atrial septum, the right atrium is situated next to the root of the
aorta. The right ventricle, which is the most anterior part of the heart, is
situated adjacent to the sternum. Anterior and to the left of the root of
the aorta are situated the pulmonary valves and the right ventricular out
let region. The ventricular septum separates the right ventricle from the
left ventricle. The cranial part of the posterior outline of the heart is oc
cupied by the left atrium. The pulmonary veins from the right and left
lungs connect to the posterior portion of the left atrium. The left ventri
cle lies anterior and slightly to the left of the atrium. In a frontal view
most of the left border of the heart consists of the left ventricle (Fig. 17
a-d). A series of transaxial MR images (Fig. 18) displays the morphol
ogy and position of the cardiac chambers. Examination of these imag
ing facilitates understanding of the anatomy of the cardiac contours as
depicted on plain radiographs.
Right atrium
The right atrium is best visualized by angiocardiography with injection
of contrast medium either into the right atrium, superior vena cava, or
inferior vena cava. The right atrium is almost globular in shape with an
appendage (auricle), projecting anteriorly, cranially and leftward from
the body of this chamber. The superior vena cava and inferior vena cava
open into the right atrium at the upper and lower edge of the posterior
wall. The tricuspid valve lies at the front and to the left of the center of
the right atrium. The coronary sinus opens into the posterior wall of the
right atrium between the tricuspid orifice and the inferior vena cava.
Opacification of the right atrium with contrast medium demonstrates the
thickness of the lateral wall against the air-filled right lung. The combined
thickness of the right atrial wall and adjacent pericardium is less than 4 mm.
785
Figure 18. Series o f ECG gated spin echo images extending from the base to the mid
portion o f the heart displays the cardiac chambers and great vessels.
A = aorta; I = inferior vena cava; LA = left atrium; L V = left ventricle; RA = right
atrium; RO = right ventricular outflow tract; R V = body o f right ventricle.
Arrows = pericardium; curved arrow = atrial septum; arrowhead = coronary sinus
Right ventricle
The internal anatomy of the right ventricle is demonstrated by angiog
raphy after injection of contrast medium into the right side of the heart
or into the superior vena cava or inferior vena cava. In frontal views the
right ventricle is triangular, with the apex pointing downwards to the left.
The pulmonary orifice is seen cranially. Prominent trabeculations are
characteristic for the right ventricle. The tricuspid and pulmonic valves
are separated by a tunnel of muscle (crista supraventricularis or in-
fundibulum). The right ventricle is not usually border-forming on a
frontal view of the chest. In a lateral view, the anterior border of the right
ventricle forms the anterior outline of the heart.
786
THE HEART
Left atrium
The left atrium is not globular like the right atrium, but more flattened
anteroposteriorly. Four pulmonary veins empty in to the posterior aspect,
two on each side. The mitral orifice lies in the caudal, anterior part of the
left atrium, slightly to the left. Like the right atrium, the left atrium has
an appendage (auricle), which, in a frontal view, constitutes the border
of the left side o f the heart between the left ventricle and the pulmonary
artery.
In a lateral view, the posterior outline of the left atrium is clearly seen
where it lies adjacent to the anterior wall of the contrast-filled esopha
gus. The left main bronchus usually runs along the upper posterior part
of the left atrium.
Left ventricle
The left ventricle (Fig. 14) has an elliptical shape with the apex anteri
orly, inferiorly and to the left. The aortic and mitral orifices lie near the
base of this chamber. The mitral valve is bicuspid, the aortic valves, tri
cuspid. The ventricular septum runs obliquely from right posterior to left
anterior, and constists of a muscular and a membranous part.
The internal anatomy of the left ventricle is demonstrated by angiog
raphy. Injection o f contrast medium into the left ventricle is an impor
tant part of coronary angiography. The mitral valves are assessed by left
ventricular angiography, which permits observation of the flow of un
opacified blood from the left atrium into the left ventricle in order to eval
uate the size of the mitral orifice.
Coronary arteries
The right and left coronary arteries (Fig. 14 c, d) arise from the aorta.
The left coronary artery arises from the aortic bulb to the left, posteri
orly. The right coronary artery arises from the right part of the aortic bulb
with its opening in the front, and slightly to the right.
From its aortic origin, the left coronary artery courses to the left. The
main trunk bifurcates into the left anterior descending artery (LAD), and
the circumflex artery (CX).
The LAD proceeds along the front of the heart, where it provides a
number of parallel branches to the interventricular septum (septal
branches) and large branches coursing over the anterior surface of the
left ventricle (diagonal branches) and supply the anterior and lateral walls
787
of the left ventricle.

The CX courses on the posterior side o f the heart towards the left,
where it provides one of several large branches to the posterior lateral
wall of the left ventricle (obtuse marginal branches).
The right coronary artery (RCA) courses from the aorta onto the right
side of the heart, and then continoues on the lower surface of the heart.
During its course, the artery provides several branches, including one to
the sinus node. The posterior descending branch and posterolateral
branches arise from the distal RCA and run on the posterior surface of
the heart, supplying the posterior portion of the ventricular septum and
the posterior wall of the left ventricle.
Dominance of the coronary arteries is designated by the arterial sup
ply to the posterior wall of the left ventricle. Right dominance is defined
by origination of the posterior descending and posterolateral branches
from the RCA. Left dominance is defined by orgination of these branches
from the CX. Balanced dominance (co-dominance) results from origi
nation of the posterior descending branch from the RCA and posterolat
eral branches from the CX. Roughly 80% of humans have a right dom
inant circulation and 10% have left dominant circulation. About 10%
have balanced dominance.
Pericardium
The pericardium is a two-layered sac that surrounds the heart. The two
layers of the pericardium are covered by a serous membrane. In the min
imal space between the two membranes, there is normally about 20 ml
clear fluid.
The pericardium completely surrounds the heart, and extends along
the pulmonary veins, azygos vein, superior vena cava, and inferior vena
cava. The pericardium also covers the pulmonary trunk up to the bifur
cation into the right and left pulmonary arteries, and the caudal 2 cm of
the ascending aorta.
The pericardium is not visible as a separate structure on the chest ra
diograph, but represents the true border of the heart shadow, together
with epicardial fat, against the air in the lungs. The normal pericardium
is easily identified on computed tomography and MRI. Pericardial fat
pads are frequently seen, most commonly at the base of the heart.
788
THE HEART
PATHOLOGY
The diagnosis o f congenital heart disease is usually established during
infancy or early childhood. The congenital heart diseases are therefore
described in the chapter on Pediatric Radiology.
The enlarged heart

Enlargement o f the heart may be generalized or involve only one or two
chambers. Enlargement may also involve predominantly one chamber
initially with secondary effects on other chambers. Several methods of
measuring the volume of the heart exist.
The simplest and most usual method is to measure the greatest trans
verse diameter o f the heart in a frontal picture, and relate this to the great
est internal width of the thorax (Fig. 19). When the size of the heart is
normal, the heart's greatest transverse diameter is less than half the max
imal internal diameter of the thorax. In Scandinavia, it has also been usual
to calculate the volume of the heart in millilitres. For this purpose, frontal
and lateral views of the chest are required. A normal heart resembles an
ellipsoid, and the volume of the ellipsoid can be calculated when the axes
are measured. The definition of the axes is shown in Fig. 20 a, b. The
axes are multiplied by each other and by a constant to determine the to
tal volume of the heart. The constant (usually 0.40) compensates for ra
diographic magnification. In order to relate the heart’s total volume to
the size of the body, the total volume is divided by the body surface ex
pressed in square metres, calculated from height and weight. The nor
mal upper limit for women is 450 ml/m2, while a volume of over 500
ml/m2 should be regarded as enlarged. A relative heart volume between
500 and 550 ml/m2 body surface is regarded as borderline in men.
However, there are considerable sources of error connected with the
method, and differences in measurement of 15 % must be accepted as
within the margin of error. Because 2D echocardiography and MRI dis
play the invididual chambers, these methods provide accurate measure
ments of chamber volume and myocardial mass. Assessment of cardiac
volumes is most frequently done using 2D echocardiography.
General enlargement of the heart

General enlargement of the heart (enlargement affecting all cardiac
chambers) is seen in a number of different diseases of the heart and lungs
- see description of these in appropriate sections.
789
790
THE HEART
Figure 21.
Slight to moderate left ventricular
enlargement with rounded and low-
lying heart apex.
Left ventricular enlargement

Enlargement of the left ventricle is due either to hypertrophy or dilata
tion. If the enlargement of the left ventricle or silhouette is considerable,
it is invariably due to dilatation. The most common sign of enlargement
of the left ventricle is an elongation of the longest axis of the left ven
tricle. The apex is also seen to be rounded and low-lying. These changes
are seen in a frontal view (Fig. 21). In the lateral view, left ventricular
enlargement is indicated by the posterior border of the left ventricle ly
ing behind the barium-filled oesophagus. The lower posterior part of the
left ventricle is also frequently seen projected behind the outline of the
inferior vena cava, where this crosses the right diaphragm.
The ejection fraction of the left ventricle (expressed by the relation
ship between the stroke volume and the end diastolic volume) is a reli
able index of left ventricular function. The ejection fraction is normally
between 60 and 75 %. In diseases affecting the left ventricle, the ejection
fraction is reduced either by reduction of stroke volume or by an increase
in end-diastolic volume. The ejection fraction and the end-diastolic vol
ume can be estimated using angiocardiography, by calculating the vol
umes at end diastole and end systole. However, it is becoming increas
ingly more common to calculate these values using echocardiography.
The most accurate and reproducible measurement of ventricular volume
can be provided by cine MRI. The most frequent causes of left ventric
ular enlargement are mitral and/or aortic valvular insufficiency, dilated
cardiomyopathy, ischemic cardiomyopathy, and decompensated aortic
791
Figure 22.
a) Generally enlarged heart with
large left atrium. The left atrium
is projected over the right
atrium and makes the outline
(black arrow).
b) Lateral view - generally en
larged heart with large left
atrium, which bulges backwards
considerably (black arrow).
stenosis and hypertension.

The most common signs of
enlargement of the left atrium
(Fig. 22 a, b) are backwards
displacement of the contrast-
filled esophagus, elevation
of the left main bronchus,
dislocation of the right mar
gin of the left atrium poste
rior to the right atrium (dou
ble contour sign), or dilata
tion of the left auricle. The
left atrium is the heart chamber where isolated enlargement of the heart
is easiest to detect. The size of the left atrium can be more precisely de
termined by 2D echocardiography.
The most common cause of enlargement of the left atrium is mitral
valve disease. Another frequent cause is resistance to left ventricle fill
ing caused by disease which reduces compliance, such as aortic steno
sis and hypertrophic cardiomyopathy. Enlargement of the left atrium may
occur secondary to hypertrophy and/or dilatation of the left ventricle.
792
THE HEART
Right ventricular enlargement

The most common radiological sign of enlargement of the right ventri
cle is filling of the retrosternal clear space with increased contact o f the
right ventricle with the posterior border of the sternum. Normally, less
than one-third o f the posterior border o f the sternum should be in con
tact with the right ventricle. Assuming a normal position of the sternal
border, enlargement of the right ventricle increases the area of contact
between the sternum and the right ventricle. On the frontal view, right
ventricular enlargement displaces the left border of the heart directly lat
erally in contradistinction to the left ventricular enlargement, which
causes the border to extend both laterally and caudally.
Two-dimensional echocardiography can provide a qualitative assess
ment of right ventricular size but is not reliable for measuring volumes
of the right ventricle. Cine MRI, and ultrafast CT can provide accurate
measurement of right ventricular volumes. The most frequent causes of
enlargement of the right ventricle are rheumatic heart disease affecting
the tricuspid valve, advanced mitral stenosis (due to pulmonary arterial
hypertension), and longlasting pulmonary hypertension, frequently ac
companied by simultaneous pulmonary or tricuspid insufficiency.
Right atrial enlargement

Enlargement of the right atrium seldom occurs as an isolated phenome
non. The most common radiological sign is that the right outline of the
heart is projected far rightward, over the right lung. With substantial en
largement there is elongation of the right atrial margin so that this mar
gin comprises more than 60% of the length of the mediastinal cardio
vascular silhouette. Right atrial enlargement can also obliterate the ret
rosternal clear space as depicted on the lateral film.
Enlargement o f the right atrium is readily demonstrated by echocar
diography, ultrafast CT and MRI. The most common cause of enlarge
ment of the right atrium is tricuspid insufficiency, usually caused by
rheumatic heart disease. Acquired tricuspid stenosis seldom occurs.
Acquired valvular diseases
Mitral valve disease

Mitral stenosis is usually caused by rheumatic heart disease and rarely
by congenital defects or left atrial myxoma. Mitral regurgitation has
793
Figure 23.
a) Mitral insufficiency - enlargement o f the left atrium with backwards dislocation o f
the contrast-filled esophagus.
b) Mitral defect with enlargement o f the left atrium (oblique view). The enlarged left
atrium dislocates the contrast-filled esophagus backwards.
many etiologies, including mitral valve prolapse, spontaneous chordal

rupture, bacterial eondocarditis, post infarctional papillary muscle rup
ture or dysfunction and rheumatic heart disease.
In the acute phase of rheumatic fever, the chest radiograph is normal.
If cardiomegaly ocurs, it is usually due to pericardial fluid as a result of
pericarditis. Enlargement of the heart not due to pericarditis is, at this
stage, most often caused by an acute involvement of the mitral valves,
resulting in mitral insufficiency.
When chronic changes develop, there is scar formation and retraction
of the cusps, which become thickened. At the same time, fibrosis devel
ops in the surrounding papillary muscles. A combination of stenosis and
insufficiency is usually seen. In late stages, calcification of the cusps may
occur.
Stenosis of the mitral valve causes increased mean pressure in the left
atrium, which is transmitted retrogradely to the pulmonary veins (pul
monary venous hypertension), eventually resulting in interstitial and later
alveolar edema. At a later stage, as a result of the development of pul
monary hypertension, pulmonary insufficiency, dilatation of the right
ventricle, and tricuspid insufficiency develope.
794
THE HEART
Figure 24.
Considerably enlarged heart with
"mitral configuration ". All parts of
the heart are enlarged. Special ac
centuation o f upper left heart out
line, considerably dilated vascular
structures in the right hilar region.
The initial radiological finding is enlargement of the left atrium (Fig.

23 a, b). The left auricle is frequently dilated and is seen as a lateral evagi-
nation in the segment of the left cardiac margin between the pulmonary
artery and the left ventricle on the frontal radiograph. At the same time,
there is elevation of the left main bronchus. The esophagus is dislocated
posteriorly and to the left. There may be signs of pulmonary hyperten
sion or edema and subsequently, right ventricular enlargement (Fig. 24).
Calcification of the valves may be difficult to detect in frontal and lat
eral views, but are readily identified if present, on fluoroscopy and on
CT scans. In some cases, calcification on the wall of the left atrium may
occur. This is usually found in the posterior part of the atrial wall.
On the basis of frontal and lateral views of the heart, it is sometimes
possible to determine whether the dominant abnormality is mitral steno
sis or insufficiency. If there is enlargement of both the left atrium and
left ventricle, mitral insufficiency is likely to be the most important com
ponent, if it is possible to exclude the simultaneous presence o f an aor
tic valve disease.
The definitive diagnosis of mitral valve disease is established by left
ventricular angiography and echocardiography. In the left ventricular an
giography, the left ventricle is catheterized, and contrast medium is in
jected. When normal mitral valves open, non-opacified blood flows from
the left atrium into the left ventricle and causes a void (wash-in defect)
in the contrast pool of the left ventricular chamber. In mitral stenosis
795
there is restriction of the wave front o f unopaficied blood flow into the
left ventricle. In mitral insufficiency, there is regurgitation o f contrast
medium from the left ventricle to the left atrium during systole.
Echocardiography is ideal for evaluation of the mitral valve morphol
ogy and motion. M-mode echocardiography allows the study of reduc
tion in DCR (diastolic closure rate), and also permits demonstration of
thickening of both the anterior and posterior cusps of the mitral valve.
Echocardiography also provides a visual demonstration of the left atrium,
making it possible to calculate its volume. The existence of thrombi in
the left atrium can also be visualized by the same technique.
Echocardiography is the most important modality in the diagnosis of mi
tral defects of non-rheumatic etiology.
Tricuspid valvular defects

Tricuspid valvular defects arise either as a consequence of a purely
rheumatic process involving the valvular apparatus, or by the tricuspid
valve becoming insufficient because of dilatation of the right ventricle.
The most important radiological sign is an enlarged right atrium. As
tricuspid defects are seldom seen as isolated phenomena, the diagnosis
is difficult to make on the basis of conventional radiography with frontal
and lateral views of the heart. Calcification of the tricuspid valve is ex
tremely rare.
It is easiest to examine the tricuspid valve by echocardiography. In the
presence of a tricuspid defect, cardiac catheterization with insertion of a
catheter through the tricuspid orifice to the right ventricle is difficult. An
enlarged right atrium makes it difficult to insert the tip of the catheter
through the tricuspid valves, especially if stenosis is also present.
Aortic valvular disease
Aortic stenosis
Aortic stenosis can occur either on a rheumatic basis or as a result of cal
cification in adult life of congenitally abnormal valves, usually bicuspid
valves. Aortic stenosis on a rheumatic basis is frequently accompanied
by aortic insufficiency. In rheumatic aortic valvular disease, however,
concomitant abnormalities of the mitral valves are always present and
frequently dominate the clinical features and the radiographic findings.
796
THE HEART
Figure 25.
Lateral view o f the heart with
calcification o f the aortic valve
cusps (black arrows).
The aortic valves are frequently calcified (Fig. 25). During the com
pensated phase, there is hypertrophy of the left ventricle but usually ra
diographic signs of enlargement of the left ventricle. In the decompen
sated phase, moderate enlargement of the heart may be present, but the
left ventricle size may be increased considerably in the presence of si
multaneous aortic insufficiency. In aortic stenosis, the ascending aorta
is dilated (post-stenotic dilatation). Echocardiography provides a good
view of the aortic valves, and the degree of restriction of motion can be
assessed. The pressure gradient between the valves can be estimated by
mesuring the peak velocity of blood flow using Doppler echocardiogra
phy. Echocardiography has reduced the necessity of catheterization of
the left ventricle, which is beneficial, as this may be difficult to perform
through a stenotic aortic orifice.
Aortic insufficiency
The radiographic features are different for acute and chronic aortic in
sufficiency. Acute aortic insufficiency is usually caused by bacterial en
docarditis, and produces a rapid incrase in the left ventricle end-diastolic
pressure, with development of pulmonary edema. In the acute phase, the
size of the heart will be normal in most patients, but if heart failure de
velops there will be pulmonary edema and redistribution of flow to the
pulmonary vessels in the upper part of the lungs. Acute aortic insuffi-
797
Figure 26.
Aortic insufficiency —injection o f
contrast medium into the ascend
ing aorta immediately above the
aortic valve with regurgitation o f
contrast into the whole left
ventricle (black arrows). Aortic
insufficiency grade III.
ciency is one of the causes of pulmonary edema in a patient with a heart

of normal size.
Chronic aortic insufficiency is most often a result of congenital valvu
lar defect or rheumatic heart disease. Bicuspid valves are the most com
mon form of congenital anomaly. Rheumatic heart disease usually leads
to destruction of the valvular apparatus, often with adhesion of the com-
misures, resulting in combined aortic stenosis and insufficiency. The mi
tral valves are frequently also involved.
The diagnosis and the amount of regurgitation from the ascending aorta
to the left ventricle in diastole can be estimated by Doppler echocardio
graphy. The thickening and limitation o f the aortic leaflets can also be
established by echocardiography. Two-dimensional echocardiography
is used to determine the size of the left ventricle and left ventricular func
tion. Cine MRI has been used to identify valvular regurgitation due to
the signal void caused by the regurgitant jet (Fig. 12).
Right-sided cardiac catheterization is usually performed in addition to
left ventricular angiography in order to evaluate the right-sided valve and
pulmonary arterial pressure. Left ventricular angiography is used to as
sess the function of the left ventricle. Preoperatively, coronary angiog
raphy will nearly always also be done to exclude significant stenoses.
Aortic insufficiency is graded angiographically (grades I-IV), according
to the amount of contrast medium refluxing into the left ventricle after
injection of contrast medium into the ascending aorta (Fig. 26).
798
THE HEART
Ischemic heart disease
Angina pectoris
Angina pectoris is a clinical syndrome, characterized by retrosternal
chest pain with typical radiation to the left arm. When surgery is con
sidered in these patients, coronary angiography is carried out in order to
identify the sites and severities of stenoses in the coronary arteries. In
the presence o f severe stenosis (> 85% reduction in luminal diameter)
or occlusion, collateral vessels are frequently present originating from
the ipsilateral or contralateral coronary artery.
Evaluation o f regional and global function of the left ventricle is an
integral part of angiography in the assessment of a patient with angina
pectoris. The global function of the left ventricle is provided by mea
surements of the ejection fraction and the end-diastolic pressure and re
gional function defined by wall motion. Assessment of left ventricular
function can also be made by echocardiography. Ventricular function
can also be studied using scintigraphy techniques and/or isotope ven
triculography (Fig. 16 a, b). At present, neither echocardiography nor
scintigraphy can provide the necessary morphological information on
the condition of the coronary arteries.
Infarct
Myocardial infarction is ischemic necrosis of the heart muscle leaving
fibrotic scar tissue. Currently, many infarcts are treated with throm
bolytic therapy, which may attenuate the severity and extent of the in
farction.
Uncomplicated infarction causes no changes in the chest radiograph.
If an earlier infarct has led to the development of an aneurysm, this may
appear as a bulging of the outline of the heart (Fig. 27). Calcification
rarely marks the site of prior infarctions or aneurysms. In some cases
acute infarction causes pulmonary venous hypertension or edema, usu
ally with a normal heart size.
In left ventricular angiography, the infarcted region usually shows no
wall motion (akinesis), paradoxical motion (dyskinesis) or severe re
duction in wall motion (hypokinesis). Multiple or large infarcts reduce
the ejection fraction of the left ventricle and increase end-diastolic pres
sure. Dilatation of the ventricle may develop, producing the features of
ischemic cardiomyopathy. Coronary angiography usually demonstrates
799
Figure 27.
PA view o f the heart with large left
ventricular aneurysm with massive
bulging o f the left outline o f the
heart.
high degrees of stenosis, or possible occlusion, of the arteries that sup

ply the infarcted area.
Complications o f infarction
A number of complications may occur secondary to myocardial infarc
tion, including cardiac rupture. This leads to cardiac tamponade, and
these patients die so quickly that angiography and echocardiography are
seldom carried out.
Aneurysms of the left ventricle may develop after large transmural in
farcts. The diagnosis can be evident on the radiograph, where there is a
focal bulging (evagination) of the normal contour of the heart, most fre
quently in the apical region (Fig. 27). During fluoroscopy, reduced, pos
sibly paradoxical, movement of the aneurysmal area is seen. The diag
nosis is otherwise made by left ventricular angiography, 2D echocar
diography, or MRI (Fig. 10).
Large infarctions that include the ventricular septum may lead to rup
ture of the ventricular septum. This is a complication with high mortal
ity if the rupture occurs in the lower posterior part, but a slightly better
prognosis if the rupture occurs in the anterior part of the ventricular sep
tum. The chest radiographs show an enlarged heart with pulmonary
edema. Right-sided cardiac catheterization demonstrates signs of left-to-
right shunt with highly oxygenated blood in the right half of the heart.
The diagnosis is easily made by left ventricular angiography, where a
leak of contrast from the left to the right ventricle is seen, and by echocar
diography.
800
THE HEART
Thrombi in the left ventricle, usually at the apex, are also seen as a
complication o f infarction. This diagnosis can be made by left ventricu
lar angiography, 2D echocardiography and MRI.
Other heart diseases

There are a number of other diseases that are confined to the myocardium,
including different types of cardiomyopathy. The major types of car
diomyopathies are: dilated (congestive), hypertrophic, restrictive, and
obliterated forms.
Cardiomyopathy may be caused by infection, collagen vascular dis
eases, atherosclerosis, or metabolic diseases. Use of alcohol and drugs
may produce dilated (congestive) cardiomyopathy. Endomyocardial fi
brosis also causes a form of cardiomyopathy. However, most cases of
dilated cardiomyopathy are idiopathic.
In the dilated form of cardiomyopathy, the heart is considerably en
larged, and there is also pulmonary venous congestion and/or edema.
Echocardiography, angiography, and isotope ventriculography can be
used to assess ventricular function and thereby document the severity of
dilated cardiomyopathy.
Two dimensional echocardiography and MRI are used to evaluate the
severity and distribution of hypertrophy throughout the left ventricle in
hypertrophic cardiomyopathy. Most patients have asymmetric thicken
ing of the ventricular septum with or without obstruction of the subaor-
tic region. MRI has been useful for quantifying myocardial mass in this
disease.
Tumors in the heart are rare and are usually benign. The most com
mon types are myxoma of the left atrium and lipoma of the right atrium.
In a chest radiograph the heart is either normal in size, or there is slight
enlargement of the left atrium. On echocardiography, it may be difficult
to differentiate between an intra-atrial myxoma and a thrombus. MRI has
recently been shown to be a very effective method for demonstrating the
presence and extent of intracardiac and paracardiac tumors (Figs. 7, 8).
The diagnosis can also be made by angiography, but here too, it may be
difficult to distinguish between a thrombus and a tumor. On MRI the sig
nal intensity of thrombus is usually lower than that of most, but not all,
cardiac tumors.
801
Pericardial diseases
Pericardial cysts
Pericardial cysts are congenital and filled by clear serous fluid. They may
communicate with the pericardial space. About 2/3 of all pericardial cysts
are found caudally and anteriorly on the right side. On the chest radi
ograph, it is impossible to differentiate between cysts and pericardial fat
pads, but the differential diagnosis is readily established by 2D echocar
diography, computed tomography, or MRI. Pericardial diverticula are
less common than pericardial cysts. These are true diverticula, contain
ing all the layers of the pericardium.
Pericardial tumors
Pericardial tumors are very unusual. Mesothelioma is the most frequently
seen malignant tumor. Dermoid is a benign tumor of the pericardium.
Metastases are seen more often. In most respects, the clinical and radi
ological picture resembles that seen with an ordinary pericardial effu
sion. A pericardial tumor is suggested by a hemorrhagic pericardial ef
fusion. The hemorhagic effusion can be defined as such by MRI, when
it causes bright signal on T1-weighted spin echo images. Pericardial tu
mors are best demonstrated by MRI.
Pericardial fluid
Pericardial effusion may be caused by a number of conditions, the most
common being cardiovascular, infectious, malignant, metabolic, or ia
trogenic in origin. Common causes are congestive heart failure, uremia,
acute viral pericarditis, and myocardial infarction. When investigating a
patient suspected o f having a dissecting aneurysm in the ascending aorta,
echocardiography can be used to define a pericardial effusion, which in
dicates leakage into the pericardium and the danger of development of
cardiac tamponade.
In ordinary chest radiographs, pericardial fluid is diagnosed on the ba
sis of a generally enlarged heart without any special part of the heart pre
dominating (Fig. 28). A heart surrounded by considerable amounts of
pericardial fluid can be compared visually to a suspended water bag. The
diagnosis is otherwise difficult to make with certainty on the chest radi
ograph, but easy to make using echocardiography, computed tomogra
phy (Fig. 29) and MRI (Fig. 6). Rapid production of pericardial fluid may
802
THE HEART
Figure 28.
Pericardialfluid with general,
considerable enlargement o f the
heart. No part o f the heart is par
ticularly enlarged.
Figure 29.
a) Pericardial fluid shown by ultrasound. The pericardial fluid is seen between the
markers. The fluid belt is wider posteriorly (+), less marked anteriorly (x).
b) Computed tomography-pericardial fluid. The chambers o f the heart are filled with
contrast medium while the pericardial fluid is seen as a low-attenuated belt around
the whole heart.
lead to cardiac tamponade. In the presence of clinical symptoms of peri
cardial tamponade, drainage may be done using percutaneous catheter
placement (see chapter on Interventional Radiology).
Pericarditis
Previously, tuberculosis was a frequent cause of pericarditis, but this is
rare today. Frequent types are purulent and uremic pericarditis. A not un
usual type of non-purulent pericarditis is seen after heart surgery (post
pericardiotomy syndrome), which is stated to occur in about 10% of all
patients who have undergone heart surgery. In most cases, however, there
are only small amounts of fluid, which it is not necessary to remove from
the pericardial space. Reactive changes after radiotherapy may also re
sult in collections of fluid in the pericardium.
803
If pericarditis heals with fibrosis or calcification, the pericardium be

comes stiff, reducing the capablity to expand in diastole. The result of
this is reduced filling of both ventricles (constrictive pericarditis). This
diagnosis may sometimes be evident on chest radiographs due to calci
fication of the pericardium. Calcificaton in this disease is usually initially
evident in atrioventricular and interventricular grooves of the heart.
Computed tomography and MRI can establish this diagnosis by show
ing thickening of the pericardium (Fig. 5). Normal pericardial thickness
on these studies is less than 4 mm. Secondary signs of this disease are
dilated inferior vena cava and right atrium with a normal size and some
times tubular-shaped right ventricle.
Percutaneous transluminal coronary angioplasty

(PTC A)
Stenosis and occlusion of the coronary arteries results in reduced pres
sure peripheral to the lesion, and reduced myocardial blood flow with
poor oxygenation of the jeopardized region of the myocardium. As a con
sequence of this, angina pectoris develops. Treatment may be either sur
gical, by aortocoronary bypass, usually autologous veins from the as
cending aorta to the affected coronary artery peripheral to the stenosis
or occlusion, or by dilatation of the arterial stenosis or occlusion.
During the last 10-15 years, modem interventional radiology has de
veloped alternatives to surgical treatment. Transluminal angioplasty of
the coronary arteries was first carried out by Andreas Gruntzig in 1977.
The method consists of introducing a narrow catheter, on which a balloon
is mounted, into the area in the coronary artery where there is stenosis (or
occlusion). The catheter is then placed in the center of the narrow area,
and the balloon inflated to a diameter corresponding to the original di
ameter of the artery. The atheromatous (or calcified) masses forming the
stenosis are thus pressed flat, and the artery regains a larger diameter, re
sulting in a return to normal of the peripheral circulation (Fig. 30 a-c).
The first years after it was introduced the method was used only in pa
tients with simple, short stenosis, centrally placed in the coronary arter
ies. Now, since the development of modem balloon catheters, a consid
erably larger number of patients can be treated, even when the lesions
are in several coronary arteries, and are relatively peripheral. Re-steno-
804
THE HEART
Figure 30.
a) Selective arteriography left coronary
artery. Subtotal stenosis (arrow) o f the
artery supplying the anterior wall o f
the heart (LAD).
b) Balloon catheter inserted into the left
coronary artery to dilate the subtotal
stenosis. Outline o f balloon marked by
arrows.
c) Angiography to check result o f dilata
tion - the calibre o f the artery has re
turned to normal.
sis occurs in about 30 to 50% of the cases, but if this occurs, repeat di
latation of the same vessel can be carried out. Acute complications of the
procedure, such as occlusion and development of infarcts, may take
place. Sudden death has also occurred, but is today rare.
In the USA as well as in Europe, it is now as common to employ coro
nary angioplasty as it is to perform an aortocoronary bypass.
Fibrinolysis
Acute infarction may be caused by thrombi in the coronary arteries. When
acute occlusion caused by thrombi occurs, treatment with fibrinolytic
agents to dissolve the thrombus, thus re-establishing circulation in the
coronary artery, may be indicated. Both systemic and local intraarterial
treatment have been used. Systemically, heparin and large doses of strep
tokinase and tissue plasminogen activator (TPA) have been given intra
venously to induce lysis of the thrombus. Local intra-arterial use of strep
tokinase (or urokinase) is a possible treatment, especially when the con-
805
diton has lasted for less than four hours. Local intra-arterial infusion with
fibrinolytic agents often lasts for several hours. Angiography is carried
out during this period to follow the effect on the thrombus and possible
retraction or dissolution of the thrombus. As complications such as bleed
ing are not unusual with this type of treatment, these patients must be
carefully monitored.
Valvuloplasty
It has now become possible to dilate stenotic cardiac valves using large-
diameter balloon catheters. This was performed initially in pediatric car-
dioradiology, where much experience has been accumulated with di
latation of pulmonary stenosis. For mitral valvuloplasty, the balloon
catheter is introduced percutaneously via the femoral vein up to the right
atrium. With the aid of a long, curved needle, the atrial septum is punc
tured and the balloon catheter is passed into the left atrium, and advanced
caudally towards the left ventricle, so that the balloon is positioned in
the mitral orifice. When the balloon is inflated, any adhesions between
the cusps will be broken, and the excursion of the leaflets improved. This
is a safe type of treatment with a relatively low incidence o f complica
tions.
An attempt has also been made to use a method employing a similar
balloon catheter in aortic stenosis. The catheter is introduced retrogradely
from the femoral artery to the aortic orifice, which is dilated. Aortic valve
dilatation is now almost abandoned because of a very high recurrency
rate.
Pericardial drainage
When large amounts of fluid collect in the pericardium, especially when
the amount of fluid is so great that there is danger of cardiac tamponade,
drainage is indicated. It is easiest to carry out pericardial drainage under
the guidance of ultrasound, employing a puncture below the ensiform
process. It is usually preferable to puncture the fluid-filled pericardial
space in the area near the right atrium. In experienced hands, this is a
safe method of treatment without appreciable complicatons. As the fluid
usually sinks down so that the belt of fluid is widest posteriorly, it is best
to use a relatively long catheter, which can be positioned with the tip at
the back of the pericardial space. When the fluid is hemorrhagic, and
large in volume, there may be doubt whether one of the chambers or ap-
806
THE HEART
Figure 31.
After drainage o f pericardial exudate
under the guidance o f ultrasound.
Some air has entered the pericardial
space, which is seen as a double out
line on the left side (black arrows).
pendages of the heart has been punctured instead of the pericardial space.
In these cases, the hemoglobin content o f the fluid will, however, rapidly
differentiate between pericardial fluid and venous blood. If the my
ocardium should be punctured accidentally, so that the tip of the catheter
enters the right atrium, complications such as bleeding into the pericar
dial space usually do not occur because the pressure in the right atrium
is low. In some cases, where pericardial fluid is formed rapidly, perma
nent drainage may be indicated and the catheter can be left in the peri
cardial space. However, it is usually preferable to remove the catheter
once drainage is completed (Fig. 31).
807
Chapter 20
The peripheral vessels
Christoph L. Zollikofer and Frode Laerum
VASCULAR IMAGING
Arterial system
The classic approach for imaging of the aorta and peripheral arterial sys
tem has been angiography performed by means of injection of contrast ma
terial through a direct needle puncture or an intraarterial catheter. However,
non-invasive means of investigation of the peripheral arteries are being in
creasingly used before the more invasive angiographic procedures.
Clinical examination and non-invasive angiologic techniques such as
oscillometry and Doppler pressure measurements are the first steps in
the evaluation of the most common pathology of the vascular system: ar
terial occlusive disease.
For vascular imaging the new non-invasive modalities like ultrasound,
computed tomography (CT) and magnetic resonance imaging (MRI)
have partly replaced angiography for diagnostic purposes.
As a screening tool ultrasound has gained an important role in the
workup of aneurysmal disease including dissections of the aorta, pelvic
and peripheral vessels. The patent lumen, mural thrombus and dissec
tion flap are well demonstrated (Fig. 1). The relatively new techniques
of colour doppler and duplex scanning furthermore allow flow mea
surements and are used to assess stenosis and occlusions of peripheral
arteries and for follow-up studies after bypass procedures. Colour
doppler is the non-invasive method of choice for evaluation of athero
sclerotic disease of the neck vessels and for peripheral AV-malforma-
tions and AV-fistulas. Duplex and colour doppler scanning is also used
in diagnosing venous pathology such as deep vein thrombosis and ve
nous valve incompetence.
809
Figure 1. Ultrasound study o f abdominal aneurysms.

A, B) Infrarenal atherosclerotic aortic aneurysm o f 4 cm diameter and 8 cm length in
transverse (A) and longitudinal (B) sections. The amount o f thrombus and the
patent lumen are well demonstrated.
C) Transverse scan o f abdominal aorta o f a type В dissecting aneurysm showing the
dissection flap (arrows).
Figure 2. CT o f atherosclerotic aneurysm are well seen (A = aorta, LRA = left renal
artery, RRA = right renal artery, LRV = left renal vein, VC = vena cava, U = Ureter
Computed tomography is used to substanciate ultrasound findings in

greater detail. Since it is not affected by overlying air or bone CT is an
excellent method o f demonstrating pathology of the aorta and pelvic ves
sels such as aneurysms, dissections, rupture, thrombus formation and cal
cification as well as paravascular structures (Fig 2). Volume scanning
and 3D reconstruction make CT an important alternative to invasive an
giography as a preoperative diagnostic tool in occlusive and aneurysmal
disease of the aorta and pelvic vessels. CT is also used to demonstrate
pathology involving the vena cava and large central veins, particularly
810
THE PERIPHERAL VESSELS
in connection with thrombus formation or extrinsic compression by tu

mor etc.
MR-angiography (MRA) finally has the great advantage that vascular
structures may be seen in great detail without using contrast material.
Using special techniques blood flow can be quantified and flow direc
tions can be determined. MRA has the advantage that any plane in all 3
dimensions may be selected and for example the aorta may by imaged
in its entire saggital course. With fast sequences excellent images o f the
neck and head vessels as well as the peripheral arteries may be gener
ated, however, the role of MRA in the periphery has not been established
yet because of its limited availability and expense.
Although non-invasive evaluation and imaging play an important role
for screening and assessment of aortic and peripheral vascular pathol
ogy, angiography is still the gold standard and is indispensible for per
cutaneous interventions. Recent advances using digital imaging and sub
traction techniques render difficult recanalisation and embolisation pro
cedures easier, faster and safer. Furthermore the amounts o f contrast
material required can be reduced for both diagnostic and interventional
procedures.
Techniques fo r arteriography
Percutaneous puncture and catherization of the arterial system
(Seldinger technique; Fig. 3): The approach to the arterial system is se
lected according to the clinical signs and location of the target organ re
spectively. Because of its superficial anatomic location the common
femoral artery is the usual site for arterial puncture. Following local anes
thesia and a small skin incision, the artery is punctured using a thin-
walled needle with a 1 - 1.2 mm outer diameter and a central mandril
(Fig. 3). Some needles are additionally covered with a Tefion-sheath ac
cepting a .038 guidewire. The needle is advanced into the artery at an
angle of approximately 45 degrees. After removing the mandril the nee
dle is pulled back till a pulsating backflow is seen. Then a guidewire with
a flexible tip (usually a J-guidewire) is advanced into the vessel. Under
manual compression the needle is withdrawn and an angiographic
catheter is advanced over the guidewire into the artery and positioned at
the desired location. The guidewire is then pulled back and the catheter
is checked for backflow and carefully rinsed with saline. The position of
the catheter is once more controlled under fluoroscopy using manual in-
811
Figure 3. Schematic drawing o f the Seldinger technique.

1) Puncture o f the artery.
2) Removal o f the mandril.
3) Withdrawal o f the needle until pulsating backflow o f blood is seen.
4) Advance o f the guidewire.
5) Withdrawal o f needle while compressing artery and holding guidewire in place.
6) Advance catheter over the guidewire.
jection of contrast material. For thoracic aortography 5 or 6 F catheters,

100 cm long which allow flow rates of up to 30 ml per second are used.
For abdominal and peripheral angiography 4 and 5F catheters o f length
of 60 cm, are used. Commonly a Pigtail configuration with multiple side-
holes is preferred for flush injection in the aorta. The contrast material
is commonly injected with a power injector. For selective femoral or
carotid angiography a hand injection usually is sufficient.
If the femoral arteries cannot be punctured, e.g. post-operatively or in
occlusive disease when the femoral artery itself is occluded or in ob
struction of the distal aorta and/or the pelvic arteries, an alternative ac
cess route has to be used. Such access sites are the axillary and brachial
artery or a translumbar approach to the abdominal aorta. Because of the
higher complication rate of axillary or brachial approach, we prefer
translumbar aortography.
812
Radiologic documentation of the contrast injection is performed with

digital substraction angiography if available, otherwise with 100 mm
spotfilming or conventional film changing techniques (Figs. 11 - 14).
The rate of contrast injections has to be tailored according to the filming
technique (DSA requires lower injection rates) and the speed of blood
flow. For thoracic aortic injections rates of 25 to 30 ml per second and
for the abdominal aorta 18 to 25 ml per second are adequate. For pe
ripheral run-off studies of the pelvic and femoral arteries, flow rates of
8 to 12 ml per second are sufficient using 80-100 ml of contrast for bi
lateral visualisation of the lower extremity arteries down to the feet. The
frame rate for thoracic aortography is usually 2 to 4 frames per second;
for abdominal aortography 2 per second. For the extremities, according
to the speed of blood flow, one to two frames per second is generally
used for the pelvis and from one film per second to one film every 3 sec
onds is used in imaging of the calves.
Complications
Complications can be caused by a) the puncture (bleeding, hematoma,
pseudoaneurysms, AV-fistula, spasm, thrombus formation and periph
eral embolisation), b) guidewire and catheter manipulation (perforation,
dissection of the intima, spasm, embolization of plaque or air embolism)
and c) contrast material: allergic or toxic systemic (cardiac, renal toxic
ity). With an adequate puncture and catheter manipulation technique and
the use of non ionic or low osmolarity contrast materials, complication
rates in angiography using a femoral approach are less than 1.8%.
Venous system
Ascending phlebography (venography)

The most common method of visualization of the lower limb veins from
the level of the foot to the lower cava is ascending phlebography (Fig. 4).
Although in several ways now challenged by duplex ultrasound, this method
is still considered the ’’gold standard” for an overview of the morphology
of the lower extremity veins and their valves and flow patterns. Only veins
draining blood mixed with contrast are visualized. The deep femoral and
the internal iliac veins are often not opacified. Incompetent valves or ve
nous obstruction may cause collateral circulation and drainage to superfi
cial veins. This may prevent filling of the more important deep veins.
813
Figure 4.
A - E ) Normal phlebography o f the lower extremity.
The examination is done in ordinary fluoroscopy rooms by manual ex
posures of films at various levels and in different projections during hand
injection of 5 0 -1 0 0 cc of a contrast medium via a cannula inserted into
a dorsal foot vein. The medial vein of the big toe is usually preferred,
since this is most often the easiest vein to puncture. More lateral dorsal
foot veins may also be chosen where a retrograde insertion may then se
cure a better filling of the deep calf veins. The application o f a hot, wet
towel can help to locate the vein by inducing venodilatation. Tilting the
x-ray table also increases the prominence o f veins by raising hydrosta
tic pressure. In edematous feet, prolonged firm compression o f the ap
propriate area of the dorsum of the foot is necessary. Nitroglycerine paste
is employed by some to obtain local distension of subcutaneous foot veins
for easier puncture. A rubber tourniquet is used at supramalleolar level
to force the contrast medium into the deep veins. This may sometimes
obstruct the filling of the anterior tibial vein. Tourniquets may also be
employed at higher levels. The examination is done with the fluoroscopy
table at 45°-60° in a semierect position, until the contrast column reaches
the pelvis. The table is then lowered, and the extremity passively raised
while the patient does a Valsalva manoeuvre to maximize contrast fill
ing during radiography of the pelvic and lower caval veins. It is impor
tant to carry out the examination on a non-weight bearing, relaxed ex
tremity, since the deep veins will otherwise be compressed by limb mus
814
cles. The calf veins should be imaged in three projections, lateral oblique,
anteroposterior and medial oblique, the veins above the knee require one
or at most two projections.
Only water-soluble radiographic contrast media can be used for phle
bography. Complications are rare, and are mostly related to the contrast
media employed. One should be prepared for the immediate manage
ment of possible anaphylactoid reactions. Nausea, vasovagal reactions
and injection pain may be encountered.
To avoid post-phlebographic thrombosis the contrast medium em
ployed should be of low osmolality, preferably non-ionic. Ionic contrast
media of higher osmalality are associated with an incidence contrast-in
duced thrombosis of 10-60%. To lessen this risk, hyperosmolar contrast
media should be diluted to a concentration of 200 mgl/ml, or alterna
tively heparin prophylaxis should be administered.
Extravasation of contrast medium at the puncture site may occur by
displacement of the cannula or failed venous puncture. This is usually
no problem if a low-osmolar contrast medium is employed. With high
osmolarity, pain and even skin necrosis may occur.
While ascending phlebography of the lower limb is still the most im
portant diagnostic test for deep venous thrombosis, it has a limited role
in the diagnosis of primary venous insufficiency. Secondary venous in
sufficiency caused by post-thrombotic obstruction of inflow to the large
veins in the pelvis, or venous anomalies like hypoplasia, valvular dys-
or aplasia or Klippel-Trenaunay syndrome may require phlebography to
demonstrate venous morphology.
Other phlebographic techniques o f the lower limb
Retrograde phlebography
This technique is employed to demonstrate valvular incompetence at the
upper femoral level. The common femoral vein is antegradely punctured
with a plastic cannula and contrast medium injected during a Valsalva
manoeuvre of the semi-erect patient. The degree of contrast back-flow
down through incompetent valves into the veins of the thigh may then
be visualized (Fig. 5).
815
Figure 5.
Retrograde phlebography showing incompetent
valves at the upper femoral level. Grade I incom
petence is present if the contrast column passes
retrograde and ju st below the inguinal ligament,
grade II i f to the midline, grade III i f to a level at
the knee, and grade IV to a level below the knee.
Isometric phlebography
Visualization of the long saphenous vein for evaluation o f its suitability
as a graft in arterial reconstruction surgery, is achieved by contrast
medium injection into a foot vein in the supine patient during isometric
tension of the limb muscles. This is achieved by pulling on a band pass
ing beneath the soles of the feet.
Videophlebography
This is used for functional studies of venous flow patterns.
Intraosseus phlebography
With this technique a cannula is directly inserted into the medullary space
of the greater femoral trochanter or lateral malleolus, in order to visual
ize the pelvic veins or lower limb veins. The procedure requires general
anaesthesia, and is rarely used.
Upper extremity venography

The veins of the upper extremity and the communication with the supe
rior vena cava are phlebographically examined on ordinary fluoroscopy
tables by hand injection of contrast medium. First the basilical vein is
cannulated. The indication of the examination will often be suspected
axillary or subclavian vein thrombosis or tumorous obstruction. Images
816
of the extremity, shoulder and mediastinum are then taken. No tourni

quet is applied. The risk of postphlebography thrombosis is probably less
than in the lower extremities possibly due to a higher thrombolytic ac
tivity in the venous intima of the arms. The volume of contrast medium
required is variable. 20-50 ml is usually sufficient. If a pump injector is
employed, a flow rate of 8 ml/s may be used. Images of the brachial, ax
illary, subclavian and brachiocephalic veins and superior vena cava are
then taken. In suspected superior vena cava obstruction the veins of both
arms may be simultaneously injected with contrast.
Cavography
The Seldinger technique is usually used during angiography o f the infe
rior vena cava. The common femoral vein is punctured at the groin, and
a Pigtail catheter is inserted with its tip placed at the bifurcation. Serial
exposures during injection of 40-80 ml of contrast medium at a flow-
rate of 15-20 ml are employed. The patient should perform a Valsalva
manoeuvre, by forced expiration against a closed glottis. Using digital
subtraction angiography (DSA), the concentration of the contrast
medium, as opposed to the volume, can be substantially lowered.
Combined pelvic and caval vein angiography may be performed by con
comitant injection of contrast medium through plastic cannulae inserted
into both common femoral veins at the groin.
Ultrasound
Ultrasound imaging may be used for the non-invasive examination of veins
and their surrounding tissues, either by grey-scale real-time imaging of the
morphology, or by combining the image with pulsed Doppler determina
tion of vascular flow. In this so-called duplex scanning, the two-dimen
sional grey-scale image is combined with the flow velocity signal depicted
as superimposed color information, as a spectral curve, or as sound.
Ultrasound is operator-dependent, however in skilled hands it is very
useful for venous examinations. In some centres it is the most frequently
used diagnostic tool for the depiction of deep venous thrombosis. There
is a wide range of indications for ultrasound mapping of peripheral as
well as central veins.
Low frequency transducers (2.3 MHz) are used to examine the iliac
veins and inferior vena cava and high-frequency transducers (7.5-10
MHz) are used for superficial veins. Other veins are interrogated by mid
817
range transducers of 5-7.5 MHz. Color-Doppler is used to localize the

paired deep veins below the knee, to diagnose venous back-flow and
valvular incompetence. The ultrasound image will also reveal surround
ing soft tissue processes which affect the veins, like hematomas, Baker
cysts of the knee, or tumours.
Duplex ultrasound scanning of the lower extremities may be used in
patients with a clinical suspicion of deep venous thrombosis, in those with
suspected or proven pulmonary emboli, in unexplained leg swelling af
ter orthopedic, pelvic or vascular surgery, and in those with unexplained,
chronic leg swelling. The two limbs should be compared at the same sites.
It is preferable to start in the groin and move sequentially down to the
posterior tibial veins at the ankle. The popliteal veins are best studied in
the prone position with the feet supported by a pillow. For the external il
iac to the popliteal veins, normal venous flow should be spontaneous and
vary with respiration. During inspiration, the flow will diminish as the in
tra-abdominal pressure exceeds that o f the inferior vena cava. The poste
rior tibial veins may be undetectable. Compression of the foot should then
be employed, resulting in an easily detectable surge. While deep venous
thrombosis in the veins between the knee and inguinal ligament may be
reliably diagnosed using ultrasound, the calf is rather more difficult and
even more dependent on the skill and experience of the sonographer.
There is a high false positive rate below the knee.
Duplex ultrasound is useful in following-up of patients undergoing an
ticoagulant or fibrinolytic therapy. Assessing venous patency or caval
placements is done in a rapid non-invasive way. Venous duplex scan
ning is also effective in revealing the presence and anatomical distribu
tion of valves in chronic venous insufficiency.
Magnetic Resonance Imaging (MRI), Computed tomography

(CT)
These two imaging modalities have a role in venous imaging similar to
their value in imaging arteries. In particular, involvement of the vena
cava by intraluminal masses like thrombi or ingrowing tumours, and
caval displacement, compression or obstruction from surrounding
processes is well shown. CT examinations require the use of contrast me
dia for venous opacification.
In magnetic resonance angiography (MRA) the vessels may be im
aged and the flow rate determined directly, without the use of paramag-
818
Figure 6.
1 Aorta ascendens
Schematic drawing o f 2 A. coronaria dxt.
normal anatomy o f the 3 A. coronaria sin.
aorta and peripheral ar 4 Truncus brachiocephalicus
5 A. carotis communis dxt.
teries. 6 A. subclavia dxt.
7 A. vertebralis dxt.
8 A. carotis interna dxt.
9 A. carotis externa dxt
10 A. carotis communis sin.
11 A. subclavia sin.
12 A. vertebralis sin.
13 A. axillaris
14 A. brachialis
15 A. radialis
16 A. interossea
17 A. ulnaris
18 Aorta descendens
19 Aorta abdominalis
20 Truncus coeliacus
21 A. hepatica communis
22 A. lienalis
23 A. mesenterica superior
24 A. mesenterica inferior
25 A. renalis dxt.
26 A. renalis sin.
27 A. iliaca communis
28 A. iliaca externa
29 A. iliaca interna
30 A. femoralis communis
31 A. profunda femoris
32 A. femoralis superficialis
33 A. poplitea
34 A. tibialis posterior
35 A. fibularis
36 A. tibialis anterior
netic contrast media. This technology is likely to develop further and be
come considerably more important and useful than today.
NORMAL ANATOMY
The aorta and peripheral arteries

The thoracic and the abdominal aorta and its branches are schematically
depicted in Fig. 6.
The ascending thoracic aorta originates at the annulus of the aortic
valve and gives off the right and left coronary artery. The aorta ascends
towards the right and swings approximately at the level of the 5th tho
racic vertebra in an arch-like curve (aortic arch) posteriorly to descend
to the left of the vertebral column (descending aorta). From the aortic
arch the neck vessels originate in the order right brachiocephalic trunk
(which bifurcates into the right subclavian and right common carotid
819
artery), left common carotid artery and left subclavian artery. The aorta
has three main points of fixation: At the level of the aortic valve, the bra
chiocephalic vessels and ligamentum arteriosum and at the diaphrag
matic hiatus. The descending aorta is the direct continuation of the aor
tic arch distally beyond the origin of the left subclavian artery and gives
off the intercostal arteries in pairs before penetrating the diaphragm
through the hiatus to become the abdominal aorta.
The first anterior branch of the abdominal aorta is at the level of about
T12 to LI. This is the celiac trunk which divides into the left gastric, the
splenic and common hepatic artery. About one centimeter lower than the
celiac trunk is the origin of the superior mesenteric artery and the right
and left renal arteries arise, another one to two centimeters caudally. At
the level of L3 to L4 the inferior mesenteric artery originates anterolat-
erally to the left. Other important branches are the paired lumbar arter
ies. The aorta then bifurcates at L4 to L5 into the right and left common
iliac arteries which divide into the internal and external iliac arteries. The
internal iliac artery commonly divides into an anterior division (giving
off the inferior gluteal and obturator artery and the internal pudendal and
visceral artery to the urogenital organs) and the posterior division (ili
olumbar and superior gluteal arteries). At the level of the inguinal liga
ment the external iliac artery becomes the common femoral artery which
bifurcates into the superficial and deep femoral artery.
The superficial femoral artery after passing through the adductor hia
tus becomes the popliteal artery which trifurcates below the knee into
the anterior tibial artery and the tibioperoneal trunk which divides into
the peroneal and posterior tibial arteries. The anterior tibial artery which
runs in the anterior muscular compartment through the interosseous
membrane ends distally in the dorsalis pedis artery. The posterior tibial
artery supplies the plantar aspect of the foot.
In the upper extremities the blood supply originates in the right and
left subclavian artery which give origin to the vertebral arteries on each
side. Other branches of the subclavian artery are the thyreocervical trunk,
the internal mammary artery and the costocervical trunk. At the lateral
end of the first rib the subclavian artery becomes the axillary artery which
becomes the brachial artery laterally to the teres major muscle. The
brachial artery gives off the profunda brachii artery and bifurcates in the
region of the elbow into the radial and ulnar arteries. The latter also gives
origin to the interosseous artery. In the hand the radial artery forms the
820
deep and the ulnar artery the superficial palmar arch.
The vena cava and peripheral veins

The veins of the lower extremity and the vena cava are depicted schemat
ically in fig. 7. In the lower extremity, the venous anatomy can be di
vided into foot veins, the superficial and the deep axial system, and the
perforating (communicating) veins.
The veins of the foot are characterized by two plantar and two dorsal toe
veins merging into the dorsal metatarsal veins, which then unite and form
the superficial dorsal venous arch. This arch proceeds in a medial direc
tion and flows into the long saphenous vein anterior to the medial malle
olus. The lateral extension of the dorsal arch joins the short saphenous vein
which in turn merges with the popliteal vein. Foot vein valves are, con
trary to the situation proximally, directed towards the saphenous system.
The veins of the sole comprise a plantar cutaneous arch draining into
lateral and medial marginal veins and from there into the short and long
saphenous systems. The deep plantar veins arise at the fourth metatarsal
system and at the medial malleolus join the posterior tibial veins. These
deep plantar veins have a large central plexus, which has a capacity in
excess of that needed to drain the foot, and have not got a recognized
function. There are numerous valveless communicating veins between
the major foot veins. The dorsal foot vein is an extension of the anterior
tibial vein.
The superficial veins

The great saphenous vein forms in front o f the medial malleolus by union
of the medial marginal vein and the dorsal superficial arch. It runs in the
superficial fascia on the medial side of the leg up to the knee and then
behind the femoral condyles and again medially in the thigh. In the groin,
it courses deeply to join with the femoral vein at the foramen ovale.
Venous valves are numerous in this vein, and almost invariably there is
a valve at the junction with the femoral vein.
The short saphenous vein starts behind the lateral malleolus, runs back
towards the posterior midline, piercing the fascia relatively low in the
calf and usually joins the popliteal vein. However, in one-third of cases
it may also continue up the thigh to join with the deep femoral vein, the
iliac system, or it may join the great saphenous or a gastrocnemius vein
at the popliteal level of the knee.
821
Figure 7.
Vena cava inferior
Schematic drawing o f the left pelvic and
i. ■Common iliac v.
■Internal iliac v.
lower extremity veins. The deep leg veins
from the level o f the popliteal vein are
- External iliac v. paired (not shown). The gastrocnemius
- Common femoral v. veins are paired and duplicated; there are
- Great saphenous v. several soleal veins.
- Deep femoral v.
- Superficial femoral v.
The deep veins (Fig. 7)
Two posterior tibial, two peroneal
- Popliteal v. and two thin anterior tibial veins
■Gastrocnemic v. possess many valves. They run
■Anterior tibial v. along the corresponding arteries as
-Soleus v. venae comitantes in the muscular
- Peroneal v.
compartments of the leg. They join
■Posterior tibial v.
the popliteal vein at the lower
popliteal fossa. From the soleus
muscles, short veins, sinusoids with
rather narrow outlets and mostly no
valves, join the deep calf veins. Two
paired, gastrocnemius veins come
from the corresponding muscle bodies to join with the popliteal vein.
They are usually smaller than the sinusoids and contain valves. The
popliteal vein is usually single and lies under the nerve but superficial to
the artery in the popliteal fossa. It continues medially upwards through
the adductor hiatus and becomes the superficial femoral vein in the ad
ductor canal. In the femoral canal, the superficial femoral vein contains
1-3 valves and receives the deep femoral vein to form the common
femoral vein. Usually there is a valve at the origin of both of these veins
before they merge. The common femoral vein passes medial to the artery
and nerve under the inguinal ligament and becomes the external iliac
vein. In two thirds of cases, a valve is seen in the common femoral vein.
It receives the great saphenous vein medially.
Communicating veins
More than a hundred communicating veins, often called perforators, tra
verse the deep fascia of the leg, linking the axial veins of the deep and
superficial systems to one another. These veins are of functional impor-
822
Figure 8.
Some perforating vein groups
important fo r surgical treatment o f
venous insufficiency, seen from
behind. (Dodd's group are venae
comm.fem. med. intermedia, Boyd’s
are the w . comm, cruris intermed.,
and Cockett's group empty into a vein
o f the vv. tib. post.). The levels o f two
dorsal perforators are also indicated,
the upper communicating with a
gastrocnemius vein.
tance, since incompetence will

lead to bidirectional flow, local
cutaneous venous hyperten
sion, and varicosities (Fig. 8).
Pelvic veins
(Dorsal view)
The valveless external iliac
veins join the internal iliac
veins to form the common iliac vein. In thrombotic occlusion o f the ex
ternal iliac vein, collateral vessels may arise from the the internal pu
dendal vein and rectal vein plexus into the internal iliac. In mesenteric
vein hypertension collateral flow may occur in the opposite direction.
Collaterals may also form via epigastric veins to the internal mammary
vein, or par-umbilical veins in the abdominal wall.
The inferior vena cava

The inferior vena cava forms in front of the fifth lumbar vertebra by union
of the two common iliac veins. It receives segmental, small lumbar veins
draining the muscles and skin of the back. The ascending lumbar veins,
ending in the azygous vein on the right side and in the hemiazygous vein
on the left, form an anastomosis between the common iliac vein and the
lumbar veins. This is an important collateral route of circulation between
the inferior and superior vena cava. The right testicular vein arises from
the pampiniform plexus and empties into the vena cava, while the left
testicular vein drains into the left renal vein. In the female, the two ovar
823
ian veins have similar courses parallel to the cava.

The right renal vein is shorter and thicker than the left, the latter re
ceives the left testicular and suprarenal veins and crosses in front of the
aorta to join the inferior vena cava. The short, right suprarenal vein plugs
directly into the cava.
The inferior vena cava is situated to the right of the aorta, in front of
the vertebral column. From the renal level, it proceeds upwards slightly
to the right. It receives 2-3 short, but large hepatic viens just before pierc
ing the diaphragm at the caval hiatus and ending in the right atrium.
Veins o f the upper extremity and the shoulder

The deep veins of the arms follow the arteries as subfascial venae comi-
tantes. They are paired and possess multiple anastomoses. The proximal
brachial vein, the axillary and the subclavian vein are unpaired.
The larger subcutaneous veins may show considerable variations.
They start with the basilic vein on the dorsal ulnar side of the lower arm,
and the cephalic vein on the radial side. They proceed upwards to the
front of the arm. In the cubital fossa these two veins are connected by
the ulnar/proximal median cubital vein. If a median brachial vein is pre
sent, it will divide into a median cephalic and a median basilic vein in
the cubital fossa, replacing the median cubital vein. The basilic vein pro
ceeds in the medial bicipital cleft, then turns through the fascia into the
depth to join with the axillary vein. The cephalic vein runs on the lateral
side of the upper arm, in the lateral bicipital cleft, then between the del
toid and lateral pectoral muscle, passes under the clavicle and descends
to empty into the axillary vein. The subclavian vein proceeds in front of
the scalene muscle to join with the internal jugular vein forming the bra
chiocephalic vein.
The thoracoepigastric veins and the lateral thoracic vein both drain
into the axillary vein and are collateral pathways for abdominal wall veins
and the 6-7 upper intercostal spaces, respectively.
DISEASES OF THE ARTERIAL SYSTEM
Arterial occlusive disease

Arterial occlusive disease may be divided into acute and chronic.
Peripheral arterial occlusive disease is commonly staged according to
the Fontaine classification into four degrees:
824
I: Asymptomatic atheroslerotic lesions

II: Intermittent claudication
a) mild (free walking distance > 100-2 0 0 m)
b) severe (walking distance less than 100 m)
III: Rest pain
IV: Trophic changes with necrosis and gangrene.
Acute arterial occlusions

These occlusions are due to arterial emboli or acute thrombosis in ap
proximately 90%. Other etiologies are dissections of the arterial wall
(traumatic or spontaneous), external compression,spasm (trauma, iatro
genic, drugs) or hemodynamic problems.
The majority of arterial emboli originate in the left heart (86%). Other
sources are aneurysms and ulcerative plaques of large arteries. Usually
the emboli get trapped at arterial bifurcations and cause further throm
bosis by apposition or stagnation of blood flow. The most frequent lo
cation of arterial emboli is the common femoral artery (46%). On arte
riography a fresh embolus shows a smooth cut-off of the contrast col
umn and few or no collaterals (Fig. 9 A). A special form of peripheral
embolism is cholesterol embolism caused by showers of cholesterol crys
tals released from atherosclerosis of the aorta and pelvic vessels which
lead to microemboli in digital arteries (blue toe syndrome).
Acute and subacute arterial thrombosis is caused by atherosclerosis
in over 90%. Rarely inflammatory processes, trauma, hematologic dis
eases or interventional procedures are the cause. The clinical signs de
pend on the location and extent of the thrombosis, however they are gen
erally less severe than with acute embolic disease. On arteriography also
an acute thrombotic occlusion may show a relative sharp cutt-off of the
contrast column and few collaterals unless there is a pre-existing stenotic
lesion (Fig. 9 B).
Chronic arterial occlusive disease

Chronic arterial occlusive disese leads to progressive stenosis and/or oc
clusions and is due mainly to obliterative arteriosclerosis. It usually starts
after the age of 40 and is dependent on certain risk factors such as smok
ing, diabetes, hypertension, hyperlipidemia etc. The sites of predilection
are the arteries of the pelvis and lower extremities, the origins of the neck
vessels and the carotid bifurcation.
825
Figure 9.
Angiograms o f acute ar
terial occlusion.
A) Acute embolic occlu
sion at the typical lo
cation o f the trifurca
tion ju st below the
knee joint. There is a
typical cut-off o f the
contrast column and
only a fe w collaterals
are seen.
B) Acute thrombotic oc
clusion o f the superfi
cial fem oral artery
secondary to athero
sclerotic stenosis. Note
contrast around fresh
thrombus (arrows) and
tortuous collaterals as
seen in pre-existing
stenosis.
Atherosclerosis of the thoracic aorta leads mainly to elongation and

calcification of the aortic wall as well as ectasia. This may be recognised
on the chest X-ray. Atheromatous plaques and ulceration may lead to pe
ripheral and cerebral emboli. The primary imaging method for arte
riosclerotic disease of the thoracic aorta is Computed tomography (Fig.
10). Thoracic aortography is used to demonstrate the arteriosclerotic dis
ease at the origin of the neck vessels or to further clarify aneurysms and
search for embolic sources. Arteriosclerosis of the abdominal aorta in
volves mainly the infra-renal portion and often continues into the pelvic
arteries. Stenosing plaques are found particularly at the aortic bifurca
tion, the distal common and proximal external iliac artery. The primary
screening test for aorto-iliac disease is colour doppler ultrasound (Fig. 1).
CT is mainly used for further work up in aneurysmal disease (Fig 2). For
the exact diagnosis and extent of aorto-iliac disease, many vascular sur
geons still need aortography as the prime diagnostic tool, especially if an
operative or percutaneous interventional therapy is considered (Fig. 11).
The role of MRI in atheroslcerotic disease of peripheral arteries has not
yet been fully established apart from diagnostic use in aorto-iliac
aneurysms and dissection particularly in patients with contra-indications
to the administration of contrast medium. However, rapid advances in
826
Figure 10.
Thoracic aortic
aneurysm
A) Chest X-ray
showing aortic
aneurysm with
somewhat lobu-
lated margins in
the arch and the
proximal de
scending aorta.
B,
C) CT at the level o f
the arch and
aortopulmonary
window showing
true size o f the
aneurysm and
marginal throm
bus formation.
Figure 11. Aorto-

gram o f the same
patient as in fig. 2.
AP (A) and oblique
(B) projection. The
oblique projection
shows the relation
o f the renal arteries
to the neck o f the
aneurysm including
the kinking o f the
aorta better than
CT. This however,
can also be demon
strated in a similar
fashion with 3D-re-
construction o f spi
ral CT (fig. 24).
technology may change this pattern in the near future.

Occlusion of the distal aorta usually starts at the bifurcation and may
extend proximally to the origin of the inferior mesenteric artery, or if the
latter is occluded, to the oring of the renal arteries (Fig. 12). Occlusion
proximal to the renal arteries is extremely rare. The etiology o f the dis
tal occlusion is a pre-existing stenosis or massive embolism. This if of
ten called the Leriche-syndrome. Originally however, this term was used
for a complex o f symptoms in young men with occlusion of the aortic
827
Figure 12.
Translumbar aortography in acute
occlusion o f the infrarenal aorta.
The intercostal arteries (arrows)
serve as major collaterals.
Figure 13. Translumbar aortogra

phy fo r bilateral iliac occlusion
demonstrating the main collaterals.
The internal iliac arteries are also
markedly diseased, the left is com
pletely occluded. The distal filling
o f the femoral arteries is estab
lished via intercostal arteries (not
visulized) to the superficial circum
flex iliac (SCI) and from the 4th
and 5th lumbar and the iliolumbar
arteries. Further collateralization
is via the middle sacral artery (MS)
and the inferior mesenterica artery
(IMA) feeding the hemorrhoidal ar
teries to the branches o f the inter
nal iliacs (I), particularly the infe
rior gluteal and the obturator
artery (O). The latter shows collat
erals to the medial fem oral circum
flex artery (FC). E l = external iliac
artery, CF = common fem oral
artery.
bifurcation consisting of erectile impotence, weakness of the lower ex

tremities and cold and pulsless feet. The symptoms of occlusion of the
distal aorta or the iliac arteries depend on the extent of the occlusion and
828
the collateral circulation as well as the associated peripheral disease. The

most important collaterals are the visceral arteries particularly the infe
rior mesenteric artery, the intercostal and lumbar arteries as well as
branches of the internal iliac, the common femoral and the deep femoral
artery. For planning therapy, angiography must show the extent of the
stenoses or occlusions, the collaterals and the peripheral outflow (Fig. 13).
The angiographic signs of arteriosclerosis in the aorta and pelvic ar
teries are irregular contour and filling defects caused by atheromatous
plaques. Stenoses are often eccentric and multiple projections may be
needed to show the significance of a lesion (Fig. 14). The stenosis may
be relatively smooth, short or quite diffuse. Other reasons for arterial
stenoses are dissecting aneurysms, aortitis/arteritis, perivascular fibro
sis, tumor compression or postradiation fibrosis and congenital hy
poplasia or so called abdominal coarctation. Additional atheroslerotic
disease at other sites in the periphery or the visceral arteries may point
to the correct diagnosis. Small aneurysms from ulcerated plaques as well
as larger aneurysms are further atherosclerotic findings.
In peripheral arteriosclerosis the upper extremities are involved to a
significantly lesser degree than the lower extremities. In particular, the
proximal lesion of the subclavian artery is often not symptomatic be
cause of well developed collaterals. An occlusion of the proximal sub
clavian artery however may lead to the subclavian steal syndrome with
reversal of the flow in the vertebral artery secondary this collateral sup
ply to the arm. This may lead to cerebral hypoperfusion with neurologic
symptoms. Occlusive disease of the forearm and finger arteries is usu
ally atheroslcerotic in nature, rarely embolic, traumatic or secondary to
Buerger's disease. Arteriosclerosis is the most common cause of the sec
ondary Raynaud phenomenon.
In the lower extremities the major site for atherosclerotic disease is the
superficial femoral artery especially in the region of the adductor canal,
the popliteal artery and the trifurcation. In diabetes, the small arteries of
the calf and feet are particularly involved and there is often combined
disease in the femoral, popliteal and calf arteries as well as changes in
the deep femoral artery. The main arteriographic findings again are
stenoses, occlusions and collateral vessels. According to the clinical find
ings, retrograde aortography to demonstrate the distal aorta and the iliac
and peripheral arteries of both legs or a direct antegrade femoral arteri
ogram for unilateral disease is performed. If femoral pulses are absent,
829
Figure 14.
Angiography o f pelvic and peripheral
arteries.
A) Oblique view shows severe stenoses
especially in the right external iliac
artery.
B) There is diffuse bilateral disease
with occlusion o f the left superfreial
femoral artery.
C) Diffuse bilateral disease o f the
popliteal arteries and occlusion o f
the posterior tibial arteries. There
is slower flow on the right than on
the left probably secondary to the
more severe iliac disease.
a translumbar or a transaxillary
approach may be needed. It is
important that the angiogram
demonstrates the location and the
length of the stenoses and occlu
sions for optimal planning o f the
therapeutic procedure. Apart
from the narrowing itself, the
significance of stenosis may be
better appreciated by the pres
ence of collaterals, poststenotic
dilatation or differences in con
trast flow. The length of an oc
clusion may be angiographically
overrated in the early phase be
cause of the stasis proximal to the
occlusion and flow through col
laterals distal to the occlusion.
Typically a thrombotic occlusion
develops by begining proximal
to a stenosis and propagating re-
grogradely until it reaches the
closest large collateral (Figs. 13,
14).
830
Retrograde aortography ofpelvic (A) and fem oral arteries (B) in patient with dilative
atherosclerosis. There is incomplete filling distally due to extremely slow and turbulent
flow.
A special form of peripheral arteriosclerosis consists of elongation and

kinking of the iliac arteries and the so called dilating form of arte
riosclerosis with aneurysmal ectasia. Angiographically the latter shows
a typical sequence of aneurysmal ectasia and relative stenosis (Fig. 15).
Because of turbulence and slow blood flow there is an increased thrombo
embolic risk. Finally there may be steal syndromes, e.g. of the internal
iliac artery caused by an external iliac artery occlusion with consequent
erectile impotence or a reversal of flow in the inferior mesenteric artery
secondary to obstruction of the proximal abdominal aorta.
Monkeberg’s medial sclerosis is primarily not a stenosing process but
characterized by massive diffuse calcification of the arterial wall. It may,
however, be combined with stenosing arteriosclerosis and is seen in di
abetes, hyperparathyroidism (patients on hemodialysis) and in vitamin
D hypovitaminosis.
Arterial disease o f inflammatory nature (arteritis)

In contrast to atherosclerosis only about 5 % of all arterial diseases are
of a non-degenerative, inflammatory origin.
Thromboangitis obliterans (Buerger's disease) is an inflammatory
process involving primarily peripheral arteries of medium and small cali
bre in young men. Accordingly the symptoms involve mainly the calf and
feet or hands with claudication, rest pain and coldness, as well as dysaes-
thesia and motor-disturbance. The etiology most likely is an immune-me-
831
Figure 16.
Arteriography o f the
femoro-popliteal arteries
in Buerger's disease.
There is a chronic
occlusion o f the right
popliteal artery with nu
merous corkscrew collat
erals (A). Note the
"string o f pearls"
changes in the small
muscular branches on
the left (B) with absence
o f atherosclerotic
changes in the popliteal
artery.
diated inflammatory reaction to various noxious substances particularily

nicotine. On angiography streched vessels and segmental peripheral oc
clusions in the region of the calf and feet or of the smaller branches of the
deep femoral artery are seen. Corkscrew collaterals representing vasa va-
sorum along the occluded vessel are fairly typical (Fig. 16). The diagno
sis is made more likely in the presence of additional disease in the upper
extremity in young, usually male patients under the age of 40 with a his
tory of smoking and lacking arterioslerotic disease in other larger vessels.
Takayasu's arteritis is a non specific aortitis and arteritis of elastic ar
teries which is most likely to be auto-immune related. There is a predilec
tion for young women who have fever, myalgia, dizziness and an increased
blood sedimentation rate. Most commonly the brachiocephalic arteries are
involved frequently with long fusiform stenoses particularly involving the
carotids (so called aortic arch syndrome or pulsless disease type 1). A sec
ond type involves mainly the abdominal aorta and its major branches par
ticularly the renal arteries. A third type is a combination of type one and
two and in a fourth type finally also the pulmonary arteries are involved.
832
Figure 17.
Abdominal aortography
showing bilateralfibro-
muscular dysplasia with
typical "string o f
pearls”- like changes o f
the renal arteries.
Other arteritides may be caused by a number of diseases causing steno

sis and occlusion such as periarteritis nodosa, giant cell arteritis, as well
as specific arteritis in tuberculosis, lues and other infectious diseases. In
these cases, not only stenotic areas, but frequently micro- or macroa
neurysms are seen.
Fibromuscular dysplasia
This disease is seen mainly in younger women between 20 and 40 years
of age. Fibromuscular dysplasia involves mainly medium sized arteries
such as the renal and internal carotid artery and there is an increased in
cidence of cerebral aneurysms. Rarely the vertebral artery, the iliac and
subclavian arteries or visceral arteries are involved. According to
histopathologic and angiographic findings various types are differenti
ated. The most frequent form is the medial fibromuscular dysplasia which
exhibits the "string of pearls" arteriographic sign (Fig. 17). Short focal
lesions are seen in medial hyperplasia or intimal fibroplasia.
Vascular compression syndromes

Thoracic outlet syndrome: These compression syndromes may involve
the sublcavian artery as well the subclavian vein (inlet obstruction). The
cause of vascular compression may be a cervical rib or fibrous band, a
costo-clavicular compression between the clavicle and the first rib and
finally a compression between muscular structures such as the scalene
833
Figure 18.
Digital subtraction angiogra
phy o f left arm in thoracic
outlet syndrome.
A) Normal subclavian arterio
gram.
B) Severe stenoses o f the
sublcavian artery at the
level o f the clavicle (c)
crossing the first rib (r)
with elevation o f the arm.
C)Note thromboembolic
changes in the arm with oc
clusion o f the radial artery
(arrows).
Figure 19. Cystic ad

ventitial degeneration o f
popliteal artery.
A) Femoral arteriogram
shows eccentric
smooth stenosis
above the knee joint.
B) CT at same level
shows crescent like
stenosis due to low
attenuation cystic de
generation o f the ar
terial wall (Cy).
V =femoral vein.
or the pectoralis minor muscle. The diagnosis is made by subclavian ar

teriography (arm phlebography) with provocation by special manoeu
vres with an elevated or extended arm. Various degrees of stenosis or
complete occlusion may be seen during these manoeuvres (Fig. 18). Fur
thermore poststenotic dilation or thrombotic layers within the lumen may
834
Figure 20.
Secondary Raynaud's syndrome in 36-year old
smoker with Buerger's disease. Arteriogram o f
lower arm and hand shows diffuse distal disease
with occlusion o f both palmar arches, multiple
digital arteries and distal occlusion o f the ulnar
artery.
be seen. Complications such as arterial

emboli with secondary Raynaud syn
drome may be the first clinical signs.
In the lower extremity the entrapment
syndrome o f the popliteal artery is mainly
seen in young men and is caused either by
an abnormal course of the popliteal artery
or an abnormal origin of the medial head o f
the gastrognemius muscle. Finally a cystic
degeneration o f the adventitia may cause
filiform smooth stenosis of the popliteal
artery (Fig 19), more rarely in the external
iliac and common femoral artery. In this
disease young men are mainly affected.
Both diseases can be reliably diagnosed by
computed tomography or MRI. Further ar
terial compression syndromes may be
caused by external compression from tu
mors, bony structures or hematomas.
Raynaud's syndrome
The primary Raynaud syndrome or Raynaud’s disease due to central dis
turbance of peripheral vasomotor regulation causing vasospasm has to
be differentiated from the secondary Raynaud phenomenon caused by
various underlying vaso-occlusive diseases.
The primary vasospastic Raynaud's disease occurs mainly in young
patients who frequently suffer from migraine and who may have a pos
itive family history. There is typically a generalized symmetric hypocir-
culation which may be triggered by coldness or agitation. The progno
sis is usually relatively good.
835
In contrast, secondary Raynaud’s phenomenon is usually asymmetric or

unilateral and of longer duration and trophic disturbance may be found.
The main etiologies are atherosclerosis, Buerger's disease and arterial em
boli as well as changes secondary to arteritis, trauma etc. On arteriography
stenoses and occlusions of palmar and digital arteries are seen (Fig. 20).
Traumatic arterial perfusion disorders

Closed arterial injuries after trauma, operations or interventional proce
dures may cause acute ischemia by infection, laceration or dissection of
the arterial wall leading to thrombotic occlusion. Early angiography is
indicated especially in acute aortic rupture secondary to deceleration
trauma which causes a typical lesion (intimal tear or false aneurysm) in
the area of the ductus ligament. Open arterial trauma may lead to com
plete transection or a false aneurysm. The brachial, femoral and popliteal
arteries are the most frequently involved. Chronic repeated trauma may
also cause occlusion as in for instance, the Hypothenar-Hammer-syn-
drome with its typical occlusion of the ulnar artery in workmen using
carving knives or pneumatic drills.
Aneurysms
Classification
Aneurysms may be divided into 3 different types true, false and dissect
ing aneurysms.
a) True aneurysms are localised outpouchings, saccular or spindle shaped
which involve all three layers of the arterial wall. The pathogenesis is
mainly a degeneration of the media and in 70% to 80% the etiology
is atherosclerosis. Other causes are congenital weakness of connec
tive tissue (Marfan-, Ehler-Danlos-syndrome); cystic medial necrosis
or post-stenotic. Rarely it may be due to an infection such as lues.
b) False aneurysms represent aneurysms caused by an interruption of
the intima and media leading to a localised and usually asymmetric
outpouching in the arterial lumen which is bounded only by adven
titia or surrounding connective tissue. The etiology is usually trauma,
iatrogenic or infectious and is rarely atherosclerotic.
c) Dissecting aneurysms are caused by a dissection of the arterial wall,
usually the intima and/or media, with formation of a false lumen be
tween the arterial wall layers. This false lumen may thrombose or
836
may continue to be perfused, especially if there is a distal re-entry

into the true lumen. Frequently the true lumen is compressed by the
false lumen. The etiology and pathogenesis is usually a degenerative
process due to a primary or secondary weakness of the vessel wall as
in Marfans, cystic medial necrosis, hypertension or atherosclerosis.
Less frequently it is seen after iatrogenic manipulations (puncture,
catheter interventions etc.), in coarctation and trauma.
Aortic aneurysms
The majority of thoracic aortic aneurysms are due to atherosclerosis and
trauma. The atherosclerotic aneurysm usually involves the descending
aorta frequently extending into the abdominal aorta. Often parts of the
aneurysms contain thrombus. Diameters above 5 - 6 cm have a high in
cidence of rupture and are an indication for operation. Traumatic
aneurysms are typically located in the region of the ligamentum arterio-
sum (above 80%) (Fig. 21). Only about 7 to 10% survive the first 24 hours
if not treated. In less than 20% the rupture is immediately above the aor
tic valve which leads to pericardial tamponade from which patients rarely
recover. Rupture in the area of the descending aorta at the diaphragmatic
hiatus is extremely rare (1%). Chronic traumatic aneurysms in the region
of the isthmus show a typical ring or crescent like calcification.
Figure 21. \H U K ltn
Acute traumatic rupture o f the aorta. ь 25-SEP
Thoracic aortography shows false
aneurysm (arrows) in typical location
o f the arch in the region o f the ductus
ligament.
837
Figure 22.
Schematic drawing o f
dissecting aneurysms.
A) Type A with dissec
tion beginning ju st
cranial to the right
coronary artery
and re-entry in the
descending aorta.
B) Type В dissection
originating distally
to left subclavian
artery.
C) Type A dissection
with thoracoab
dominal extension
to the aortic bifur
cation.
About 25 % o f aneurysms in the thoracic aorta are dissecting aneurysms

in older patients with hypertension and atherosclerosis. According to the
Stanford classification two types are distinguished (Fig. 22): Type A:
Originating in the ascending aorta, usually cranial to the right coronary
artery and type В originating distal to the left subclavian artery. Type A
may be limited to the ascending part o f the aorta or may involve the aor
tic arch with or without the brachiocephalic vessels or may continue to
the descending aorta and even to the abdominal aorta. Occasionally the
dissection may extend retrogradely into the coronary artery and the si
nus of valsalva which may lead to myocardial infarction and/or aortic in-
suffiency. The type В dissection may similarly continue to dissect more
distally. Type A dissection must be operated on immediately. Type В
dissections are usually managed conservatively unless there is involve
ment of the renal or visceral arteries or danger of aortic rupture.
Mycotic aneurysms are usually located in the ascending aorta and are
caused by bacterial endocarditis or after a composite graft. Other infec
tious mycotic aneurysms have a predilection for the descending aorta.
The radiologic work-up in thoracic aneurysms in non-acute situations
usually starts with CT or MRI especially if contrast injection is con
traindicated (Figs. 10, 25). These modalities may show the amount of
thrombus and the extent of the perfused lumen as well as the relation
ship of the aneurysm to the neighbouring organs. CT and MRI are also
used for follow-up examinations. Echocardiography may be used for
838
screening aneurysms in the region of the sinus of valsalva and the as
cending aorta or for aortic dissection. In acute situations angiography is
still the method of choice for evaluation of traumatic aneurysms and type
A dissecting aneurysms, or in type В if possible involvement of visceral
arteries is not exclued by CT. Aortography usually shows aortic insuff-
icency and the involvement of brachiocephalic or coronary vessels in a
better degree in type A dissection. Also in an acute traumatic aneurysm
the lesion may be better shown on angiography than CT especially if
there is only a localised intimal tear. This situation may change with the
use of rapid spiral CT scanning, however.
Aneurysms of the abdominal aorta are caused mainly by atheroscle
rosis and may be seen in the plain film in up to 80% because of calcifi
cation of the aortic wall. 95% of the aneurysms are located below the re
nal arteries and in 18 % the bifurcation and iliac arteries are also involved.
The danger of rupture ranges from 10% with a diameter of 5.5 cm up to
40 to 80% with a diameter of 8 cm. Penetrating ulcerated plaques also
increase the rate of rupture.
Atherosclerotic abdominal aneurysms also represent a frequent source
of peripheral macro-emboli (10%) as well as cholesterol showers lead
ing to the blue toe syndrome.
The inflammatory aneurysm is a special form of atherosclerotic
aneurysm possibly caused by an auto-immune process. It typically occurs
in men after the fifth decade and may lead to obstruction of the ureters.
Localised dissecting aneurysms of the aorta are extremly rare in the
abdominal aorta and are usually extensions of a type В dissection.
Mycotic aneurysms have no pathognomonic signs but usually occur
rapidly as a complication of an infection, i.e. spondylodiscitis. They have
a high rate of rupture and no other signs of atherosclerosis are usually
seen if they occur in the younger patients.
For the radiologic work-up in abdominal aortic aneurysms ultrasound
is the prime screening method in the acute as well as chronic stage for
all types of aneurysm. It shows the perfused lumen and its clot content
as well as identifying a dissecting membrane (Fig. 1). CT is used for pre
operative evaluation especially with regard to the dimensions of the
aneurysm, its relationship to visceral arteries and the differentiation of
perfused from thrombosed lumen in atherosclerotic and dissecting
aneurysms (Figs. 2 and 23). It may also demonstrate the signs o f an im
minent rupture or "leaking” external to the calcified media. Angiography
839
Figure 23.
CT o f dissecting aortic
aneurysm type A.
A) Scan at level o f pulmonary
artery bifurcation shows
dissection in ascending and
descending aorta with
partially thrombosed lumen
in the ascending aorta.
B) Scan at level o f origin o f
superior mesenteric artery
again shows dissection flap
(arrows) and both the true
and false lumen patent.
A B C
Figure 24. 3D-reconstruction o f spiral CT in patient with atherosclerotic abdominal
aneurysm (A) and a patient with common iliac artery aneurysm (В, C).
A) 3D shows the kinked infrarenal neck o f the aneurysm with the aneurysm itself involv
ing mainly the distal aorta and the bifurcation. Arrows mark the renal arteries.
B) 2D-reconstruction shows the perfused lumen o f the aneurysms and the calcifications
in the arterial wall. No major thrombus is seen.
C) 3D-reconstruction shows the relation o f the internal and external iliac arteries to a
better degree and the tortuous external iliac arteries are depicted in their entire
length.
840
bloodflow, whereas the false lumen (FL) with slow flow shows increased signal inten
sity. Note the narrowed origin o f the SMA which is supplied from the true lumen.
VC = vena cava.
is used mainly to show the origin of the renal arteries and the "neck” of
the aneurysm for possible cross clamping (Fig. 11). In the future the use
of spiral CT with 3D-reconstruction may obviate the need for preopera
tive angiography (Fig. 24). MR may be used to demonstrate differences in
flow between the true and false lumens in dissecting aneurysms (Fig. 25).
In inflammatory aneurysms, CT shows a horse-shoe shaped 2 to 3 cm
thick highly enhancing fibrotic cuff which typically spares the dorsal aor
tic wall (Fig. 26).
Aneurysms in peripheral arteries

Aneurysms of peripheral arteries are of atherosclerotic origin in the ma
jority of cases. Less frequently they are post-traumatic, post-operative
(grafts) or occur after an arterial puncture for angiography or percuta
neous intervention. Very rarely they are mycotic. Characteristically ath
erosclerotic aneurysms are found in the popliteal artery (26%) or the in
guinal region (17 %). They are often symmetric and rarely are they found
in the upper extremities particularly the brachiocephalic and subclavian
841
Figure 26.
Inflammatory aneurysm
o f abdominal aorta.
A) CT shows typical
densely-enhancing
horseshoe-like cu ff o f
tissue around the aor
tic aneurysm
(arrows).
T = thrombus,
Ao = perfused aortic
lumen.
B) Abdominal aortogram
in same patient shows
aneurysm which
angiographically cannot be distinguished from common atherosclerotic aneurysm.
artery. They may thrombose especially in the popliteal artery and pre
sent with acute or chronic ischemia. They also represent a source of ar-
terio-arterial emboli.
If a palpable pulsating mass is found ultrasound and color-doppler are
the best methods for screening to show the dimensions of the aneurysm
and the extent of thrombosis. Angiography is indicated only in the con
text of pre-therapeutic diagnosis of other aneurysms and demonstration
of the general status of the peripheral vasculature.
Vascular anomalies (malformations)
Classification
There is no simple classification. Because of the various clinical and an
giographic manifestations a vast number of descriptive terms has been
arbitrarily used. A rational classification of hemangioma and vascular
malformations has been proposed by Mulliken and co-workers based on
endothelial characteristics. Two main groups of vascular anomalies may
be distinguished according to these authors, the pediatric cutaneous vas
cular lesion (hemangioma) and vascular malformations,
a) Pediatric cutaneous vascular lesions or pediatric hemangioma usually
appear within the first months of life. They are not present at birth
and more than 90% of the pediatric hemangiomas regress sponta
neously by the age of 5 to 7 years. The majority should not be treated
to allow for the natural history of involution. Only if they produce
symptoms such as eyelid hemangioma or subglottic hemangioma etc.
842
do they need to be treated. Steroid therapy usually proves successful

within a couple of weeks in the treatment of pediatric hemangiomas
in contrast to arteriovenous malformations which do not respond to
steroids.
b) Vascular malformations are present at birth whether or not clinically
evident and grow with the child. Vascular malformations can be cat
egorised into arterio-venous malformations (AVMs), capillary mal
formations (formerly cavernous or capillary hemangioma), venous
malformations, congenital arteriovenous fistula (AVF) and lymphatic
malformations. Mixed malformations are also grouped under the
common term vascular malformations.
Post-traumatic AVF or large AVF-like shunts in renal cell carcinoma or

other tumors are different because they are acquired. Most AVF are of
the acquired type. Vascular malformations include also those entities
which occur in syndromes like the Klippel-Trenaunay or Parkes-Weber-
syndrome as well as cutaneous capillary malformations such as naevus
flammeus.
Work-up fo r vascular malformations

Colour doppler imaging is the first step in the investigation of a
suspected vascular malformation. Both, high flow lesions (AVM, AVF)
and low flow lesions (capillary and venous malformations) are easily di
agnosed. Though CT can be useful, MR is the preferred non-invasive
tool for distinguishing between high and low flow lesions and for deter
mining relationship to adjacent structures (Fig. 27). Angiography or di
rect puncture in venous or lymphatic malformations is then performed
to define the angio-architecture, particularly the degree and site of AV-
shunting, the presence of aneurysms, venous outflow and the potential
route of access for endovascular therapy.
On angiography capillary malformations usually show slow flow with
delayed filling of a sponge like vascular mass with minimal or absent
AV-shunting.
Arterio-venous malformations (AVM) show meandering and dilated
feeding arteries and early venous filling (Fig 27). Depending on the de
gree of AV-shunting there may be very rapid flow.
50% of AVMs occur in the region of the head and neck and other pre
ferred locations are the extremities and branches of the internal iliac
843
Figure 27.
28-year old male with
A VM above the right
knee.
А, В) T1 weighted MR-
image in transverse
(A) and coronal
plane (B) showing
the low-signal vas
cular spaces o f the
A VM (arrows) in
the vastus medialis
muscle.
C, D) Early (C) and late
(D) arterial phase
o f femoral angio
gram showing the
dilated feeding
artery (arrows)
and early filling o f
the accompaning
veins (arrowheads)
joining the super
ficial fem oral vein
(FV).
artery. In Rendu-Weber-Osier disease they may be seen also in the gas

trointestinal tract and in the lungs.
In venous malformations the supplying arteries are of normal size and
AV-shunting usually is minimal or absent. There is contrast pooling in
the late phase in the dilated abnormal venous structures. Often venous
malformations are incompletely filled on arteriography when closed sys
tem venography or direct puncture of the pathologic venous structure is
thus needed. Venous malformations may be very large and may occur in
connection with syndromes such as Klippel-Trenaunay or Parkes-
Weber-syndrome. Venous malformations often show calcifications
within them (phleboliths).
Arteriovenous fistulas are pathologic connections between artery and
vein with direct AV-shunting. The shunts have a tendency to increase
844
Figure 28.
Iatrogenic fistula o f the deep femoral
artery after thrombectomy with Fogarty
balloon. Selective DSA o f deep femoral
artery (A) shows arteriovenous fistula
(F) with immediate filling o f the deep
femoral vein (V).
over time and large fistulas may lead to left heart failure.
Angiographically these lesions are best evaluated with digital sub
traction angiography because of the very fast blood flow. The most fre
quent causes are iatrogenic i.e. punctures for biopsy (liver, kidney) and
other frequent causes are trauma or rupture of an aneurysm into a neigh
bouring vein (Fig. 28).
Diseases of the venous system
Deep venous thrombosis (DVT)

Deep venous thrombosis is considered to have an incidence of about one
per 800-1000 inhabitants per year in Western Europe, but the incidence
varies considerably in different parts of the world. As many as one-third
may develop pulmonary embolism. The clinical diagnosis of DVT is very
unreliable, and is said to be as accurate as tossing a coin in terms of sen
sitivity and specificity. An accurate diagnosis is required to start therapy
without delay. Also, anticoagulant and thrombolytic therapy carry po
tential risks which demand clear indications before commencing treat
ment. The standard therapy is bed-rest and heparin treatment if the DVT
is above the level of the knee. In extensive cases or in young patients
with iliofemoral thrombosis, fibrinolytic therapy may often be chosen.
Surgical thrombectomy or local fibrinolysis is not often employed.
Surgical thrombectomy may be combined with a temporary a/v fistula
845
Figure 29.
The occurence o f thrombi in per cent from 338 patients
with D V T (after H.E. Schmitt 1977).
16
33
to protect thrombogenic surfaces from rethrom-
46 bosing. Local fibrinolysis may be combined with
a caval filter or balloon obstruction to prevent
45 pulmonary emboli. Recurrent pulmonary em
boli may require the insertion of a caval filter.
Predisposing conditions for DVT are malig
65
nant disease, surgery or other trauma, immo
bility, age and coagulation disorders. The well
66
known Virchows triad of stasis o f blood, inti-
83
mal injury and hypercoagulability is still valid.
83 C onsequences o f D V T
73 Deep venous thrombosis carries the short term
77
risks of pulmonary embolism, pain and swel
83
ling of the limb, venous gangrene or limb loss,
or proximal extension of the thrombus into the
inferior vena cava. It is considered that 80% of
thrombi will resolve by lysis if left untreated.
About three weeks after an acute episode of
DVT, the amount of remaining thrombus is un-
likely to change much.
The long term risks of DVT are post-thrombotic syndrome with valve
destruction or incompetence, eventually leading to venous obliterations and
collateral vessel formation. The result may be secondary varicosis, cuta
neous ulcerations, and claudication. Rethrombosis with the danger of re
current pulmonary embolism and pulmonary hypertension may also occur.
Location a n d frequency o f D V T (Fig. 29)

In a large study of more than 3000 lower extremities suspected of DVT,
60% actually had the disease. In 4/5 cases, the calf veins were throm
bosed, in 3/5 the popliteal and femoral veins. The external iliac was throm
bosed in 1/3 and common iliac in 1/5 of the cases. The most frequent
thrombosis is considered to be in the soleal venous plexus. However, due
to their narrow mouths into the deep veins, embolization of thrombi may
846
Figure 30.
Pelvic vein spur (arrow) in a patient
with acute DVT o f the leg veins.
not be frequent from this site. In au

topsy material, the second most
frequent site of thrombi is the foot
veins. The significance of foot vein
thrombi is unclear, however their
presence reveals that the patient
suffers thromboembolic disease.
This may be of importance if there
is suspicion of pulmonary em
bolism. Thrombosis of the left limb
is 1.5 times more frequent than in
the right. The reason for this is con
sidered to be the slight obstruction
of the common iliac vein by inden
tation from the crossing iliac
artery. At this point, there is in
aproximately 20% of the popula
tion a web formed by local endo
thelial proliferation (Fig. 30). This
web may be like a ring, or even a bridge over the venous lumen which cre
ates a double-lumen.
Diagnosis
The diagnosis of DVT is accomplished by ascending phlebography or
ultrasound examination.
Direct phlebographic signs of deep venous thrombosis are accom
plished by visualization of an intraluminal filling defect in two projec
tions of a contrast filled vein. A thin lining of contrast around the fresh
thrombotic mass is called the "railroad track sign" (Fig. 31 A, B). The
protruding top of a thrombus may "float" on the top of an occluded seg
ment, or propagate from a venous lumen into a non-occluded vein. Care
should be taken not to mistake an in-flow phenomenon caused by the jet
from a non-opacified vein, for a thrombus.
847
Figure 31.
A, B) Direct signs o f a fresh deep venous thrombosis, intraluminal contrast defects, in
the popliteal vein and leg vein (arrows).
C) Indirect sign o f extensive thrombosis o f leg veins; no filling ofposterior tibial or
peroneal veins, massive collateral circulation via superficial veins.
Figure 32.
KNEHASEN MED KOMPR,
Grey-scale ultrasound examination
o f the popliteal fossa with the vein
(V) and artery (A).
Uncompressibility o f the popliteal
vein indicates thrombosis o f the
popliteal vein.
Indirect signs of acute deep venous thrombosis are segmental inter

ruptions of the veins and collateral circulation. In total occlusion, only
superficial veins may be seen (Fig. 31 C). Often indirect and direct signs
848
of DVT will be present at the same time.

On ultrasound, non-compressibility of thrombosed venous segments
is a most important indirect diagnostic sign (Fig. 32). The direct visual
ization of a thrombus within the venous lumen is the most obvious means
of diagnosing deep venous thrombosis. The usual appearance of an acute
thrombus is hypoechoic, although very fresh thrombi also may be hy
per-echoic. With organization or during lysis, the thrombus again be
comes more echogenic. The importance of concomitant examination of
local venous flow by duplex-scanning is stressed. Determination of vas
cular flow direction velocity and waveform is useful in distinguishing
arteries from veins.
Lack of spontaneous flow in the major veins is a sign of obstruction
(with the exception of the tibial and peroneal veins). Absence o f phasic
flow with respiration also suggests abnormality of the venous outflow.
When a large vein is occluded, no flow is detected. It is worth re
membering that collateral veins in a similar orientation may mimic a
patent vein. Collateral veins, however, usually have continuous flow, not
influenced by respiration. Continuous venous flow in one limb and not
in the other may be a sign of thrombotic obstruction.
Venous throm bosis o f the upper extrem ity

The clinical signs of obstructed venous return include oedema o f the up
per extremity, pain, cyanosis and distended superficial veins. The etiol
ogy may be obstructing tumours in the mediastinum, a cervical rib, ex
ostosis or trauma causing thrombosis, or effort thrombosis. Iatrogenic
thrombosis of the axillary or subclavian vein is frequently seen follow
ing the insertion of central venous or pacemaker catheters.
Phlegmasia cerulea dolens

In about one per cent of patients with lower limb DVT, the extensive is
chemic thrombotic state of phlegmasia cerulea dolens appears, in which
the arterial flow is compromised by profound venous out-flow obstruc
tion and resulting venous hypertension. Venous gangrene may then oc
cur and in this situation there is a high mortality rate. Limb salvage is
more likely achieved by performing immediate venous thrombectomy
than by heparin treatment. This condition is distinguished from the more
common phlegmasia alba dolens ("painful white inflammation") with se
vere thrombotic masses throughout the extremity veins.
849
Figure 33.
Incompetent perforating veins on the dorsal/lateral
side o f the leg (arrows).
Venous insufficiency
In western communities, chronic venous
insufficiency affects about 2.5 per cent of
the population, and has significant socioe
conomic consequences. The pathophysiol
ogy o f chronic venous insufficiency in
volves incompetence of valve segments
with associated reflux, obstruction of the
vein lumen, or a combination of these re
sulting in peripheral venous hypertension
(Fig. 33). Ablative surgical management is
effective for disease in the superficial and
communicating systems, while deep ve
nous reconstructive surgery must be con
sidered experimental.
Primary varicose venous disease

This is a primary non-thrombotic venous
defect involving the valve cusp or valve
ring which prevents apposition of the valve
cusps. Normally,ascending phlebography
is of limited value except in some rare cases
for exact localization of incompetent perforating veins prior to ligation.
The preoperative diagnosis is made by clinical examination supplemented
by various methods for measuring venous pressures and ultrasound
(Doppler or colour-Doppler duplex scanning). The latter will accurately de
tect the presence or absence of valvular reflux at anatomically identified
sites, with quantitative measurements of reflux severity.
,
Secondary varicose venous disease postthrombotic syndrome
Secondary varicose vein disease may result from valve destruction due
to scarring and organization of thrombus, or obstruction of vein seg
ments. A number o f valveless collateral veins will form after obstruction
has occurred. If they appear as cork-screw bundles in the path of the ob-
850
Figure 34.
Post-thrombotic occluson o f the left common iliac
vein. Note recanalisation by developed collateral
veins.
structed vein, this is claimed to indicate that

the recanalization originates from the vasa
vasorum of the venous wall. A decrease in
the number of venous valves will be visi
ble. Destroyed valves are recognizable as
stiff, scarred webs. On phlebography re
canalized veins look like tubes with irreg
ular wall patterns resembling the loosening
bark of a tree, due to organized thrombotic
material adherent to the walls. Obstructed
veins are seen as segmental interruptions or
irregular deviations from the venous path
(Fig. 34). Increased collateral/superficial
venous flow and varicose superficial veins
often dominate the picture.
Retroperitoneal fibrosis
Retroperitoneal fibrosis is an idiopathic
process which can obstruct the retroperi
toneal urinary tract. It may also cause ob
struction of the inferior vena cava. Ascen
ding lumbar veins will often act as the main
collateral pathways (Fig. 35).
Tumours, hematomas and Baker

cysts
Neoplastic masses along the major veins
may obstruct the flow and cause peripheral
venous hypertension or thrombosis. Pri-
Figure 35. Collateral circulation in the ascending

lumbar veins following occlusion o f inferior vena
cava by retroperitoneal fibrosis. Pelvic venography
and cavography by contrast injections into both
femoral veins.
851
Figure 36.
A) Valve aplasia.
Huge tubular veins
in a young man
with extensive vari
cosities.
В, C) Klippel-Trenaunay
syndrome in the left
lower limb with a
large lateral ve
nous trunk arising
from the level o f
the popliteal vein.
mary tumours of the venous walls (rhabdomyosarcoma) are rare.

Ingrowing tumour masses into the vein lumen are called tumour thrombi.
Hematomas may clinically mimick a DVT, and may cause venous ob
struction by external compression. The lumen will appear dislodged or
stretched, thinner, or even occluded with a tapered end of the venous
segment passing into the hematoma. A similar stretched, or tapered and
occluded appearance may be presented by Baker’s cysts of the knee, in
the poplietal fossa. A ruptured Baker’s cyst is often mistaken for acute
DVT, however a carefully obtained clinical history and ultrasound ver
ification of the diagnosis, should prevent unnecessary ascending phle
bography.
Anomalies
Pelvic vein webs are described above. The popliteal and superficial
femoral veins may often be duplicated. Venous hemangiomas occur, as
described earlier in this chapter.
Venous dysplasia, valvular aplasia, is a rare anomaly consisting of
tubular veins lacking valves and inherited. It presents mainly in young
men as multiple bilateral varicose veins in the lower limbs (Fig. 36 A).
In Klippel-Trenaunay syndrome, flat haemangiomas of the skin are
present together with a very large lateral venous trunk in the thigh
852
(Fig. 36 В, C). This trunk may empty at different proximal levels. Trophic
alterations of the limb may result.
INTERVENTIONAL PROCEDURES IN PERIPH

ERAL VESSELS
Percutaneous revascularisation of arteries

The basic and most popular percutaneous revascularisation technique of
the distal aorta, the pelvic and peripheral arteries is percutaneous trans
luminal balloon angioplasty (PTA) where balloon catheters are guided
past the stenosis and through occlusions with the help of a guidewire. In
addition numerous other mechanical devices for recanalisation such as
rotating or pulsating wires and catheters, atherectomy devices and aspi
ration catheters have been developed. Furthermore, thrombolysis with
Urokinase and less frequently rtPA is used to dissolve and recanalise
thrombo-embolic occlusions. All of these methods are generally used in
combination with balloon angioplasty. Other new developments are
Laser angioplasty to remove plaque material or endovascular stents for
the treatment of recurrent or residual stenosis and complications after
PTA or surgery. Adjunctive therapy to prevent acute or delayed throm
botic occlusion and /or restenosis consists of inhibition of platelet ag
gregation by plateled inhibitors such as salicylic acid (SSA), Heparin to
avoid acute thrombosis and vaso dilators to avoid mechanically induced
spasm. As a general principle 5,000 units of Heparin are given intraar-
teriarly during the procedure. To prevent arterial spasm oral calcium an
tagonists or intraarterial nitroglycerine or lidocaine may be given. After
successful revascularisation plateled aggregation inhibitors (SSA) are
given in uncomplicated cases. Heparinisation for three days followed by
oral warfarin is advocated after recanalisation of complete occlusions or
in patients with increased risk of peripheral embolisation. Oral antico
agulation is also indicated after stent procedures in patients with insuf
ficient run-off. Other regimens for the prophylaxis of thrombosis and re
currence pre- and post-treatment consist of a combination of SSA and
Dipyridamole.
Percutaneous transluminal ballon-angioplasty

Balloon dilation is based on Gruntzig’s original concept using a non com
pliant balloon mounted on a double lumen catheter. One lumen allows
853
Figure 37. Balloon catheters o f 4, 8 and

6 mm diameter.
the balloon catheter to be ad

vanced over a guidewire and per
mits injection of contrast material
while the second lumen serves to
inflate the balloon to a predeter
mined diameter. The pathomor-
phologic mechanism by which
PTA works maybe described as a
’’controlled traumatic injury” con
sisting mainly of rupture o f the in-
timal and medial layers as well as
stretching of the arterial wall lead
ing to a more or less free arterial
lumen followed by a healing
process which results in a smooth inner surface.
Modem balloon catheters are usually made from Polyethylene or
Polyethylene-Teraphthalate or Polyurethane and Nylon compounds
which allow inflation pressures of approximately 5 to 20 atmospheres, ac
cording to material and balloon diameter. Various shapes and profiles al
low safe dilation of large diameters such as occur in the aorta down to the
very small calibres which occur in the tibiofibular arteries (Fig. 37). There
is a wide variation in the preferred timing of ballon inflation lasting any-
were from around 20 seconds to several minutes. Usually 20 to 60 sec
ond inflations applied to overlapping segments are used. In very resistant
lesions prolonged inflation of the balloon over several minutes may be of
benefit but can be applied only if sufficient collateral flow distal to the oc
cluding balloon is present. For this reason continuous monitoring of the
peripheral blood flow using oscillometry of the toes is very useful.
According to the site of the lesion an ante- or retrograde arterial punc
ture in the groin is selected. We always use a hemostatic sheath for easy
catheter exchange, protection of the arterial wall from insufficient bal
loon deflation and for control injections with contrast material. After an
initial control angiogram the obstruction is traversed with a guidewire
under fluoroscopy followed by the balloon catheter. The balloon size is
selected according to the estimated original lumen size. Balloon dilation
854
Figure 38. Various guidewires (A) (from left to right standard 0.035 J-wire, floppy
Benson cerebral-wire, Terumo-wire and .021 steerable wire with flexible gold tip) and
angiographic catheters (B) (from left to right Cobra, headhunter, sidewinder, Pigtail).
is always monitored under fluoroscopy and the results checked with an

angiogram after deflation of the balloon. To pass irregular stenoses or
occlusions various guidewires with different shapes and steering quali
ties are available. A steerable 0.035 torque control wire which protrudes
beyond a soft tipped 4 or 5F angiocatheter with a slight curve at the dis
tal end is best suited for traversing a total occlusion. Lately hydrophilic
wires have become very popular (Fig. 38). If a lesion cannot be passed
with a guidewire other mechanical devices such as rotating wires, drills
or rotablators may be tried. Finally local or regional thrombolysis and/or
percutaneous aspiration thromboembolectomy (PAT) is increasingly
used to recanalise acute and subacute occlusions (see below).
The indications for PTA of aortoiliac and femoral angioplasty range
from claudication to rest pain and gangrene. The ideal lesion is a short
concentric stenosis whereas long eccentric lesions are less ideal. Iliac oc
clusions and femoral occlusions longer than 10 cm are no longer felt to be
contra-indications. Distal popliteal and tibioperoneal lesions have also be
come treatable lesions with modem low-profile balloon catheters espe
cially for limb salvage (Figs. 39 + 40). The success rates in aortoiliac dis
ease as well as in the femoro-popliteal territory are high at 95 and 87%,
respectively. The patency rates are between 80 and 90% and 60 to 70%
after 5 years. The complication rate is approximately 5% but with only
1% requiring surgery. Hematomas and peripheral embolisation are the
most frequent complications, of which the latter may by treated with PAT
or fibrinolysis during the intervention. Stenosis of the subclavian artery
can also be dilated with a success rate of over 90%. Increasingly lesions
of the carotid and vertebral arteries are treated with PTA.
855
Figure 40. Patient with stage IV disease

and threatened limb.
Figure 39. Patient with Fontaine IIB
A) Angiogram shows total occlusion at
claudication.
trifurcation.
A, B) Angiogram before (A) and after (B)
B) After recanalisation o f fibular artery
recanalization with a J-guidewire
with Terumo-guidewire and 2.5 mm
and balloon dilation showing a
PTA balloon there is good patency o f
good result.
fibular artery.
Laser angioplasty
Laser angioplasty uses laser energy to remove atheromatous material
mainly by evaporation secondary to high local temperature. The most
common laser systems are the Argon-Laser, the Neodynium Yag-Laser
and the Xenonchloride-Excimer-Laser. Various systems to deliver the
laser energy to the target site such as bare fibre optics, metal caps (hot
tip), sapphire tips and balloons (hot balloon) have been used. The main
problem with the laser technique lies in the steering of the probes (per
foration), the limited diameter of the recanalised lumen and the high costs
of the laser systems and probes. Since most occlusions can be recanalised
with cheaper systems and longterm results are no better than those of
balloon angioplasty, this technique is of limited value as of yet.
856
Figure 41. Removal

o f postsurgical inti-
malflap.
A) Simpson
atherectomy
catheter. The
inflated bal
loon (B)
presses the
atheroma (A)
into the win
dow o f the
housing with
the rotating
knife (K).
В, C) Angiograms o f popliteal artery showing obstructing intimal flap (arrow) before
treatment (B) and after removal by the atherectomy catheter (C) with a smooth
lumen.
Drills and atherectomy catheters

For chronic, hard and calcified lesions which cannot be managed with
conventional guiedwires, various rotating devices have been developed.
Of the various systems so far only the Rotacs system and the Simpson-
atherectomy-catheter have been used successfully in large numbers. The
Rotacs system consists of an electrically driven rotating catheter (outer
diameter 2,2 mm) made from steel coiled-wires with an inner lumen that
allows the introduction of exchange wires and the injection of contrast
agents. It is covered with a highly flexible Teflon-shrinking tube and has
an olive shaped blunt tip. The motor unit, offering a continously variable
speed range up to 500 rpm is battery operated. The overall success rate
of the Rotacs-system is about 78% with a 66% success rate after previ
ously failed conventional techniques.
The Simpson atherectomy catheter can be used only for stenosis, inti
mal flaps or after an occlusion has been passed with a wire because the ro
tating atherectomy knife is contained within a cylindrical housing with a
longitudinal window. A balloon opposite this window serves to press the
latter snuggly against the atheromatous plaque so that the advancing ro
tating blade may cut the atheroma protruding into the window (Fig. 41 A).
The results of the Simpson-catheter unfortunately are not significantly su
perior to conventional balloon angioplasty. It can be a very helpful tool
when used to treat eccentric stenoses or intimal flaps (Fig. 41 В, C).
857
Figure 42.
Patient with acute
embolus in trifur
cation treated with
percutaneous aspi
ration embolec-
tomy.
A) Thin walled 8F
endhole
catheter and
60cc syringe to
supply suction.
В, C) Angiograms be-fore and after removal o f embolic occlusion involving the trifur
cation with three passes o f catheter aspiration.
Percutaneous aspiration thromb-embolectomy (PAT)

PAT is an effective and relatively simple technique for removing fresh
and older clot as well as embolic material. Depending on the size of the
blocked arterial lumen a thin walled, non-tapered catheter of 4 to 9F is
advanced through a hemostatic sheath. The catheter is applied to the
thromboembolic occlusion and a negative suction is generated with a
large (60 cc) syringe. The catheter is withdrawn keeping the suction con
stant. In fresh embolic occlusions PAT alone may restore the entire lu
men with only a few passes (Fig. 42). In thrombotic and subacute oc
clusions PAT may be combined with local thrombolysis and PTA is per
formed where additional stenotic lesions are found. We also use PAT
regularly to extract distal emboli during PTA or fibrinolysis. The com
bination of local thrombolysis and PAT considerably reduces the amount
of fibrinolytic drugs required and speeds up the procedure.
Fibrinolysis/thrombolysis
Percutaneous intraarterial thrombolysis is used to recanalise thrombotic
occlusions. The lytic drug may by infused over a catheter or a perfusion
wire placed proximal to the occlusion (regional fibrinolysis). Today how
ever, it is often preferred to infuse the fibrinolytic drug directly into the
thrombotic occlusion thereby reducing the amount of fibrinolytics nec
essary for recanalisation because of the prolonged contact o f the acti
vated plasmin with the thrombus (local thrombolysis). The agent most
widely used today is Urokinase. For regional fibrinolysis a typical dose
is 50,000 to 100,000 units of urokinase per hour (Fig. 43). In local fibri-
858
Figure 43.
Patient with threat
ened limb from
acute occlusion o f
superficialfem oral
artery and poor
distal run-off
C, D) Follow-up angiogram 12 hours after infusion o f a total o f 1.2 million units o f

urokinase shows restoration o f patency including tibiofibular artery.
nolysis the usual dosages are about 5,000 to 20,000 units per cm o f oc
clusion, depending on the age and degree of organization of the throm
bus. The other (much more expensive) agent currently used is rt-PA,
however, no definite advantages of its use in peripheral occlusive dis
ease have yet been proven. In local fibrinolysis a 5F angiocatheter is usu
ally introduced 3 to 4 cm into the clot and increments of 5,000 to 10,000
units of Urokinase are infused. Under fluoroscopic control the catheter
is slowly advanced distally into the occlusion. The thrombus should not
be traversed before most of the proximal clot has been lysed to prevent
distal embolization. Combining this method with PAT may significantly
speed up the procedure and reduce the dose of Urokinase.
Recently the so-called pulse-spray method has been advocated. This
technique uses a catheter with multiple tiny side-holes to disperse small
volumes of highly concentrated fibrinolytic drug into a 5 to 10 cm long
occluded segment. A further development is the microporous balloon
catheter where the balloon is perforated by numerous holes of micro
scopic size. With a mixture of fibrinolytic drug and saline the balloon is
inflated with a comparatively low pressure of one to two atmospheres
leaking the drug by multiple small jets o f highly concentrated Urokinase
or rt-PA into the clot. The clot is infiltrated and compressed against the
arterial wall at the same time (Fig. 44). In our experience this method
speeds up the lytic process and has been especially useful in older clots
and/or chronic occlusion with soft non-organised thrombus. Again this
method may be sucessfully combined with PAT and conventional PTA.
859
Figure 44. Patient with subacute ischemia o f left leg due to occlusion o f a superficial
femoral artery.
A) 25 cm occlusion o f SFA from origin to the adductor canal. Distal SFA filled via
collateral (arrow) from deep fem oral artery (DFA).
B) After recanalization with guidewire a microp ore-balloon is progressively ad
vanced distally infusing 5,000 to 10,000 units o f urokinase every 1 to 3 minutes.
The balloon (arrows) is placed ju st above the distal stenosis in the adductor
canal region and partial lysis is noted proximal to the balloon.
C) After infusion o f 300,000 units o f urokinase within 60 minutes the lumen has re
canalised, however, there are still some filling defects.
D, E) After additional PTA with a conventional 6 mm balloon there is a widely patent
femoropopliteal artery with only minimal wall irregularities.
Figure 45. Endo-
vascular stents used in
the arterial system.
A, B) Balloon-expand
able Palmaz and
Strecker stent.
C) Self-expandable
Wallstent.
Standard local fibrinolysis has a success rate of over 80% in the

femoro-popliteal territory. Best results are achieved if the thrombus is
less than 3 months of age and easily passable with a guidewire. The com
plications in regional fibrinolysis are about 10 to 15% whereas for local
fibrinolysis they are reduced to about 6%. The main complications con
sist of hematoma formation and distal embolisation for the latter method.
Hemorrhage is rarely seen in local fibrinolysis if dosages of 400,000 to
500,000 units o f urokinase are not exceeded. Local fibrinolysis has also
860
been successfully used for recanalisation of iliac occlusions and in throm

bosis of hemodialysis shunts.
Intraarterial stents
To overcome the problem of insufficient PTA due to elastic recoil, inti-
mal flaps, persistent flow obstructing plaques and restenosis following
PTA, endovascular stents have been developed. Most widely used in the
arterial system are the two balloon expandable stents designed by Palmaz
and Strecker and the self-expandable Wallstent (Fig. 45). These stents
consist of a fine mesh of metal filaments or of thin-walled stainlesss steel
tubing with staggered rectangular slots in the case of the Palmaz-stent.
Mounted on a balloon catheter or a special introducing instrument, the
stents can be released at the desired site via a percutaneous inguinal ap
proach. The expanded metal stents are strong enough to withstand the
recoiling forces of the arterial wall and to keep the lumen well open. The
results in the iliac arteries have been excellent with patency rates of over
90% after 5 years. The stents are especially valuable in the management
of complex iliac lesions and iliac occlusions (Fig. 46 A, B). In the femoro-
popliteal axis intimal hyperplasia is a yet unsolved problem and leads to
reobstruction in 40 to 60% (Fig. 46 C, D). The more distal the stents are
placed respectively the smaller the vessel diameter, the more likely is the
development of intimal hyperplasia. This process is even more likely if
there is an insufficient distal outflow. Therefore, great care should be
taken when considering patients for femoro-popliteal stenting and other
means such as repeated balloon dilation and percutaneous atherectomy
should be tried first.
Embolization procedures
Embolization procedures are an important alternative to surgical treat
ment for arterial bleeding, aneurysms, arteriovenous fistulas and mal
formations (angiodysplasias), as well as tumors of the peripheral vascu
lature. The main indications are:
- Treatment of iatrogenic and traumatic bleeding including AV-fistu-
las and aneurysms especially in the pelvis and in the extremities.
- Congenital AV-malformations and fistulas,
- to stop bleeding of tumors especially in the urogenital tract and for
chemo-embolisation of bone tumors (Osteosarcoma) and primary
or secondary tumors of the liver
861
Figure 46.
Stenting fo r iliac and femoral
occlusions.
A, B) Occlusion o f external
iliac artery (A) recanal-
izsed with guidewire and
stented with two over
lapping 7 mm Wallstents
(B).
С , D) Patient two years after
femoropopliteal stenting
showing a second recur
rence o f intimal hyper
plasia within the stented
segment. Patient had
been dilated one year
before. Angiogram
shows marked irregular
ities o f the lumen and
stenosis due to initimal
hyperplasia (C). After
PTA there is a good
result (D).
Technique and embolisation material

A high quality (super selective) angiogram is a prerequisite for any type
of arterial embolisation. The catheters through which the embolic mate
rial will be administered, should be guided as close as possible to the
lesion in order to spare non involved arteries and tissue. Torque control
catheters of 4 and 5F with an inner lumen of .035 or .038 inches (0,9,
1,0 mm) are used together with special steerable wires. Guidewires with
hydrophilic coating have greatly improved the trackability of peripheral
arteries. For access to small and tortuos vessels catheters of 2.7 to 3F size
862
Figure 47.
Embolization materials.
1) Gianturco coils.
2) Polyvinyl alcohol (Ivalon) -parti
cles o f various sizes.
3) Gelfoam particles.
Figure 48.
Patient with inter
mittent bleeding
causing swelling
o f thigh and drop
o f hemoglobin af
ter total hip-pros-
thesis.
A) Antegrade arte
riogram shows
false aneurysm
fed by a deep
femoral artery
branch.
B) After filling the aneurysm with 7 coils and gelfoam plus blocking the feeding artery
with two additional coils the bleeding has stopped. Note the coils filling the
aneurysm (arrow) and the additional coils (arrowhead) occluding the feeding artery.
accepting .016 to .018 guidewires may be used coaxially through con

ventional 4 and 5F angiographic catheters.
There is a great number of embolization materials (Fig. 47), the most
important being: mechanical devices such as stainless steel coils and de
tachable balloons; reabsorbable material such as gelatin sponge
(Gelfoam) and occlusion gel (Ethibloc); non resorbable materials such
as polyvinyl alcohol (Ivalon), silicon spheres; liquid material such as tis
sue glues (Bucrylate), sclerosing agents, absolute ethanol; autologous
material such as blood clot, muscle, fat etc. and finally chemo-embolic
agents. No single embolization material can be used optimally for all
clinical conditions. For any clinical situation several embolization ma
terials may be required. For larger vessels, aneurysms and large AV-con-
nections, coils and detachable balloons are the agents of first choice (Fig.
48). For medium-sized arteries Gelfoam and tissue adhesives (Bucrylate)
are often used. Hemorrhage of small arteries and AV-malformations as
863
Figure 49.
Embolization o f
A VM in the vastus
medialis muscle o f
the right thigh
(same patient as in
fig- 27).
A, +B)
Superselective
catheterisation o f
arterial branch
feeding the A VM
(B)
tent o f the malfor
mation with tortuous arterioles and cirsoid early draining veins to a much better
degree than the nonselective arteriogram (A).
C) Arteriogram after superselective embolisation with Ethibloc shows the A VM and
main filling artery blocked. A small branch barely visible before is now seen to be
feeding a small non-occluded part o f the A VM.
well as tumors are treated with particulate matters such as Ivalon,

Gelfoam, Ethibloc, Bucrylate, ethanol or minicoils (Fig. 49).
Complications of embolization procedures in the peripheral arterial
system usually result from ischemia and infarction of the target organ.
Reflux of embolization material or passage through to the venous side
with unintended occlusion of non target vessels (i.e. peripheral ischemia,
lung embolism) are other sources of complications. With a meticulous
technique the complication rate should stay below 5%. However, pain,
soft tissue swelling and fever, which constitute postembolizsation syn
drome may last for 2 to 10 days and are seen quite commonly.
INTERVENTIONAL PROCEDURES IN THE

VENOUS SYSTEM
PTA and stenting of obstruction in arterio-venous fistu-

lae in patients on hemodialysis
Obstruction of venous outflow is by far the most common problem en
countered in patients with hemodialysis access fistulae. Most stenoses
occur within a few centimetres of the venous anastomoses in Cimino-
shunts, or in grafts at the site of the proximal anastomosis. In approxi
mately 21 % of all venous outflow lesions, however, the stenoses occur
in the brachiocephalic vessels. A stenosis at the arterio-venous anasto-
864
Figure 50.
PTA o f venous outflow
stenosis in hemodialy
sis shunt.
A) Shuntogram with
proximal compres
sion shows widely
patent A V-anasto-
moses but multiple
stenoses o f the ve
nous outflow tract
close to the anasto
mosis.
B) Afterfirst dilation
suboptimal result.
C) Good result after
prolongued dilation with high pressure (12 atmos.) fo r 6 and 10 minutes. Prolonged
balloon dilatation in venous outflow stenoses often improves dilation results.
mosis is much rarer than venous outflow obstruction. Balloon dilation

particulary of venous outflow stenosis and stenosis of graft anastomoses
has been used with increasing frequency during the past decade. The
route of access to a lesion requiring balloon angioplasty depends on its
location, and the exact anatomy of the venous outflow tract including the
arterio-venous anastomosis has to be studied before any percutaneous
intervention. The approach to the stenotic lesion can be either antegrade
or retrograde and is chosen so as to allow sufficient space for the ma
nipulation of guidewires, and angiographic and balloon catheters through
the stenosis via a hemostatic sheath. The balloon sizes are generally 5 to
7 mm for veins below the elbow, 7 to 10 mm for those in the upper arm
and 10 to 12 mm for the subclavian and brachiocephalic veins. For a
stenosis of the arterio-venous anastomosis smaller balloon sizes accord
ing to the diameter of the artery may have to be chosen. As with any PTA
procedure 5,000 units of Heparin are given after introducing the sheath
but nothing further in the way of anticoagulation is usually necessary.
Although patency rates have been somewhat disappointing ranging from
42 to 45% at one year and as low as 12 to 38% at two years, PTA remains
the treatment of first choice for failing hemodialysis fistulae (Fig. 50).
Repeat dilation of venous outflow obstructions in the native outflow vein,
and/or at the arteriovenous or graft anastomoses may be necessary to
keep the fistula functioning for hemodialysis.
865
Figure 51.
Patient eight months after placement o f
a 10 mm Wallstent fo r tight recurrent
stenosis in the basilic vein.
A) Recurrent stenosis from intimal hy
perplasia at the efferent end o f the
stent (arrow) and moderate intimal
thickening within the stent (arrow
heads).
B) A second 10 mm Wallstent has been
placed overlapping the first one via a
femoral approach with good immedi
ate result. Patient died two months
later from underlying disease with
functioning shunt.
In spite of the higher recurrence rates with PTA, agressive angiography

coupled with angioplasty at the first sign of fistula dysfunction may pro
long the life of a fistula for several years. Recently intravascular stents have
been tried in an attempt to improve upon the results of PTA alone. In gen
eral however, primary stenting without a previous trial of conventional
PTA is not recommended since a stent cannot usually prevent later resteno
sis from intimal hyperplasia. Exceptions to this rule may be cases where
PTA has proved ineffective owing to the elastic recoil of the stenosis or
where the recanalisation of chronically occluded central veins is required.
As is the case with PTA, access to the lesion depends on the location
of the stenosis and for central and proximal peripheral lesions we prefer
a femoral approach. We always predilate the stenotic segment before
stent implantation and repeat dilation of the stented segment immedi
ately following stent release is also performed if adequate stent expan
sion seems delayed.
Though the initial technical and clinical success rate after stenting of
hemodialysis outflow stenosis is very high, restenosis at some point af
ter stenting (usually between 4 and 12 months) almost invariably occurs.
However, restenosis caused by intimal hyperplasia can usually be redi
866
lated quite easily by balloon angioplasty. Since patients on chronic hem-

dialysis are likely to have multiple surgical procedures during their life
time it is important to perform percutaneous transluminal procedures
whenever possible (Fig. 51).
PTA and stenting of benign and malignant obstructions

of the vena cava and large veins
There are various causes of obstruction or stenosis of the vena cava and
large veins. Those seen most frequently include compression by malig
nant disease, fibrous reactions after radiation therapy and the sequelae
of deep vein thrombosis and from indwelling central venous catheters.
Other causes for venous obstructions include trauma, infection, post-sur
gical complications, venous anomalies such as webs or venous spurs and
finally stenoses of the liver veins or the intrahepatic segment o f the IVC
in Budd-Chiari syndrome. The sites most frequently involved in these
conditions are the superior and inferior venae cavae (including the pelvic
veins). The operative treatment of stenotic or occlusive venous disease
is often difficult and involves major vascular surgery in the case o f the
venae cavae and other large central veins. In malignant obstruction
surgery is not justified in view of the dismal prognosis of the underlying
disease. Therefore interventional techniques such as percutaneous trans
luminal angioplasty and stenting have been recently introduced as both
curative and palliative forms of treatment.
Since most obstructions are caused by external compression or fibrotic
changes which do not respond well to PTA alone, angioplasty is practi
cally always backed up by an endovascular stent. Inflow obstructions of
the superior or inferior vena cava (superior vena cava and inferior vena
cava syndrome) are excellent indications for stenting since the majority
of the patients will respond by rapid regression of the symptoms of in
flow obstruction within hours (Fig. 52). Clinical relief of symptoms can
be expected in 70 to 100% of the subjects in malignant disease and in
close to 100% in benign obstructions. Long-term patency in SVC and
IVC stenting for malignant disease ranges from 86 to 100%, though the
length of patient survival rarely lasts more than two years. If acute throm
bosis or restenosis occurs a second procedure using local thrombolysis
or redilatation and additional stent placement can be performed. Although
there is only limited data on long-term patency for benign lesions this will
probabely be above 90% (Fig. 53).
867
Figure 52.
Patient with severe superior V. cava syndrome from mediastinal metastases secondary
to carcinoma o f the breast
A, +B)
Phlebography o f both arms shows tight stenosis o f right brahiocephalic vein and
occlusion o f the left brachiocephalic vein.
C) After stenting with a 12 mm Wallstent on the right and guidewire recanalization
and stenting with a 10 mm Wallstent on the left there is good drainage. Patient was
free o f symptoms within hours.
Provided a stenosis or occlusion of the vena cava or a large vein can be

passed using a guidewire and a preliminary dilatation of the lesion with
a balloon catheter allows enough expansion of the lesion to permit stent
implantation, practically any malignant or benign venous obstruction
may be stented. It is important, however, to ensure that adequate blood
flow will exist through the stented area which means adequate inflow and
outflow. Generally a femoral approach is employed for stenting but an
internal jugular approach is sometimes necessary. For very tight lesions
or chronic occlusions of the brachiocephalic vessels a double approach
from the arm and the femoral vein (the so called pull-through method to
stabilise the guidewire from both ends) may be necessary. If significant
thrombosis distal to the obstruction is found on phlebograhy, local throm
bolysis with Urokinase should be performed before stent placement to
prevent pulmonary emboli and/or early reocclusion.
PTA and stent implantation for palliation in malignant disease and as
curative treatment in benign conditions should be regarded as the method
of choice in view of its success compared to surgical alternatives.
868
Figure 53. Patient with

veno-venous bypass fo r
trauma to common
femoral vein during op
eration fo r varices.
Massive right leg
swelling two months af
ter corrective surgery.
A) Crossover retro
grade phlebography
shows subtotal steno
sis o f right commom
femoral vein.
B) After placement o f a
10 mm Wallstent the
antegrade flow o f the
femoral vein is re-es
tablished.
Chapter 21
The lymphatic system
Elias Zerhouni
The lymphatic system functions is the main immunologic surveillance

mechanism of the body. The lymphatic system consists of a rich network
of interconnected lymphatic vessels which exist in virtually every tissue
of the body. Interstitial fluids, normal and abnormal cells, microorgan
isms and antigens are carried through lymphatic channels to loco-re
gional lymph nodes which function as peripheral lymphoid organs.
Lymphatic fluid eventually returns to the venous circulation mainly via
the thoracic duct which drains in the right subclavian vein. The spleen,
a lympho-reticular organ serves as a major site of clearance for circulat
ing microorganisms, antigens, damaged and abnormal circulating cells.
Enlargement of lymph nodes, spleen, thymus or liver is one o f the most
common clinical findings and can be secondary to an increase in the num
ber of normal cells such as lymphocytes and macrophages during anti
genic stimulation, infiltration by inflammatory cells, proliferation of ma
lignant lymphocytes or macrophages, infiltration by metastatic malig
nant cells and infiltration by lipid-laden macrophages in lipid storage
diseases. It is therefore not surprising that lymph node involvement can
be observed in a wide spectrum of infectious, autoimmune and neo-plas
tic disorders (Table 1). Under 30 years o f age 80% of lymphadenopathies
are benign whereas in patients older than 50 years, only 40% are benign.
871
Table 1. Pathologic conditions in which lymph node involvement

can be observed.
INFECTIOUS DISEASES
a - Viral infections: infectious hepatitis, infectious mononucleosis,
AIDS, rubella, varicella, herpes
b - Bacterial infections: Streptococci, staphylococci, salmonella, bru
cella, listeria monocytogenes, pasteurella pestis, cat-scratch dis
eases, yersinia
с - Fungal infections: coccidiodomycosis, histoplasmosis
d - Chlamydial infections: lymphogranuloma venereum, trachoma
e - Mycobacterial infections: tuberculosis, leprosy
f - Parasitic infections: trypanosomiasis, microfilarissis, toxoplasmosis
g - Spirochetal infections: syphilis, yaws, leptospirosis
MALIGNANT DISEASES
a - Hematologic: lymphomas, leukemias and malignant histiocytosis
b - Metastatic: (common) melanoma, tumors of lung, breast, prostate,
gastrointestinal tract, kidney and head and neck. Seminona, Kaposi's
sarcoma
ENDOCRINE DISEASES: hyperthyroidism

LIPID STORAGE DISEASES: Gaucher, Niemann-Pick diseases
DISEASES OF UNKNOWN ETIOLOGY: sarcoidosis, amyloidosis,
giant follicular lymph node hyperplasia (Castleman's disease), lym-
phomatoid granulomatosis, familian mediterranean fever, sinus histio
cytosis, muco-cutaneous lymph node syndrome
ROLE OF DIAGNOSTIC IMAGING

The radiologist is often called upon to help evaluate diseases involving
the lymphatic system. Imaging is primarily used to
- detect the presence of lymphatic system involvement in regions in
accessible to physical examination
- stage the extent and degree of lymphatic involvement

- guide and perform image guided tissue sampling whenever necessary
to obtain a specific diagnosis in regions inaccessible to excisional
872
THE LYMPHATIC SYSTEM
biopsy or for staging purposes in malignancies

- to assess the level of response to therapy by monitoring size changes
and other features such as signal intensity, contrast uptake and meta
bolic activity.
MODALITIES
Conventional radiography
The imaging test most often required in the evaluation of lymphatic sys
tem disease is the chest radiograph. Because the lungs are open to the at
mosphere and frequently subject to infection, thoracic lymph nodes can
be slightly larger than in other organs and are more often calcified. For
interpretation purposes, an upper size limit of 1 cm is generally accept
able. Although the total number of thoracic lymph nodes is about 100,
only a few can be assessed by conventional radiography. Moderately
large (2-3 cm at least), hilar, mediastinal, paracardiac and paraspinal
lymphadenopathy can often be detected by postero-anterior and lateral
projection radiography. A contour abnormality is most often the key find
ing in such cases. The following anatomic regions should be most par
ticularly examined because they almost always contain lymph nodes in
close proximity with pleural/lung reflections that are tangential to the X-
ray beam. These are: the aorto-pulmonary window, the right tracheo
bronchial angle, the upper paratracheal regions bilaterally (Fig. 2 a), the
subcarinal angle, the right cardiophrenic angle, the paraspinal reflection,
the posterior junction line and the azygo-esophageal reflection line. The
right bronchus intermedius, as well as the posterior aspects o f the left
main bronchus and right upper lobe bronchus are best assessed on lat
eral views where they present easily seen interfaces with aerated lung.
In patients with well inflated lungs the retrosternal pre-aortic clear space
helps evaluate the anterior mediastinum for masses or adenopathy. In
other regions of the body, plain radiography is often ineffective in as
sessing lymphatic system disease because of lack of soft tissue contrast.
Nonetheless, plain abdominal radiographs can be helpful in evaluating
the liver and spleen for enlargement. Calcified or previously opacified
lymph nodes can be effectively followed by plain radio-graphy.
873
Figure 1. Normal lymph node.

a) CT scan. Note small sharply de
fined node in pretracheal retro-
caval space.
b) MRI scan. T1 -weighted series.
Same node (arrow) appears low
in signal intensity due to long
Tl o f normal lymphoid tissue.
Lymphangiography
The technique of lymphangiography, once very popular in the evalua
tion of various lymph node beds such as the lower extremities and ab
domen to the level of the cistema chyli is being abandoned in most cen
ters in favor of computed tomography. At a few oncologic centers, lym
phangiography is still preferred for the management of certain
lymphomas such as Hodgkin's disease because opacified lymph nodes
can be assessed repeatedly by simple radiographs over a period of sev
eral weeks and involvement of normal sized lymph nodes can be specif
ically detected by the pattern of opacification. In addition, unlike non-
Hodgkin's lymphoma where peripheral nodes such as mesenteric and
peripancreatic nodes are more often involved but cannot be visualized
by lymphography, Hodgkin's disease involves axial lymph nodes such
as para-aortic and iliac groups which are opacifiable. Using fine local
dissection of superficial lymphatics after coloration of the interstitial flu
ids by a vital dye, lymphatics can be visualized and cannulated with very
fine needles. Lipid based iodinadated contrast agents or even radioactive
874
Figure 2.
Metastatic disease in mediastinal
lymph nodes.
a) Plain film. Note right paratracheal
mass.
b) CT scan. Note ill-defined, matted
group o f precarinal lymph nodes
and
c) right paratracheal adenopathy.
agents can then be injected for

evaluating lymph flow and in
termediary lymph nodes. The
difficulty of successful cannula-
tion has limited the utilization of
this technique to a few well
skilled radiologists.
Computed tomography
The advent of computed to
mography (CT) has revolution
ized the imaging assessment of
the lymphatic system. The high
tissue density contrast between
lymph nodes and the fat that of
ten surrounds them is large
enough to identify some of the
normal and most of the enlarged
lymph nodes in all body regions
(Figs. 1,2). The cross-sectional
plane of imaging and the uti
lization of fast dynamic intra
venous contrast-enhanced CT
permits easy differentiation of
blood vessels from lymph nodes in most cases provided sufficient fat
surrounds the lymph node. There are, however, several limitations to CT.
After initial optimism, it has become clear that CT cannot reliably de
tect the presence of small focal or diffuse disease in the liver or spleen
875
Figure 3.
a) CT with contrast enhancement
shows no obvious lymph node.
b) T2-weighted MR scan shows ob
vious bright lymph node in right
hilum.
thus limiting its potential in accurate staging of lymphomas. In the ab

sence of surrounding fat, CT fails to detect many lymph nodes (Fig. 3).
Furthermore, CT cannot differentiate malignant from reactive lymph
nodes on the basis of density or appearance and its accuracy in cancer
staging is thus limited. Size being the only criterion CT can rely upon
for assessing normal and abnormal nodes in early metastatic involve
ment, microscopic or minimal macroscopic disease cannot be detected.
CT is useful in monitoring the response of lymph node masses to ther
apy by monitoring size changes, however, it cannot differentiate resid
ual active disease from fibrotic residual lymph nodes (see below). Despite
its limitations, CT remains the best method for imaging the lymphatic
system because of its relative ease o f use and interpretation. In addition,
because it can help direct precisely needle biopsy to lesions as small as
1 cm in regions of difficult access, CT has become a good management
tool by helping provide direct histologic confirmation in a minimally in
vasive fashion. This latter role is bound to grow further in the future as
familiarity with such techniques develops but also because an increas
ing number of molecular genetic markers that provide very specific and
sensitive diagnoses with minute amounts of tissue material are being dis-
876
Figure 4.
a) T1-weighted and
b) T2-weighted MR scans show a
large metastatic lymph node in
the right hilum with typical high
signal intensity on T2-weighted
scan. Note also a smaller node in
the precarinal region that re
mains dark on the T2-weighted
scan. This low signal would
suggest that this node is normal
or fibrotic. However, at patho
logic examination, microscopic
disease was found. M RI is not
reliable in excluding the pre
sence o f minimal disease in
metastatic nodes.
Figure 5.
a) CT scan shows two small calcified
lymph nodes.
b) MRI scan suggests that a larger node
with central fa t is present and does
not clearly detect calcification.
(Courtesy o f Dr. Richard Webb, UCSF)
877
covered at a rapid pace.

Several more specific contrast agents for CT o f the reticulo
endothelial system have also been investigated. Lipid based agents such
as EOE-13 have been tested in animals and humans. These contrast agents
increase the density of the liver and spleen as they are picked up by the
reticulo-endothelial cells. This type of agent has not, however, gained
wide acceptance. Attempts have also been made at developing methods
to visualize lymph nodes of the mesentery by using orally administered
oily based iodinated agents with very limited success.
Magnetic resonance imaging

MRI is an imaging technique with greater tissue contrast capabilities than
CT. As with CT, lymph nodes can be distinguished from surrounding fat
by their different relaxation characteristics. Lymph nodes have much
longer T 1-relaxation times than fat and thus appear as low intensity struc
tures on T1-weighted images. However,the T2 relaxation times are sim
ilar and lymph nodes are not always distinguishable on T2-weighted se
quences and are best visualized on T 1-weighted sequences (Fig. 1). With
the advent o f MRI, it was hoped that specific differences in tissue sig
nals will be found between malignant and non-malignant tissues, because
tissue parameters such as the T l- and T2-relaxation times vary as a com
plex function of water content, protein composition and structure. Even
though statistically significant differences in both the Tl and T2 relax
ation times o f malignant and non-malignant nodes do exist, the overlap
between signal characeristics is such that diagnostic utility is limited in
the individual patient (Fig. 4). MRI can to some extent differentiate fi-
brotic lymph nodes which exhibit low signal intensity on T2-weighted
series from inflammatory or neoplastic nodes which appear much
brighter and this has found some limited use in the differentiation of
retro-peritoneal fibrosis from tumor, post-radiation fibrosis from recur
rent tumor in lymphomas, rectal and uterine cervical cancers.
Microscopic disease is not detectable and calcification may not always
be detected with MRI (Fig. 5). Because of these limitations, as well as
the greater cost and longer examination times of MRI, CT remains the
preferred method of investigation for lymph node pathology except in
patients with allergy to iodinated contrast agents. In the evaluation of the
liver and spleen, MRI is equally accurate to CT and in selected instances,
can show diffuse or small multifocal involvement of the liver and spleen
878
Figure 6. Untreated Hodgkin's disease in anterior mediastinum (arrows).

a) T1-weighted scan
b) T2-weighted scan. Note high but heterogeneous signal intensity on T2-weighted
scan, typical o f active lymphoma.
Figure 7. Evolution o f treated Hodgkin's disease. A series ofT2-weighted M RI scans

at time o f diagnosis (a); 6 weeks (b); 3 months (c) and 1 year (d) after initiation o f
therapy. Note the decreasing signal intensity typical o f fibrosis and the parallel change
in size typical o f good therapeutic response.
that cannot be detected with CT. In evaluating liver and spleen, it is felt
that MRI and CT play complimentary roles and are often used jointly in
patients with known malignancies in whom accurate evaluation of the
liver and spleen is necessary. MRI is very effective in the evaluation of
the bone marrow. Fatty marrow is easily differentiated from red marrow
879
and the normal conversion patterns of red fatty marrow with aging have
been well described. MRI is considered accurate in evaluating the pres
ence or absence of diffuse or focal bone marrow disease. In many cases,
the MR examination may be positive for metastatic disease to the bone
marrow before radionuclide bone scanning. In primary bone marrow dis
eases such as myeloma, lymphoma and leukemia, MR imaging of the
bone marrow is the most accurate method to stage and follow bone mar
row involvement.
MRI can also be useful in the management of patients with known
lymphoma in whom partial regression of tumor masses is often observed.
These residual masses most often represent the fibrotic residual of a ster
ilized tumor mass. It can, however, also represent residual active disease.
With CT, it is impossible to differentiate fibrosis from residual active
disease. With MRI, significant differences in the signal intensity pattern
of fibrosis and residual tumor have been demonstrated on T2-weighted
series (Figs. 6 and 7). MRI is thus used at several centers as a method of
monitoring the residual masses in patients with known lymphomas. If
the signal intensity of these masses is low on T2-weighted series, they
are presumed to represent residual fibrosis. However, if the signal in
tensity remains high beyond six months following initial therapy they
are considered to represent residual disease and further diagnostic steps
are undertaken. More importantly, reappearance of high signal intensity
foci in a previously fibrotic appearing mass is a reliable sign o f tumor
recurrence.
To enhance the detection and assessment of lymphatic system pathol
ogy, multiple contrast agents are being investigated for use with MRI.
MRI has the distinct advantage of greater sensitivity to smaller amounts
of contrast agent as compared to computed tomography. Because of this
increased sensitivity, efforts have been directed to the development of
superparamagnetic iron oxide particles which are cleared from the blood
stream by the reticulo-endothelial system. The presence of a superpara
magnetic particle reduces signal intensity considerably due to a marked
shortening of the T2 relaxation time. In the liver and spleen, the retic-
ulo-endothelial system effectively clears such agents and leads to a
marked decrease in the signal intensity of normal liver and spleen, thus
enhancing the detection of underlying pathology. In addition, since the
clearance from the blood stream is not immediate, these agents can be
used to measure perfusion in various organs. If made small enough, these
880
superparamagnetic iron oxide particles can leave the vascular space be
fore trapping by reticular endothelial cells and can penetrate the inter
stitial extra-cellular space. Since foreign particles in the interstitial space
are primarily cleared through the lymphatics, these particles eventually
accumulate in the lymph nodes. Early clinical trials have shown that nor
mal lymph nodes will readily accumulate these particulate contrast
agents whereas lymph nodes involved by metastastic disease do not. It
is hoped that these newer agents will enable more accurate assessment
of loco-regional lymph nodes, thus facilitating the staging of various
types of cancers.
Radionuclide methods
Because of the superb sensitivity of radionuclide imaging, albeit at lower
spatial resolution, the lymphoreticular system has been extensively im
aged with multiple radioactively labeled agents. Using reticulate agents
such as Technetium 99m sulfur colloid particles, the liver and spleen can
easily be demonstrated. Using smaller particles, bone marrow uptake can
be improved, however, bone marrow imaging with radionuclide tech
niques has not gained wide acceptance because of the inconsistency of
uptake. Over the years, many efforts have been expended in the devel
opment of more specific agents including labeled monoclonal antibod
ies and cells such as leukocytes in the hope of using immunological
mechanisms for agent localization. These efforts have generally failed.
A notable exception is the use of Gallium 67 scanning which appears to
more reliably detect areas of disease activity in both inflammatory and
neoplastic processes. For example, in the management of lymphoma,
Gallium 67 scanning is reliable at assessing the disease after therapy.
Over the past few years, the use of single photon emission computed to
mography (SPECT) has improved the spatial resolution of radionuclide
methods. Progress in radiochemistry and labeling agents may lead to an
increased use of SPECT for assessing diseases of the lymphatic system.
More recently, the development of metabolic agents such as FDG-glu-
cose with positron emission tomography (PET) offer the hope of directly
observing the metabolic activity of diseased tissues. Already, prelimi
nary studies show that positive FDG-glucose imaging in lymph nodes
correlates highly with the presence of metastatic disease. This concept
is being used in lung, colorectal and breast cancer as a new method of
detecting lymph node involvement. Greater experience will be needed
881
to assess the diagnostic accuracy o f such approaches. With the advent of

total body high resolution efficient PET scanners, it is possible that can
cer staging may be more accurately performed with PET in the future.
The specificity of the metabolic activity associated with increased up
take of FDG-glucose, however, needs to be ascertained before wide
spread clinical use.
PATHOLOGY
Malignant lymphomas
Malignant lymphomas represent the most common neoplasm in patients
between the ages of 20 and 40 years. The two major variances of ma
lignant lymphoma are non-Hodgkin's lymphoma and Hodgkin's disease.
Although both of these tumors infiltrate reticular endothelial organs, they
are distinct from the biological and clinical standpoints.
Imaging is primarily required to detect nodal and extra nodal disease
in regions inaccessible to physical examination. In two thirds of patients
the disease is suspected by the presence of asymptomatic peripheral
adenopathy that persists over 4 to 6 weeks. Constitutional symptoms such
as fever and night sweats known as В symptoms occur in 25 to 30% of
patients with Hodgkin’s disease and in a lower percentage of patients
with non-Hodgkin's lymphoma. Once the diagnosis is established by
lymph node biopsy, imaging is required for full evaluation. Treatment
of lymphomas can be highly effective if delivered properly with over 80%
and 50% disease free survival being reported for Hodgkin's and non-
Hodgkin's lymphomas, respectively. It is important to understand that
imaging is primarily needed to determine whether the disease is at a lo
calized stage that could be treated with radiation therapy, a very effec
tive approach. If the disease is at a more advanced stage, it is now es
tablished that radiotherapy is not indicated and chemotherapy alone en
tails a similar or better prognosis than radiotherapy or combination
therapy in most cases. The Ann Arbor staging system is the most com
monly used scheme and can serve as a guide for imaging interpretation
(Table 2).
882
Figure 8.
Examples o f lymphadenopathy in
lymphomas.
a) CT scan showing enlarged
right and left anterior parac
ardiac nodes. This localiza
tion is very suggestive o f
Hodgkin's disease.
b) CT scan showing retro-crural
adenopathy (arrows) in non-
Hodgkin's lymphoma. In the
retroperitoneum, nodes larger
than 6 mm are considered
abnormal.
c) CT scan o f retroperitoneum, showing a common pitfall mimicking adneopathy, the
crus o f the right hemidiaphragm (arrow).
Table 2. Ann Arbor staging system fo r lymphomas
Stage 1: Involvement of a single node region or single extralymp

hatic site
Stage 2: Involvement of two or more nodal regions on the same side
of the diaphragm; can include localized involvement in a
single extralymphatic site
Stage 3: Involvement of nodal regions or extranodal sites on both
sides of the diaphragm
Stage 4: Disseminated involvement to one or more extralymphatic
organs with or without lymph node involvement
B: Denotes the presence of constitutional symptoms
E: Denotes involvement of extralymphatic sites
CT is the main method of imaging for staging lymphomas. Several dif

ferences in the natural history of Hodgkin's and non-Hodgkin's lym
883
phomas need to be appreciated for the judicious use of imaging. Hodgkin's

disease involves predominantly the axial lymph node groups such as me
diastinal, paracardiac and paraaortic regions (Fig. 8). Over 60% of pa
tients with Hodgkin's disease present with mediastinal lymphadenopathy.
Non-Hodgkin’s lymphomas predominantly involve peripheral nodal re
gions such as epitrochlear, mesenteric and Waldeyer’s ring lymph nodes.
Only 20 % of non-Hodgkin's lymphomas exhibit mediastinal lymph node
involvement. In addition, Hodgkin's disease is more frequently localized
and spreads by contiguity to adjacent nodal regions with infrequent
"skipped” nodes. Non-Hodgkin’s lymphoma is more frequently multifo
cal or diffuse and can easily spread to non-adjacent regions. Thus, in non-
Hodgkin’s lymphoma it is necessary to scan the entire body for accurate
staging whereas in Hodgkin's disease involvement is generally contigu
ous. The great majority of involved nodes are enlarged and detectable
with CT which exhibits accuracy’s in the 80 to 90% range for staging of
lymphomas. Microscopic disease and diffuse liver, spleen and marrow
involvement, cannot be detected with CT. Gallium 67 scanning has been
advocated for the detection of occult disease but does not seem to be use
ful except in the context of following up residual disease and detecting
recurrence, however, it is indicated prior to therapy to determine if the
lymphoma is Gallium avid. MRI has been advocated in the detection of
liver and spleen involvement but does not appear efficacious without the
use of contrast agents which are still under experimental development.
On the other hand, MRI is sensitive to the presence of gross bone mar
row involvement. When staging by imaging indicates localized disease
in Hodgkin’s lymphoma, staging laparoscopy may then be considered to
exclude occult splenic or abdominal lymph node disease because no
imaging technique is accurate enough to exclude such eventuality if the
disease is adjacent to abdominal structures. For non-Hodgkin’s lym
phoma the incidence of localized disease is less than 10% and except for
low and intermediate grade types, systemic therapy is almost always
used. A common problem in the management of lymphoma is the fre
quent occurence of partial regression of tumor masses raising the possi
bility of incompletely treated active disease versus residual masses. MRI
can help evaluate and monitor such residual masses by virtue of the dif
ferent signal intensity of fibrosis and active tumor on T2-weighted im
age sequences. It has been shown that residual fibrosis exhibits uniform
low signal intensity because of its low T2 relaxation times whereas resid
884
ual tumor exhibits high or mixed signal intensity due to its higher water
content and longer T2 relaxation times (Figs. 6 and 7). Thus, MRI can
help monitor response to therapy in such cases and help assess early re
currence in residual masses which are commonly the site of relapsing
lymphoma. Gallium 67 scanning is also used extensively for this pur
pose with fibrotic lesions exhibiting no activity. Both MRI and Gallium
67 scanning suffer from false positive results in the first 6 months fol
lowing initiation of therapy because of necrosis and inflammatory reac
tions. More recently, PET scanning with FDG-glucose as a marker for
assessment of non-aerobic metabolism has been proposed for the eval
uation of the problem of partial regression in lymphoma and is still be
ing investigated.
Hodgkin’s disease involves the thorax in over 60% of cases with the an
terior medastinum, tracheo-bronchial, paratracheal and hilar nodes in
volved in 50%), 45 %, 40% and 25 % of cases, respectively. Non-Hodgkin's
lymphoma involves the same nodal groups in less than 15% of cases.
Paraesophageal, posterior mediastinal and pleural involvement are, how
ever, more common in non-Hodgkin’s than in Hodgkin's lymphoma.
Calcification of lymphomatous masses is distinctly unusual in untreated
lymphoma but can be present in post treatment CT studies most partic
ularly after radiation therapy. Non-Hodgkin's lymphoma are more com
mon in the abdomen and involve intestinal structures and other extra
nodal sites in a higher proportion of cases. It is, however, unusual to de
tect extra nodal masses without some associated lymphadenopathy in
lymphoma, whereas other types of focal masses do not exhibit signifi
cant adenopathy. Thus, when confronted with a mass associated with sig
nificant adenopathy and the possibility o f lymphoma, surgical excisional
biopsy rather than image guided needle biopsy should be undertaken be
cause diagnosis and cell typing of lymphoma usually requires larger tis
sue samples.
Metastatic nodal disease

In every neoplasm, involvement of loco-regional and distant lymph
nodes is associated with a worsened prognosis. In several cancers, the
presence of lymph node metastasis is a critical element of staging and
determines in many cases the feasibility of surgical resection. The im
pact of imaging on the most commonly encountered cancers will be re
viewed here.
885
Figure 9.
American Thoracic Society map o f
mediastinal lymph nodes fo r lung
cancer staging and reporting.
L. SUBCLAVIAN
ARTERY
AOR TA
LIGAMENTUM
ARTERIOSUM
L. PULMONARY
ARTERY
Primary lung cancer

Except for small cell lung cancer which is almost always disseminated
by the time of initial diagnosis, nodal staging is a critical element in the
staging o f lung cancer. To facilitate assessment of mediastinal lymph
nodes, a standardized map of the different nodal stations has been de
veloped by the American Thoracic Society and is used as part of the new
International Lung Cancer TNM staging system (Fig. 9). CT and MRI
have been investigated extensively as staging modalitites. CT and MRI
exhibit similar accuracy in assessing mediastinal lymph nodes. Initially,
high sensitivities and specificities in the 80 to 90% range were reported
with CT scanning but with increasing experience and better designed multi
at best are now observed. This is primarily due to the higher than sus
pected incidence of microscopic disease, the existence of skipped nodal
regions and, the higher incidence of enlarged reactive lymph nodes simu
lating metastatic disease most particularly in patients with associated pneu
monitis or prior granulomatous infection. MRI signal intensities have not
proven helpful in the differentiation of metastatic versus reactive nodes.
Recent and still preliminary data with FTG-glucose PET scanning sug
gests that such differentiation may be achievable in lung cancer.
Nonetheless, despite these limitations, CT remains important for the man
agement of the lung cancer patient because the current surgical staging
scheme adopted in 1984 no longer considers low ipsilateral or subcarinal
adenopathy a cause for non-resectability. Only positive contralateral, high
886
Figure 10.
Coronal Tl-weighted M RI showing
extensive metastastic peribronchial
and paratracheal adenopathy in
patient with right upper lobe carci
noma.
mediastinal or distant nodes contraindicate surgery. Thus, CT is important

in identifying such nodes and prompts nodal sampling with medi
astinoscopy prior to curative surgery if distant or contralateral disease is
found. On the other hand, most surgeons consider a negative CT scan suf
ficient to proceed directly to surgical exploration since full ipsilateral nodal
resection is routinely undertaken in most cases. Technically, the use of
thinner 4-5 mm sections from the arch of the aorta to the lower lobar bi
furcations are important in detecting enlarged nodes and avoid partial vol
ume averaging of vascular structures and nodes. Likewise, contrast en
hancement most particularly with rapid or single breathhold continuous
spiral scanning is also preferable whenever possible and necessary when
mediastinal fat is limited in amount. Although no specific nodal size can
be reliable, it is generally agreed that sharply marginated nodes smaller
than 1 cm are considered normal, nodes between 1 and 1.5 cm are suspi
cious and larger nodes are definitely abnormal. The appearance of lymph
nodes is sometimes useful with nodes exhibiting a central lucency and
sharp margins considered benign and those appearing irregular, adherent
to adjacent clustered nodes considered probably malignant. In the patient
with allergy to contrast and in patients with lesions suspected of invading
critical structures such as the heart, great vessels, esophagus, vertebral bod
ies or superior sulcus, MRI is indicated because blood vessels, airways and
adjacent masses can easily be differentiated in multiple imaging planes
(Figs. 3 and 10).
887
Breast cancer
Despite the critical importance of lymph node dissemination in this dis
ease, no method of imaging has been effective in staging cancerous nodes
in breast cancer. Most surgeons do not feel that axillary lymph node imag
ing is necessary. However, for advanced lesions, CT scanning of the chest
to assess internal mammary lymph nodes has been advocated. More re
cently, research using PET scanning and labeled metabolites such as
FDG-glucose or MRI with lymph node specific contrast agents have been
investigated. In the absence o f a reliable method for detecting micro
scopic disease in lymph nodes, it is doubtful that imaging methods can
obviate the need for surgical nodal sampling.
Head and neck tumors

In head and neck tumors, assessment of deep lymph nodes is essential.
Both CT and MRI are being extensively used for such purposes. With
CT, contrast enhancement is essential in assessing nodes of the neck re
gion. Some investigators report that the pattern of enhancement of lymph
nodes may be helpful in differentiating benign from malignant nodes
with rim enhancement being suggestive of malignant disease. In the neck,
nodes greater than 1 cm are considered abnormal.
Colorectal cancer
The presence of more than 4 malignant lymph nodes has a significant detri
mental effect on the prognosis of the patient with colorectal cancer. A re
cently conducted prospective multiinstitutional clinical trial in the United
States comparing CT and MRI in the staging of colorectal cancers showed
that both modalities are not very accurate in staging lymph node extension
with CT showing a slightly better performance albeit not statistically sig
nificant. Normal nodes are smaller in the mesentery and retroperitoneum
than in the mediastinum. Nodes larger than 6 mm should be considered
suspicious especially if clustered and with ill defined margins. Peripan-
creatic and portocaval nodes are commonly involved in more advanced
stages of colonic cancer and should be specifically sought by using thin
ner sections in the pancreatic regions as well as excellent intestinal opaci
fication throughout the bowel. At least 16 ounces of oral contrast should
be administered prior to CT examination. Although, monoclonal antibody
imaging has been experimentally successful in the detection and staging
of colorectal malignancies it has not gained widespread acceptance.
888
Prostate cancer
Extension of prostate cancer to the regional nodes most commonly in the
internal iliac chain is an absolute contraindication to prostatectomy for
cancer. Imaging methods, however, have had limited success in reliably
detecting nodal invasion preoperatively except in the most advanced
cases. Imaging may be useful in staging the transcapsular extent of the
prostatic tumor and the possible involvement of the neurovascular bun
dles which, optimally, should be spared at surgery. During such imag
ing evaluation, iliac lymph nodes can be visualized and nodes larger than
1 cm are considered highly suspicious for metastatic disease. Needle
biopsy can then be used to assess these lymph nodes. In practice, how
ever, because o f the high rate of false negative nodal examinations, sur
gical sampling with immediate frozen section diagnosis remains the pre
ferred approach.
CONCLUSIONS
Imaging of the lymphoreticular system remains a real challenge in prac
tice. Detection and assessment of pathologic involvement of lymph
nodes is dependent on the presence of gross enlargement of nodes.
Diffuse infiltration of spleen, liver and bone marrow are frequently un
detected with all techniques. Clearly, further research and development
are needed to enable detection of earlier stages of disease in lymph nodes.
Imaging, despite its low accuracy when compared to histologic exami
nation, remains, however, the best method for the staging and monitor
ing of known neoplasms with CT remaining the most efficacious method
to date. Research in newer and more specifically targeted agents with
both MRI and radionuclide methods may, in the future, enable better
evaluation of this important system. In the meantime, because of the de
velopment of molecular markers which can be detected through DNA
analysis after amplification with the PCR reaction, the presence of dis
ease may reliably be assessed on small samples of tissue.It is therefore
likely that more efficient image-guided needle biopsy methods that can
rapidly acquire samples from multiple locations in the body will be im
plemented in clinical practice to supplement imaging.
889
Chapter 22
The gastrointestinal tract
Richard M. Mendelson
UPPER GASTROINTESTINAL TRACT
General considerations
Many authorities now advocate flexible oesophago-gastro-duo-
denoscopy (OGD) as the primary imaging modality in patients with up
per gastrointestinal symptoms. In locations where endoscopy is freely
available there has been a decline in the number of contrast studies per
formed. While some radiologists may strive to maintain their erstwhile
role in the luminal GI tract, it is more appropriate to define strategies for
the investigation of upper GI symptoms based on the relative strengths
of radiology and endoscopy in given clinical situations. Moreover, it
must be realised that in many parts of the world - both "developing" and
"developed" - such pragmatic considerations as cost and availability will
be the predominant factors in the choice of primary investigation. The
advent of endoscopy has had the desirable side-effect of encouraging ra
diologists to optimize their own techniques with the development of dou
ble-contrast and then biphasic barium studies. There has also been a shift
among GI radiologists towards functional or dynamic studies (for ex
ample videofluoroscopy of swallowing disorders) and imaging modali
ties such as CT and US that can define extramural disease.
In an attempt to best reflect the relative strengths of OGD and barium
studies in patients presenting with various symptom complexes, Table 1
provides a suggested policy for primary investigation, the reasons for
which are given in the appropriate sections of the following text.
891
Chapter 22
The gastrointestinal tract
Richard M. Mendelson
UPPER GASTROINTESTINAL TRACT
Many authorities now advocate flexible oesophago-gastro-duo-
denoscopy (OGD) as the primary imaging modality in patients with up
per gastrointestinal symptoms. In locations where endoscopy is freely
available there has been a decline in the number of contrast studies per
formed. While some radiologists may strive to maintain their erstwhile
role in the luminal GI tract, it is more appropriate to define strategies for
the investigation of upper GI symptoms based on the relative strengths
of radiology and endoscopy in given clinical situations. Moreover, it
must be realised that in many parts of the world - both "developing” and
’’developed” - such pragmatic considerations as cost and availability will
be the predominant factors in the choice of primary investigation. The
advent of endoscopy has had the desirable side-effect of encouraging ra
diologists to optimize their own techniques with the development of dou-
ble-contrast and then biphasic barium studies. There has also been a shift
among GI radiologists towards functional or dynamic studies (for ex
ample videofluoroscopy of swallowing disorders) and imaging modali
ties such as CT and US that can define extramural disease.
In an attempt to best reflect the relative strengths of OGD and barium
studies in patients presenting with various symptom complexes, Table 1
provides a suggested policy for primary investigation, the reasons for
which are given in the appropriate sections of the following text.
891
Table 1. Suggested primary imaging modality
Symptom complex BA OGD
DYSPEPSIA *
"Simple" +
"Com plicated"
REFLUX OESOPHAGITIS +
DYSPHAGIA +
HAEMATEMESIS/MELAENA
PREVIOUS GASTRIC SURGERY
- for recurrent disease +
- for anatom y / emptying +
Notes:
BA = barium study; OGD = oesophagogastroduodenoscopy
* Complicated dyspepsia is used here to indicate features which, when one or more are
present, may be expected to be associated with a high prevalence o f gastric pathology
(thus requiring biopsy) and it is therefore rational for OGD to be the primary imaging
modality. These features are:
Age > 40-45 years

Constant daily pain
Weight loss
Vomiting
Past history o f gastric ulcer
Previous gastric surgery
Absence o f these features is denoted as "simple" dyspepsia.
Investigation of dysphagia
Dysphagia may be due to abnormalities of function (neuromuscular) or
structure. Endoscopy and radiology are complementary investigations
but a contrast swallow is the investigation of first choice since it allows
dynamic study of neuromuscular function, as well as the detection of
structural abnormalities in the pharyngo-oesophageal segment such as
webs, that may be missed endoscopically, and diverticula that may pre
sent a hazard to endoscopy. In addition, mild strictures and Schatzki rings
can be overlooked by modem thin-calibre fibrescopes. Radiology is of-
892
THE GASTRO-INTESTINAL TRACT
ten able to define the length of an endoscopically impassable stenosing

lesion and to provide information about extrinsic compressions.
Endoscopy will usually be required for biopsy of radiologcally demon
strated strictures and for radiologically negative dysphagia.
Although it is useful to distinguish abnormalities of the oropharyngeal
and oesophageal phases of swallowing, it is recognized that the level of
obstruction cannot reliably be determined by the patient’s subjective site
of’’sticking”. Up to one third of patients with oesophageal causes of dys
phagia have symptoms referred to the neck. In addition, hypopharyngeal
and oesophageal abnormalities often co-exist. Prominence of the
cricopharyngeus (cricopharyngeal bars) and Zenker's diverticula are as
sociated with gastro-oesophageal reflux and other distal abnormalities
such as Schatzki rings and hiatus hernia; reflux may present with globus
sensation, sore throat and hoarseness. A significant proportion o f patients
with gastro-oesophageal reflux present with pharhyngeal symptoms.
Radiological examination therefore should include all phases o f swal
lowing, although in practice the study is tailored to the patient’s symp
toms with emphasis on a particular region. In addition, gastric fundal le
sions and even gastric outlet obstruction should be excluded, since these
may present as "dysphagia”.
Oropharyngeal swallowing - examination techniques

Ideally the examination should be recorded dynamically with cineradi
ography or videofluoroscopy, since the examination may then be re
played, frame by frame, to assess oropharyngeal function. In addition,
subtle abnormalities such as webs may only transiently be visible dur
ing the passage of a liquid bolus. The use of a 105 mm camera is much
less satisfactory; a frame rate of only 6 per second is usually obtainable.
Many centres have set up ’’dysphagia groups" - multidisciplinary spe
cial interest groups, comprising radiologists, speech pathologists, dieti
cians, neurologists, laryngologists, gastroenterologists, etc. - to assess
patients with oropharyngeal swallowing difficulties. This is of particu
lar importance where aspiration is a problem, not only in determining
the cause and degree of dysfunction but, by testing the patient with var
ious consistencies of bolus and assessing compensatory mechanisms,
therapeutic and dietary manoeuvres can be instituted to minimise the
problem.
893
A "routine” examination in a patient with dysphagia likely to be o f

oropharyngeal origin may be as follows:
1) If there is no history to suggest aspiration, anteroposterior and lateral
views of the pharynx at rest are obtained after coating with high-den-
sity barium. A lateral view is also taken with phonation o f ”eeee” or
during a Valsalva manoeuvre to distend the pharynx. In certain pa
tients vocal cord movement should be observed in frontal projection
during phonation of ”ee”.
2) If the study is to particularly assess aspiration, the patient can be ex
amined sitting in a special chair in front of the fluoroscopy table.
Varying consistencies of bolus are used ranging from non-ionic iod-
inated contrast (ionic contrast such as Gastrografin must never be used
if there is a risk of aspiration), through low-density barium, varying
thicknesses of puree mixed with barium, to barium "cookies”. Solid
boluses are given with extreme caution if aspiration is seen with thin
ner liquids. The latter are more likely to be associated with aspira
tion. Some workers start with thicker and then gradually decreasing
consistencies until the patient is seen to aspirate. The effect of head
and/or body position and the use of ice may also be tested. In such a
way it is possible to assess the type of dietary manipulation required
in, for example, a stroke patient with swallowing difficulties, to al
low discontinuation of nasogastric tube feeding while minimizing the
risk of aspiration.
Videofluoroscopic recording allows review of:

- tongue movement and bolus formation
- palatal dysfunction which may result in posterior leakage into the
pharynx from the mouth and nasal regurgitation-epiglottis and la
ryngeal movement during swallowing, particularly laryngeal eleva
tion and closure and epiglottic tilt thus preventing laryngeal penetra
tion and aspiration
- pooling and retention of contrast in the valleculae and/or pyriform
fossae
- whether laryngeal penetration/aspiration is detected and cleared by
the patient
- the temporal relationship of aspiration to swallowing (before, during
or after)
894
THE GASTROINTESTINAL TRACT
- the function of the pharyngo-oesophageal segment which includes the

cricopharyngeal sphincter - this must open completely in time with
the passage of the bolus
Compensatory mechanisms employed by the patient should be observed,

such as abnormal palatal descent to prevent posterior leakage and en
largement of Passavant's cushion.
3) Where the clinical features point to an oesophageal cause of dyspha

gia and the study is not specifically directed to assessing the oropha
ryngeal phase of swallowing, initial inspection of this phase prior to
examining the oesophagus may be modified by asking the patient to
take a small sip of high-density barium under fiuorosocpy to exclude
aspiration or major or high obstruction. As this results in coating of
the oropharynx, frontal and lateral views of the pharynx may be ob
tained at this time. Detailed assessment of the oesophagus (see below)
is then often best performed before returning to the examination of
the pharyngo-oesophageal segment for functional and structural ab
normalities with videofluoroscopy and/or rapid-sequence camera,
since the lower density barium (100% w/v or less) used for the
pharyngo-oesophageal segment sometimes interferes with coating by
the high-density barium used for the double-contrast oesophagram.
The pharyngo-oesophageal segment is examined in lateral, frontal and
oblique projections with liquid boluses. Evidence of cricopharyngeal
dysfunction is looked for, as well as structural abnormalities such as
webs and diverticula. Sometimes solid boluses (marshmallows or bar
ium-soaked bread, for example) may be indicated to show hold-up
due to subtle strictures or webs.
895
Oropharyngeal dysphagia: pathologic conditions
Neuromuscular disease
Many patients requiring assessment have been victims of stroke or head
injuries. Bulbar palsy leads to a lower motor neurone lesion resulting in
abnormality o f the pharyngeal phase of swallowing. Pseudobulbar palsy
affects the upper motor neurons and primarily causes problems with oral
initiation of swallowing. Disorders of deglutition affect 20-40% of pa
tients with unilateral stroke.
It is seldom possible to diagnose specific diseases from the radi-
ographically observed dysfunction o f swallowing, but one can often de
termine the pathophysiological mechanisms involved. Some specific
neuromuscular disorders and the observed signs at videofluoroscopy are
shown in Table 2.
Table 2. Some specific neuromusuclar diseases associated with oropha

ryngeal dysphagia.
Disease Notes/radiographic abnormality
Motor neurone disease (ALS) Oropharyngeal muscle atrophy

Pharyngeal paresis
Nasopharyngeal regurgitation
Airway penetration
Compensatory extension of head/neck
Multiple sclerosis Dependent on site and extent ofdemyelination
Parkinson's disease "Dysphagia" common. Dysfunction of oral initiation
i.e. bolus formation; hesitancy and repetitive tongue
movement; delayed swallow reflex; vallecula pooling
and airway penetration; aspiration may be "silent".
Poliomyelitis (bulbar) Pharyngeal muscle paresis; aspiration. Pharyngeal
muscle atrophy in "post-polio syndrome".
Myasthenia gravis Fatigueing of pharyngeal muscles during repetitive
swallowing.
Myopathies May affect bulbar muscles. Striated muscles of
cervical oesophagus may also be affected with redu
ced peristalsis. Cricopharyngeal "chalasia" in myoto
nic dystrophy.
896
Figure 1.
Cricopharyngeal webs extending from
the anterior wall at level indicated by
large arrow. Note "jet"phenomenon
below the webs and prominent
cricopharyngeus impression posteriorly
(white arrow).
Figure 2.
Cricopharyngeal diverticulum
(arrowed). Note marked associated
prominence o f cricopharyngeus and
luminal narrowing.
Structural abnormalities
Cricopharyngeal prominence ("pharyngeal bar")

The posterior indentation at approximately C5/6 level by cricopharyn
geus muscle normally effaces as a bolus passes through. Mild persistent
indentation may be normal but more obvious prominence may be seen
897
in some patients with dysphagia (Figs. 1, 2). There is association with

distal oesophageal disease, especially gastro-oesophageal reflux (GOR),
and other pharyngeal abnormalities. A spectrum o f cricopharyngeal ab
normalities can be seen with GOR. It is likely that acid reflux leads to
oedema, spasm and/or hypertrophy o f cricopharyngeus; this in turn raises
pharyngeal pressure proximal to the upper oesophageal sphincter and
hence the association of GOR with a (usually small) pulsion-type
Zenker's diverticulum. Other causes o f cricopharyngeal prominence in
clude intrinsic cricopharyngeal disease, and neuromusuclar diseases af
fecting the oropharynx.
Cricopharyngeal webs
These mucosal folds occur on the anterior wall at the hypopharynx/oe-
sophagus junction. Often they are thin and asymptomatic, but they may
be circumferential and cause luminal narrowing (Figs. 1 and 14). A char
acteristic "jet effect" may be seen on contrast swallow when a large bo
lus passes through a web. Differentiation must be made between webs
and the submucosal venous plexus which is a normal structure on the an
terior wall. The latter causes an impression that is effaced as the bolus
distends the lumen. Large boluses and dynamic imaging, such as video
fluoroscopy, may be required to detect webs since they may appear tran
sient during a contrast swallow. Sometimes webs are associated with
iron-deficiency, glossitis and pharyngeal atrophy (Plummer-Vinson or
Paterson-Kelly syndrome). Web-like stenoses may also be seen in vari
ous bullous skin diseases, such as epidermolysis bullosa.
Pouches and diverticula

The most significant lesion is the hypopharyngeal (Zenker's ) diverticu
lum, that occurs at the junction of hypopharynx and oesophagus at
Killian's dehiscence between the horizontal and oblique fibres of the
cricopharyngeus muscle (Fig. 2). This pulsion diverticulum starts pos
teriorly and enlarges posterolaterally, usually to the left. Dysphagia oc
curs as the pouch fills preferentially with food and obstructs the lumen
of the oesophagus. There is typically regurgitation of pouch contents and,
often, aspiration as the pouch overflows. A plain radiograph o f the tho
racic inlet may show an air-fluid level in the diverticulum. There is usu
ally a prominent cricopharyngeal impression, which may be related to
the association with raised pharyngeal pressure which causes the diver
898
ticulum. The association with distal oesophageal disease, particularly

gastro-oesophageal reflux, has been described above.
Lateral pharyngeal protrusions (pharyngoceles or ears) extend from
the tonsillar fossae, valleculae or pyriform sinuses. They are not usually
true diverticula, are rarely of significance and are associated with glass-
blowing and trumpet-playing. True lateral diverticula are rare and may
communicate with the lumen by a neck. Lateral diverticula may also arise
at the pharyngo-oesophageal junction in a weak triangular area caudal
to the transverse portion of cricopharyngeus muscle; this corresponds to
the passage for the inferior laryngeal nerve.
Pharyngeal tumours
The large majority are carcinomas. They may be diagnosed endoscopi-
cally, but radiographically they are best seen on double contrast pharyn-
gograms as masses within the lumen and/or deformity. Smaller lesions
may be demonstrated as irregularities of the mucosa. Multiple projec
tions are needed for optimal demonstration, including distended views
as described above. CT is useful for staging.
Pharyngeal foreign bodies

In adults most commonly the problem is one of an impacted fish or
chicken bone. A lateral radiograph of the neck taken at soft tissue expo
sure may show a radio-opaque foreign body, but many such bones are
poorly opaque. Evidence of perforation should be sought, including ex
traluminal gas and widening of the prevertebral soft tissues. A contrast
swallow is performed with a small volume of low-density barium, or wa
ter-soluble non-ionic contrast if perforation is suspected. If no foreign
body is seen, a small cotton ball or marshmallow soaked in barium may
show it.
The oesophageal phase of swallowing - examination

techniques
Contrast studies
The examination is multiphasic - double-contrast erect views to show
mucosal detail; single-contrast distended views to best show strictures,
rings and hiatus hernias; single boluses with the patient recumbent to as
sess motility; occasionally mucosal relief views for varices and oe
899
sophagitis. If the examination is part of a study of the stomach and duo

denum, it is best to complete the double-contrast views o f these organs
before returning to the oesophagus to perform the single-contrast phase,
since the thinner barium used for the latter will interfere with obtaining
the optimum coating of the stomach and duodenum.
Evidence of gastro-oesophageal reflux is also sought. Spontaneous re
flux during the examination is noted. If this does not occur, reflux is pro
voked by tilting the patient head down and then by turning the patient
from prone to supine, left-side down to fill the gastric fundus with bar
ium, and then supine LAO to submerge the cardia. If no reflux occurs, a
water-siphon test is undertaken. Many normal invididuals will reflux a
little contrast in this situation, but will rapidly clear the oesophagus again
in a swallow or two. True "refluxers" on the other hand tend to have less
effective peristalsis and delayed clearance.
Hypotonic drugs commonly used in upper GI barium studies have an
effect on oesophageal motility and/or the lower oesophageal sphinc
ter,and should therefore be avoided when the primary purpose of a study
is to assess these functions. Hyoscine butylbromide (Buscopan) reduces
peristalsis and decreases lower oesophageal sphincter pressure.
Glucagon has little effect on oesophageal motility but also reduces
sphincter pressure.
Radionuclide scintigraphy
Radionuclide oesophageal transit studies provide a simple, cheap and
non-invasive method of diagnosing motility disorders as well
as unique quantitative information on oesophageal emptying. Boluses of
99mTc-sulphur colloid are given diluted in water, and time-activity curves
generated over different segments of the oesophagus and the stomach
are obtained. Although good sensitivity and specificity have been re
ported compared with manometry, some authors have questioned the re
liability and reproducibility of the technique.
Oesophageal manometry
This study remains the gold-standard for oesophageal motility disordes,
but is not widely available. Contrast studies, performed as outlined
above, correlate well with manometry and provide a satisfactory screen
ing examination in most situations.
900
Normal oesophageal motility

Primary oesophageal peristalsis is induced by a swallow at the pharyngo-
oesophageal junction. Caudad progression of a bolus is achieved by a
wave of inhibition preceding the bolus and a wave of contraction behind
it. This is seen radiographically as a V-shaped stripping wave. Normally
all of a liquid bolus is stripped, but some proximal escape may be seen
at the level of the aortic arch even in normal individuals, which is then
cleared by secondary peristalsis. This phenomenon increases in fre
quency with age. The lower oesophageal sphincter (LOS) segment is 3-
4 cm in length and is an area of high resting pressure (which aids in the
prevention of gastro-oesophageal reflux) that falls prior to the arrival of
a bolus to allow its passage. In some normal individuals a little retro
grade propulsion of the bolus occurs at the sphincter. As the LOS seg
ment relaxes and distends with the bolus the lower oesophageal ampulla
is seen radiographically. Secondary peristalsis is also a propulsive wave
that occurs to clear the oesophagus o f any retained bolus. This is induced
by oesophageal distension and initiates around the level of the aortic arch.
Tertiary contractions are non-propulsive and cause a variable degree of
narrowing of the lumen. Non-segmenting contractions occur in a signif
icant proportion of swallows in normal individuals, but increase with age
and in conditions that increase the irritablity of the oesophagus, such as
oesophagitis. Segmenting tertiary contractions that obliterate the lumen
are almost invariably associated with disorders that significantly affect
primary peristalsis.
Pathological conditions of the oesophagus
Oesophageal motility disorders

The barium swallow is a simple and sensitive method of assessment of
oesophageal motility and has been shown to correlate very well with the
’’gold-standard” of oesophageal manometry. Patients with motor disor
ders of the oesophagus present with dysphagia and/or chest pain. Primary
disorders of oesophageal motility include achalasia, diffuse oesophageal
spasm, nutcracker oesophagus, and a collection of conditions grouped
as a "non-specific oesophageal motility disorder” (NEMD - with which
presbyoesophagus may be included). In addition, there is a miscellany
of often systemic conditions that cause secondary motility disorders, in
cluding systemic sclerosis (CREST syndrome), diabetes and neurologi-
901
Figure 3.
Longstanding achalasia with compli
cating squamous oesophageal carci
noma. Note dilated lower oesophagus
with beaking o f gastro-oesophageal
junction and hold-up o f barium above.
There is an extensive irregular neoplas
tic mass in the proxim al oesophagus
causing luminal narrowing and thick
ened folds, and displacing the trachea
anteriorly (arrows).
cal disorders. Reflux oesophagitis is associated with disordered motility,

including diminished peristalsis, delayed bolus clearance and decreased
LOS pressure. Debate continues as to whether this is secondary or
whether "refluxers" have a primary oesophageal motor disorder. A sig
nificant number of patients with "atypical" non-cardiac chest pain prove
to have GOR or oesophageal motility disorders.
Achalasia can present at any age but is commonest in the 30-50 year
age group. Dysphagia may initially be intermittent and eventually is per
sistent. Patients often develop manoeuvres to empty the oesophagus and
relieve symptoms. Oesophageal dilatation is mild in the early stages,
which may make radiographic diagnosis difficult, but is progressive. On
plain radiography there may be an air-fluid level in the oesophagus, the
level of which reflects the degree of hold-up above the LOS and thus
902
Figure 4.
Endoscopic ultrasound images
in patient with pseudo-achala-
sia due to carcinoma at the
GOJ. (a) asymmetrical trans
mural tumour (T). Concentric
rings are artefacts from the
endoluminal probe within the
oesophagus (oe); ao=aorta.
(b) peri-oesophageal nodal
metastases (N). Note circum
ferential oesophageal wall
thickening due to tumour with
loss o f normal ultrasonic
layers (compare with Fig. 8).
severity. A gastric air bubble is often absent. Contrast swallow with the
patient erect demonstrates a variable degree of dilatation of the oesoph
agus above a beak-like narrowing at the lower oesophageal sphincter.
The sphincter opens intermittently under the force of the hydrostatic pres
sure of the barium column above it to allow bolus passage. The distal
two-thirds of the oesophagus, which contains smooth muscle, is aperi-
staltic. The abnormalities of peristalsis and of the sphincter are present
even in the early stages of the disease. A variant known as ’’vigorous
achalasia” is described in which there are repetitive tertiary contractions
which may be associated with chest pain; the degree of dilatation is typ
ically less with this variant. Some authors dispute its existence as a sep
arate entity. There is an increased incidence of squamous carcinoma of
the oesophagus in achalasia (Fig. 3).
903
Secondary or pseudo-achalasia is a syndrome similar to achalasia due

to tumours at or around the gastro-oesophageal junction and is related to
destruction of the intramural myenteric plexus. The commonest cause is
adenocarcinoma of the stomach. A mass may be detected on imaging by
endoscopic ultrasound (Fig. 4) or computed tomography. Amyl nitrite
inhalation may also distinguish true from pseudo-achalasia, having no
effect on the sphincter in the latter. Rarely other tumours may cause sec
ondary achalasia as a non-metastatic manifestation of malignancy.
Infestation with Trypanosoma cruzi (Chagas' disease) causes a disorder
identical to idiopathic achalasia.
Diffuse oesophageal spasm presents with intermittent dysphagia
and/or chest pain. Radiographically there are segmenting tertiary con
tractions ("corkscrew” oesophagus; Fig. 5) interspersed with normal
peristaltic waves (c.f. vigorous achalasia). The diagnosis should only
be made in the absence of gastro-oesophageal reflux, since this can lead
to a similar pattern of contractions. Also, it should be noted that simi
lar appearances can be seen in asymptomatic elderly patients (presby-
oesophagus).
Nutcracker oesophagus is not a radiological diagnosis. There are su
pernormal high amplitude primary peristaltic contractions seen on
manometry which have no radiological correlate; patients present with
atypical chest pain. Presbyoesophagus is a term best reserved for asymp
tomatic elderly patients with abnormalties of motility which include di
minished primary peristalsis, tertiary contractions and delayed transit.
Non-specific oesophageal motility disorder (NEMD) is a miscellany
of abnormalities of oesophageal contractions and LOS behaviour seen
in patients with dysphagia and/or atypical chest pain which cannot be
easily categorised into any of the above disorders.
Systemic sclerosis/CREST syndrome involves the oesophagus and is
associated with LOS incompetence allowing free reflux and resultant oe
sophagitis. There is absent peristalsis in the smooth muscle part of the
oesophagus and often mild oesophageal dilatation. As a consequence of
the severe oesophagitis, strictures occur frequently associated with
Barrett's mucosa. Sacculation may be seen in the region o f the stricture
904
Structural causes of oesophageal dysphagia
Benign strictures
Commoner causes of oesophageal strictures are listed in Table 3.
Varieties of peptic strictures are dealt wiht under Gastro-
oesophageal Reflux Disease. Radiation, caustic and post-infective stric
tures are described in the relevant sections. Bullous skin diseases, espe
cially epidermolysis bullosa and pemphigoid, are associated with prox
imal oesophageal strictures or web-like narrowing.
905
Table 3. Causes o f oesophageal strictures
Benign Site Features, comments
Peptic
reflux oesophagitis distal, near GOJ,
above hernia smooth tapering
Barrett's oesophagus more proximal deep ulcer; reticular mucosa
Nasogastric intubation distal long strictures; history
Schatzki ring GOJ symm etrical 2-4 mm long
Caustic single or m ultiple, long history
Radiation related to portal tapered, history
Skin diseases high strictures or w ebs; bullous
diseases
Drug ingestion above left atrium history, enteric KC1 especially
Post-infective usually mid Candida, ТВ
Benign tu m o u rs variable subm ucosal lesion;
smooth m uscle
tum ours co m m o n e st
Malignant
C arcinom a
Leiom yosarcom a
Extrinsic
Lym phom a
Benign tumours
Benign mucosal tumours do not cause luminal narrowing. The com
monest are squamous papillomas seen as small polypoid lesions on dou
ble contrast radiography. Submucosal benign tumours are much more
common; the vast majority of these are leiomyomas. Unlike their coun
terparts elsewhere in the GI tract, oesophageal smooth muscle tumours
are hardly ever malignant, nor do they ulcerate. They may be an inci
dental finding or cause dysphagia. Being of smooth muscle origin they
occur in the mid or distal oesophagus. In profile they appear radi-
ographically as smooth filling defects with right angle or slightly obtuse
re-entrant angles at their borders. En face, the tumour appears to widen
the lumen. Endoscopic ultrasound is useful in confirming the diagnosis.
Other benign submucosal tumours (fibromas, neural tumours, duplica
tion and retention cysts, lipomas) are rare.
906
Figure 6.
Ulcerating and stricturing squamous
carcinoma o f the distal oesophagus.
Note shouldered margins.
Oesophageal carcinoma
Radiology has an important role in diagnosis, staging and post-treatment
follow-up of this common neoplasm.
Diagnosis
Most neoplasms are squamous carcinomas; the minority are adenocar
cinomas arising in Barrett's oesophagus. Most patients present with ad
vanced disease. Tumours are infiltrating (irregular narrowing with nodu
larity +/- ulceration and shouldered margins), polypoid (intraluminal fun-
gating), ulcerative (relatively flat with ulceration), varicoid (resembling
varices, with thickened serpiginous folds due to submucosal spread) or
a mixture of any of these types (Figs. 3 and 6). Satellite lesions may be
seen due to vertical submucosal spread. Occasionally "early" lesions are
seen as small protrusions, plaque-like lesions with or without ulceration,
sessile polyps or focal nodules. A superficial spreading variety is also
seen, comprising coalescent raised lesions and/or shallow ulceration. In
907
most cases of advanced carcinoma the radiological diagnosis can confi

dently be made. All lesions, however, should be subjected to endoscopy,
biopsies and cytological brushing.
Staging
While surgery remains the mainstay of treatment in resectable carcinoma
and arguably provides the best palliation for squamous and adenocarci
noma, palliative surgery is associated with significant morbidity and
mortality. Other treatment options are becoming more widely accepted.
These include chemo/radiotherapy (which may be used preoperatively
or palliatively in combination with endoscopic techniques to provide pa
tency); endoscopic laser treatment and endoscopic stenting, including
the use of the new metallic expandable stents. Therefore, the purpose of
staging is to assess local resectability and, in those patients treated by
non-operative means, to direct therapeutic options and provide baseline
information and monitoring. Ideally accurate staging should prevent un
necessary surgery in those patients with unresectable tumours, while not
denying surgery to those with potentially curable lesions. Staging is di
rected to the determination of depth of wall penetration, invasion of ad
jacent structures (tracheobronchial tree, pericardium or aorta), involve
ment of regional nodes and distant metastases.
Computed tomography and endoscopic ultrasound are the most accu
rate methods of staging oesophageal carcicnoma. Occasionally the mul-
tiplanar imaging potential of MR may be advantageous. Although CT is
far more widely available the results for T and N staging have been
largely disappointing. This is particularly true for gastro-oesphageal
junction carcinomas. Estimation o f local spread at CT depends on the
identification of transgression of mediastinal fat planes. Unfortunately,
these planes are often lacking in these frequently wasted patients. Wall
thickening beyond the normal of 3 mm is non-specific, and may repre
sent tumour or benign disease. Demonstration of the depth of wall inva
sion is not possible at CT. In addition, identification of nodal metatasis
is entirely dependent on the visiualisation of enlarged nodes, those with
a short-axis length greater than 10 mm being taken as abnormal. CT can
demonstrate local invasion of the tracheobronchial tree, seen as im
pingement or bulging of the posterior wall of the carina or left main
bronchus; tumour abuttment alone is not a specific sign. Identification of
aortic involvement is more difficult. Picus showed that if there is an arc
908
Figure 7.
CT at level o f carina showing
asymmetrical mass (m) o f oe
sophageal wall in contact with
descending aorta over arc o f ap
proximately 90 % (arrows) indi
cating tumour invasion is likely.
of contact of 90° or greater between the tumour and aorta, then invasion
is very likely (Fig. 7). Less than a 45 degree arc means no invasion.
Unfortunately, a large group of tumours are indeterminate. Loss of the
triangular fat space between oesophagus, aorta and spine has been re
ported to be a reasonably accurate predictor of aortic invasion. The CT
protocol should be directed towards local staging and identifying distant
metastases. Distention of the oesophagus with gas is useful as well as,
occasionally, decubitus scans. A dynamic incremental scanning tech
nique with intravenous contrast is used to detect liver metastases. EUS
has been found consistently superior to CT in T and N staging, but is of
limited availability. The accuracy o f EUS in T staging is due to the fine
detail achievable in imaging the 5-layer structure of the wall. This struc
ture is a constant finding in the normal upper GI tract (Fig. 8).
A review of several studies showed EUS to be 85 % and 75 % accurate
and CT to be 60% and 74% accurate in the T andN staging, respectively,
of oesophageal carcinoma (although there is an indication that improved
equipment and techniques may be leading to better CT results). There
are two major drawbacks to EUS staging. Firstly, stenosing lesions can-
909
Figure 8. Normal endoscopic ultrasound appearance o f

stomach wall, showing 5 layer structures; b=wall o f water-
distended balloon used fo r acoustic coupling. Concentric
rings are scanning artefacts from endoluminal transducer. 1
and 2=mucosal layers; 3=hyperechoic submucosa;
4=hypo-echoic muscularis propria; 5=adventitia/serosa.
(Reproduced with permission o f Australasian Radiology).
not be passed by the EUS endoscope in up to about 50% o f patients.

Although this can be a problem, often in practice staging o f only the prox
imal aspect of these stenosing tumours is not associated with much in
accuracy, since the advanced nature o f these lesions can still be discerned.
"Miniprobes" are now available which can be passed through the biopsy
channel o f a conventional flexible endoscope and thence through a
stenotic oesophageal lesion, but experience with these is as yet relatively
limited. The second problem with EUS is the difficulty in distinguish
ing benign from malignant nodes, thus reducing the specificity of N stag
ing. Specificity for nodal malignancy ranges from 54 to 72%. With the
exception o f coeliac lymph nodes, which are classified as distant metas
tases in oesophageal carcinoma, M staging with EUS is not possible, only
limited views of the liver being obtained. A combination o f EUS and CT
is thus required for complete TNM staging. EUS may also be used to
monitor response to chemo/radiotherapy of oesophageal carcinoma and
the detection of submucosal recurrence following surgery.
Oesophageal bolus obstruction

In adults, bolus obstruction is usually related to a lump of meat or in
gested bones but there is often an underlying motility disturbance or stric
910
ture. The impacted material is obvious on a contrast swallow. Water-sol

uble contrast medium should be used initially if perforation is suspected.
Even when this is not the case it is probably best to use non-ionic water
soluble contrast, since if there is complete obstruction the patient is at
risk for aspiration. In addition, endoscopy is usually required to remove
the bolus, and the presence of barium in the oesophagus obscures endo
scopic view. Various ’'radiological" manoeuvres have been attempted to
facilitate onward passage of the bolus. A hypotonic agent may be given
to relax the oesphagus combined with an effervescent agent. Although
Glucagon has been most often used, some authors advocate Buscopan
since this relaxes the oesophageal body as well as the LOS. There is a
potential danger to this technique as overdistension may lead to oe
sophageal laceration. Once the acute episode is over and spasm and
oedema have settled the patient should be investigated for underlying oe
sophageal pathology.
Gastro-oesophageal reflux (GOR) disease

Most patients with symptoms of GOR disease do not require investiga
tion. Indications for investigation include: if the diagnosis is in doubt;
for exclusion of co-existent gastro-duodenal disease; failure of response
to conventional medical treatment; imaging of complications. Since each
of the various modalities available tends not to address all o f the aspects
of GOR disease, patients who do require investigation often are subjected
to a combination of complementary tests. Investigations are directed to
wards answering several interrelated questions.
Is reflux present? Is there oesophageal dysmotility?

The gold-standard for assessment o f reflux episodes is ambulatory pH
monitoring. However, this is not universally available. Scintigraphy us
ing 99mTechnetium sulphur colloid provides a test of acceptable sensi
tivity and specificity compared with pH monitoring and is superior to
contrast radiography in this aspect, although some authors have ex
pressed doubts regarding its specificity. Assessment of reflux at barium
studies should be directed not only towards the identification of reflux,
but also towards the rate and efficiency of clearing of the refluxate from
the oesophagus, abnormality of which may point to an associated motil
ity disorder. All individuals have episodes of reflux associated with tran
sient falls in LOS pressure but are able to clear the refluxate rapidly. Most
911
Figure 9.
Relatively mild reflux oesophagitis. Note
"smudged" appearance o f mucosa and thick
ened longitudinal folds. In this patient there is
a small hiatus hernia and mild stricture
(arrowed).
patients with symptomatic reflux have normal LOS pressure but exhibit
diminished clearance. There is controversy as to whether this represents
a primary oesophageal motor disorder (for which there is recent evi
dence) or is secondary to associated oesophagitis. A proportion of symp
tomatic refluxers have reduced gastric emptying. Other oesophageal
motility disorders seen in GOR include an increase in frequency of ter
tiary contractions - usually non-segmenting, but occasionally segment
ing, in which case differentiation from diffuse oesophageal spasm must
be made in older patients - and transient contractions o f the muscularis
mucosae leading to transverse striations, so called oesophageal "shivers"
or "feline" oesophagus.
912
Spontaneous reflux during a barium study is seen in less than 50% of

symptomatic refluxers. When seen it correlates well with symptomatic
GOR. However, as stated previously, it can occasionally be seen in nor
mal individuals and, therefore, it is necessary to assess oesophageal clear
ance when it occurs. The oesophagus should be cleared in two or three
swallows at twenty-second intervals when the patient is slightly head-
down. If spontaneous reflux is not seen, a provocation test may be per
formed. Unfortunately, all such manoeuvres, while increasing sensitiv
ity, also significantly decrease specificity. Many radiologists have ceased
using them. The water siphon test is the simplest that may be performed;
a small amount o f reflux is often seen in normals and once again, vol
ume clearance of any refluxate must be assessed. Recent evidence sug
gests that combining identification o f reflux with abdominal compres
sion with a measurement of the internal calibre of the oesophagus at the
cardia of greater than 2.5 cm gives an accuracy of 80% for GOR.
Is there oesophageal injury?

Endoscopy and/or contrast radiography are used to image oesophagitis
and the other complications associated with GOR.
Oesophagitis
Endoscopy is superior to radiology in the diagnosis of oesophagitis.
Barium studies are accurate for moderate and severe grades of oe
sophagitis, but are insensitive for mild oesophagitis and also are associ
ated with significant false positives. The technique should be multipha-
sic, including double- and single-contrast examinations. Although dou
ble contrast films best demonstrate ulceration, most false-positives occur
due to over-reading of thickened folds and granular mucosa. The mildest
changes of oesophagitis (Fig. 9) include a loss of smoothness, or "smudg
ing" of the mucosal surface, a finely nodular or granular mucosal pattern
in the distal third of the oesophagus and oedematous longitudinal folds
(exceeding 2 mm in thickness in the distended oesophagus or 3 mm on
mucosal relief films). The granular pattern must be distinguished from
Candida oesophagitis which tends to be better defined, from glycogenic
acanthosis (a normal finding manifest as well-defined, usually small nod
ules, more prominent in the mid-oesophagus) and from undispersed ef
fervescent agent. A characteristic oesophago-gastric fold may be seen,
consisting of a prominent gastric fold continuing proximally to the
913
Figure 10.
Reflux oesophagitis showing nodular, mildly
narrowed distal oesophagus with saccula
tion above a hiatus hernia (arrowed).
squamocolumnar junction where it may appear as a polypoid lesion. This

is inflammatory in nature and probably represents localised gastritis.
However, the appearance is often sufficiently worrying to warrant en
doscopy and biopsy to exclude tumour.
More severe changes include restricted distensibility, due to spasm and
oedema, and punctate erosions or linear ulcers, often with a radiolucent
halo of oedema. Other causes of ulceration, such as opportunistic infec
tions and drugs tend to produce their own patterns (see below). The sever
est grades of oesophagitis (Figs. 10-12) demonstrate multiple erosions
or ulcerations, plaque-like "pseudomembranes" which may mimic can-
914
Figure 11. Hiatus hernia (diaphrag Figure 12. Barrett's oesophagus.

matic hiatus arrowed), tapered peptic Stricture above the GOJ with associ
stricture, and oesophageal ulceration ated moderately large ulcer (ar
(white arrows). rowed). The oesophagus above the
stricture is nodular with thickened
folds indicating oesophagitis. Below
the stricture there is a reticular mu
cosal pattern.
915
dida or infiltrative carcinoma, nodularity, a severely distorted scarred

mucosal pattern and strictures. Scarring may lead to stricturing, saccu-
lations or wall puckering.
Strictures and rings

Radiology can demonstrate subtle strictures and Schatzki rings, which
may be missed with modem "skinny” endoscopes. Although symptoms
of dysphagia may be due to reflux oesophagitis without stricture forma
tion, such a history without obvious narrowing on the semi-prone single
contrast views taken with maximal distension with a liquid bolus, should
lead to an examination with marshmallows or a bread bolus. Most re
flux-associated strictures occur in the distal oesophagus near the gastro-
oesophageal junction. A hiatus hernia is almost invariably present.
Typically, the stricture is smooth and tapered in appearance (Fig. 11). It
is reasonable policy that most strictures should be inspected endoscopi-
cally and biopsied to exclude malignancy. This is certainly true if there
is assymmetry and irregularity. More proximal strictures should raise the
possibility o f Barrett's oesophagus (Fig. 12).
A typically long distal oesophageal stricture may be seen in patients
who have had a nasogastric tube in situ. While this usually occurs after
relatively prolonged intubation, and is probably due to reflux, sometimes
stricturing is seen after a short episode.
Schatzki rings are mucosal rings at the gastro-oesophageal junction.
Although recent evidence suggests that these rings may not be associ
ated with GOR, it is convenient to consider them here. They have a char
acteristic appearance, being symmetrical with a longitudinal extent of no
more than a few millimetres, and they will be missed radiologically if
only erect double contrast views are obtained. Full column semi-prone
head-down views are required (Fig. 13); an examination with a solid bo
lus may be needed. They may be asymptomatic or be associated with in
termittent bolus obstruction. As a general rule, rings with a calibre of 13
mm or less tend to be symptomatic. Oesophageal webs, occuring more
proximal than Schatzki rings, may also be associated with GOR.
Barrett's (columnar-lined) oesophagus

In Barrett's oesphagus there is progressive columnar metaplasia of the
distal oesophagus associated with chronic GOR and oesophagitis. Its im
portance is in its malignant potential; dysplastic change is the precursor
916
Figure 13.
Schatzki ring at the GOJ shown on single
contrast full-column view with patient semi-
prone. The lesion was not visible on a double
contrast erect oesophagogram.
of oesophageal adenocarcinoma. This usually occurs around the squamo-

columnar junction. Endoscopic surveillance, with multiple biopsies, is
increasingly recommended to detect severe dysplasia and early neo
plastic change. Barrett's oesophagus has been more frequently recog
nised in recent years. A prevalence of about 10% is reported in patients
investigated for GOR. Contrast oesophagography is insensitive in the di
agnosis, but there are features which may be identified which put the pa
tient in a high risk group, and should be reported as such. These features
are: a "high" stricture, i.e. 5 cm or more proximal to the gastro-oesophageal
junction; ulceration (especially deep) in the body of the oesophagus; a
reticular mucosal pattern, especially when located immediately distal to
a stricture (Fig. 12). The last sign was originally reported as highly spe
cific for Barrett's oesophagus, but this has been questioned; it is also an
917
insensitive sign, being present in 5-30%. The presence of a distal peptic

stricture and/or reflux oesophagitis places the patient in a moderate risk
category for Barrett's oesophagus, one study reporting a 16% incidence
in this group.
Oesophageal intramuralpseudodiverticulosis
This is an uncommon condition o f somewhat obscure aetiology which
is probably part of the spectrum o f GOR disease. Multiple tiny flask-like
outpouchings are seen in the wall of the oesophagus which represent di
lated ducts of mucus glands (Fig. 14). They may be diffuse or segmen
tal and may only be seen on single-contrast, only entry of the thinner bar
ium into the invaginations being possible. The great majority of cases
are associated with strictures, often of the proximal oesophagus.
Outpouchings may be localised to the area of the stricture. A case of peri-
oesophageal abscess has been reported in this condition.
Is there a hiatus hernia?

The presence or absence of a hiatus hernia is really only relevant in two
respects. Firstly, if surgery is contemplated for GOR disease. Secondly, it
is unusual for the more severe grades of oesophagitis to be present in the
absence of a hiatus hernia. The exact relationship of hernias to GOR dis
ease is uncertain. The presence of a hernia appears to facilitate reflux. On
the other hand, when severe oesophagitis has been present for some time,
longitudinal scarring of the oesophagus may lead to shortening and the
appearance of a hernia. Radiology is more sensitive than endoscopy for
the demonstration of hiatus hernia. However, a small hernia can be demon
strated in a large number of normal individuals, especially in the semi-
prone head-down position. Oesophagitis is present in only a small num
ber of subjects with hiatus hernias. It has been suggested that hiatus her
nias should be ignored unless they are present at rest in the supine position.
Are the symptoms due to reflux?

This largely lies outside the ambit of the radiologist. Oesophageal pH
monitoring can correlate symptoms with objective episodes of reflux,
and may pinpoint the cause of symptoms in patients without overt oe
sophageal lesions. A Bernstein test can be performed, when the response
of the patient can be assessed to the instillation into the oesophagus of
dilute hydrochloric acid. Acidified barium can occasionally be used, and
918
Figure 15. Candida oesophagi

tis (HIV-positive patient).
Figure 14. Intramural pseudo- Multiple linear punctate and
diverticulosis o f the upper oe comma-shaped plaques are
sophagus (arrows) with associ shown in longitudinal
ated stricture. Note also orientation.
cricopharyngeal web (arrow
heads).
919
is sometimes useful in patients with globus pharyngeus; observed reflux

of acidified barium may mimic the patient's symptoms.
Non-reflux related oesophagitis
Infectious oesophagitis
Opportunistic infections of the oesophagus usually occur in immuno
compromised individuals. They have been increasingly associated in re
cent years with HIV infection (AIDS). Main causes are Candida, Herpes
simplex and Cytomegalovirus (CMV). Candida oesophagitis is often as
sociated with oral candidiasis. Double contrast oesophagography
demonstrates, with a 90% sensitivity, discrete plaques or small nodules,
usually in the proximal or mid-oesophagus. These are typically separated
by normal mucosa and may be orientated in the long axis of the oe
sophagus (Fig. 15). Severe infection, as sometimes seen in HIV patients,
manifests as a diffuse "shaggy" oesophageal contour due to plaques and
pseudomembranes, especially seen when the lumen is collapsed. Herpex
simplex oesophagitis causes discrete superficial ulcers of various shapes,
often stellate and often surrounded by a halo of oedema in the mid-oe
sophagus on a background of normal mucosa. Clustering may occur. This
entity may occasionally be seen in immunocompetent patients and re
quires differentiation from medication-induced oesophagitis (see be
low). The history will usually help.
CMV oesophagitis is usually associated with AIDS. Although the ra
diological picture may be indistinguishable from herpes oesophagitis,
the appearance in other patients is more typical; flat, large ulcers are seen
with associated oedema. Giant ulcers may be present up to several cen
timetres in size. It is now recognised that the HIV virus itself may cause
discrete oesophageal ulceration relatively early in the course of the dis
ease. Tuberculous oesophagitis is rare and is characterised, usually in
the proximal half of the oesophagus, by ulceration, wall thickening and
sinuses and fistulae to trachea or bronchus. Patients often present with
strictures. Radiological appearances may be indistinguishable from car
cinoma. Oesophageal involvement may also be related to narrowing or
displacement by caseating tuberculous nodes in the mediastinum.
920
Figure 16.
Oesophageal ulceration due to medication
(Doxycycline). Note multiple irregular superficial
ulcers surrounded by haloes o f oedema.
Drug-induced oesophagitis
Oesophagitis related to drug ingestion is
due to a local irritative effect and there
fore usually occurs at the sites of physio
logical hold-up, such as the aortic arch or
the level of crossing of the left main
bronchus or, in patients with heart dis
ease, often above a dilated left atrium. The
commonest causes of medication oe
sophagitis are antibiotics, particularly
tetracycline and doxycycline, frequently
in young patients. The oesophagitis re
sults in odynophagia. Superficial ulcers
are seen in the mid-oesophagus which
may be of various configurations (Fig.
16). The ulcers heal on drug withdrawal.
Those ulcers that result from slow-release
potassium supplements tend to occur in an
older age group, are larger and hence may
heal with scarring and stricture formation.
An apparent stricture may be present in
the acute phase due to spasm and/or
oedema. Various other tablets have been
reported to cause oesophagitis.
Caustic oesophagitis
Lye (alkalis) are the commonest causes of
caustic oesophagitis, usually ingested in the form of drain cleaners, re
sulting in liquefaction necrosis. While acids can produce oesophageal
damage, they tend to predominantly affect the stomach. Chest radi
ographs and supine and erect or decubitus abdominal films should be
performed to detect signs of perforation, such as pneumomediastinum or
921
pneumoperitoneum, as well as evidence of a dilated oesophagus or em

physematous gastritis. Contrast studies may be required. If perforation
is suspected, water soluble contrast should initially be used. In the acute
phase, abnormal oesophageal motility is seen, either spasm or atony
(which may presage perforation). Barium studies are not very sensitive
for the detection of mild mucosal changes in this condition. Severer forms
are seen as oedema, ulceration and sloughing of mucosa. Submucosal
contrast may result from the latter. Later, fibrosis occurs which pro
gresses to stricture formation. Strictures are typically long and may be
single or multiple.
Radiation-induced oesophagitis
Radiotherapy to the mediastinum can result in acute and chronic effects
to the oesophagus; these have been reported following doses of 45-60
Gy over 6-8 weeks. A combination of radiotherapy and chemotherapy
is more likely than radiotherapy alone to cause oesophageal injury.
Abnormal motility, which may be segmental and related to the radiation
portal, with or without mucosal oedema, is seen within 4-12 weeks of
radiotherapy. Ulceration, and pseudo-diverticula occur mainly when a
mass has been causing extrinsic compression on the oesophagus. Fistulae
between oesophagus and airway are uncommon. Oesophageal strictures
form some months after completion of radiotherapy and are tapered and
occur within the radiotherapy portal.
Oesophageal diverticula
Most oesophageal diverticula are acquired false diverticula, and so com
prise outpouchings of mucosa with or without submucosa. Although
there is controversy as to whether those around the level of the carina are
due to traction, and thus true diverticula, it is now thought that the ma
jority are of the pulsion variety. Other common sites are at a level be
tween the aortic arch and the left main bronchus and in the distal oe
sophagus (epiphrenic). Pulsion diverticula tend to change shape and size
and move longitudinally with oesphageal peristalsis. Epiphrenic diver
ticula may be multiple, are associated with GOR and hiatus hernias and
are presumed related to dysmotility. Oesophageal diverticula hardly ever
cause symptoms.
922
Figure 17.
Spontaneous oesophageal perforation.
Sudden onset o f pain during a meal, (a)
Water soluble contrast swallow shows
an ovoid filling defect (upper border
shown by large arrow) due to intra
mural haematoma, and linear collec
tion o f submucosal contrast (small ar
row). (b) CT o f same patient shows gas
in mediastinum (arrowed) indicating
that there has been a transmural
perforation.
Oesophageal perfora
tions
Perforations may be trans
mural or intramural. The
great maj ority are caused by
instrumentation or dilata
tion. Non-iatrogenic causes
include vomiting and for
eign body impaction. Truly
spontaneous transmural per
forations (Boerhaave’s syn
drome) and intramural lacerations or haematomas do occur, but often there
is a history of vomiting as a precipitating factor. Intramural haematomas
occur in patients on anticoagulant drugs or with bleeding diatheses.
Occasionally, oesophageal injury is a result of penetrating or blunt com
pression trauma. Most iatrogenic injuries occur at the cricopharynx or
923
distal oesophagus. Spontaneous perforations tend to be sited in the dis

tal oesophagus. Boerhaave's syndrome is usually a dramatic event asso
ciated with vomiting, severe chest pain and collapse, but occasionally it
is relatively insidious.
Plain chest radiographs will only be abnormal in transmural perfora
tion; signs may include mediastinal widening, pneumomediastinum, sur
gical emphysema in the neck, loss of the left paraspinal line, a V-shaped
lucency at the left base due to air between the left margin of the de
scending aorta and the left diaphragmatic pleura, an air-fluid level in the
mediastinum, and a left pleural effusion or hydropneumothorax. A right
pleural effusion may be seen if the perforation is in the more proximal
oesophagus. To demonstrate a small transmural perforation a contrast
study needs to be performed with meticulous attention to detail. Views
are taken with the patient recumbent in supine, and prone-oblique pro
jections, using water-soluble contrast medium. If this is negative, low
density barium should be used. Intramural perforations will be demon
strated as submucosal haematomas or dissections (Fig. 17 a); there may
be narrowing of the lumen by the mass effect of the haematoma seen as
a long smooth filling defect in the mid and lower oesophagus; clot may
be present within the lumen if the haematoma has ruptured through the
mucosa or there may be a double lumen due to contrast entering the sub
mucosa - so called "double-barrel” appearance.
CT is often useful to examine for mediastinal collections in transmural
perforations or to confirm the diagnosis, when contrast studies are equiv
ocal or a small leak has sealed, by demonstrating air or oral contrast
within the mediastinum (Fig. 17 b). In addition, there are reports of char
acteristic findings of submucosal haematomas, including high attenua
tion blood within the wall of the oesophagus.
Mallory-Weiss lacerations
These are relatively superficial tears occurring in the distal oesophagus
around the gastro-oesophageal junction, limited to the mucosa, with or
without submucosal involvement, following vomiting and presenting as
acute GI haemorrhage. Barium studies are usually negative but in view
of the presentation, endoscopy is in any case the investigation of first
choice.
924
Oesophageal varices
Although an optimal barium swallow technique is probably as accurate
as endoscopy in the diagnosis of varices, if these are suspected clinically
then, even in the patient who is not acutely bleeding, endoscopy is the
preferred examination, since it allows assessment of other mucosal le
sions related to portal hypertension and also offers the option of injection
sclerotherapy. However, if a barium study is used, then a single contrast
technique is performed with the oesophagus collapsed - mucosal relief
views. Hyoscine butylbromide is given to relax the body of the oesoph
agus, the mucosa coated with barium and multiple views taken in various
supine-oblique and prone-oblique projections, with the patient in a
Trendelenburg postion. A Valsalva manoeuvre may be used to distend the
varices. The varices are seen as serpiginous filling defects usually along
the line of the longitudinal folds in the distal oesophagus. Distinction must
be made from the rare varicoid carcinoma; unlike varices the configura
tion of the latter will not change with oesophageal distension.
STOMACH AND DUODENUM
Imaging techniques
Contrast studies
The routine contrast examination for gastroduodenal disease is the dou-
ble-contrast barium meal (DCBM); this has been found consistently su
perior to single contrast studies. There are many variations in technique
for performance of the DCBM, but a frequently used method is a bipha-
sic one that incorporates elements o f the single contrast examination. The
single contrast barium meal is occasionally justified in very elderly, sick
or immobile patients and can be used to answer specific questions, such
as determining the presence of gastric outlet obstruction. Water-soluble
iodinated contrast media are used where there is suspected perforation
or where a recent anastomosis is being tested. The commonest such con
trast is 76% sodium methylglucamine diatrizoate ("Gastrografin").
However, this is contra-indicated if there is a risk of airway aspiration
or suspicion of an oesophago-tracheal fistula, since its hyperosmolality
can precipitate pulmonary oedema. Non-ionic iodinated contrast media
are then used (or, alternatively, low-density dilute barium, with caution).
925
Figure 18.
Supine double contrast view
o f gastric body and antrum
showing mosaic-like areae
gastricae.
The aim of the DCBM is to see, by appropriate positioning, all parts

of the oesophagus, stomach and proximal duodenum in double contrast
with good mucosal barium coating, adequate gaseous distension and hy
potonia. A measure of good coating is the visualisation of the areae gas
tricae, which are seen as a mosaic-like pattern in the stomach (Fig. 18).
These represent the areas about 1-4 mm in diameter, in the centre of
which, the gastric glands open. Their visualisation depends on radi
ographic technique, barium density and the amount of mucus in the stom
ach. They are most often seen in the gastric antrum and body. Although
controversial there is a suggestion that an increase in size o f the areae
and their presence in the proximal stomach are associated with increased
acid production. Focal abnormalities of the areae are more important;
distortion or enlargement may be seen in gastritis around an ulcer or due
to superficial infiltration by carcinoma, and may be the only subtle clue
to this. Other anatomical features seen in the stomach on DCBM include
the rugal folds and the cardia. The folds in the antrum are effaced with
distension by gas; if they persist this suggests antral gastitis. The rugae
in the fundus and proximal body should be smooth and relatively straight
in the distended stomach. The appearance of the cardia is variable; it may
appear en face as a rosette which may be flat or have elevated margins;
it may possess a hooded fold - the "burnous sign"; or it may be seen as
a crescentic line.
926
The modem biphasic barium meal should include double and single
contrast oesophagograms, compression views of the gastric antrum and
duodenal cap as well as double contrast images of the stomach and duo
denum, and an assessment of oesophageal motility. As part o f the DCBM
it is important to ensure that the second and third parts of the duodenum
have been outlined. It is possible to obtain good double-contrast dis
tended views of the descending duodenum. It is rarely necessary nowa
days to perform a hypotonic duodenogram using a tube method.
If the examination is being performed for suspected gastroduodenal
perforation, a water-soluble contrast is used. Profile views of the filled
stomach are obtained. The patient is then turned onto the right side to
allow duodenal filling and turned through 360°. If no obvious ex
travasation o f contrast is seen, the patient should remain on the right side
for ten minutes or so and then re-fiuoroscoped. If no perforation is seen
but is still strongly suspected clinically, delayed films may show con
trast excreted through the urinary tract, since Gastrografin is absorbed
from the peritoneal cavity. However, this sign is not specific for per
foration since inflamed or ischaemic mucosa can allow absorption and
thus renal excretion.

CT is useful in gastroduodenal disease for staging of neoplasms and as
sessment of extramural disease. The patient should be fasted so that solid
food in the lumen does not cause confusion with pathological filling de
fects. Distension of the gut with oral contrast medium is essential. Dilute
(3 %) Gastrografin or dilute barium sulphate suspension is used. As well
as positive contrast, a gas-forming agent can be given to distend the stom
ach and duodenum. Sometimes this can be given in lieu o f the final cup
of contrast. A hypotonic agent may also be administered if gas is used.
This distension allows recognition of wall thickening and intraluminal
filling defects. If there is a suspicion of wall thickening the patient can
be rescanned in a decubitus or prone position as appropriate to show the
distended non-dependent wall of the viscus, for example right-side up
for lesions at the cardia. Normally, a dynamic sequential scan following
intravenous bolus administration of contrast is used to show vascular
structures and for the identification of liver metastases. Recent CT tech
nological advances allow helical (spiral) CT images of the upper ab
domen to be obtained with a single breath-hold.
927
CT is also a useful technique in suspected gastroduodenal perforation,

being able to detect very small volumes of free intraperitoneal gas or io-
dinated contrast.
Ultrasonography (US)
Conventional US has little place in gastroduodenal disease in adults, al
though wall thickening due to gastric carcinoma and inflammatory dis
ease in the antrum can often be seen. Real-time US can also be used to
study antropyloric emptying and motility non-invasively. Endoscopic ul
trasound (EUS) is accurate in the T and N staging of gastric adenocar-
cioma and the confirmation of linitis plastica. It may also be used to de
tect and stage gastric lymphoma, and image submucosal tumours such
as smooth muscle lesions and distinguish them from extrinsic impres
sions seen at endoscopy or barium studies.
Nuclear medicine scintigraphy

Applications of nuclear medicine techniques in the gastroduodenal re
gion include gastric emptying studies and, occasionally, detection of duo-
denogastric bile reflux. The former is performed with either a solid or
liquid phase test meal or both. Serial imaging is performed with com
puter acquisition and time-activity curves are generated to calculate gas
tric emptying rate. Bile reflux into the stomach is assessed by injecting
intravenously a Technetium-labelled iminodiacetic acid derivative (e.g.
HID A). This tracer is excreted by the liver into the bile duct and thence
the duodenum. If there is significant retrograde passage of tracer into the
stomach this can be quantitated.
Investigation of dyspepsia
Dyspepsia means different things to different individuals. It has been
carefully defined as intermittent or continuous pain, discomfort or nau
sea that is referable to the upper gastrointestinal tract, which is present
for at least a month, is not precipitated by exertion and is unrelieved
within five minutes by rest. This definition will include patients with or
ganic gastroduodenal disease, GOR disease, various forms of non-ulcer
dyspepsia and biliary tract disease. If one considers patients with gas
troduodenal dyspepsia of age greater than, say, 45 years or with symp
toms that include one or more of constant daily pain, weight loss, vom
iting, a past history of gastric ulcer or gastric surgery, then these patients
928
by virtue of their age and/or symptoms, may be expected to have an in

creased probability of gastric pathology - either benign or malignant -
compared to younger patients whose symptoms do not have any of the
above features. If endoscopic and radiological services are of equal avail
ability it is reasonable for endoscopy to be the primary investigation in
the former group (since all of this group require investigation and are
likely to need biopsies). Where endoscopic services are limited, a care
ful biphasic barium meal should be performed. A barium study may be
the initial examination in the latter group. It has been suggested that this
latter group may not require initial investigation at all, and that it is ac
ceptable to treat empirically for dyspepsia and to reserve investigation
for those with refractory symptoms. In patients with barium-negative
dyspepsia consideration should be given to other causes of symptoms
such as biliary or pancreatic disease (and US should be performed.) The
relationship of non-ulcer dyspepsia to Heliobacter pylori gastric infec
tion remains to be finally clarified. Some patients will respond to eradi
cation of these organisms.
Pathology
Hiatus hernias and gastric rotations
Sliding hernias
The gastro-oesophageal junction is above the diaphragm (Figs. 11, 19).
The size of the herniated proximal stomach is variable. Small sliding hia
tus hernias are a very common finding and are often asymptomatic. The
major association of sliding hiatus hernias is gastro-oesophageal reflux
(see above).
Para-oesophagueal hernias
These are much less common (about 5%). In this case the gastro-oe
sophageal junction lies below the diaphragm but all or part of the gas
tric fundus is above the diaphragm and lies adjacent to the distal oe
sophagus - usually to the left. Most para-oesophageal hiatus hernias are
non-reducible. They may be recognised on a chest radiograph by an air-
fluid level behind the heart, the nature of which may be confirmed by re
peating the radiograph after the patient takes a few mouthfuls of barium.
Most patients with para-oesophageal hernias are asymptomatic, but corn-
929
Figure 19.
Sliding hiatus hernia. Area o f
narrowing is arrowed at level
o f diaphragmatic hiatus.
There is a benign gastric ul
cer (small arrow) on the
lesser curve, presumed due to
recurrent mechanical trauma
at the hiatus.
plications are mechanical. Dysphagia may occur when the intrathoracic

portion of the stomach fills during a meal and obstructs the distal
oesophagus. Obstruction of the herniated portion o f the stomach may
cause strangulation and perforation. An acute torsion may occur.
Mixed hernias
In this case the oesophagogastric junction is in the thorax but much of
the rest of the stomach also lies in the chest adjacent to the distal oe
sophagus. A variant of this is the intrathoracic stomach. This is associ
ated with partial twisting of the stomach so that the fundus lies behind
the heart, the greater curvature is cranial, and the antrum passes through
the diaphragm (Fig. 20). When the fundus lies at a level inferior to the
body, distension of the former with food may cause obstruction to the
antrum. Similarly obstruction may occur when a herniated fundus re
turns into the abdomen (Fig. 21). Other viscera, particularly the trans
verse colon, may also be herniated. Although the intrathoracic stomach
is prone to volvulus, chronic volvulus usually only causes mild symp
toms. However, acute torsion presents as an emergency.
The stomach can undergo two main types of rotation and these are of
ten associated with herniation of the stomach. Organo-axial rotation is a
930
Figure 20.
Intrathoracic stomach. The GOJ
is in the thorax (curved arrow),
the gastric fundus lies behind the
heart, the greater curve is upper
most, due to organo-axial rota
tion and the antrum passes
through the diaphragm (straight
arrow).
Figure 21.
Intrathoracic stomach with axial
rotation, but fundus has returned
to infradiaphragmatic position
with resulting partial obstruc
tion. The nasogastric tube
demonstrates the position o f the
GOJ (arrowed).
twist along the long organic axis o f the stomach - that is the line drawn
from the fundus to pylorus. The resulting configuration depends on the
original orientation of the stomach. If the stomach was horizontally ori
entated, then the result is a reversal o f the normal lesser and greater curves
(Fig. 20). When the stomach is more vertically orientated the fundus lies
to the right and the antrum points to the left - so called "mirror-image"
stomach. Organo-axial rotation is only rarely associated with severe
symptoms. Mesentero-axial rotation is less common but much more of-
931
Figure 22.
Varioliform erosive gastritis.
Multiple punctate erosions
are seen in the gastric antrum
and body, each surrounded by
a halo o f oedema.
ten associated with obstruction and strangulation. The stomach rotates

around an axis joining greater and lesser curves and perpendicular to its
long organic axis so that the resulting configuration is an "upside-down"
stomach. Total volvulus is a rotation greater than 180° with obstruction
at GOJ and/or gastric outlet. The patient has sudden epigastric pain, retch
ing without vomitus and collapse. Ischaemia and necrosis o f the stom
ach result. A chest radiograph may show air-fluid levels in the upper ab
domen and the mediastinum. A contrast study shows tapering obstruc
tion of the distal oesophagus.
Gastritis
Radiology is limited in the diagnosis of gastritis and other superficial
mucosal disease, but certain patterns are recognisable based on the pres
ence of erosions, thickening or atrophy of folds, hyper-rugosity and wall
thickening. Disturbance of the areae gastricae pattern is a further indi
cation of mucosal disease.
Erosive gastritis may be acute or chronic and may be asymptomatic
or accompanied by dyspeptic symptoms or bleeding. Causes include al
cohol, aspirin and other non-steroidal anti-inflammatory drugs, but many
are idiopathic. Two patterns of erosive gastritis are seen. The so-called
932
varioliform gastritis comprises multiple aphthous erosions surrounded

by a mound of radiolucent oedema, usually orientated along the longi
tudinal folds and tending to be concentrated in the antrum (Fig. 22). A
similar appearance may be seen in Crohn's disease affecting the stom
ach. The second pattern is of flat erosions without a halo of oedema, but
tending to have the same distribution of varioliform gastritis. This vari
ety is more difficult to diagnose on DCBM. Distinction must be made
from barium precipitates.
Hypertrophic gastropathy is a group of entities characterised radio-
logically by hyper-rugosity of the stomach. Such conditions include hy
peracidity states such as Zollinger-Ellison syndrome and chronic renal
failure, Menetrier's disease and hypertrophic gastritis, and are mimicked
by infiltration with lymphoma or submucosal spread of carcinoma.
Gastric atrophy, such as occurs in pernicious anaemia, is associated
with loss of folds on the greater curvature and in the fundus and reduc
tion of the areae gastricae.
Eosinophilic gastritis is a condition characterised by peripheral
eosinophilia, a history of allergy and protein-losing enteropathy. The
stomach only is involved in about half the patients with eosinophilic gas
troenteritis. The usual site is the antrum and in the acute stage demon
strates enlarged rugal folds. In the chronic phase there is a contracted
nodular antrum.
Corrosive gastritis
Corrosive damage to the stomach is usually due to acid ingestion, but
sometimes alkalis can affect the stomach as well as, more typically, the
oesophagus. The radiological findings depend on the stage of damage.
Acutely there is gastric atony, rugal swelling, ulceration, pneumatosis
or perforation. These may be visible on plain radiographs. Gradually
scarring occurs with resultant deformity and contraction of the stomach
(Fig. 23).
Gastric ulceration
On double-contrast barium meal (DCBM), gastric ulcers are seen as
niches or collections of barium. When viewed en face, ulcers on the pos
terior (dependent) wall are apparent as barium collections when full of
contrast, or ring shadows when empty, with or without radiating folds
(Fig. 25 a). On the non-dependent (anterior) surface they are seen en face
933
Figure 23.
Stomach o f a young man
approximately 3 weeks after
Formalin ingestion. The
stomach is contracted with
sacculation and ulceration
and antral narrowing.
There is also narrowing and
spiculation o f the proximal
duodenum. GOJ and
pylorus are arrowed.
Figure 24.
Benign gastric ulceration.
Two ulcers (arrowed); that
on the lesser curve is empty
o f barium and seen almost
in profile as a curvilinear
outpouching —note that the
edges (and those o f the ul
cer in Fig. 19) do not pro
trude into the lumen - com
pare with Fig. 26. The pos
terior antral ulcer contains
barium.
934
Figure 25.
a) Benign posterior wall
gastric ulcer showing
radiating folds extending to
ulcer crater.
b) Malignant antral ulcer with
thickened margin and folds
amputated short o f the
ulcer crater.
as ring shadows.
Anterior wall lesions
may not be easily seen
without erect and prone
compression views. In
profile ulcers are seen as
barium-filled collections
extending beyond the lu
men or, if empty, curvi
linear lines of barium
(Figs. 19, 24). The ma
jority of benign gastric
ulcers occur on the lesser
curve or in the antrum
(usually posterior wall).
Greater curve ulcers are
more suggestive of ma
lignancy, but even benign ulcers in this site may have a malignant ap
pearance. There appears to be an association between non-steroidal anti
inflammatory drug therapy and benign greater curve ulcers which may
progress to gastrocolic fistulae. Pyloric and prepyloric ulcers are usually
935
Figure 26.
Gastric diverticulum just dis
tal to the cardia. Note the
gastric folds running into the
lesion aiding the distinction
from gastric ulceration.
small and benign. Size is not a good indicator of benign or malignant na
ture; giant ulcers are often benign. Features on barium meal that help dis
tinguish benign and malignant gastric ulcers are listed in Table 4. As ul
cer healing occurs the crater diminishes in size and the oedematous edges
disappear. The radiating folds become more apparent as scarring pro
gresses. As re-epithelialisation occurs the crater may end up as a small
residual depression (an ulcer scar) or as an area of flat mucosa with ra
diating folds.
Gastric diverticula are not-infrequently misdiagnosed as gastric ulcers.
These true (congenital) lesions occur on the posteromedial wall just dis
tal to the cardia (Fig. 26). The typical site and often the demonstration
of gastric folds running into them will help distinguish these non-con-
sequential lesions from ulcers.
936
Figure 27.
Malignant gastric ulcer.
Although a typical site (lesser
curve, incisural) fo r a benign ul
cer, note the margins protruding
into the lumen, characteristic o f a
malignant lesion (arrowed).
Figure 28.
Malignant gastric ulcer seen en
face. The ulcer crater is empty o f
barium and the raised margins
typical o f malignancy are clearly
shown (arrows).
Table 4. Benign versus malignant gastric ulcers (Figs. 19, 24-28)
Feature Benign Malignant

Size N ot a good indicator Not a good in d ica to r
Site m ajority lesser curve o r antrum variable
Shape round, oval, linear irregular
Areae gastricae extend to crater* cease away from crater
Edges + /- ulcer mound/ collar raised edges
w ith central and protruding into lumen
symmetrical niche.
Margins of mound form
obtuse angle with
normal wall.
Hampton line
Radiating folds sm ooth, radiate to ulcer* clubbed, nodular
amputated, fused
* but not necessarily when the ulcer is surrounded by significant gastritis
937
If a gastric ulcer is diagnosed on barium meal the question of further

investigation prior to treatment will depend on a) the degree of radio
logical confidence that it is benign, and b) the prevalence of gastric can
cer and, particularly, "early" gastric cancer in that community. Laufer
introduced the concept of confidence levels in relation to radiological di
agnosis o f a benign gastric ulcer and found that, if the radiologist is con
fident o f the benign nature o f an ulcer then he/she is rarely wrong.
Subsequent studies have confirmed the reliability of a radiological diag
nosis of a benign gastric ulcer by DCBM and have suggested that en
doscopy and biopsies can be reserved for equivocal or malignant-ap-
pearing ulcers or those that do not completely heal on follow-up imag
ing after ulcer therapy. However, partly due to the oft-quoted ability of
malignant ulcers to heal on modem ulcer therapy, many gastroenterolo
gists prefer to perform endoscopy on all radiologically diagnosed gas
tric ulcers. In communities where "early" gastric cancer is common, it is
pmdent to follow this policy. It must be remembered that malignant
change may be patchy and, therefore, multiple biopsies from all areas of
the ulcer rim and crater and, preferably, cytological bmshings should be
obtained. Where "early" gastric cancer is not prevalent a reasonable cost-
effective policy for a radiographically benign gastric ulcer is to perform
endoscopy/biopsy where available prior to therapy and follow-up (if con
firmed benign) to complete healing by subsequent DCBM examinations.
Gastric carcinoma
Diagnosis
The diagnosis of gastric carcinoma is usually made by endoscopy or bar
ium meal. "Early" gastric cancers (EGC), i.e. those limited to mucosa
+/- submucosa regardless of the presence of lymph node metastases) are
prevalent in some communities, such as Japan, but are relatively un
common in most Western societies. They can appear as Type I (poly
poid), Type II (superficial; Type Ila elevated; Type II b flat; Type II с
depressed), or Type III (excavated). Mixed types occur. The surface of
early polypoid lesions on DCBM is lobular or granular and simulates the
areae gastricae. Differentiation is required from adenomas and hyper
plastic polyps (see below). Type II lesions are seen as flat mucosal ele
vations. Where a central depression is present (i.e. superficial erosion)
this is irregular in outline with an uneven surface. Folds radiating to-
938
Figure 29.
Diffuse infiltrative gastric car
cinoma, causing obstruction
at the antrum.
wards the lesion may show evidence of infiltration such as nodularity,

amputation or fusion. Type III lesions demonstrate deeper excavations.
Advanced gastric cancers are more common than EGC in Western so
cieties. These involves the muscularis propria or deeper layers. They may
be classified on gross radiological appearances as polypoid, ulcerative
with raised margins (Figs. 25 b, 27, 28), a larger infiltrative and ulcerat
ing type, and a diffuse infiltrative type (often seen as a constricting tu
mour in the antrum) (Fig. 29). These correspond to Borrman types 1-4,
respectively. Linitis plastica is a diffuse infiltration, predominantly sub
mucosal, which is manifest on contrast studies as a poorly distensible -
so-called "leather bottle"-stomach. This not infrequently may be over
looked endoscopically and, to a lesser extent, radiographically.
Advanced ulcerative or raised cancers are often large and obvious radi-
ologically. All lesions need endoscopic biopsy for confirmation.
Staging
The need for staging of gastric carcinoma is less obvious than for oe
sophageal lesions. However, in communities where EGC is prevalent, it
is useful to help determine therapy and prognosis, particularly where
non-surgical endoscopic treatment is contemplated. Where advanced le
sions are more prevalent it could be argued that surgery, whether for at
tempted cure or palliation, is the treatment of choice and that pre-oper
ative staging does not influence management. However, surgeons' prac
tices differ; if staging is required then this is best achieved by CT or EUS
for local staging, and dynamic enhanced or helical CT (or conventional
939
US) for distant metastases. EUS has been shown consistently superior
to CT for local staging, but is of limited availability. CT visualises the
thickened gastric wall and its relationship to adjacent structures, but is
unable to determine the depth of wall invasion. CT can detect lymph
node enlargement but is non-specific, unable to distinguish reactive from
malignant nodes. The criterion for enlargement is usually taken as > 10
mm. Since metastases can also be present in non-enlarged nodes, CT is
not very sensitive. When performed optimally CT, using either a dy
namic sequential technique with bolus contrast enhancement or the
newer spiral (helical) techniques, is relatively accurate (probably in the
region of 90%) at showing whether the patient has liver metastases or
nor, but is significantly less sensitive at demonstrating all lesions in an
individual patient. Moss has suggested a CT staging scheme for gastric
carcinoma (Table 5).
Table 5. CT Staging o f gastric carcinoma (after Moss et al)
Stage 1
Intraluminal m ass without wall thickening (i.e. < 10 mm thick).
No m etastases.
Stage II
Wall thicken in g > 1 0 mm w ithout tu m o u r extension or m etastases.
Stage III
Thickened w all w ith adjacent organ involvem ent but no d istant metastases.
Stage IV
Distant m etastases with thickened wall.
The accuracy of EUS in T and N staging of gastric carcinoma is sim

ilar to its accuracy in oesophageal carcinoma and significantly better than
dynamic CT, being 80-90% for T and 75% + for N in most series. Once
again, there is difficulty in distinguishing benign from malignant nodes
although positive and negative predictive values of 87.5 % and 82 % have
been achieved for nodal metastasis. EUS is highly accurate in distin-
guising EGC from advanced cancer. In linitis plastica EUS demonstrates
a diffuse thickening of the submucosa and muscularis propria layers.
940
Figure 30.
Submucosal smooth muscle tumour
o f the gastric body (seen in single
contrast) exhibiting central ulcera
tion (arrowed). Note otherwise
smooth surface and right angled
conjunction with gastric walls.
Other gastric tumours
Submucosal tumours
Although many cell types can give rise to suomucosai tumours in
stomach, the vast majority are smooth muscle lesions - leiomyomas,
leiomyoblastomas and the malignant leiomyosarcomas. Radiology es
sentially cannot distinguish these three lesions. Most smooth muscle tu
mours are fundal, rounded and often exhibit central ulceration (Fig. 30).
The latter accounts for the frequent presentation of bleeding. Size is vari
able. As for all submucosal lesions they appear on DCBM as smooth sur
faced with normal overlying mucosa. In profile the margins are at right
angles or obtuse to the line of the gastric wall. Much of the bulk of the
tumour may be exophytic to the stomach - an "iceberg” phenomenon.
EUS is useful for confirming the origin of the tumour from muscularis
propria and distinguishing between a submucosal and an extrinsic mass
(Fig. 31). For larger lesions where malignancy is suspected, EUS or CT
are helpful in assessing infiltration o f adjacent structures.
Haematogenous metastases from malignant melanoma, breast and
lung carcinoma, phaeochromocytoma and, in recent times, Kaposi sar
coma, may give rise to small submucosal tumours. These are usually
multiple and have a ’’bull’s eye” or target appearance due to central ul
ceration. Breast carcinoma may spread submucosally like scirrhous car
cinoma.
941
Figure 31.
EUS image o f submucosal
smooth muscle gastric tumour
(leiomyoblastoma), T. Lesion
seen to arise from muscularis
propria layer o f gastric wall (ar
row). W=normal wall (see
Fig. 8); b=water filled balloon
covering transducer.
(Reproduced with permission o f
Australasian Radiology).
M ucosal polyps
These occur in 1-2% of DCBMs. They appear as rounded filling defects
in the barium pool on the dependent wall or a ring-shadow on the non
dependent wall. They may be pedunculated or sessile. The majority are
hyperplastic and possibly result from regeneration following gastritis.
The minority are adenomas and are important because of their malignant
potential. In addition, there is an increased risk of carcinoma in the same
stomach when adenomas are present. Features to help distinguish be
tween hyperplastic and adenomatous gastric polyps are listed in Table
6. However, if there is any doubt, endoscopy and biopsy are recom
mended.
Table 6. Gastric polyps
HYPERPLASTIC ADENOMATOUS
Frequency >90% <10%
Size < 1 cm > 1 cm
Number multiple single or few
Site fundus, body antrum
Other gastric polyps

Although occasionally gastric adenomas occur in Familial Adenomatous
Polyposis (FAP), most gastric polyps in this condition are hamartomas.
Hamartomas are also seen in Peutz-Jegher syndrome.
942
Figure 32.
Gastric lymphoma. An infiltrative
polypoid mass involves the cardia
and proximal stomach.
Gastric lymphoma
These constitute 1-3% of all gastric malignancies. Most are o f the non-
Hodgkin’s lymphoma type, and the lesion may be localised to the stom
ach with or without regional nodes, or part of a generalised involvement.
Radiographic appearance on contrast studies is variable. Infiltrative,
nodular, ulcerative, polypoid or mixed forms occur (Fig. 32). Sometimes
the predominant sign is markedly thickened folds. The site within the
stomach is variable. Often it is not possible to distinguish lymphoma
from carcinoma. Further difficulties arise since mucosal biopsies are fre
quently negative, as much of the spread is submucosal. Distinction is im
portant since the prognosis is considerably more favourable for lym
phoma than for carcinoma. Staging of gastric lymphoma is best per
formed by a combination of CT and EUS. CT (or transabdominal US)
will determine whether there is involvement of regional nodes; CT will
define the presence of more generalised disease in other regions and will
help assess gastric transmural infiltration. EUS is accurate at mapping
out the distribution of disease within the stomach and the depth of in-
943
tramural and transmural spread. Several EUS patterns of mural spread

have been described.
The post-operative stomach

In the early post-operative period following gastric surgery, contrast
studies are required to test for anastomotic leakage (when water soluble
contrast agents should be used) and for gastric emptying.
In the late post-operative situation, modifications to the standard dou
ble contrast technique are required for satisfactory visualisation; if the
anatomy is known then this will help determine those modifications.
However, endoscopy is superior to radiology in assessing recurrent dis
ease in a gastric remnant or at an anastomosis. Radiology may still be
required to determine the anatomy, if this is uncertain, and to assess gas
tric emptying.
Duodenal disease
Contrast examination of the duodenum is part of the DCBM. Good dis
tended views are obtainable using hypotonic agents and it is now rarely
necessary to perform hypotonic duodenography using a tube technique.
Other modalities, including US, CT, endoscopy and endoscopic retro
grade cholangiopancreatography have largely surplanted duodenogra
phy in imaging periampullary and pancreatic lesions.
The duodenum, extending from the pylorus to the duodenojejunal flex
ure, is approximately 25-30 cm long and divided into four parts. The first
part (the ’’cap”) is about 5 cm in length and extends posteriorly, superi
orly and to the right from the pylorus and is triangular in shape on bar
ium studies. The proximal 2-3 cm is intraperitoneal; the rest o f the duo
denum is retroperitoneal. The second part extends from the superior duo
denal flexure, at the end of the first part, inferiorly to the inferior flexure.
At the apex of the superior flexure there is often a redundant mucosal
fold which may be mistaken for a lesion on contrast studies. On the pos
teromedial wall of the descending duodenum is the major papilla which
appears on hypotonic duodenography as a rounded or oval filling defect.
The appearance is variable but there are usually mucosal folds which
serve as landmarks, the most constant of which is a vertical fold extending
distally from the papilla and a hooded fold covering the papilla itself
(Fig. 33). The minor papilla is much less frequently seen radiologically.
The third part of the duodenum extends from the inferior flexure almost
944
Figure 33.
Normal hypotonic duodenogram
showing area o f major papilla.
Hoodedfo ld (h) covering papilla (p),
oblique folds (f), proximal longi
tudinal fo ld (pi), distal longitudinal
fold (dl) and probable site o f minor
papilla (a). The pattern o f mucosal
folds is quite variable.
horizontally and to the left across the midline. The fourth part begins
where the duodenum becomes more vertical and directed superiorly to
wards the duodenojejunal flexure. The duodenum terminates at the sus
pensory ligament of Treitz. The normal mucosal pattern o f the duodenal
bulb on DCBM is smooth and relatively featureless. A minority of pa
tients exhibit a fine recticular pattern or small punctate collections of bar
ium which are evenly spaced and appear as triangular spiculations in pro
file. The latter must be distinguished from erosions (which are irregu
larly spaced, less numerous and associated with oedema and other signs
of duodenitis) and barium precipitates (which are more dense and wash
off during the procedure).
945
Figure 34.
Brunner's gland hyper
plasia/nodular erosive
duodenitis. Note multiple
nodules in duodenal cap,
several with central ero
sion. p=pylorus.
Table 7. Duodenal "tumour-like”filling defects
BLH Brunner's Heterotopic Crohn's Nodular

glands gastric disease duodenitis
mucosa
Site Dl & D2 D1 +/- D2 juxtapyloric variable D1 +/- D2
Size 1-2 mm upto 1 cm small variable variable
Number uniform size occ. central angular thick folds thick folds
depression ulceration +/- erosions
strictures
Duodenal nodular filling defects

A guide to differential diagnosis of nodular defects is given in Table 7.
Benign lymphoid hyperplasia (BLH) may be a normal finding in a small
number o f individuals or associated with immunoglobulin deficiency and
BLH elsewhere in the bowel. Brunner's gland hyperplasia is most promi
nent in the duodenal bulb, decrasing below the papilla. Several patterns
have been described: focal hyperplasia consisting of solitary lesions or
small clusters; diffuse with innumerable small uniform nodules; multi
focal; hyperplasia with evidence of duodenitis; hyperplasia with erosive
duodenitis (Fig. 34). There is also an association with hyperacidity
states and chronic renal failure. Crohn's disease of the duodenum is
usually associated with other signs besides nodularity, including ul
ceration, thick folds and stricturing. There is often antral involvement,
as well as disease elsewhere in the GI tract. Heterotopic gastric mu
cosa is seen in about 5% of barium meals and is of doubtful patholog
ical significance, although there is some evidence that there is an as-
946
Figure 35.
Duodenal ulceration. One mod
erate sized ulcer (arrowed) and
other possible small erosions
are seen. There are oedematous
folds with linear collections o f
barium among them, some radi
ating towards a central erosion.
Note the tenting o f the base o f
the duodenal cap due to fibrotic
scairing (open arrow).
Figure 36.
Multiple duodenal erosions with
radiating and oedematous folds
and duodenal cap deformity.
Consistent with duodenal ulcer
ation and duodenitis. Note the
coarse areae gastricae in the
stomach antrum suggesting
gastritis.
947
sociation with H. pyloris infection.
Non-specific duodenitis
Although there is controversy regarding the true nature o f non-specific
duodenitis, and the natural history is somewhat different than duodenal
ulceration, it is probably part o f the spectrum of peptic ulcer disease.
Barium studies are not especially accurate, but criteria for diagnosis in
clude nodularity, thickened folds (> 4 mm thick), bulbar deformity and
punctate collections of barium with halos of oedema, representing ero
sions. There is a significant false negative rate and false positive rate for
DCBM. False positives occur particularly when the diagnosis is made
on the presence of only one radiological sign. The pattern o f duodenitis
may sometimes be predominantly nodular (Fig. 34). There is consider
able overlap with Brunner's gland hyperplasia; indeed the two often co
exist and it is not clear whether the nodules of duodenitis represent in
flammatory infiltrate or Brunner's glands.
Duodenal ulceration
Duodenal ulcers are linear, rounded or irregular in shape on barium stud
ies. About 10% are multiple and about half occur on the anterior wall,
and as such are more difficult to diagnose; compression and profile views,
including prone-oblique views are needed. When acute there may be lit
tle or no associated wall deformity. Radiating folds and cap deformity are
more commonly seen when the ulcer is more longstanding (Figs. 35,36).
The healing process causes fibrosis, deformity andpseudodiverticula (Fig.
37). The base of the pseudodiverticulum, when present, points to the ul
cer crater. Deformity of the cap is assumed to be related to a past history
of duodenal ulcer. When distortion is severe it is often difficult to be def
inite as to whether an ulcer is currently present. It is usually satisfactory
in these circumstances, if the patient has appropriate symptoms, to as
sume the presence of an ulcer and treat accordingly. In particular, the pres
ence of a pseudodiverticulum usually means that there is an ulcer.
Approximately 5% of duodenal ulcers occur distal to the cap: most of
these occur on the medial wall proximal to the papilla of Vater. They are
often difficult to demonstrate radiologically due to accompanying spasm
and oedema. In these circumstances healing often leads to stricturing.
Ulcers distal to the papilla should suggest Zollinger-Ellison syndrome.
948
Figure 37.
Gross deformity o f the
duodenal cap due to
chronic duodenal ulcera
tion. Note pseudodivertic-
ula (arrows). u=ulcer.
C om plications
Acute bleeding presents as haematemesis and/or melaena. Radiology
plays little part in the initial diagnosis; occasionally angiography is re
quired for diagnosis when endoscopy is unsucessful or equivocal, or for
therapeutic intervention when endoscopic treatment fails or surgery is
contraindicated. Labelled red-cell nuclear medicine scanning may also
sometimes be indicated prior to angiography to localise a source of blood
loss. However, its accuracy in the upper GI tract has been questioned.
Ulcer perforation presents as an "acute abdomen"; usually free in-
traperitoneal gas is seen under the diaphragms on plain abdominal radi
ographs. A water-soluble contrast meal may be required for confirma
tion. An ulcer may penetrate into adjacent structures: involvement of the
pancreas may present as an acute pancreatitis; penetration into the bile
duct will also present acutely with gas seen in the biliary system on plain
films. In the chronic stage the healing process may give rise to duodenal
or gastric outlet obstruction, seen on plain films as a distended stomach,
easily confirmed on a contrast study. In some cases obstruction may be
at least in part due to oedema in the acute phase and may resolve with
conservative management.
Zollinger-Ellison syndrome
This syndrome is due to the hypersecretion of gastric acid in response to
a gastrin-secreting tumour. The tumours are usually in the pancreas, but
a significant proportion are extrapancreatic. Occasionally there is diffuse
islet-cell hyperplasia. Between 40 and 70% of tumours are malignant,
but slow growing. Metastases are often evident at the time of diagnosis.
949
Although 75% of associated peptic ulcers are gastric or in the duodenal

bulb, distal duodenal ulcers and/or multiple ulcers should suggest the di
agnosis. Other signs on GI contrast studies include excess fluid residue
and hyper-rugosity in the stomach, duodenitis with erosions and
Brunner's gland hyperplasia, a dilated descending duodenum with thick
ened folds, and jejunal fold thickening with increased small bowel fluid
and rapid transit. Reflux oesophagitis is also commonly present.
Coeliac disease
Duodenal abnormaliaties seen on DCBM may be the first clues to the di
agnosis, particularly in those patients presenting atypically. The charac
teristic finding is the so-called "bubbly bulb", due to multiple small de
fects in a mosaic-like pattern. The appearance is similar to heterotopic
gastric mucosa (see above), but is more diffuse. Thickened folds in the
descending and distal duodenum may also be seen.
D uodenal changes in pancreatic disease

Duodenography in pancreatic pathology has become much less impor
tant since the advent of more specific imaging modalities for pancreatic
disease. However, abnormalities of the descending duodenum are ap
parent in both inflammatory and neoplastic disease o f the pancreatic
head. Signs o f pancreatic disease include those of pancreatic enlarge
ment, such as widening of the duodenal loop, stricturing, and a mass im
pression on the second or third parts of the duodenum; these are non
specific and seen in both inflammatory and neoplastic disease. Other
signs are nodularity and mass indentation of the wall o f the duodenum;
these are suggestive but not diagnostic of neoplastic pancreatic disease
as are spiculation and tethering o f folds. Inflammatory masses tend to
lead to more smooth impressions and thickened folds but these signs,
too, are by no means specific. Similarly, non-specific, is the "inverted 3
sign", due to a mass impression on the medial wall of the descending
duodenum which is tethered at the site of the major papilla.
Blunt duodenal trauma

Duodenal laceration/perforation
Bowel or mesenteric injury occurs in about 5% of cases of significant
blunt abdominal trauma. Duodenal injury (perforation or haematoma) is
usually the result of a deceleration force when the body is restrained by
950
a seat belt. Fixation of the second and third parts of the duodenum
retroperitoneally to the posterior abdominal wall leads to a propensity to
shearing injury. In addition, compression of the third part of the duode
num can occur where it overlies the spine. Early diagnosis of duodenal
perforation is essential since delay is associated with increased mortal
ity. CT is the investigation of choice in blunt upper abdominal trauma
when hepatic, splenic, pancreatic, renal, duodenal or mesenteric injury
is suspected and the patient is haemodynamically stable. In patients who
are unstable diagnostic peritoneal lavage (DPL) or urgent surgery is in
dicated. DPL has largely been replaced by CT in stable patients, but in
some centres this is still performed, although the sensitivity is less in
retroperitoneal trauma to the duodenum than in intraperitoneal injury.
When lavage is undertaken this should preferably be after CT to avoid
errors in interpretation of fluid or gas in the peritoneum. CT is performed
using oral contrast (3 % Gastrografin), administered by a nasogastric tube
if necessary which allows aspiration of the stomach at the end of the pro
cedure. Approximately 250 ml are given 30-40 minutes before the scan,
and a further similar volume immediately prior to it. Scans are performed
using an intravenous contrast bolus-enhanced dynamic incremental
technique. Contiguous slices are obtained from the diaphragm to the
pelvis and then at intervals in the pelvis. Images are viewed at appropri
ate soft tissue windows; in addition, lung windows are recorded for the
upper slices to help exclude basal lung pathology, haemothorax or pneu
mothorax. The findings in duodenal trauma include haemoperitoneum
and/or retroperitoneal fluid (both of which are non-specific), extralumi
nal gas (a sign formerly regarded as reasonably specific for hollow vis-
cus perforation but recently there have been doubts raised as to its speci
ficity), extravasation of contrast medium (specific but infrequent), a "sen
tinel clot" (a high-attenuation blood clot seen adjacent to the involved
bowel), thickened bowel wall, or mesenteric infiltration (a non-specific
sign). The reported sensitivity of CT in duodenal injury is variable in dif
ferent series, but it should be noted that the signs may be subtle. In ad
dition, distinction of duodenal from adjacent pancreatic contusion may
be impossible on CT.
Duodenal haematoma
In distinction to duodenal perforation, intramural haematoma may pre
sent late - up to one or two weeks following the injury. Haematoma is
951
commoner in children than in adults, in whom duodenal and small bowel

perforations are more likely. The signs on contrast studies (and on CT)
include partial or total obstruction from the mass effect of the haematoma
and a "stacked coin" or "picket-fence" appearance of thickened trans
verse folds. Symptoms usually subside on conservative management.
Spontaneous intramural duodenal haematoma occurs in patients on an
ticoagulants and in those with bleeding diatheses. Signs are essentially
the same as for the traumatic variety.
Superior mesenteric artery syndrome

This is a controversial condition manifest by partial obstruction in the
third part of the duodenum where it passes between the aorta and the su
perior mesenteric artery. It is reported to occur following marked weight
loss from a variety of causes and also in patients in body casts. Vomiting
is a prominent feature. Barium studies show partial obstruction with
proximal dilatation of the second part of the duodenum. There is often
"to-and-fro" peristalsis within the dilated segment. The diagnosis is ap
parent when the obstruction is seen fluoroscopically to be relieved when
the patient is turned prone. However, CT or US may be needed to ex
clude a mass lesion at the root o f the mesentery causing obstruction.
Duodenal diverticula
These are frequent findings on upper GI barium studies. They are re
garded as acquired pulsion-type diverticula, and may be single or mul
tiple. The commonest site is the medial wall of the descending duode
num. Their nature is usually obvious; differentiation from ulcers is made
by the appearance of mucosal folds extending into the mouth of the le
sion and variability of shape during the examination. Pseudodiverticula
are associated with duodenal ulceration and most commonly occur in the
bulb. Duodenal diverticula are nearly always asymptomatic, but occa
sionally give rise to complications: diverticulitis may occur and duo-
denocolic fistula has been reported to follow this; this may be more com
mon with laterally placed diverticula. Obstruction is rarely seen when
inspissated food impacts inside the lesion. There is evidence that peri
ampullary diverticula are associated with an increase in the incidence
of common duct calculi and a recurrence of calculi following chole
cystectomy.
952
Congenital abnormalities
Occasionally congenital abnormalities may present in adulthood.
Annular pancreas causes narrowing of the lumen of the descending duo
denum due to a ring of pancreatic tissue. There is usually a defect on the
lateral wall of the duodenum associated with an ’’hour-glass” type stric
ture. Patients may present with duodenal obstruction, pancreatitis or pep
tic ulceration. An intraluminal diverticulum, due to an incomplete con
genital web, may cause obstruction to the second or third parts of the
duodenum and is seen as a ”wind-sock” filling defect within the lumen.
Duplication cysts manifest as submucosal or extramural masses.
Duodenal neoplasms
Tumour-like filling defects in the duodenum are dealt with above. True
primary neoplasms of the duodenum are rare. Usually endoscopy and
biopsy are necessary for diagnosis. Adenomas tend to occur in the first
or second parts and may be sessile or pedunculated, appearing as filling
defects or ring shadows on barium studies. In polyposis syndromes they
may be multiple. They have significant malignant potential. Similarly
villous adenomas are of high malignant potential and should be removed;
these appear as cauliflower-shaped filling defects, usually near the
papilla. Other benign neoplasms include smooth muscle tumours and
lipomas.
Primary malignant neoplasms are most commonly adenocarcinomas,
but lymphomas, smooth muscle tumours and carcinoids are also seen.
Adenocarcinomas are polypoid, ulcerating or stricturing. There is a
propensity for the peri-ampullary region. Peri-ampullary carcinomas
may arise from duodenal mucosa, the Ampulla of Vater itself, from pan
creatic tissue or from the bile duct. There is an association o f peri-am
pullary duodenal carcinoma with familial polyposis, particularly
Gardner's syndrome. Duodenal lymphomas have similar characteristics
to small bowel lesions (see below). Duodenal carcinoid tumours have
variable malignant potential. Ectopic islet-cell tumours occur in the duo
denal wall and are associated with ulcers. Secondary malignant tumours
affecting the duodenum usually result from direct spread from neigh
bouring organs such as colon, gallbladder, pancreas and right kidney.
953
Figure 38.
Normal enteroclysis demonstrat
ing catheter in first jejunal loop
and well distended jejunum and
proximal ileum with normal pat
tern o f valvulae conniventes.
THE SMALL INTESTINE

The length of the small intestine varies among indidviduals between 3-
10 metres. Fully distended as in an enteroclysis examination the calibre
of the upper jejunum is 3-4 cm, the lower jejunum 2.5-3 cm and the ileum
2-2.5 cm. The values for a "follow-through" type examination are 3 cm
for the jejunum and 2.5 cm for the ileum. The wall thickness is measur
able when, on a contrast examination, two loops are parallel over a length
of 4 cm during compression; the combined thickness o f the apposing
walls should not exceed 2 mm. The normal mucosal pattern o f the small
bowel depends on the method o f examination. On enteroclysis, when
there is optimal distension, the transverse mucosal folds (valvulae con
niventes) occur at a density of 6-12 every 5 cm length o f bowel and are
up to 2 mm thick; they extend "ladder-like" across the whole width of
the lumen (Fig. 38). The folds are more prominent in the jejunum and
are often absent in the distal ileum. On small bowel meal (follow-
through) examination the mucosal pattern is feathery due to secondary
mucosal folds, which are effaced on enteroclysis.
Imaging techniques
In recent years there has been an increasing emphasis on the usefulness
of CT in the diagnosis of small bowel disease and, with regard to con
trast studies, more widespread use of enteroclysis techniques.
954
Plain radiographs
These are of limited use in non-acute disease (see chapter on the Acute
Abdomen) but may be of help in patients with abdominal pain when sub
acute or recurrent obstruction is suspected.
Contrast studies
It is no longer appropriate to perform a follow-through examination as
an adjunct to a barium meal, merely obtaining a few delayed spot films
of the small bowel during the transit of barium. This is an inaccurate ex
amination and, when performed after a double contrast barium meal, is
usually technically inadequate as the high density barium does not lend
itself to this application. The choice of barium study is between an en-
teroclysis examination (small bowel enema - SBE -; intubation study)
and a dedicated small bowel series (small bowel meal). There is contro
versy as to which is the superior study for routine use. Some radiologists
perform enteroclysis on all patients; others perform small bowel meals
almost exclusively; still other use enteroclysis selectively. Each type of
examination has its advantages and disadvantages. Although it is diffi
cult to perform prospective comparative trials, there is a widespread con
sensus that enteroclysis is the more accurate examination, particularly
for the depiction of proximal disease, skip lesions, subtle strictures and
mucosal abnormalities. The infusion of contrast at enteroclysis leads to
continuous flow through the small bowel with resultant maximal disten
sion allowing detection of mild narrowing and the examination of indi
vidual loops with compression. However, enteroclysis requires greater
technical skill, more radiologist's and room time, the relative discomfort
of the passage of a nasojejunal tube, and greater radiation exposure. Many
radiologists argue that, when performed with due attention to detail, the
small bowel meal is sufficiently accurate and is arguably less demand
ing on patient and radiologist. Contraindications to both techniques in
clude suspected bowel perforation and large bowel obstruction. In the
latter, antegrade administration o f barium may worsen the problem when
the barium becomes inspissated proximal to an obstructing lesion.
However, small bowel obstruction is not a contraindication since in these
circumstances the contrast remains sufficiently thin in the already fluid
laden small bowel to avoid exacerbation of the obstruction.
The small bowel meal is performed on a fasting patient. Purgatives to
clear the caecum and terminal ileum of faces are desirable, but not uni
955
versally used. Dilute barium sulphate suspension (about 45% w/v) to a

volume o f 300-600 ml is taken orally by the patient. Rapid and contin
uous gastric emptying is important to ensure a non-interrupted barium
column in the small bowel. Therefore, the patient drinks lying on his/her
right side and the rate of drinking is kept sufficent to maintain some bar
ium at the pylorus. Metoclopramide 10-20 mg orally may also be used.
The upper GI tract is screened and spot films taken to exclude gross gas
troduodenal pathology. Films o f the small intestine are taken at ten min
utes (supine) and then at 20 minute intervals (prone) until the terminal
ileum is reached. Any abnormality is fluoroscoped with compression and
spot films obtained. The terminal ileum is always screened with and with
out compression. Several variations on this techique are employed, such
as the use of hurrying agents, e.g. metoclopramide, or cholecystokinin,
or a "peroral pneumocolon" procedure.
The small bowel enema (SBE) or enteroclysis examination is per
formed following bowel preparation to clear the right colon o f faecal ma
terial. A nasojejunal tube is placed under topical anaesthesia. Various
types are employed, the commonest being the size 12 French Bilbao-
Dotter tube or a variation thereof. Others include balloon catheters de
signed to prevent reflux of barium into the duodenum and stomach. Some
radiologists use a single-contrast dilute barium technique; others chase
the barium with water to obtain a double-contrast effect in the jejunum;
still others perform a biphasic examination using methylcellulose or air
to provide double-contrast. There is little objective evidence that any
technique is significantly superior. Intermittent fluoroscopic screening is
carried out with spot films of jejunum and ileum with compression to
separate individual loops. Filled and collapsed views of the terminal
ileum are obtained. Whichever method of enteroclysis is employed it is
axiomatic that accuracy depends on the two factors of maximal disten
sion and compression views of individual loops.
In the context of the post-operative patient with a small bowel which
is slow to become normally motile, some authors believe that a water-
soluble small bowel follow-through using hyperosmolar contrast such as
Gastrografin will accelerate the process of recovery. This is presumed to
relate to the distension of the bowel caused by drawing into the lumen
of fluid by the hyperosmolar agent.
Signs of disease to observe on contrast studies include:
Lumen changes: strictures, dilatation, compression, pseudodiverticula
956
Figure 39.
Ultrasound o f thickened bowel.
Relatively hypoechoic thick walls
(arrowed) with echogenic lumen.
Appearances are nonspecific - in
this case, Crohn's disease o f the
ileum.
Wall abnormalities: wall thickening as evidenced by displacement of ad

jacent bowel loops.
Mucosal fold abnormalities: thickened folds, nodularity, crowding of
folds, fold effacement. Submucosal oedema or infiltration tends to pro
duce straight, thickened folds.
Ulcerations: aphthoid, transverse, longitudinal, "cobblestone” pattern
(ulceronodular change produced by intersection of longitudinal and
transverse ulceration with intervening oedema).
Nodules andfilling defects: lymphoid hyperplasia, small and large nod
ules, polyps.
Sinuses and fistulae: to other parts of the bowel, other hollow organs or
skin.
Ultrasonography
Bowel imaging with ultrasound suffers from limitations by the presence
of bowel gas and faeces. However, abnormal bowel loops can be imaged
when there is thickening of the wall; these have a sonolucent periphery,
due to oedema or infiltration, and echogenic centre (Fig. 39). Extramural
abscesses can be seen as usually relatively sonolucent masses contain
ing internal echoes (Fig. 43). Omental and mesenteric masses may be
identified, as well as enlarged lymph nodes, which are usually sonolu
cent.
957
Computed tomography
The ability of CT to demonstrate bowel wall thickening, extramural and
mesenteric disease has seen its increasing use in suspected small bowel
pathology. It is necessary to give adequate oral contrast to provide good
lumenal distension (with the exception of high-grade small bowel ob
struction, where there is often already distension by fluid content). Up
to a litre or more of dilute water-soluble contrast or dilute barium is given
in divided doses, starting about one hour prior to the scan. A hurrying
agent such as sorbitol or metoclopramide may be added to the contrast.
A dynamic bolus contrast-enhanced examination is performed. It may
be necessary to obtain additional cuts through an area of interest, or to
scan with thinner slices to provide greater resolution o f the bowel wall.
New generation scanners have the ability to acquire images o f large vol
umes in a single breath-hold using helical scanning technology, and this
may prove to be the technique o f choice. Inflammatory diseases or is-
chaemia tend to cause symmetrical bowel wall thickening with homo
geneous attenuation or a "double halo" or "target" appearance on en
hanced images, whereas neoplastic lesions are associated with asym
metrical, iregular thickening.

The development of MR applications in the abdomen has been limited
by motion artefacts, limitations in tissue contrast and, to some extent, by
the lack of an ideal oral contrast agent - particularly a "negative" agent.
Fat suppresion and the increasingly wider availability o f fast pulse se
quences (including echoplanar techniques) are likely to result in consid
erable increase in utility of MR in the GI tract. There is preliminary ev
idence that MR can help distinguish active inflammation from fibrosis
in inflammatory disease and accurately delineate enteric fistulae and ab
scesses.
Pathology
Inflammatory diseases
Crohn's disease
Suspected Crohn's disease is one o f the commonest indications for con
trast studies of the small bowel in the developed world. The role of ra
958
diology encompasses diagnosis, assessment of extent and distribution of

disease and the imaging of complications. Although the sensitivity of en
teroclysis is reported as extremely good in detecting Crohn's disease, the
radiographic features often do not correlate well with disease activity.
Ultrasound examination is useful in demonstrating thickened bowel wall
and it has been suggested for screening patients for a demonstrable cause
of abdominal pain.
The features seen on small bowel contrast studies can be classified as
superficial, transmural and extramural abnormalities.
Superficial abnormalities: "Early” changes that are described include
thickened folds (which are straight, due to submucosal oedema), aph-
thoid ulcers, punctate collections of barium and small nodules. These
may occur alone or in combination. However, these have not conclu
sively been shown to progress to the typical more advanced changes of
Crohn's disease and many patients with such signs as aphthoid ulcers
may have inflammatory diseases o f other types, such as Yersinia infec
tion; other signs may represent normal variants. True superficial abnor
malities in Crohn's disease include aphthoid (Fig. 40) and "punched-out"
ulceration, mucosal granularity and transverse and longitudinal ulcers
(Fig. 41). The latter may be short or long and usually occur along the
mesenteric border where they are associated with contraction and con
cavity of that border. Cobblestoning is frequent. Abnormal mucosal folds
are seen; these are thickened and may be nodular, especially when as
sociated with aphthae. Thickened folds are often an early sign of recur
rent disease proximal to a surgical anastomosis. When disease is long
standing the folds may become effaced.
Transmural abnormalities (Figs. 41-43): Crohn's disease is typically
a transmural process; the signs associated with this constitute the clas
sic features of this disease. Deep ulceration is seen as fissure (transverse,
"rose-thom") ulcers and penetrating, discrete ulcers. It may be difficult
to distinguish fissure ulcers and barium trapped in troughs between oede-
matous folds. Large excavated ulcers are very unusual and suggest an al
ternative diagnosis. Cobblestoning is a feature of intersecting longitudi
nal and transverse ulcers, with intervening heaped-up oedematous mu
cosa. Deep ulceration may result in the sinuses and fistulae characteristic
of severe Crohn's disease. Thickened bowel wall may be manifest as sep
aration of loops. Luminal narrowing is nearly always present to some de
gree and may be due to spasm and oedema during the acute phase, or
959
Figure 40.
Aphthoid ulceration o f terminal
ileum (small arrows). Note also
"cobblestoning" (larger ar
rows).
Figure 41.
Typical features o f Crohn's dis
ease o f the distal ileum includ
ing fissure ulcers (small ar
rows), longitudinal ulcers (ar
rowhead), "cobblestoning"
(open arrows), aphthoid ulcers
(curved arrow) and stricturing.
ic=ileocaecal valve.
compression from mesenteric disease, or, later, due to fibrotic strictures.

Crohn’s disease typically affects the bowel asymmetrically involving the
mesenteric aspect and adjacent mesentery more severely than the an-
timesenteric border; as fibrosis occurs, shortening o f the mesenteric side
leads to redundancy of the antimesenteric border and, thus, sacculation.
A typical feature of Crohn’s disase is a gradation of abnormalities along
the affected segment of bowel; this may help in the differentiation from
other pathologies, such as tuberculosis.
Extramural abnormalities: Mesenteric inflammatory masses and ab
scesses may produce compression and displacement of bowel loops.
Fibrosis in the mesentery, as stated above, leads to shortening of the
mesenteric and redundancy of the antimesenteric border.
960
Figure 42.
Crohn's disease o f distal ileum
with stricturing and sacculation
on the antimesenteric aspect
(curved arrows), andfisssure
ulcers (small arrows). Open ar
row points to ileo-caecal valve.
Figure 43.
Ultrasound image demonstrates
pelvic abscess and enterocuta-
neous fistula complicating
Crohn’s diease. Abscess (ar
rows) contains internal echoes.
Hyperechoic foci (arrowhead)
represent gas in bladder (b)
wall.
The distribution of small bowel Crohn's disease is best assessed by en

teroclysis. The terminal ileum is nearly always involved in small bowel
disease and is the only site in up to 30% of patients. "Skip" lesions are
seen in up to 20%. Crohn's disease is typically asymmetrical - both cir-
cumferentially and longitudinally. Recurrent disease following bowel re
section almost always involves the pre-anastomotic segment.
Complications of Crohn's disease are mainly related to its transmural
nature. Strictures often lead to obstructive symptoms. It may be ex
tremely difficult to distinguish bowel narrowing due to active Crohn's
961
Figure 44. Same pa

tient as Fig. 43. CT o f
pelvis demonstrates
thickened loop o f ileum
(small arrows), fistula
to bladder (arrowhead)
and gas in bladder wall
(curved arrow) and in
non-dependent aspect
o f bladder itself. More
cranial image better
showed associated ab
scess.
disease from fibrotic strictures, when other signs of activity, such as ul
ceration, are absent. There are preliminary data that MR may be useful
in this distinction. Extramural complications often require ultrasound
and/or CT for imaging. Sinuses and fistulae are common; fistulae may
communicate with other loops of small bowel, colon, urinary or genital
tract or skin. Enteroclysis will usually demonstrate such complications,
but ultrasound or CT will demonstrate the extent of the disease and as
sociated abscesses (Fig. 43). Sinograms may be helpful when there is cu
taneous communication. Cross-sectional imaging is particularly useful
in the diagnosis and management of abscesses complicating Crohn’s dis
ease. Many o f these patients are young, and it is therefore reasonable to
perform ultrasound initially to try to avoid ionising radiation, although
a negative examination should usually be followed by CT since this is
superior in the detection of abscesses, which may be interloop, intra- or
retroperitoneal in site. CT is also the investigation of choice in suspected
enterovesical fistula (Fig. 44). There is growing evidence of the sensi
tivity of MR in the detection of fistulae and abscesses related to Crohn's
disease. As well as demonstrating these complications, CT in Crohn's
disease will show the thickened bowel wall, mesenteric streaking and,
sometimes, mesenteric nodules due to mildly enlarged lymph nodes.
The differential diagnosis of Crohn's disease on contrast studies is
wide. There is usually no problem in the appropriate clinical setting
where there are typical changes and distribution of disease. Difficulties
occur when there is sparing of the terminal ileum, diffuse disease or there
are atypical signs. Small bowel tuberculosis (ТВ; see below) may be in
distinguishable from Crohn’s disease and must be considered where ТВ
962
Figure 45.
"Backwash ileitis" due to ulcera
tive colitis. Note features o f
chronic ulcerative colitis in right
colon, patulous ileocaecal valve,
dilated distal ileum with granular
mucosa.
is endemic. Features that favour ТВ include a relatively abrupt change

from normal to abnormal bowel, predominantly transverse ulcers
(Japanese authors suggest that longitudinal ulcers are not a feature of
ТВ), and marked caecal involvement with disproportionately less ter
minal ileal disease. Large excavated ulcers and discrete larger nodules
without signs of mucosal inflammation favour lymphoma. Carcinoid pro
duces a severe desmoplastic reaction in the mesentery, but does not usu
ally lead to mucosal ulceration. Primary adenocarcinoma of the ileum
may mimic Crohn's disease, but typically demonstrates the shouldered
stricturing of a neoplasm. Acute infections (such as Yersinia) are not typ
ically transmural processes. Ischaemic segmental strictures are often sus
pected by the history. Aphthoid ulcers are non-specific, occurring in a
variety of pathologies including infections, such as Yersinia and ТВ, and
lymphoma. "Backwash ileitis" is seen in ulcerative colitis when the
whole of the colon is involved; the distal ileum is of normal or dilated
calibre, the mucosa is granular but of smooth contour (Fig. 45).
963
Figure 46.
Graft-versus-host dis
ease in a bone marrow
transplant recipient.
There are several loops
o f ileum which demon
strate a featureless ap
pearance - "ribbon
bowel".
Miscellaneous inflammatory disorders

Behget's disese may affect the small bowel and produce changes similar
to Crohn's disease. "Ring ulcers" have been descibed in the distal ileum
and there is often a colitis. Long-standing use of non-steroidal anti-in-
flammatory drugs (NSAIDs) may result in a variety of small bowel ab-
normaltiies, including malabsorption, blood and protein loss, inflamma
tion and ulceration. Single or multiple strictures, often short and web
like in configuration can give rise to obstructive symptoms. Other drugs,
especially slow-release potassium-supplements may also lead to small
bowel strictures. Graft-versus-host disease (GVHD) in bone marrow re
cipients can involve any or all parts o f the bowel. In the small intestine
fold thickening evolves into a featureless appearance with fold efface-
ment ("ribbon bowel") on barium studies (Fig. 46). Acute GVHD is in
distinguishable from viral enteritis on radiological findings alone and,
indeed, these often co-exist. Gastric involvement and prolonged mucosal
coating favour a viral pathology. Eosinophilic enteritis is characterised
by episodic abdominal pain, diarrhoea and eosinophilia. Contrast exam
ination demonstrates extensive or segmental thickened valvulae con-
niventes with moderate stricture formation. There is often nodularity or
narrowing of the gastric antrum and enlarged or nodular rugal folds. In
some patients there is oesophageal and/or colonic involvement.
964
Figure 47.
Chronic ileocaecal tuberculosis.
The caecum and ascending colon
are retracted craniad and are fi
brotic, scarred and sacculated
(curved arrows). The terminal
ileum in this patient is relatively
patulous (straight arrows) and
probably nodular. v=ileocaecal
valve.
Infections
Tuberculosis
Tuberculosis, worldwide, is the most common chronic inflammatory dis
ease of the small bowel. In addition, it is now increasingly seen in the
developed world in association with HIV infection in immunocompro
mised hosts. The radiological features may be indistinguishable from
Crohn’s disease. Less than 50% of patients have demonstrable pulmonary
involvement. The ileocaecal region is the commonest site in the bowel.
Ulcerative and hypertrophic forms have been described. Early signs in
clude thickening of the mucosal pattern and nodularity in the terminal
ileum. In the acute phase there is spasm of the caecum with a narrowed
and ulcerated distal ileum. Ulcers are transverse or circumferential in ori
entation. Occasionally large cavitating ulcers are seen which mimic those
seen in lymphoma. Later the caecum becomes contracted and retracted
in a cephalic direction as the hypertrophic granulomas lead to fibrosis
(Fig. 47). The ileocaecal valve may be patulous, but as the disease pro
gresses it may narrow. Strictures of the distal ileum are typical short and
’’hour-glass” in configuration. Complications include fistulas and perfo
rations which are usually localised. CT will demonstrate the thick-walled
965
bowel and may show tuberculous ascites and lymph node enlargement,
which is typically greater than that seen in Crohn's disease, or an in
flammatory mass that may surround the ileum. Nodes may be necrotic
(caseating) and/or calcified. Other features that help distinguish Crohn's
disease and tuberculosis are listed under Crohn fs disease.
Other chronic infections such as South American Blastomycosis and
disseminated Histoplasmosis can simulate Tuberculosis and Crohn's dis
ease in the ileocaecal region. Actinomycosis has a particular propensity
to form sinuses and fistulae in the right iliac fossa.
Yersinia Enterocolitica Infection

This causes a self-limiting terminal ileitis or mesenteric adenitis. The
distal 10-15 cm of ileum are involved, but the colon may also be abnor
mal. Aphtoid ulcers and lymphoid hyperplasia may be demonstrated on
contrast studies. Ultrasound examination, often performed for suspected
appendix inflammation, may show a circumferentially thickened distal
ileal wall and/or hypoechoic regional mesenteric lymph node enlarge
ment. Patients with iron-overload syndromes may be susceptible to more
severe, even life-threatening, infection.
Giardiasis
Giardia lamblia infestation produces non-specific radiological changes.
The proximal small bowel is maximally affected, where there is thick
ening of the valvulae conniventes. Giardiasis is associated with nodular
lymphoid hyperplasia in patients with hypoglobulinaemia.
Strongyloidiasis
This may be asymptomatic when infestation is mild or produce symp
toms related to the upper GI tract, often simulating peptic ulcer. Small
bowel motility disturbances and hypersecretions may occur. On small
bowel follow-through examinations there is a malabsorption pattern.
Severe, even overwhelming, infestation is seen in immunosuppressed
patients. Ulceration occurs in the proximal small bowel leading to stric
tures and loss of normal mucosal fold pattern (Fig. 48).
AIDS-related infections
A variety of opportunistic pathogens may affect the small intestine in
AIDS patients. It may be difficult to separate out the features of indi-
966
Figure 48.
Strongyloidiasis affecting
the distal duodenum and
proximal jejunum. There
are multiple strictures
and loss o f normal folds.
St=stomach.
Figure 49.
Nodular filling defects in
small bowel o f AIDS pa
tient (some o f which are
arrowed) are consistent
with the submucosal de
posits o f Kaposi sar
coma. Disease was pre
sent elsewhere in the
bowel. Although unveri
fied in this patient, the
thickened folds and poor
coating probably repre
sent co-existent oppor
tunistic infection - most
likely Cryptosporidium.
vidual organisms, since many produce similar radiographic abnormali

ties and since there may be multi-organism involvement (Fig. 49).
However, there are characteristic patterns that may be recognised radi-
ographically based on the distribution of disease, the presence of distor
tion of folds, nodularity and changes in small bowel calibre. Commoner
pathogens include Cryptosporidium, Mycobacterium avium intracellu
larae (MAI) and Cytomegalovirus (CMV). Cryptosporidium is a proto
zoan that causes a cholera-like syndrome. It predominantly affects the
proximal small bowel and on contrast studies causes thickened folds, a
dilated lumen or spasm, nodular duodenal folds and hypersecretion lead
ing to poor mucosal coating. Gastric involvement may also be seen,
967
where it is commonly associated with CMV infection, and leads to antral

narrowing. Small bowel changes similar to Cryptosporidium may also
occur in giardia, hookworm, strongyloides, CMV and Isospora infec
tions. Mycobacterial infections of the small bowel may be related to
Mycobacterium tuberculosis or atypical mycobacteria such as MAI. The
latter causes a disseminated disease affecting lungs, liver, spleen, mar
row and lymph nodes, as well as the GI tract. In the small bowel MAI
leads to radiographic features similar to Whipple’s disease. There is mild
dilatation, thickened folds and fine nodularity. In the ileum, particularly,
a pattern may be seen consisting of prominent folds without wall thick
ening. CT scanning demonstrates mesenteric and retroperitoneal nodal
enlargement, splenomegaly and ascites.
CMV affecting the small intestine causes a diffuse inflammation which
may include the large bowel. CMV is associated with a vasculitis and
therefore ischaemic necrosis and subsequent perforation is not uncom
mon. Radiographic changes may be diffuse or limited to the distal ileum,
where it causes thickened walls and narrowing, sufficient to produce ob
struction, submucosal nodularity and ulceration. Adenopathy is not a fea
ture on CT scanning.
Other sm all bowel infections and infestations

In acute enteric infections such as Salmonella and Helicobacter
(Campylobacter) apart from the occasional need for plain flms, radio
logical investigation is rarely performed. Severe Salmonella infections
are associated with a variable ileus on plain radiographs. In typhoid, plain
films may be taken for the suspected complication of perforated bowel.
Contrast radiography is rarely indicated in typhoid but demonstrates
nodular thickening of the ileum, due to enlarged Peyer’s patches, a di
lated lumen and ulceration. Roundworm (Ascaris) infestation, when
heavy, may be identified on plain radiographs by a tangle of worms out
lined by gas in the lumen of the bowel. They may be associated with
bowel obstruction. Barium studies will also outline them as filling de
fects and can also give rise to opacification of the GI tract of the worms.
Ascaris may infest the bile duct. Hookworm infestation is accompanied
by a normal barium study or non-specific changes of coarsened mucosal
folds. Tapeworms can give rise to bowel obstruction. Rarely they may
be seen on contrast examination as long linear radiolucent filling defects
within the barium. Whipple's disease is a systemic disease caused by an
968
unknown organism but classified as an infective disorder, in part due to

its response to antibiotic therapy. The characteristic cells that are seen
on small bowel and lymph node biopsy are "foamy macrophages". Radio-
graphic changes on barium studies include thickened folds with a vari
able degree o f dilatation of the lumen. These features are predominantly
seen in the jejunum. On double-contrast enteroclysis tiny nodules of 1-
2 mm are seen representing swollen villi. CT or ultrasound demonstrate
abdominal lymph node enlargement in about half of the patients. The
nodes may be of low attenuation on CT and are echogenic on US.
Malabsorption
In adults the most common causes of malabsorption are coeliac disease
(non-tropical sprue) and tropical sprue but other specific entities leading
to malabsorption include systemic sclerosis (q.v.), jejunal diverticulosis
(q.v.), Whipple's disease (q.v.), small bowel resections and blind-loop
syndromes. In most cases of malabsorption, when the clinical, bio
chemical and histological diagnosis of sprue is straightforward, radiol
ogy plays little part. Indications for imaging in adult patients with sus
pected coeliac disease, to exclude morphological abnormality, include:
atypical presentation or equivocal small bowel histology; unresponsive
ness to a gluten-free diet or recurrence of symptoms after initial response
(to exclude lymphoma or ulcerative jejuno-ileitis - see below); elderly
patients presenting with recent onset of symptoms; patients with other
disease states such as scleroderma, a history of abdominopelvic radio
therapy, etc. Radiological investigations include small bowel contrast
studies and, in selected patients, CT examination. Findings in adult sprue
on barium studies depend on the method used. If a dedicated per-oral
small bowel meal is performed a "sprue or malabsorption pattern" will
be evident, which is non-specific (Fig. 50). This comprises dilatation,
segmentation and flocculation. The jejunum is moderately dilated and
hypomotile with associated slow transit of barium. Excess fluid in the
lumen leads to segmentation of the barium column into separated clumps
(this sign is not prominent with the use of modem barium suspensions)
and flocculation of barium in severe disease. A mold-like configuration
of barium in the lumen is due to fold effacement (the "moulage" sign).
The valvulae conniventes are of normal thickness unless there is hy-
poalbuminaemia. Transient non-obstructive intussusceptions are seen in
20%. Enteroclysis demonstrates diagnostic signs in 75% o f patients with
969
Figure 50.
Barium "follow-through "in patient
with gluten-enteropathy. The je
junum is mildy dilated with slightly
thickened fo ld s, segmentation and
flocculation o f barium.
adult coeliac disease. The jejunal folds are fewer than normal, three or
less per inch length being highly suggestive of the diagnosis. There may
be jejunization of the ileum, i.e. a greater number of folds per unit length
than normal. Intussusceptions are not seen on enteroclysis. In approxi
mately 10 % a 1-2 mm polygonal mosaic mucosal pattern is seen. Double
contrast studies of the duodenum may show a "bubbly bulb" appearance
and/or Brunner’s gland hyperplasia.
Complications of coeliac disease include ulcerative jejunoileitis, stric
tures, small bowel neoplasms (lymphoma or, less commonly, adenocarci
noma), cavitating mesenteric lymph node syndrome, splenic atrophy and
oesophageal carcinoma. Ulcerative jejunoileitis is a very severe disease
which may present de novo or in patients with a known history of coeliac
disease. Acute symptoms may be due to haemorrhage, obstruction or per
foration. Barium studies, if performed, will show areas of stricturing and
thickened folds and often deep ulceration. This entity is probably part of
the spectrum of small bowel lymphoma. Short strictures, frequently mul
tiple, are seen in the chronic form of the disease. Lymphoma complicat
ing coeliac disease is usually multifocal or diffuse. Differentiation radio
970
logically from ulcerative jejunoileitis may be difficult, and indeed the

two may coexist. CT examination will show any mesenteric nodes, but
the presence of enlarged nodes in coeliac disease is not specific to lym
phoma. CT or ultrasound scanning will also demonstrate the splenic at
rophy that complicates coeliac disease. Cavitating mesenteric lymph
node syndrome is a rare and usually fatal complication. Enlarged mesen
teric nodes undergo cavitation and there is villous and splenic atrophy.
CT scanning will demonstrate the enlarged nodes with diminished cen
tral attenuation; there may be fat/fluid levels within them.
Tumours
A variety of benign tumours occur including adenomas, leiomyomas and
vascular tumours. These are most common in the jejunum, whereas ma
lignant lesions, with the exception of adenocarcinoma, are more com
mon in the ileum. Adenomas may be part of polyposis syndromes but
are less frequent than in the duodenum. Pre-operative diagnosis of ma
lignant small bowel tumours used to be achieved only in the minority of
cases. A combination of enteroclysis and CT scanning can now detect
and suggest the diagnosis in the majority of tumours. Lipomas, leiomy
omas, leiomyosarcomas and carcinoid tumours can give a characteristic
pattern on CT. Adenocarcinoma and lymphoma are more difficult to di
agnose specifically.
Carcinoid tumours
The majority of small bowel carcinoids occur in the distal ileum.
Tumours are considered malignant if there is local invasion or distant
metastases, since differentiation on histological criteria may be difficult.
Lesions larger than 2 cm in size are consistently malignant. Up to 70%
of carcinoid tumours are invasive when discovered. Radiological signs
may be due to the primary lesion, seen as a filling defect or annular le
sion on barium examination, or due to the secondary mass in the mesen
tery which typically provokes a dense desmoplastic response with re
sultant stretching, angulation and kinking of bowel with involvement of
more than one loop, fixation and rigidity. Interference with mesenteric
blood supply may lead to thickening of folds due to arterial ischaemia
or venous oedema. CT scanning is useful in demonstrating the secondary
mesenteric effects and often leads to a definitive diagnosis. Small ill-de-
fined masses in the mesentery exhibit a stellate or spoke-like configura-
971
Figure 51.
Carcinoid tumour. CT
scan showing mesenteric
mass (arrowed) with
stellate stranding caus
ing retraction o f an adja
cent sm all bowel loop in
the right iliac fossa with
resultant small bowel ob
struction (note dilated
loops).
tion with stranding extending out to involve adjacent bowel loops and
frequently exerting a retractile effect on them (Fig. 51). Mesenteric nodal
enlargement and hepatic metastases may be detected.
Small bowel lymphoma

Lymphomas (usually non-Hodgkin's type) consitute about 40% of small
bowel malignancies and most frequently affect the ileum. They may be
primary lesions or part of a disseminated disease. Multifocal abnormal
ities occur in 10-15%. There is a broad spectrum o f radiological ap
pearances; lymphoma is a great mimicker. The following signs (Fig. 52),
or a combination thereof, are seen on small bowel barium studies: nar
rowing of the lumen with mucosal destruction and shallow ulcers; bowel
wall thickening with a normal or dilated lumen; broad-based ulceration
which can lead to large cavitating or excavating extraluminal masses -
these may fistulate; if these cavitating masses appear to be in the line of
the lumen, then they are termed "aneurysmal dilatations"; multiple nod
ules of varying sizes; mesenteric masses; non-specific thickening of mu
cosal folds. Differentiation from other pathologies, particularly Crohn's
disease, may be difficult. Strictures occur in a large number of small
bowel diseases, although they are relatively uncommon in lymphoma.
Nodular changes in lymphoma may simulate the "cobblestoning" seen
in Crohn's disease. The broad-based ulceration in lymphoma may be con
fused with sacculation seen in Crohn's disease. Aneurysmal dilatations
are characteristic of lymphoma, the affected segment being aperistaltic,
thick-walled and containing an amorphous collection of barium. This
972
Figure 52.
Small bowel non-
Hodgkin’s lymphoma. (a)
Enteroclysis examination
demonstrates a segment
o f ileum in the right iliac
fossa with wall thicken
ing, destruction o f the
normal fo ld pattern and
aneurysmal ulceration
(arrowed) and mass ef
fect; (b) CT demonstrates
marked wall thickening
and aneurysmal luminal
dilatation, containing
contrast.
feature may mimic a dilated segment proximal to a stricture due to other

pathologies. A large excavated mass may also be seen in malignant
smooth muscle tumours of the small bowel.
CT scanning is useful, both in the differentiation of small bowel tu
mours and in staging. Lymphomas on CT may appear as large, some
times annular, masses which may be single or multiple, with narrowing
or enlargement of the lumen. Characteristically there is homogeneous
wall thickening (> 2 cm) associated with a normal or enlarged lumen,
i.e. aneurysmal ulceration (Fig. 52). CT will also allow detection of ab
dominal lymphadenopathy and staging of the lesion. Sonography may
demonstrate circumferential wall thickening, with or without an extra
mural mass and mesenteric nodes.
973
Mediterranean lymphoma or alpha-heavy chain disease is associated

with diffuse plasma cell infiltration of the duodenum and jejunum.
Contrast studies demonstrate thickened folds in the proximal small in
testine which may be nodular. Double contrast examinations may reveal
a mosaic pattern of fine granular elevations. These may be seen as "sand
like nodularities" on follow-through type studies, which may also show
a sprue pattern in the ileum. Abdominal lymphadenopathy is visible on
CT or ultrasound examination.
Adenocarcinoma
Small bowel adenocarciomas are most common in the jejunum and usu
ally demonstrate a similar pattern on barium studies to colonic carcino
mas (q.v.) - often a short annular constricting lesion with local destruc
tion o f the mucosal pattern and shouldered margins or, more rarely, a
polypoid intraluminal mass. Enteroclysis is 85% sensitive in diagnosis;
sensitivity is less on follow-through type examinations. CT appearance
is of a soft tissue concentric or eccentric mass with or without mesen
teric nodal enlargement, usually less than that seen in lymphoma. There
is an increased incidence in Coeliac disease, Crohn's disease and Peutz-
Jegher syndrome.
Smooth muscle tumours

Leiomyomas tend to be "dumb-bell" shaped tumours, mainly in the je
junum. Leiomyosarcomas are seen on barium studies or CT as large
masses displacing loops of bowel, often with large excavated contrast-
containing cavities.
Metastatic deposits
Haematogenous
Haematogenous metastases occur to the antimesenteric border of the
bowel. Most commonly the primary tumours are malignant melanoma,
bronchial or breast carcinomas. Melanoma metastases appear on con
trast studies as multiple submucosal polypoid nodules, often with cen
tral umbilication - so called "target lesions". They are more common in
the stomach than the small intestine. Sometimes they may reach a large
size but despite this, obstruction is infrequent. However, lesions may be
come pedunculated and intraluminal with growth and lead to intussus-
974
ception. Ulceration and bleeding are frequent. CT may show the lesions
to be more extensive than is apparent on enteroclysis, although small le
sions will not be seen. A thickened bowel wall may be visualised at CT
which may mimic a primary neoplasm. In addition, a linitis plastica ap
pearance may be evident in the small bowel. Metastases from bronchial
carcinoma may be single or multiple and may exert a desmoplastic ef
fect on the bowel. There is a propensity to localised or (rarely) free per
foration. Breast carcinoma metastases are cellular submucosal masses.
They are relatively rare in the small bowel in comparison to the stomach.
Intraperitoneal seeding
This is more frequent than haematogenous spread. Seeding tends to oc
cur where ascitic fluid accumulates in the peritoneal recesses, such as at
the ileocaecal region, between mesenteric folds and in the pelvis. In con
tradistinction to haematogenous metastases, these lesions are seen on the
mesenteric surface of the bowel. Commoner primary tumours are carci
nomas of the ovary, cervix and colon. As well as seeding, direct spread
of tumour to small bowel can occur from pelvic malignancies. Only those
lesions large enough to cause alteration in the lumen contour and/or
changes in the mucosal pattern can be demonstrated by barium studies.
The mucosal folds are preserved, but there is tethering of the mucosa
which is seen as a "tacked down" appearance in profile, the folds tend
ing to be distorted in a radial pattern extending from a central point out
side the wall formed by the lesion which may be associated with kink
ing, angulation or stricturing of bowel loops. There may be rounded pro
trusions into the lumen. Larger metastases in the peritoneum can involve
several small bowel loops on the mesenteric border. A lateral film with
contrast in pelvic loops is often useful in demonstrating the tethering.
Small peritoneal seedings cannot be seen on contrast study or CT, but
the latter is superior to enteroclysis in showing mesenteric and omental
deposits. Soft tissue masses may be seen separating or displacing loops
and there may be ascites. Pseudomyxoma peritonei from mucin produc
ing ovarian cystadenocarcinomas is recognisable on CT scanning when
there are septations in ascites and cystic masses with solid components,
with or without abdominal lymphadenopathy.
975
Figure 53.
Benign lymphoid hyperplasia o f
distal ileum. Ileocaecal valve is
arrowed.
Kaposi sarcoma
The multiple submucosal, often umbilicated, nodules in this HIV-related
condition are more common in the stomach and duodenum than in the
small bowel. The lesions are discrete and there is preservation of mu
cosal folds between nodules (Fig. 49) (c.f. lymphoma).
Peutz-Jegher syndrome
In this hereditary condition hamartomatous polyps occur in the stomach,
small bowel and colon. These are seen as filling defects of variable size
on contrast studies. There is an association with gastrointestinal carci
nomas as well as other malignant tumours, notably o f pancreas, breast
and reproductive organs. Removal o f polyps is advocated.
Miscellaneous small bowel abnormalities
Benign lymphoid hyperplasia

Small 1-2 mm nodules represent hyperplastic lymphoid follicles, They
are frequently demonstrated on contrast studies of the distal ileum in
young adults and may be regarded as a normal variant (Fig. 53). In older
individuals there is an association with Yersinia and other infections,
Crohn's disease, lymphoma and polyposis syndromes. Diffuse lymphoid
976
Figure 54.
Jejunal diverticulosis on
enteroclysis examination.
Multiple moderate-sized
and large diverticula
present.
hyperplasia is seen in immunodeficient individuals.
Jejunal diverticulosis
These are acquired pseudodiverticula and are seen in middle aged and
elderly patients. Although mostly asymptomatic, a variety of complica
tions do occur. The diverticula tend to be larger and more frequent in the
proximal small intestine. Multiple diverticula may be recognisable on
plain radiography as containing short gas/fluid levels. On barium exam
ination they are seen as multiple barium-containing outpouchings on the
mesenteric surface (Fig. 54). They may be missed on a follow-through
type examination; enteroclysis is more sensitive due to the luminal dis
tension achieved and the opportunity for compression. Small bowel di
verticula are seen in about 2% of enteroclysis examinations. Patients may
present with a malabsorption state or vitamin В 12 deficiency due to bac
terial overgrowth in the diverticular lumen. Rarely diverticulitis may oc
cur which results in haemorrhage or perforation. Strictures or adhesions
from diverticulitis may lead to recurrent bowel obstruction. Other asso
ciations include volvulus, pneumoperitoneum without peritonitis, and a
chronic pseudo-obstruction syndrome due to hypomotility.
977
Figure 55.
Systemic sclerosis com
plicated by adhesive ob
struction. Grossly dilated
proxim al jejunum ex
hibits crowding o f nor
mal thickness folds and
sacculation. Adhesive ob
struction was also pre
sent in the left iliac fossa
related to previous
surgery.
Systemic sclerosis
Gut involvement is very common. The oesophagus, small bowel and
colon may be abnormal. The small bowel is affected in over 40% of
cases. There is vasculitis associated with atrophy o f mucosal and sub
mucosal layers of the wall and replacement of the smooth muscle with
collagen. There is resultant hypomotility; this and the reduced absorp
tive function of the mucosa may lead to a malabsorption state. Barium
examination demonstrates often marked dilatation o f the lumen which
particularly affects the descending duodenum and proximal jejunum.
There is atony with associated delayed transit. Sacculations occur on the
antimesenteric side of the bowel, although this feature is more commonly
seen in the colon. A characteristic sign is a "hide-bound" appearance of
the valvulae conniventes (Fig. 55); in a dilated segment the folds are
packed close together, there being more per unit length of intestine, but
they are of normal uniform thickness.
Meckel's diverticulum
The "rule of twos" is usually quoted, that is that Meckel's diverticulum
occurs in 2% of the population, 2 feet from the ileocaecal valve and is
978
Figure 56.
Meckel's
diverticulum
(arrowed)
demonstrated
on enteroclysis
in a young
patient with
recurrent
melaena.
usually 2 inches long. In fact, the site and dimensions are somewhat vari
able. O f those individuals with this congenital abnormality approxi
mately 20-40% will develop symptoms, most commonly melaena.
Ectopic gastric mucosa, which is mainly responsible for the propensity
to bleed, occurs in 20% of all diverticula, but in about 70% of those that
bleed in adults and a higher percentage in children. No single imaging
method is entirely reliable at detecting Meckel's diverticula. Nuclear
medicine studies are valuable; technetium pertechnetate is given intra
venously and is taken up by normal and heterotopic gastric mucosa. The
diverticulum is seen as focal uptake, usually in the right lower quadrant
of the abdomen. In patients who have bled the test has an approximate
sensitivity of 85% for detection overall, but only 60-70% in adults. If
there is active bleeding Tc-colloid may detect the region of extravasa
tion. Small bowel barium meal is unreliable in the detection of Meckel's
diverticulum since peristalsis tends to empty the lumen of the lesion
which fills only transiently. Enteroclysis is more sensitive due to the
greater luminal distension achieved and ability for compression under
careful fluoroscopy (Fig. 56). Recognition depends on finding a blind-
ending sac on the anti-mesenteric side of the ileum which occasionally
contains a gastric rugal pattern. A typical triradiate fold pattern is de
scribed at the base of the lesion due to folds occurring at right angles to
those in the ileum. Even if there is no filling of the lumen of the lesion,
a large diverticulum may be recognised by its mass effects on the neigh
bouring loops.
979
A characteristic finding on angiography is described in Meckel's di

verticulum. There is persistence o f a separate vitelline artery to the di
verticulum arising from the distal ileal artery, often terminating in a group
of tortuous vessels. Angiography performed during an episode of bleedig
may, o f course, show extravasation of contrast at the diverticulum.
Other complications of Meckel’s diverticulum besides bleeding in
clude diverticulitis, volvulus and intussusception.
Small bowel obstruction - the role o f radiology

The plain radiographic findings in acute small bowel obstruction (SBO)
are discussed in the section on the Acute Abdomen. When clinical fea
tures and plain abdominal radiographs show high-grade SBO, patients
are either subjected to early surgery or given a trial of conservative ther
apy. Arguably, no further imaging is required. If further radiological
studies are needed in patients undergoing initial conservative manage
ment, CT scanning has advantages over enteroclysis (which is the alter
native study). In high-grade obstruction CT can confirm or refute ob
struction (versus pseudo-obstruction), can define the approximate level
of obstruction and may determine the cause. Adhesive obstruction is usu
ally a diagnosis of exclusion of other causes, particularly the failure to
show a mass lesion at the point of transition of proximal dilated to col
lapsed distal bowel. CT is potentially of particular use in patients with
SBO who do not have previous risk factors for adhesions; in these cir
cumstances CT is of clinical relevance in showing the cause of obstruc
tion. Such demonstrable causes include internal or external hernias, in
flammatory disease, such as appendiceal or diverticular abscess or tu
mours. Even in patients with likely adhesive obstruction it may be argued
that CT is useful in excluding other causes and complicating factors, such
as volvulus, closed-loop obstruction or strangulation which will neces
sitate early surgical intervention. Intravenous contrast enhancement
should be used and this facilitates determination of strangulation due to
vascular compromise. The CT signs of bowel ischaemia are described
later. Enteroclysis is accurate in diagnosing obstruction, determining the
level and grade and sometimes demonstrating the cause. However, there
are disadvantages of enteroclysis in high-grade SBO: surgeons do not
like barium in the bowel when they operate; examination is time-con
suming when there is hypoperistalsis in long-standing obstruction; dilu
tion of the barium by the time it reaches the point of obstruction often
980
makes the examination non-diagnostic, particularly when loops of di

lated barium-containing bowel overly this point.
In the case of lower grade or subacute or intermittent obstruction, the
role of CT is still evolving. Consensus suggests that enteroclysis in these
situations is still the examination of choice. The overdistension of the
bowel during this study allows recognition of subtle strictures and lo
calisation of adhesions. Particular indications for small bowel barium
study include :
i) inconclusive plain film findings; ii) when there is an underlying or pre
vious significant clinical problem such as a history of surgery for ma
lignancy or radiotherapy, i.e. there are several potential causes for ob
struction - simple adhesions, metastases or local tumour recurrence, ra
diation enteritis - which are demonstrable by enteroclysis; iii) to help
determine the suitability of continued conservative management or to
confirm adhesions in those patients who may not require surgery and, iv)
to determine the cause in patients with intermittent low-grade obstruc
tion during an asymptomatic phase.
In some patients with no relevant past history in whom an acute dis
tal SBO is suspected on plain film criteria, it is appropriate to perform a
single contrast retrograde enema to exclude a caecal mass lesion.
Small bowel adhesions

Enteroclysis is the examination of choice due to the ability of this tech
nique to maximally distend individual loops and allow compression un
der fluroscopy (Fig. 57). A delayed film at 18 to 36 hours may be useful
when transit is slow, since it may be easier to visualise the point of ob
struction free of overlapping loops of barium-containing bowel. Several
patterns of adhesions can be seen. Single band adhesion is most com
monly associated with high-grade obstruction; there is loop fixation at
the site of obstruction where there is a sudden cut-off, dilated bowel with
normal folds being present to this point. This appearance may be con
fused with metastatic disease. Lower grade obstruction due to a single
band is seen as abrupt narrowing with collapsed or normal bowel dis-
tally separated from the proximal dilated loops by a short compressed
segment where the folds are retained but crowded or flattened. Multiple
band adhesion is demonstrated as luminal narrowings over a relatively
short length of bowel. Fixity of loops and adherence to the abdominal
wall may be apparent. Normal folds are present. Extensive adhesions
981
Figure 57.
Multiple band adhesions o f small
bowel in left iliac fossa causing re
traction, tenting andfixation o f sev
eral adjacent loops.
manifest as fixation of longer segments of bowel to the abdominal wall

and involvement of adjacent loops. Fixation often occurs to posterior
wall structures. There is deformity and displacement of bowel and re
stricted distensibility, such that a mesenteric mass may be simulated in
massive adhesions. Tenting adhesions are described when there are mul
tiple scattered lesions causing fixation between loops or the abdominal
wall which do not cross the lumen but cause tenting or retraction of one
wall of the bowel.
The diagnosis of adhesive obstruction on CT examination is essentially
one of exclusion of other pathologies, although clues such as tethering or
angulation of loops and mesenteric bands may be apparent. CT is useful
in acute high-grade obstruction for the reasons stated previously.
982
Figure 58.
Acute small bowel ischaemia.
Small bowel barium study
shows partial functional
obstruction, proxim al to
diffuse spastic narrowing o f
ileum with thickened folds and
thick walls. There is a "picket
fence”pattern in places
(arrowed). c=colon.
Figure 59.
Small bowel ischaemia. Same
patient as Fig. 58. CT after in
travenous contrast. Note "tar
get”sign in thickened ileal
loops in right iliac fossa (ar
rowed), oedema in adjacent
mesentery and fluid filled ob
structed bowel to left o f mid
line. Bowel had returned to
normal a fe w weeks later on
follow up contrast study (pa
tient then asymptomatic).
Vascular disease
Acute ischaemia
Acute arterial ischaemia of the small intestine is due to relatively large
vessel thrombo-embolic occlusion or (more commonly in most reported
series) is non-occlusive in origin. The latter is related to low-flow states
as in shock, congestive heart failure, etc. In occlusive ischaemia, plain
radiographs are often disappointing: focal dilatation, wall thickening,
"thumbprinting" or a "gasless" abdomen may be evident. In more ad
vanced disease when infarction has taken place, intramural gas and/or
portal vein gas may be seen. There is rarely an indication for barium stud
ies, but these will show local spasm, submucosal haemorrhage or oedema
(manifest as a "picket-fence" pattern of thickened and rigid mucosal
folds) or "thumbprinting" (Fig. 58). In reversible ischaemia improvement
983
may be seen on follow-up studies with or without the development of an

ischaemic stricture. CT scanning with intravenous contrast bolus en
hancement is the procedure of choice in the acute phase. Findings in
clude possible demonstration of the intravascular thromboembolus in,
for example, the superior mesenteric artery (SMA). Features of bowel
ischaemia on CT are often non-specific, but in the correct clinical con
text are highly suggestive. These include concentric wall thickening ex
ceeding 3 mm, which may be of high attenuation (presumably due to
haemorhage), or a region of intramural low attenuation - the "target sign"
of contrast-enhanced inner and outer layers of the wall sandwiching a
thickened low-attenuation submucosa (Fig. 59). More specific signs, in
dicating bowel infarction, include intramural gas (for which CT is highly
sensitive, but images may have to be scrutinized on wide windows) and
portal vein gas. Angiography in occlusive ischaemia will demonstrate
the obstructed vessel, and will also provide opportunities for radiologi
cal intervention.
In non-occlusive ischaemia arteriography will not demonstrate main
vessel obstruction, but there will be diffuse splanchnic spasm, with gen
eralised narrowing of SMA branches, slow flow and poor distal filling
with or without vessel beading. Intra-arterial vasodilators may be bene
ficial.
Focal ischaemia of small bowel occurs in strangulation due to hernias,
adhesive bands, volvulus, trauma or vasculitis. Segmental changes in the
bowel wall are seen as described above on CT, which may also enable
the cause to be determined when there is a mechanical reason for stran
gulation.
Acute mesenteric venous thrombosis affecting the superior mesenteric
vein may be idiopathic, related to intra-abdominal sepsis (e.g. appen
dicitis, diverticulitis), trauma or surgery, portal hypertension or a hy
percoagulability state. Plan abdominal radiographs may show segments
of bowel with thickened folds or "thumbprinting". Contrast-enhanced
CT is very useful (Fig. 60) and will often show thrombus within the vein,
mesenteric oedema and ascitic fluid. Venous ischaemia will produce
bowel wall signs on CT, as described above.
Chronic ischaemia
Occlusive arterial disease rarely will cause chronic ischaemia of the
bowel with symptoms of diarrhoea, malabsorption or mesenteric
984
Figure 60.
Venous infarction o f
bowel due to idiopathic
superior mesenteric vein
thrombosis. CT scan (af
ter IV contrast) demon
strates thrombus in su
perior mesenteric vein
(curved arrow) and
thickened loops o f small
intestine ("target sign ",
arrowed) consistent with
but not specific to is
chaemic bowel. Long
segment o f infarcted
ileum resected at la
parotomy.
’’angina”. Two of the three major mesenteric arteries must be signifi

cantly (> 50%) stenosed for symptoms to occur. Aortography is the de
finitive examination, specifically with lateral projection to show the ori
gins of the mesenteric arteries. However, duplex Doppler US and colour
Doppler imaging (CDI) are evolving as useful screening examinations
for this condition. Although sometimes limited by overlying bowel gas
and difficulty in imaging the inferior mesenteric artery, nevertheless a
normal study makes the diagnosis of mesenteric ischaemia very unlikely.
The patient is fasted for 12 hours and a Doppler survey performed of the
imaged coeliac axis (CA) and SMA to pick up local flow abnormalities.
This is considerably easier with CDI. Doppler abnormalities are docu
mented as changes in waveform, velocity, or flow direction and increased
turbulence indicating stenosis. It is fortuitous that most significant
stenoses occur in the proximal segment of the vessels. The normal wave
form in the proximal CA is a high resistance pattern with little diastolic
flow. More distally the waveform becomes a low-resistance one with
continuous diastolic flow. The SMA normally demonstrates turbulent
flow at its origin. In the fasting state there is a high resistance pattern
with minimal diastolic flow. Post-prandially there is a low resistance pat
tern with broadened systolic peaks, increased systolic and diastolic ve
locities and continuous diastolic flow. In the presene of significant steno
sis in the fasting patient there is increased maximal systolic velocity
through the area of narrowing with spectral broadening and post-stenotic
turbulence and a relatively prominent diastolic forward flow. A high ve
985
locity jet is seen on CDI. Most workers give a standard test meal and re
peat the examination after about 45 minutes, since in some patients fast
ing flow is normal and a provocation test is therefore needed. In the pres
ence o f significant stenosis the normal post-prandial change seen in the
SMA is lacking. The flow characteristics in the CA do not change sig
nificantly even in normal individuals.
Chronic radiation enteropathy

The chronic changes due to radiotherapy are related to endarteritis oblit
erans. Symptoms may develop many years after the treatment or, in some
patients, proceed without obvious pause from the acute radiation-induced
bowel symptoms commonly present during and immediately following
treatment. Most commonly treatment has been for cervical or ovarian
carcinoma. Enteroclysis is the examination of choice, although CT will
demonstrate the relatively non-specific changes of wall and mesenteric
thickening and loop fixation usually in the pelvic loops of bowel. The
signs on enteroclysis include, fold thickening, often o f the "picket-fence"
pattern indicating submucosal disease, mural thickening, mucosal "tack
ing" and angulation due to adhesions, stenoses (single or multiple), si
nuses and fistulae, and segments of bowel which demonstrate effacement
of their mucosal pattern. Hypoperistaltic segments which may be dilated
and lack mucosal folds may be seen as "pools of barium".
LARGE BOWEL
Imaging techniques
Plain radiography is useful mainly in acute disease such as obstruction,
ischaemic colitis or acute inflammatory colitis (see below). In chronic
disease it is of limited use; the extent of faecal residue may be approxi
mately assessed in patients with constipation. The double contrast bar
ium enema (DCBE) is now the contrast examination o f choice in most
patients with suspected large bowel pathology. The single contrast en
ema is undertaken if the DCBE cannot be performed or in an unprepared
colon if there is suspected large bowel obstruction or leak, in which lat
ter case a water-soluble contrast should be used. The DCBE has ben
shown to be superior to the single contrast technique in the detection of
small polyps and subtle mucosal disease. The single contrast barium en
ema may be used in the very old, disabled or ill patient where moblity is
986
limited and to exclude obstruction. Some authors advocate a biphasic

technique, a limited single contrast study of the sigmoid being performed
after the double-contrast examination. This is effective where there is di
verticular disease which may obscure polyps on the double-contrast
study.
For routine studies, single or double contrast, colon cleansing is es
sential. A variety of regimens is available, some of which require a
preparatory period of low-residue diet and then clear fluids. Laxatives
are then given which are often a combination of magnesium citrate and
Bisacodyl tablets, followed by suppositories. Colonic cleansing enemas
may be given, but an interval of at least 45-60 minutes is required before
the examination can be performed. Several regimes, for example sodium
picosulphate or oral colonic lavage solution, dispense with the need for
strict low-residue diets and cleansing enemas.
Barium is introduced via a rectal tube. Balloon retention catheters
should be avoided, as most complications of barium enema - perfora
tion of the rectum or more proximally - have occurred in assocation with
their use. If a balloon catheter is used, as when there is laxity of the anal
sphincter, this should be inflated under fluoroscopy using a low-capac
ity bulb with a valve. The bariums used for DCBE are of high density.
Low density, dilute barium should be used for the single contrast barium
studies. Ionic water soluble contrast is used when there is suspected per
foration or in obstruction when the patient is expected to be operated
upon soon after the study. Contra-indications to DCBE include obstruc
tion (use single contrast), potential technical difficulties (such as immo
bility, etc), severe inflammatory bowel disease, acute diverticulitis (use
water-soluble contrast or, preferably, CT scanning) and deep biopsy
within the last 6-7 days (superficial mucosal biopsy is not a contraindi
cation). Contraindications to single contrast barium enema include acute
severe colitis, suspected perforation (use water-soluble contrast) and re
cent deep biopsy.
Many different techniques have been described for the performance
of the DCBE. Some are complicated and depend upon the configuration
of the sigmoid loops seen during the examination. Other are simple stan
dardised methods which work in the great majority of patients. There is
an increasing tendency to use carbon dioxide instead of room air for in
sufflation since, because of its more rapid absorption from the bowel, it
causes less post-procedure discomfort. A pressure limiting system is re-
987
Figure 61.
Detail o f double
contrast examina
tion o f sigmoid
colon showing typi
cal innominate
groove pattern in
proximal loop (open
arrows) andfine
granularity o f ac
tive ulcerative coli
tis (solid arrows).
quired to give carbon dioxide; it must not be administered directly from

high pressure cylinders. Views of the large bowel taken during the DCBE
are designed to show all parts of the bowel in double contrast. Optimal
positioning for spot films is determined by fluoroscopy.
Thin grooves may be seen in profile on DCBE in the normal colon,
known as innominate lines; these are a feature of the normal mucosal
pattern but are not seen as frequently as the areae gastricae in the stom
ach. It is important to distinguish them from the granular pattern of fine
mucosal ulceration (Fig. 61). Most errors in DCBE are perceptive; mul
tiple readings by more than one radiologist significantly increase lesion
detection rate.
As in small bowel disease, transabdominal ultrasound may be useful
in the delineation of extramural disease such as paracolic abscess but its
application is limited by bowel gas. Some authors have used transab
dominal colonic sonography for the detection of neoplasms, using
colonic water enemas, but the role o f this technique is yet to be defined.
Endoluminal ultrasound is of limited availability but appears to be ac
curate in the staging of colorectal neoplasms in a similar way to upper
gastrointestinal cancer staging with endoscopic ultrasound.
CT scanning is still the method of choice in most centres for the imaing
of extramural colorectal disease. Major applications include the staging
of neoplasms and the assessment o f paracolic inflammation and ab
scesses in inflammatory bowel disease and diverticulitis. There are lim
itations to CT; bowel wall thickening is largely non-specific and in neo
plastic disease the depth of intramural invasion cannot be determined;
the demonstration of enlarged lymph nodes is also non-specific and
metastatic disease may occur in normal-sized nodes. The technique for
CT scanning in large bowel disease must include adequate oral contrast
988
administration to allow good luminal distension and opacification. Bowel

cleansing preparation may be required for imaging primary colonic dis
ease. A dose of dilute oral contrast should be given, if possible, several
hours before the examination - the evening before, if the study is sched
uled for the morning - or else a hurrying agent such as Sorbitol or
Maxolon may be added to the oral contrast. In selected patients 200-300
ml of dilute contrast may be administered by rectal catheter to opacify
the distal colon and rectum. An alternative is to insufflate the rectum with
air which provides good luminal distension and contrast. In most cases
intravenous contrast should be given to outline vascular structures and
the urinary tract. Dynamic intravenous bolus contrast techniques are used
to image gastrointestinal lesions, if possible, during the arterial en
hancement phase, since the presence, degree and pattern o f enhancement
are important parameters used in diagnosis. Dynamic techniques are also
used for detection of liver metastases in colorectal cancer staging. It may
be desirable to acquire extra scans in decubitus or prone positions, de
pending on the site of the lesion, to image subtle abnormality, and to ob
tain extra thin sections through an area of interest for better resolution.
The use of fast scanning techniques in MR imaging and the develop
ment of intraluminal contrast agents are likely to lead to wider applica
tion of this modality in large bowel disease. There is evidence of MR’s
utility in detecting fistulae and abscesses in inflammatory bowel disease.
MR suffers from the same limitations as CT in relation to bowel wall
disease. There is little advantage of MR over CT for staging colonic car
cinoma, but it does appear to be superior in invasive rectal carcinoma
staging and in the diagnosis of presacral recurrent tumour following ab-
domino-perineal resection.
Pathology
Diverticular disease
Colonic diverticula are of the acquired pulsion type. In Western societies
they are present in 30-50% of the population over the age of 50 years.
Divertiula are seen predominantly in the sigmoid and distal descending
colon and occur laterally between the mesenteric and antimesenteric tae
nia or sometimes in the antimesenteric inter-taenial area, in which posi
tion they are often small or intramural. In 10% they are seen in the right
side of the colon only, and in 17 % they are scattered throughout the colon.
989
Figure 62. Views o f a sigmoid colon diverticulum on double contrast bar

ium enema. Note in (a) the diverticulum is seen en face; it is empty o f bar
ium, the resultant ring shadow having an outer well defined rim and an in
ner rim that 'fades away”. The mouth o f the diverticulm is seen in the centre
o f the ring giving a "Mexican hat" sign. In (b) the diverticulum is seen
obliquely and protrudes beyond the lumen proving the nature o f the lesion.
The term "diverticulosis" is often used for multiple diverticula in asymp

tomatic individuals; "diverticular disease" is used when there are symp
toms and "diverticulitis" when there is associated inflammation. "Pre-di-
verticular disease" is sometimes employed to denote the appearance of
thickened circular folds in the sigmoid colon and a spikey irregular out
line along the antimesenteric ridge, changes assumed to represent the
early phase of diverticular disease. When a large number o f diverticula
are present in the sigmoid colon, often with spasm and overlapping loops,
it is easy to miss co-existing polypoid lesions. Indeed, this area is one of
the weak points of the barium enema examination. Some authors advo
cate a biphasic examination, following the double-contrast study with a
limited single contrast one with compression of the sigmoid colon, to
demonstrate small polyps as filling defects within the dilute barium. The
appearance of diverticula on barium enema depends on the angle from
which they are viewed, the degree of filling with barium and/or air, and
whether there are retained faceoliths within them. En face they are seen
as rounded collections of barium of variable size, or to contain an air/bar
ium level on decubitus or erect views, or as a ring shadow if they are
empty of barium. When viewed in profile or obliquely, diverticula ap
pear as barium-coated or barium-filled outpouchings (Figs. 62, 63).
990
Figure 63.
Double contrast barium enema
showing left sided diverticula,
some appearing as ring shadows,
others as barium filled outpouch
ings. In addition there is a peri
colic inflammatory mass causing
impression on the medial aspect
o f the sigmoid (arrowed).
Diverticulitis
Acute diverticulitis typically presents with left iliac fossa pain, with or
without a palpable mass, fever and leucocytosis. There is an increasing
tendency to investigate these patients radiologically with CT scanning,
though some authors maintain that there is a continued place for water-
soluble contrast enema, particularly if the CT is equivocal. CT has many
advantages: as well as being more comfortable for the patient, it is able
to confirm the presence of diverticula and the site of disease, demonstrate
peri-colic inflammation - assess abscess formation and help plan man
agement, whether it be medical or, in the case of abscess, surgical or per
cutaneous drainage. As well as showing even small paracolic fluid col
lections, other CT signs include wall thickening and peridiverticular in
flammatory infiltrate into the surrounding fat (Fig. 64). If CT is
unavailable, ultrasound is often able to show pericolic abscess, but suf
fers from the usual limitations of US in the presence of bowel gas. If con
servative management is undertaken, it is reasonable to perform a de
layed double-contrast barium enema when the patient has recovered, to
assess the extent of diverticular diseasee and any co-existing pathology,
since the CT appearance of wall thickening is non-specific and CT can-
991
Figure 64.
Acute diverticulitis, (a) CT scan showing sigmoid loop with marked mural thickening
and pericolic inflammation. A row o f diverticula are interconnected by linear inflamma
tory stranding (arrowed), (b) Another case. Double contrast enema showing impression
from pericolic abscess (arrowed). Gas is present in the adjacent pericolic gutter
(curved arrow), (c) Same patient as (b). Small pericolic abscess with inflammatory infil
trate into pericolic fa t and thickening o f anterior pararenal and lateroconal fascia.
not exclude colonic neoplasm.

If a contrast enema is performed during the acute attack, water-solu-
ble contrast should be used and introduced with care. If a significant leak
is present this will be seen as extravasation, contrast usually tracking par
allel to the bowel wall and sometimes forming interconnections with a
number of diverticula (see Fig. 64 a). Deformed distended diverticular
sacs may suggest microperforation. Mucosal changes that are seen in
clude the "drape sign" - the bending o f adjacent diverticula around a pre
sumed pericolic abscess and multiple crowded transverse pleat-like folds
which may be deformed into a crumpled pattern. Other signs of pericolic
inflammation include a soft tissue mass which may cause impression,
992
compression or displacement of the adjacent lumen (Figs. 63, 64), and

may have visible gas within it. Occasionally, contrast extravasates into
a definite cavity. A pattern of small bowel obstruction may be apparent
on plain radiographs or CT, due to loops of bowel adherent to an in
flammatory mass.
Other complications o f diverticular disease

Diverticulitis may cause large bowel obstruction due to a pericolic in
flammatory mass and associated narrowing and spasm. It is often very dif
ficult on contrast enema to distinguish this from neoplastic obstruction.
The strictures caused by carcinomas tend to be shouldered and associated
with destruction of mucosal folds. Acute haemorrhage from diverticulitis
may be a massive affair and is not uncommon. Contrast studies are not in
dicated. The patient will usually undergo endoscopy. If bleeding contin
ues and the source of bleeding remains in doubt or there is an indication
for non-operative intervention, then angiography is undertaken. This may
be preceded by a nuclear medicine blood pool scan. Diverticular disease
is not regarded as a cause of anaemia by occult bleeding.
Other complications of diverticulitis include spread of inflammation,
resulting in fistula formation to the urinary or genital tract or retroperi
toneal spread to the perirenal space or inferiorly to the buttock or groin
through the sacrosciatic foramen. Free perforation into the peritoneal
cavity is rare. Distant spread of infection can occur leading to portal
pyaemia and/or hepatic abscess.
Polyps versus diverticula

A frequent problem on double contrast barium enema is to distinguish
the ring shadows of polyps and diverticula (Fig. 62). A polyp will ap
pear intraluminal on all views; within the barium pool it will be seen as
a filling defect; a stalk may be present which may be seen in long or
oblique axis, or present a "Mexican-hat sign” when the stalk is seen en
face through the head of the polyp (Fig. 65). Ring shadows due to polyps
typically have an inner rim which is well-defined and an outer rim which
tends to fade away, in contradistinction to the ring shadows formed by
diverticula, which demonstrate the reverse pattern. Diverticula are usu
ally seen on at least one view as extraluminal when imaged obliquely or
tangentially, or to contain barium and/or air. The "bowler-hat" sign is a
feature of both polyps and diverticula and is due to the base o f the lesion
993
Figure 65.
View o f sigmoid/descending
colon junction showing con
stricting carcinoma (open ar
row) and "sentinel”polyp in
barium pool (solid arrows).
Note the "Mexican hat" sign
related to the latter.
being seen tangentially. However, if the "hat" always points towards the
centre of the long axis of the bowel the lesion should be intraluminal, i.e.
a polyp. This rule is useful unless the lesion lies in the midline of the
bowel or is parallel to its long axis.
Inflammatory diseases
Of the non-infective causes of inflammatory bowel disease (IBD) to af
fect the large intestine, ulcerative colitis (UC) and Crohn’s disease (CD)
are by far the commonest.In the patient with acute symptoms, the plain
radiograph may be useful. In UC, the extent of disease can sometimes
be ascertained by the distribution of faecal residue; residue is not seen
in that part of the bowel where there is active inflammation. However,
this sign is not helpful if the colon happens to be empty of faeces nor in
CD where there are often "skip" lesions. The extent and severity of the
disease may be apparent from the visualised mucosal fold pattern.
Mucosal pseudopolyposis, submucosal oedema ("thumbprinting") and
wall thickening may be seen where luminal air provides adequate radi
ographic contrast. In severe colitis, actual or impending toxic megacolon
may be evident.
Most patients with IBD can be examined by DCBE, but the bowel
preparation should be modified in patients with acute symptoms or se
994
vere diarrhoea. Contraindications to the double contrast examination in

clude severe acute colitis, and contraindications to any contrast enema
study include toxic dilatation and perforation. Some authors advocate an
’’instant-enema" in patients with acute colitis to assess the extent and
severity of the disease and to monitor progress with treatment. It is help
ful in UC where inflammation starts in the rectum and extends proxi-
mally in a contiguous fashion, but is of less use in CD. However, with
the increased availability of flexible endoscopy, the ’’instant enema” is
not commonly required. It may be of use if endoscopy is unable to reach
the proximal extent of the inflammation. The technique is performed on
an unprepared colon. Barium is run in to the splenic flexure or until fae
cal residue is encountered (if this is more distal) - in UC there is unlikely
to be active disease where there is faceal residue. The rectum is then
drained and air (or preferably carbon dioxide) is carefully introduced to
produce gentle distension. A short-acting hypotonic agent may be given.
Other modalities that are employed in the investigation of IBD include
radionuclide-labelled white cell scaning to assess activity and severity
of disease, and US or CT imaging for extramural complications, such as
abscesses and fistulae. US is hindered by the presence of bowel gas. CT
should be regarded as complementary to barium studies. It has limita
tions in milder degrees of UC where the disease affects the mucosa only,
but in more severe UC and other colitides, CT will demonstrate thick
ened bowel wall, in a distribution corresponding to the type of colitis,
and may show transmural ulcers and pericolic inflammation or abscesses.
Regarding MR scanning, see previous comments under ’’Inflammatory
bowel disease” in the section small intestine.
Ulcerative colitis
This disease is characterised by episodes of exacerbation and remission.
The rectum is virtually always involved, with a variable but contiguous
extent of the colon being affected proximally. The main categories of in
volvement are: proctitis, distal (or left-sided) colitis and so-called ’’ex
tensive” colitis. The latter term is used to denote disease radiographically
extending as far proximally as the hepatic flexure. In practice this almost
always means that the whole colon is involved. The earliest sign of UC
on DCBE is a finely granular mucosal pattern which is uniform and con
fluent. Progression is manifest as superficial erosions which give a stip
pled appearance to the mucosa (Fig. 61). As these heal a coarsely gran-
995
Figure 66.
Double contrast enema showing left
sided ulcerative colitis. Deep "collar
stud” ulcers are present on a back
ground o f abnormal mucosa.
ular appearance is seen. More

severe disease leads to deeper
ulceration, with "collar-stud"
ulcers which are due to under
mining of the mucosa and ap
pear as linear and parallel to the
long axis of the bowel (Fig. 66).
If these are long they produce a
double-track appearance to the
wall. These changes are seen on
a background of diffuse granu
larity (cf. Crohn's disease).
Extensive acute ulceration re
sults in islands of relatively in
tact mucosa between ulcers.
This intact and usually hyper-
plasic, oedematous mucosa ap
pears polyp-like on contrast
studies (and often on plain
films) - so called pseudopoly
posis. Inflammatory polyps are
seen due to masses of granula
tion tissue. The haustrations of the colon are blunted and thickened, but
become effaced when ulceration is present. (It should be noted that haus
trations are often normally absent from the left hemi-colon.) In the rec
tum, the mucosal changes described above are seen and there is thick
ening of the rectal folds. Apparent relative sparing of the rectum may be
seen in patients receiving topical steroid enema treatment.
In longstanding chronically active UC there is loss of haustral folds
and the whole affected colon becomes narrowed, shortened and feature
less ("pipe-stern" colon; Fig. 67). The rectal folds are effaced and there
996
Figure 67.
Chronic ulcerative colitis. The left
hemicolon is diffusely mildly nar
rowed and has lost haustral mark
ings. The filling defect in the
splenic flexure region was artefac-
tual.
is widening of the post-rectal space. The rectum is narrowed and conse

quently of low capacity. In total colitis "backwash ileitis" may be pre
sent manifest as dilatation, hypomotility and granularity o f the distal
ileum and incompetence of the ileocaecal valve (Fig. 45).
Intestinal complications o f ulcerative colitis

In the acute attack, plain abdominal films should be obtained. The mu-
socal edge pattern and the distribution of faceal residue should be ob
served. Sometimes an exacerbation of symptoms is associated with im
paction of faeces proximal to active colitis. A "gasless" abdomen often
points to an extensive active colitis. Dilatation of the colon, most com
monly involving the transverse colon, but affecting any segment of the
large bowel,may signifiy toxic megacolon. This is a diagnosis made on
a combination of clinical and plain radiographic criteria. The latter in
clude the presence of dilatation to a calibre of 8 cm, mucosal islands and
thumbprinting, usually associated with evidence of a small bowel ileus.
If this progresses, intramural gas followed by local or free perforation
may be apparent. When dilatation extends to 5 cm, then the patient should
be regarded at high risk for developing toxic dilatation, and frequent
monitoring with plain abdominal radiographs is called for.
997
Figure 68.
Chronic total ulcerative colitis
complicated by carcinoma. There
is an annular carcinoma o f the as
cending colon (open arrow), su
perimposed on changes o f chronic
colitis - shortened, narrowed
colon lacking haustrae. Plaque
like areas o f dysplasia were also
evident (solid arrows in sigmoid
colon; these reproduce poorly in
the illustration).
The complications of long-standing UC include benign strictures and

colonic malignancies. Benign strictures occur mostly in the sigmoid
colon and are symmetrically tapered with a uniform mucosal texture.
However, endoscopic biopsies are usually required to exclude malig
nancy and dysplastic changes. There is a significantly increased risk of
colonic neoplasm in UC; this is particularly so in patients with total col
itis of greater than 10 years duration. The presence of dysplastic mucosal
changes is associated with a high risk. Neoplasms are evenly distributed
in the large bowel and tend to be annular (Fig. 68), although scirrhous
growths are also seen. Synchronous neoplasms are relatively common.
Dysplasia can occasionally be recognised radiographically when it gives
rise to elevated plaques which appear as a nodular polygonal pattern on
double contrast views. However, radiology is insensitive in detecting
dysplasia, and monitoring of at-risk patients should be by serial colono
scopies.
An interesting and characteristic appearance may be seen on DCBE,
following healing of a severe colitis, which is usually due to UC but may
be seen with other inflamatory colitides. As ulceration heals, the hyper-
998
Figure 69.
Post inflammatory filiform
polyps in a patient with a his
tory o f previous acute colitis,
plastic mucosal islands between the ulcers undergo further hyperplasia

and may give rise to branching mucosal tags of various configurations -
often Y or V or inverted U shapes - leading to post-inflammatory fili
form ("worm-shaped") polyposis (Fig. 69).
Crohn's (granulomatous) colitis

Crohn's disease is a chronic disorder with acute exacerbations. The trans
mural nature of the abnormality explains the propensity for sinus, fistula
and stricture formation. Approximately 15% of patients with this dis
ease have colonic involvement only. The small bowel only is affected in
30%, and ileocolic involvement is present in 55%. Early changes of
Crohn's disease in the colon are similar to those previously described in
the small bowel. Discrete aphthoid ulcers may be demonstrated on DCBE
surrounded by normal mucosa (Fig. 70). The differential diagnosis of
this appearance includes Yersinia, Amoebic, CMV and other infective
colitides, Behcet's disease and ischaemic colitis. The accompanying sub
mucosal oedema is less prominent than seen in small bowel Crohn's dis
ease and the haustral pattern and mucosal folds may therefore be nor
mal. Occasionally, a granular mucosa may be seen as in UC. A subgroup
999
Figure 70.
Crohn's colitis, overview o f
colon. There are discontinuous
changes with severe involve
ment o f transverse colon (cob-
blestoning and ulceration) and
mild sigmoid disease (aphthoid
ulcers on a background o f nor
mal mucosa). Note also the ter
minal ileal stricture.
of colitis occurs in which it is impossible to distinguish, on radiographic

criteria, UC and Crohn’s disease. In some of these the distinction may
also be impossible on endoscopic and histological grounds.
More advanced disease is characterised by discontinuous, asymmet
rical changes (Fig. 70). This asymmetry is seen as involvement of one
wall with ulceration during the active phase, and, later, by sacculation
as fibrosis causes shortening of one wall and redundancy o f the opposite
wall. Large ulcers which may be of ’’collar-stud" type may be seen, as in
UC, but unlike UC the intervening mucosa tends to be normal and not
granular. Serpiginous longitudinal and transverse ulcers, with or with
out cobblestoning, strictures, fistulae and sinuses are seen as in small
bowel Crohn’s disease. Abscesses may be imaged by ultrasound, CT or
MR scanning. MR appears useful in delineation of peri-anal fistulae and
abscesses. Rectal involvement occurs in 50% of patients with colonic
disease. Inflammatory polyps and pseudopolyposis are seen as in UC.
Regression of acute changes often leads to scarring in colonic Crohn’s
disease, unlike UC which may heal to a virtually normal appearance.
Comparative features of large bowel Crohn's disease and ulcerative col
itis are summarised in Table 8.
1000
Table 8. Features o f colonic Crohn's disease & ulcerative colitis
UC CROHN'S
Rectum involved always approx. 50 %

Extent variable, proctitis to total variable
Ileum occ backwash ileitis w ith com m only involved
total UC
C ontiguity contiguous disease "skip" lesions
Background granular normal m ucosal pattern
Ulceration collar-stud on granular tend to deeper ulcers on normal
background background
Sinuses/fistulae rare common
Strictures uncommon common
Malignancy increased slightly increased
Infectious diseases
Entamoeba Histolytica
This is dealt with in the chapter on "Tropical disease".
Other infective colitides

In most patients with acute colonic infections a plain abdominal radi
ograph is the ony radiological examination performed. This may give an
indication of the extent and severity of disease and will show the devel
opment of toxic dilatation, which can occur with most o f the acute in
fections.
Shigella dysentery produces discrete aphthoid ulcers predominantly in
the left side of the colon which may progress to exensive deep ulcera
tion like UC. Salmonella colitis and Pathogenic E. eoli infection are
rarely investigated radiologically, but can produce a similar picture to
Shigella. Campylobacter infection is like UC or Crohn's disease. Toxic
dilatation can occur in any of these.
Yersinia enterocolitica affects the distal small bowel (q.v.) but occa
sionally involves the colon where it produces aphthoid ulceration; the
ulcers tend to be smaller than those seen in Crohn's disease.
Chlamydia infection causes lymphogranuloma venereum, a disease of
the tropics but also seen in immunocompromised hosts. Involvement of
the rectum occurs mainly in women but also in men practising anal re
ceptive intercourse. A chronic proctitis occurs which results in strictur
ing which may extend for a variable length up to the sigmoid colon or
1001
even more proximally. The sigmoid loop may be elevated by the fibrotic
reaction. Pararectal, paravaginal and paracolic sinuses can be demon
strated often associated with abscesses. Rectal gonorrhoea results in
small rectal ulcers usually without radiolucent halos on a background of
normal mucosa. Rarely strictures and fistulae may occur. Actinomycosis
affects the right side of the colon and distal ileum where it has a propen
sity for causing complex sinuses and fistulae and fibrous masses which
may mimic neoplasms. Mycobacterium tuberculosis infrequently causes
pure colonic disease. Ileocolic involvement has been described in the
small bowel section. Scarring of the ileocaecal region and ascending
colon, annular strictures and/or deformity of the ascending colon occur
and the picture may be indistinguishable from Crohn’s disease or from
neoplasm. Prevalence of the respective diseases in local practice will ob
viously help. Tuberculosis is suggested by circumferential or stellate ul
cers, ’’hourglass" type strictures and a constricted caecum with a patulous
ileocaecal valve. Occasionally, diffuse colonic disease will mimic UC.
Schistosomiasis affecting the bowel is usually due to S. mansoni or S.
japonicum. The appearances are described in the chapter on "Tropical
disease".
AIDS-related colitis may be due to the co-existence o f multiple or
ganisms ("gay-bowel"). CMV infection may be relatively mild, associ
ated with diffuse mucosal granularity and aphthoid ulceration, or fulmi
nant, causing multiple large discrete ulceration, submucosal haemor
rhage, toxic dilatation, pneumatosis and gangrenous necrosis. There is a
predilection for caecal involvement with deep ulcers; this may also be
seen in renal transplant patients. The haemorrhagic colitis and necrotic
features are related to the vasculitis seen in infection with this organism.
Cryposporidium and atypical mycopbacterial organisms do not produce
a specific radiological picture in the large intestine. CT may be useful in
AIDS-related proctocolitis. Inflammatory infiltrate into the perirectal fat
is seen, but in addition, CT may help distinguish neoplastic from in
flammatory disease. Diffuse mural thickening with a "target-sign"
favours inflammatory disease.
Pseudomembranous colitis is due to endotoxin-producing Clostridium
difficile and is most commonly related to the administration of broad-
spectrum antibiotics. Sigmoidoscopy is usually diagnostic, showing the
typical pseudomembranes, together with the isolation of the toxin from
the stools. The clinical course is variable. Fulminant disease may occur
1002
with toxic dilatation demonstrable on plain radiographs. Other plain ra

diographic findings in less severe disease include an adynamic ileus
(which may presage toxic dilatation), "thumbprinting”, irregularity of the
mucosal edge due to ulceration and pseudomembrane, and haustral thick
ening. If contrast studies are indicated, these show an irregular shaggy
mucosa due to confluent shallow necrotic ulceration and pseudomem
brane, elevated plaques where the ulcers are covered by pseudomem
brane, and "thumbprinting” due to submucosal oedema. The whole colon
may be affected and there may be an associated small bowel enteritis.
Occasionally there is rectal sparing.
Acute ischaemic colitis

Acute ischaemic colitis typically presents with abdominal pain and rec
tal bleeding. In the majority of patients the splenic flexure and proximal
descending colon are involved, this being the "water-shed” region be
tween superior and inferior mesenteric artery circulations. Three cate
gories of disease are described. The benign "transient” form responds to
conservative therapy and the colon returns to a radiologically normal ap
pearance. The "gangrenous" form requires surgical management. The
third "stricturing" form is more controversial and is associated with the
later development of an ischaemic stricture.
The "transient" form leads to submucosal haemorrhage or oedema,
manifest as "thumbprinting" seen on plain films and contrast studies,
mural thickening, spiculation and spasm causing narrowing of the lu
men. The "instant enema" (see under ulcerative colitis) is an appropriate
method of performing a contrast examination on these patients.
Overdistension on barium examination may cause effacement of the
thumbprinting. The mucosa may be radiologically intact, or, in more se
vere cases, there may be ulceration and, occasionally, pseudopolyps.
Transverse ridging can be seen, the presence of which may be more com
mon when the patient proceeds to the stricturing form. The colon in most
patients will return to normal at a variable rate, often up to several weeks
or months from the acute episode. Narrowing of the lumen during the
healing phase is often eccentric, tapered and associated with sacculation
(Fig. 71). There is some evidence that the latter finding may be an indi
cator of a delayed return to normal or to the formation o f a stricture.
In the gangrenous form of ischaemic colitis, plain films may show in
tramural gas or, later, free gas or gas in the portal venous system. CT
1003
Figure 71.
Ischaemic colitis involving "water
shed" region around the splenic
flexure. The proximal descending
colon is shown. There are eccentric
changes with mild narrowing, sac
culation andfine nodularity.
scanning may be useful in is

chaemic colitis, although its
role is as yet controversial. In
the diagnosis of the less severe
forms the findings are non
specific and include relatively
mild (0.5-1 cm) symmetrical
bowel wall thickening with a
"double-halo", "target" sign or
homogeneous density on in
travenous bolus contrast en
hancement. In more severe
disease, CT is sensitive in de
tecting intramural and portal
venous gas. In addition, CT
can sometimes determine the
cause of ischaemia by show
ing arterial occlusion or
thrombus in SMA or portal ve
nous system. Angiography is
seldom indicated, since the in
formation provided is infre
quently decisive; even if an occlusion is detected, this usually affects a
peripheral branch.
1004
Figure 72.
Pneumatosis cystoides coli af
fecting the sigmoid colon.
Note radiolucent gas blebs
which in profile are seen to
parallel the bowel wall. More
proximally the sigmoid is
normal.
Pneumatosis coli
Gas in the bowel wall may occur for reasons other than ischaemic necro
sis. Pneumatosis (cystoides) coli is a benign idiopathic condition asso
ciated with gas collections, usually in blebs or "cysts" within the wall
and paralleling the lumen. It is most frequently distributed in the sigmoid
and descending colon, often with rectal sparing. There is luminal nar
rowing and scalloping of the contour by the submucosal impressions of
the gas cysts but obstruction is not seen (Fig. 72). Patients are either
asymptomatic or present with intermittent abdominal pain and diarrhoea.
Occasionally, a bleb may perforate and cause pneumoperitoneum with
out peritonitis. The small bowel may be involved in addition to the colon.
A secondary form may be seen where there is a cause o f raised intralu
minal pressure in association with mucosal ulceration, such as may be
present proximal to an obstructing stricture of the colon.
Colorectal neoplasms
Detection
Colorectal cancer (CRC) is the commonest internal malignancy in many
Western countries. It occurs at all adult ages, but the incidence rises
sharply after 40 years of age. Although some individuals fall into high
or above-average risk groups (for example, prior history of colorectal
neoplasia, family history of polyposis syndromes, hereditary non-poly-
posis colorectal cancer families, first degree relative(s) with CRC,
1005
chronic ulcerative colitis) most CRCs occur in patients with no known

increased risk. As the cause of CRC is unknown, primary prevention is
unlikely to be possible in the near future for most individuals, despite
the imminent development o f molecular genetic techiques to identify
those at inherited risk. It is generally accepted that the great majority of
CRCs develop in pre-existing benign adenomas, the detection and re
moval of which should therefore effect secondary prevention of CRC.
For these reasons screening o f asymptomatic persons has been advocated
using faecal occult blood testing, flexible sigmoidoscopy, colonoscopy,
radiology or a combination o f techniques, to detect early-stage CRC and
adenomas. The role of radiography in the screening of asymptomatic in
dividuals has yet to be resolved. Some authors have advocated screen
ing with periodic DCBE every 3-5 years in combination with annual fae
cal occult blood testing commencing at the age 40-50; there is a push by
the American College of Radiology to adopt this programme but at pre
sent this is controversial.
Colonoscopy is undoubtedly superior to DCBE in demonstrating small
polyps and has the potential for polypectomy, and this is the preferred
examination (with a combination of DCBE and flexible sigmoidoscopy
an acceptable alternative to colonoscopy where this is not availble) in
persons with positive occult blood tests or, some would suggest, as a
screening technique in its own right. It is the screening procedure of
choice in high risk groups.
Leaving aside the question of screening asymptomatic individuals, it
behoves radiologists performing contrast enemas to optimise their tech
niques to enable them to pick up small cancers and polyps in patients un
dergoing studies for any indication. By diagnosing asymptomatic early
neoplasms and polyps they will be contributing to the reduction of CRC
mortality. Double reporting o f DCBEs increases the yield of these ex
aminations.
Colonic epithelial polyps

Neoplastic epithelial polyps are very common, increasing with age. Most
are in the rectosigmoid region, but there is a relative shift to the right side
of the colon with increasing age. They are multiple in about 50% of pa
tients. In those with polyposis syndromes they may be innumerable. The
importance of benign polyps lies in their malignant potential. Neoplastic
polyps are tubular adenomas (much the most common), villous adeno-
1006
Figure 73.
Polypoid carcinoma o f the
caecum (large arrows) with
synchronous sessile (small
arrow) and pedunculated
(arrowheads) sigmoid
polyps.
mas and tubulovillous adenomas. Those with villous features have a

higher malignant potential. Lesions may be pedunculated or sessile (Figs.
65,73). Villous adenomas are more likely to be sessile polyps or plaque
like when they may give rise to a characteristic "carpet-like" growth, es
pecially in the rectum or sigmoid colon, extending over several cen
timetres. The difficulties of radiological detection of small or diminutive
polyps has already been alluded to, particularly in the sigmoid colon
when there is co-existing diverticular disease and overlapping loops.
Although the double-contrast method is superior to single contrast and,
in the best of hands may detect up to 90% of polyps greater than 10 mm
in diameter, there is only a 60-70% sensitivity for smaller lesions. Some
authors advocate a biphasic technique. Combining DCBE with flexible
sigmoidoscoy increases sensitivity. How important is it to find diminu
tive polyps? The majority of distal lesions smaller than 4 mm in size are
hyperplastic and thus have no malignant potential. However, of lesions
of 4-5 mm approximately 50% will be adenomas and will have this po
tential.
In determining whether a radiologically demonstrated polyp is cur
rently benign or malignant, size is the only reliable indicator. For lesions
less than 5 mm in diameter, the presence of malignancy is so unlikely as
1007
to be virtually discounted. One to 2% of lesions o f 5-10 mm in diame

ter are malignant. About 10% of 1-2 cm polyps are malignant, while the
incidence rises to approximately 50% for polyps greater than 2 cm.
Pedunculated polyps are less likely to be malignant than sessile ones.
Indentation of the polyp base suggests malignancy. The surface pattern
of the polyp is an unreliable indicator, but ulceration suggests malig
nancy.
The radiographic features o f polyps and their distinction from diver
ticula have been discussed previously.
Polyposis syndromes
Familial adenomatous polyposis and Gardner's syndrome are associated
with multiple, usually innumerable, colonic adenomas. Carcinoma is in
evitable without colectomy. Polyps may be seen throughout the bowel
and have been desribed elsewhere in this text. In Gardner’s syndrome,
soft tissue desmoid tumours and osteomas are also seen. There is a ten
dency to develop peri-ampullary duodenal malignant neoplasms.
Juvenile polyps are a form of hyperplastic benign lesion, usually solitary
and pedunculated in the rectosigmoid area; they have a propensity for
autoamputation. Peutz-Jegher's syndrome is associated with hamar
tomas in the bowel, bur rarely malignant degeneration can occur.
Colorectal carcinoma
Diagnosis
The rectum and sigmoid regions are the commonest sites for carcinoma,
but there has been a relative shift o f distribution to the right side of the
colon in recent years. Multiple cancers are seen in about 5 % or there are
benign polyps present within the same colon, frequently so-called ’’sen
tinel” polyps that occur near the malignant tumour. The double contrast
barium enema, in the best hands, detects approximately 90-95% of
colonic cancers. Most missed tumours are in the sigmoid, often when
there is co-existing diverticular disease, and in the caecum. Plaque-like
lesions are more likely to be be overlooked than polypoid or annular ones.
The vast majority of tumours are adenocarcinomas. The radiographic ap
pearances on barium studies are:
1008
i) annular constricting lesions: the most common, seen as typically short

"apple-core" segments of narrowing with destruction of the mucosal
pattern (Fig. 65); ulceration may be present.
ii) Polypoid lesions which are fungating and intraluminal producing a
large mass with irregular surfaces and an indrawn base; these are fre
quently caecal (Fig. 73).
iii) Infiltrating, plaque-like, lesions with submucosal spread, similar to
linitis plastica. Subtle examples may be missed on barium enema, the
only clues to the presence of a lesion may be its elevated edges with
a deformity of the mucosal contour. This type of lesion is often the
one associated with malignant change in ulcerative colitis when long
and rather smooth contoured strictures may be seen.
iv)Ulcerating tumours with deep excavating craters and raised margins.
These are the least common.
v) Mixed types.
Although most carcinomas conform to these patterns, early invasive can

cers are occasionally seen. They have been classified by Japanese au
thors in much the same way as early gastric cancers, i.e. elevated or poly
poid and flat or depressed lesions. Occasionally, colonic carcinoma may
present with signs of localised or free perforation. Local perforation gives
rise to an inflammatory mass, the nature of which is difficult to assess
radioogically. Another uncommon pattern is that of ischaemic colitis
proximal to a chronically obstructing annular carcinoma, presumably due
to vascular compromise as a result o f distension of the bowel wall.
Staging
The most frequent surgical/pathological method of staging colorectal
carcinoma is by the modified Dukes classification. In recent years the
TNM method has gained increasing acceptance. A single modality that
allows accurate pre-operative staging is not available. Such staging
would facilitate appropriate therapy to be planned and monitored.
Accurate staging demands the determination of local tumour spread,
lymph node metastasis and distant (liver) metatasis. Liver imaging is
dealt with elsewhere in this publication. CT staging of the primary tu
mour (Fig. 74) and lymph node metastasis in colorectal carcinoma, while
initially encouraging, has been shown to be only 48-74% accurate. This
is due to the inability of CT to detect minor degrees of perirectal or peri-
1009
Figure 74.
CT showing rectal car
cinoma (T) infiltrating
perirectal fa t laterally
and posteriorly (ar
rows) and seminal vesi
cles anteriorly.
colic tumour infiltration and due to the incidence o f metastatic disease

in non-enlarged lymph nodes. It is possible that recent refinements in
technique have improved results, such as the use o f colonic cleansing
preparation, positional variation such as prone scans for the rectum, and
air distention of the rectum. Lowering the size threshold for diagnosing
lymph node metastasis increases sensitivity but lowers specificity.
Endorectal ultrasound using rigid probes for rectal carcinoma staging
and flexible endoscopic ultrasonography for colonic cancers has proved
promising. In rectal carcinoma accuracies of 80-90% have been
achieved. Sensitivity is higher than specificity. As in the upper GI tract
there are problems related to specificity for lymph node metastases and
to non-transversable lesions. EUS is more accurate than CT in assessing
local spread, but the advantage is less than is apparent in upper GI tract
cancer staging. There is a tendency to overstage due to the presence of
peritumourous inflammation. EUS is of particular clinical importance
because of the expanding range of treatment options for rectal carcinoma,
determined by the stage of disease. The clinical value of T-staging of
colonic cancers is less certain, and data are relatively few. MR imaging
is preferable to CT scanning for local staging of rectal cancer. Although
suffering the same limitations in its inability to assess depth of intramural
infiltration and nodal deposits, however, its multiplanar imaging poten
tial offers special advantages. Invasion into pelvic muscles and bone by
rectal tumours may be better seen by MR imaging. The use of endorec
tal coils has improved T staging, but problems remain particularly re
lated to detection of nodal metastases. The advent of pelvic phased-ar-
1010
ray coils may lead to further improvements. Early results have been re
ported using Indium-labelled monoclonal antibodies for radionuclide
imaging of colorectal cancers. There appears to be high sensitivity in the
detection o f tumour sites in the abdomen, but there is a significant false-
positive rate.
Recurrent tumours
Investigations have shown both CT and MR scanning to be able to de
tect asymptomatic tumour recurrence when the carcinoembryonic anti
gen levels are normal. Tumour recurrence after surgery for rectal carci
noma occurs in about one third o f patients within the first two years and
is most frequent in the area contiguous with the surgery. Sixty percent
of these patients will have only local recurrence. It has been shown that
resection of recurrent tumour increases survival time. It has therefore
been suggested that a baseline CT (or MR) be performed 2-3 months af
ter initial surgery, followed by imaging every 6-9 months for 2-3 years.
The protocol for imaging should be directed to the detection of both lo
cal recurrence and hepatic metastasis, since there is evidence that resec
tion of the latter, where possible, may also increase survival time. CT ac
curacy for local tumour recurrence suffers from the same limitations as
in staging the primary lesion, that is the inability to detect microscopic
invasion of perirectal or pericolonic fat and to assess metastatic deposits
in nodes of normal size. A further problem occurs after abdominoper
ineal resection for rectal cancer since there is frequently a soft tissue pre-
sacral mass due to oedema, haemorrhage, granulation tissue or fibrosis,
for many months after surgery. This is particularly so if radiotherapy has
been performed. Hence, the rationale for undertaking a post-operative
baseline study at 2-3 months. Any enlargement of the mass should be
cause for concern and lead to percutaneous biopsy. MR scanning is re
ported to help distinguish recurrent rectal tumour from scar tissue, re
current tumour having a high signal intensity on T2-weighted images.
Position emission tomography with fluorine-labelled D-glucose has re
cently been shown to be useful in this function.
Less common benign tumours

Lipomas are the second most common benign colonic tumours. They are
usually asymptomatic but can bleed or intussuscept. Most appear as sub
mucosal pedunculated lesions, often on the right side of the colon, which
1011
tend to change shape during the barium examination with posture and
compression. CT scanning is definitive in demonstrating the fatty atten
uation of the lesion. Large bowel carcinoids mostly occur in the rectum
and comprise 1-2% of polyps less than 5 mm in size. They are sessile
polyps and should be considered potentially malignant. Nearly all lesions
greater than 2 cm in diameter are malignant. Endometriosis occurs at the
rectosigmoid junction in 85% of cases, due to deposits o f endometrial
tissue in the pouch of Douglas. On barium enemas they are seen as
smooth, often scalloped, submucosal impressions on the bowel lumen
on the anterior wall of the rectum causing mild narrowing. Symptoms
are related to menstrual periods.
Prominent colonic lymphoidfollicles may be seen as a normal variant
on DCBE in young patients. Follicles less than 3 mm in diameter may
be seen in 50% of patients less than 30 years of age. However, when fol
licles of 4 mm or more are seen, usually in the rectosigmoid area, there
is an increased incidence o f inflammatory bowel disease or lymphoma.
Some authors have found a 70% incidence of colorectal neoplasia in pa
tients over 40 years of age with prominent follicles 1-3 mm in diameter,
especially when diffuse or left-sided. This finding should precipitate a
very careful search for neoplasia.
M etastases to the colon

Metastasis to the colon can occur by direct invasion from contiguous or
gans, by spread along the mesentery or its lymphatics, by intraperitoneal
seeding or less commonly by haematogenous embolisation. Typically
serosal involvement leads to a mass effect on the bowel, fixation, angu
lation, traction changes with tethering and spiculation and narrowing
(Fig. 75). En face, pleating of transverse folds which do not completely
traverse the lumen, gives rise to a "stripe sign" due to tethering.
Commoner causes of direct spread o f neoplasm to the bowel include pri
maries in the genital tract, kidney and pancreas. Peritoneal spread espe
cially involves the pouch of Douglas and thence the anterior rectal wall
(Fig. 76), but also the sigmoid, ileocoecal and paracolic regions. Omental
involvement produces an "omental cake" which typically affects the su
perior aspect of the transverse colon. US and CT will show coexisting
mesenteric and peritoneal deposits and ascites, as well as soft tissue
masses involving the serosal surfaces.
1012
Figure 75.
Serosal metastases (squamous
carcinoma, primary unknown)
involving proximal descending
colon. Note narrowing, fixa
tion, tethering and spiculation.
Figure 76.
Transperitoneal spread to
pouch o f Douglas from carci
noma o f caecum. There is nar
rowing o f the rectosigmoid re
gion with anterior spiculation.
Haematogenous metastasis, especially from breast, lung and mela

noma, produce submucosal nodules which may become circumferential
and may ulcerate.
1013
Figure 77.
MR images, T2 weighted -
(a) axial and (b) coronal -
showingfistula-in-ano track
(arrowed) running from left
to right posterior to ano-
rectum (r) but inferior to le
vator muscles (Im).
Anorectal evacuation disorders

Radiology has a role in the investigation of chronic constipation, faecal
incontinence and in various other functional anorectal disorders. In re
fractory constipation in adults a barium enema should be performed to
exclude stricturing lesions. Bowel transit studies may be undertaken by
nuclear medicine or radio-opaque marker methods. Techniques for imag
ing the anorectal region include evacuation proctography (defaecogra-
phy) and anal endosonography. Magnetic resonance imaging is useful in
staging anorectal neoplasms and assessing inflammatory conditions such
as fistulae due to its multiplanar imaging capacity (Fig. 77).
1014
Figure 78.
Evacuation proc
togram showing no
significant abnor
mality. (a) at rest
(b) during
"squeeze” or lift
(c) during straining
(d) during evacua
tion. See text fo r il
lustrated features.
Solid line depicts
level o f ischial
tuberosities.
V=vaginal contrast;
dotted line=anorec-
tal angle.
Evacuation proctography
Barium paste, the approximate consistency of soft stool is introduced
into the rectum. A vaginal marker is inserted and some workers opacify
the pelvic small bowel with oral barium. The patient is then seated lat
erally on a special radiolucent commode in front of the screening unit.
Hard copy images are obtained with a 100 mm camera, and videofluo-
roscopic recording is made at rest, during "squeezing”, during straining
without evacuation, and then during attempted evacuation (Fig. 78). The
investigation gives morphological and functional information.
Parameters that are measured include the anorectal angle, the level of the
anorectal junction relative to a bony landmark (such as the ischial
tuberosities) and the anal canal width. Changes in these parameters in
the various phases of the examination are more important than the ab
solute values. Features that are observed with each manoeuvre include
the state of opening of the anal canal, the configuration and position of
the anorectal junction, the degree of rectal mucosal prolapse and any rec-
tocele or enterocele formation. A subjective assessment is made of the
efficiency and degree of rectal evacuation.
Normally, at rest the anal canal is closed, the anorectal angle is about
90° and there is a well formed posterior impression at the anorectal junc
1015
tion from the puborectalis muscle. On "squeezing” there is contraction

of the puborectalis sling and the external anal sphincter resulting in a de
crease in the anorectal angle, elevation of the anorectal junction and fur
ther closure of the anal canal. On straining there is depression of the
anorectal junction which should be no more than 3.5 cm from its resting
position. Evacuation should proceed rapidly and efficiently and be ac
companied by relaxation of puborectalis with loss of the posterior im
pression from this muscle, effacement of the anorectal angle, depression
of the anorectal junction which should take on a funnel-like configura
tion, and opening of the anal canal. A "zone of evacuation" in the rec
tum develops as the rectum empties. Even in normal individuals, partic
ularly women, there is some anterior bulging of the rectal wall (recto-
cele) and minor rectal mucosal prolapse. Abnormal features that may be
observed are as follows:
- Weakness of the internal anal sphincter may be seen as an open anal
canal at rest with incontinence.
- Puborectalis and external anal sphincter weakness is demonstrated as
a weak "squeeze" with poor anorectal elevation and lack of anorec
tal angle change.
- Failure of relaxation or paradoxical contraction of puborectalis on
evacuation seen as lack of effacement of the anorectal angle, causing
straining against an unrelaxed pelvic floor - so called anismus or dys-
kinetic puborectalis muscle resulting in obstructed defaecation.
- Anterior rectocele formation during straining and defaecation. This
may be seen to a minor degree in normals. Larger rectoceles may re
tain barium and be a cause of incomplete evacuation. They are often
associated with other abnormalities such as rectal prolapse and per
ineal descent.
- Intussusception, or prolapse, of rectal mucosa. A minor degree is seen
in many normals. There is invagination of the rectal wall which may
be anterior, posterior or circumferential. The degree of descent is vari
able, reaching the internal anal os or, in more severe degrees, be
coming intra-anal or prolapsing externally. Intussusception is often
associated with sequestration of barium in a rectocele. When the pro
lapse spontaneously reduces after evacuation, the content of the rec
tocele may then leak out and produce incontinence.
- An enterocele, which may be suspected by separation of the posterior
vaginal wall and the anterior rectal wall during evacuation. This may
1016
be confirmed by repeating the test after opacification of pelvic small

bowel loops with oral barium. Enteroceles may be associated with
incomplete evacuation.
- ’’Perineal descent” seen as an abnormal degree of descent of the
anorectal junction with straining and evacuation. This is related to a
decrease in tone of the pelvic floor musculature and gives rise to a
sensation of incomplete evacuation. This leads to persistent strain
ing, stretching of the pudendal nerve and pudendal neuropathy and,
later, external sphincter weakness and incontinence. There is evi
dence that patients with a history of chronic constipation and strain
ing at stool may progress through this course of events since cases of
outlet obstruction constipation and incontinence demonstrate a sim
ilar pelvic floor neuropathy. A "vicious spiral" of deterioration is thus
likely to ensue.
- Features of the "solitary rectal ulcer" syndrome. This is a misnomer
since there is often focal inflammation but no ulceration and some
times there are multiple ulcers. The mechanism of damage is proba
bly due to trauma to intussuscepted mucosa during straining against
an unrelaxed pelvic floor.
Constipation
Debilitating, chronic constipation in adults may be due to a number of
systemic disorders (e.g. hypothyroidism). Idiopathic constipation may
be related to slow bowel transit, anorectal outlet obstruction or a com
bination of these. Imaging investigations after exclusion of systemic con
ditions will therefore include barium enema (for stenosing lesions and
megacolon), transit studies and evacuation proctography. Transit stud
ies may be performed by the use of radio-opaque ingested markers - se
rial radiographs are taken to assess the number of markers remaining in
the bowel - or by a nuclear medicine method. In the latter study,
11indium-labelled resin microspheres or other material are given by
mouth and images acquired serially. The radiograhic method has the
virtue of cheapness and simplicity and is a reasonable screening test. The
scintigraphic technique is more specific and allows measurement of seg
mental transit which may be important in management. The features seen
on evacuation proctography have been discussed. A subjective assess
ment of rate and efficiency of evacuation may be made as well as the
demonstration of puborectalis dysfunction and morphological abnor-
1017
Figure 79. Endo-anal ultrasound image showing relatively hypo-

echoic internal sphincter. There is a fo ca l posterior defect (long ar
rows) with a longer neighbouring segment o f thinning (short arrows).
More laterally the sphincter is normal.
malitis such as rectocele, prolapse and enterocele which may give rise
to a sensation of incomplete emptying. Recently, radio-isotope proctog
raphy has been used to permit a quantitative measure o f evacuation ef
ficiency; this also provides some morphological information.
Incontinence
Incontinence may be associated with other evacuation disorders, such as
the descending perineum syndrome or prolapse, and is accompanied by
a history o f multiparity and/or chronic straining leading to pudendal neu
ropathy and loss of anorectal sensation and deficient sphinters. Obstetric
injury or anorectal surgery may result in sphincter defects. While evac
uation proctography may help characterise some of the associated fea
tures of incontinence, the role of this examination is less clear cut than
in constipation. Endo-anal sonography has become the most useful
method of imaging the internal and external anal sphincters. Detailed im
ages may be obtained which can localise focal defects and influence man
agement (Fig. 79). Endosonography may replace needle electromyo
graphic mapping of the external sphincter. It is also useful in imaging
anorectal fistulae and abscesses, in local staging of ano-rectal carcinoma
and in imaging local recurrence after rectal surgery for neoplasms.
1018
ACUTE GASTROINTESTINAL HAEMORRHAGE

Radiology has a role in the diagnois and therapy of acute gastrointesti
nal bleeding. That role is more important in haemorrhage arising from
below the Ligament of Treitz since, when the source is from the upper
GI tract the endoscopist can make the diagnosis in most patients and of
ten institute endoscopic measures to arrest the bleeding. There is virtu
ally no place for barium studies in acute bleeding, since superficial mu
cosal lesions are not seen, the source of haemorrhage cannot be deter
mined when multiple lesions are shown and barium will obscure the field
for subsequent angiography. The major role for radiology lies with an
giography - both diagnostic and interventional. Whether angiography
should be preceded by radionuclide studies is a vexed question. Some
radiologists prefer this in haemodynamically stable patients in order to
confirm active bleeding (and thus increase the yield of angiography) and
to localize the approximate site of bleeding to save time and contrast
medium at angiography. However, as discussed below there are prob
lems and pitfalls related to isotope studies.
Two techniques of scintigraphic imaging of gastrointestinal bleeding
are generally available. Technetium-labelled sulphur colloid given in
travenously is quite rapidly taken up in the liver and spleen. This method
therefore will only detect bleeding if it is actively occurring during the
intravascular phase of the tracer. This is a problem given that, even in
patients with massive bleeding, haemorrhage is often intermittent. In ad
dition, bleeding sites in the upper abdomen may be masked by he-
patosplenic uptake. However, the technique is very sensitive, being able
to detect as little as 0.05 ml per minute of blood loss away from the back
ground of liver and spleen. Technetium-labelled red cells - now able to
be labelled in vitro - act as a blood pool agent, allowing imaging up to
24 hours or so after administration, and thus detection of intermittent
bleeding. (Indium-labelling enables detection up to 5 days but at high ra
diation dose.) The minimum rate of blood loss detectable is about 0.1 ml
per minute. Images are acquired initially at 30 second intervals for at
least 60-90 minutes. Scintigraphy with Technetium-labelled red blood
cells is a sensitive, non-invasive procedure that can be used for prolonged
surveillance of bleeding, but there are many pitfalls leading to false pos
itive results or inaccurate localisation. These may be overcome by high
labelling efficiency techniques, digital imaging for at least 90 minutes,
use of cine display to enable demonstration of changes of position with
1019
time o f areas of abnormal uptake, and strict criteria for the localisation
of a source of bleeding seen on delayed images only. This latter prob
lems arises from the rapid antegrade or retrograde movement of ex-
travasated red cells within the bowel leading to false localisation. In ad
dition, pooling can occur in the large bowel from a source more proxi
mally. Figures for correct localisation vary in the literature from 40 to
90%.
It is convenient to discuss upper and lower gastrointestinal haemor
rhage separately. It is usually possible to distinguish these on clincial
grounds and by the passage o f a nasogastric tube. Selective angiography
is performed, the choice of vessel first selected being determined by the
suspected site of bleeding. Although digital subtraction radiography
(DSA) is convenient, many radiologists prefer cut films citing the pit
falls of DSA such as artefacts due to bowel movement, lesser field of
view and decreased spatial resolution. It is estimated that conventional
angiography can detect blood loss of approxinmately 0.5 ml per minute;
DSA can probably detect 1—1.5 ml per minute. Extravasation is seen as
puddling of contrast in the early to mid-arterial phase which changes size
and shape as the series progresses. Venous bleeding is hardly ever
demonstrated.
Upper gastrointestinal haemorrhage

Patients present with haematemesis and/or melena. Occasionally, in mas
sive bleeding, red blood may be passed per rectum. Endoscopy is usu
ally diagnostic and often, if there is active bleeding, endoscopy measures
will arrest this. Angiography is required if the result of endoscopic is
equivocal or if angiographic therapeutic intervention is planned.
Haemodynamically unstable patients may be examined while undergo
ing resuscitative measures - nuclear medicine studies are not indicated
in these patients. In stable patients the question of whether to perform
scintigraphy is vexed (see above); these studies are least accurate for up
per GI bleeding.
Coeliac angiography is undertaken, followed by selective left gastric
artery (LGA) catheterisation. LGA angiography identifies about 70% of
active gastric bleeding. If no abnormality is seen, then further injections
of gastroduodenal and superior mesenteric arteries are performed to as
sess the pancreaticoduodenal arcades and other gastric vessels. It should
be noted that venous bleeding, for example, from varices, is hardly ever
1020
detected. Transcatheter intervention may be performed by intra-arterial

vasopressin infusion or embolotherapy. Vasopressin administration is
associated with complications such as hypertension, arrhythmias and
vasoconstriction that my result in tissue ischaemia and necrosis that may
affect bowel, myocardium and the periphery. The reader is referred to
specialist texts for details of dosage. The success rate of vasopressin in
arresting bleeding from gastric sources is high (75- 80%). It is usually
unsuccessful if there have been previous attempts at endoscopic heat or
electrocautery to the bleeding site, and embolotherapy is generally indi
cated. The success rate of vasopressin for arrest of pyloroduodenal haem
orrhage is low (about 30%). This may be due to the dual blood supply
of this region, penetration of ulcers into the muscular layers of the wall
or the propensity for large vessels such as the gastroduodenal artery to
be the bleeding source. Embolotherapy for gastric bleeding usually in
volves the LGA. Gelatin sponge (Gelfoam) is the most frequently used
material; this is a temporary occluding agent, allowing the body’s haemo
static mechanisms to be effective at the bleeding site. Permanent oc
cluding agents are used for malignant causes of bleeding. Embolotherapy
is successful in approximately 80%. The risk of infarction is significantly
increased if there has been a previous gastric resection. Embolisation for
duodenal bleeding sources is more challenging due to the dual blood sup
ply, whch may require occlusion of gastroduodenal artery and inferior
pancreaticoduodenal artery or branches. This is usually well tolerated
when there has been no previous surgery. Occasional complications in
clude doudenal ischaemic necrosis, hepatic or gallbladder infarction.
Success rates are quoted as 60-100% for ulcer bleeding.
Lower gastrointestinal haemorrhage

Radiologists more frequently have a role here. Endoscopy is rarely di
agnostic if the patient is bleeding significantly. However, proctoscopy
or rigid sigmoidoscopy should be performed to exclude an anorectal ori
gin. In addition, the upper GI tract is the source in about 10% of patients
with severe rectal bleeding; this should be excluded by nasogastric in
tubation or, preferably, endoscopy. Scintigraphy is at its most accurate
in the colon and may be undertaken in the haemodynamically stable pa
tient. Small bowel haemorrhage is most commonly due to anastomotic
ulcers, neoplasms, Meckel's diverticulum, arteriovenous malformations
or angiodysplasia, and varices. Variceal bleeding is not seen angio-
1021
Figure 80.
Superior mesenteric artery
angiogram demonstrating ex
travasation into a bleeding
right-sided colonic diverticu
lum (arrowed).
graphically, although the varices are demonstrable. Colonic sources of

massive haemorrhage are most commonly diverticula (Fig. 80) (80% of
diverticula are left-sided but 50% of diverticular bleeding is right-sided),
and angiodysplasia. Colonic haemorrhage arrests spontaneously in 80-
90% o f patients, but recurs in about 25%. Angiodysplasia is common in
elderly asymptomatic individuals and lesions are not uncommonly mul
tiple. Therefore, unless extravasation is seen, the angiographic demon
stration o f angiodysplasia must be interpreted with caution - it may be
an incidental finding in a patient with another cause o f bleeding. The an
giographic features of angiodysplasia are of a vascular tuft with an early
filling prominent draining vein which persists. Lesions occur anywhere
but are usually seen in the right colon. Possible transcatheter interven
tions include vasopressin infusion, embolisation or (for small bowel le
sions) aiding the surgeon in localising the appropriate segment for resec
tion (see below). Vasopressin controls bleeding in approximately 50% of
small bowel and 75% of colonic lesions. In the latter, 15% will recur fol
lowing cessation of infusion. Embolisation carries the risk of bowel in
farction; proximal occlusions are safer but less effective, most workers
aiming at occluding proximal second order branches or more distally. In
one series embolisation controlled haemorrhage in over 90%. The inci
dence of infarction is difficult to assess, but is probably about 10%. Not
1022
all of these will require urgent resection; some are relatively minor and
will lead to no sequelae or to later colonic strictures. There is no con
sensus as to whether vasopressin or embolotherapy is the initial preferred
method in colonic bleeding. Both techniques have their advocates. There
is some evidence that vasopressin is best in diverticular bleeding and em-
bolisation in others.
Angiography in recurrent obscure bleeding

Recurrent bleeding of obscure origin is often a difficult problem.
Bleeding has frequently ceased by the time that angiography has been
arranged. Attempts to increase the yield of angiography include select
ing the timing of the study by scintigraphy and pharmacoangiography.
Agents used for the latter have included heparin or thrombolytic drugs
to prolong bleeding and vasodilators, such as tolazoline, to enable an
giographic detection of extravasation. There are, of course, risks associ
ated with these techniques. However, angiography may be diagnostic
even if active bleeding is not occurring at the time. Lesion detection in
creases with age over 50 years. Neoplasms, arteriovenous malforma
tions, angiodysplasia and varices may be demonstrated. Results may be
interpreted with caution since the only conclusive evidence that a lesion
has bled is the demonstration of extravasation.
The angiographer may aid the surgeon in selecting the appropriate
small bowel segment for resection in difficult small bowel lesions. The
catheter may be left in situ in the vessel supplying that segment and meth
ylene blue instilled through the catheter to enable visual identification of
the loop.
RADIOLOGICAL INTERVENTION IN THE

GASTROINTESTINAL TRACT
As in other subspecialities, gastrointestinal radiology has seen a large in
crease in "interventional” procedures, used for diagnosis and therapy.
These may be broadly classified as follows:
Angiographic interventions
These interventions include:
i) Therapy to arrest bleeding - previously discussed
ii) Thrombolytic therapy to dissolve thrombo-emboli to the major
mesenteric vessels.
1023
iii) Transluminal balloon angioplasty and stenting for stenosing lesions

of the mesenteric vessels.
Percutaneous abscess drainage

Radiologically guided abscess drainage is now a well accepted, safe and
effective alternative to surgery in selected cases. It has revolutionised the
management of abscesses and usually obviates the need for general
anaesthetic and surgery. Imaging guidance may be by ultrasound (which
has the advantage of availability, speed and real-time interaction), CT
(which is superior in complicated cases and where safe access is poten
tially difficult), fluoroscopy, or a combination of modalities. Whereas
unilocular abscesses are easiest to treat, multilocularity is not necessar
ily a bar to percutaneous treatment. Loculi may be broken down and mul
tiple catheters may be used. Indications related to the GI tract include di
verticular, appendiceal and peri-anastomotic postsurgical absceses and
those due to Crohn's disease. Percutaneous drainage of such enteric col
lections often allows surgery to be performed, if indicated, on an elec
tive basis. Drainage is best performed under CT guidance since this al
lows better demonstration of any intervening bowel; the catheter should
not traverse the GI tract. Abscesses are often found to communicate with
the GI lumen, but even Crohn’s collections usually close without fistu
las. The technique and catheter equipment used are largely determined
by personal preference. Deep pelvic abscesses may be drained transrec-
tally with radiological guidance.
Overseeing post-procedure catheter care should be the responsibility
of the radiologist. Usually low-pressure suction and saline irrigation are
maintained. Contrast sinography is performed as required, and withdrawal
of the catheter determined on conventional surgical principles.
Drainage of abscesses associated with fistulae should be managed so
that the communication must be allowed to close prior to catheter removal.
Low-output fistulae nearly always close. High-output fistulae sometimes
close with prolonged drainage provided distal GI tract obstruction, tu
mour at the fistula site and persistent infection have been excluded.
Enteric stricture dilatation

Balloon catheter dilatation of strictures is now a well-accepted technique.
Balloons should be intrinsically safer than bougies since virtually all the
dilating force is radially distributed, whereas with bougies there is con
1024
siderable shearing stress. Gastroenterologists have largely adopted bal

loon dilatation techniques; there are advantages to both radiological and
endoscopic dilatation. The radiologist can assess the length and config
uration of the stricture and ensure the instruments remain within the lu
men. The endoscopic method allows direct mucosal visualisation and
biopsy, but with a tight lesion the view is limited to the proximal end.
The greatest experience is with oesophageal strictures. Post-surgical
strictures respond well; those due to repeated insult, such as peptic stric
tures respond less well. Response of malignant strictures is variable. The
complication of significant oesophageal rupture occurs in approximately
0.3%. Most ruptures are seen in malignant strictures. Other strictures
amenable to radiological balloon dilatation include pyloric stenosis,
stenosed gastroenterostomies and rectal and distal colonic stricures.
Placement of enteric tubes

Radiologists are often asked to place nasoenteric tubes for short or long
term feeding and hydration. This is usually straightforward under fluo
roscopic guidance.
Percutaneous gastrostomy
For long term feeding, percutaneous gastrostomy may be performed
safely and relatively simply by radiological or endoscopic methods. The
catheter can be advanced into the jejunum if required.
Fine needle aspiration biopsy (FNAB)

FNAB of bowel-related lesions may be performed under fluoroscopic,
US or CT guidance. The technique is safe and cost-effective. Sensitivity
for malignancy of around 90% should be achieved. False positives for
malignancy are extremely rare.
1025
Chapter 23
The liver, biliary tract, pancreas and

spleen
David J. Allison and

Carl-Gustaf Standertskjold-Nordenstam
The liver
MODALITIES
With the introduction of cross-sectional imaging methods such as US,
CT, and MRI, direct imaging of the liver parenchyma became possible
where previously only angiography and radionuclide imaging had been
available.
Ultrasonography
Because of the location, size and structure of the liver, US is very well
suited for imaging its parenchyma and is therefore usually the first
method employed. It is widely available, easily performed and has no
contraindications. An excessive amount of bowel gas may degrade the
study.
Ultrasound gives information on the size and structure o f the liver and
demonstrates both localized lesions (e.g. hepatic tumours, cysts and ab
scesses) and diffuse disease. Intrahepatic structures, such as portal ves
sels and biliary ducts can be identified. The vascular systems in the liver
may be studied with Doppler US, which can give important differential
diagnostic information especially when a colour-system is used (Fig. 1).
1027
Figure 1.
US o f the liver. The normal echo
pattern o f the liver is demonstrated.
The echo-free, tubular structures
within the liver are hepatic veins
(arrows).
Computed tomography
A CT study of the liver entails imaging of the entire organ from its su
perior border at the dome o f the diaphragm to its caudal tip. Contiguous
10 mm thick slices are obtained, usually before and after the intravenous
injection of contrast medium (Fig. 2). Because of its iron content, the
density of the liver is slightly higher than that of other intra-abdominal
organs, usually of the order of 65 ± 5 HU. Most pathological lesions have
a density less than that of normal parenchyma. This difference is accen
tuated following a contrast medium injection, but because of pharmaco
dynamic considerations care has to be taken to perform the enhanced
study during a narrow time window of 30-60 seconds following the bo
lus injection of contrast medium. Because of the size of the liver, the con
trast injection may have to be repeated in order to study the entire organ
but this requirement has diminished considerably since the advent of fast
CT scanning and spiral CT. Sequential scans at a single, predetermined
level after a bolus of contrast medium are useful for determining con
trast enhancement dynamics, which are of decisive importance in the di
agnosis of, for example, a haemangioma.
1028
THE LIVER, BILIARY TRACT, PANCREAS AND SPLEEN
Figure 2.
CT o f the liver, (a) Without
i.v. contrast enhancement
the texture o f the liver is
even. The blood vessels are
seen faintly as low-attenu
ating structures against the
liver parenchyma. The at
tenuation o f the liver (I) is
equal to that o f the spleen
(s). (b) After i.v. contrast
enhancement the attenua
tion o f the liver increases,
as does that o f the spleen.
The hepatic veins are now
clearly visible as highly-
attenuating (white)
structures and are well
discerned against the liver
parenchyma. On this scan
contrast medium is also
seen in the aorta (a).
The size of the liver and information on both focal and diffuse
parenchymal disease are all clearly evaluated by CT. Newer CT tech
nology has also made it possible to visualize blood vessels (CT-angio-
graphy, CT-portography) and to perform 3-dimensional reconstructions
which are important in studying anatomically complex areas, such as the
liver hilum.

MRI is, in many respects, equal to CT in imaging of the liver. It has,
however, certain advantages, that probably make it the best available
method for studying disease in this organ. The free choice of imaging
planes permits better anatomical orientation (Fig. 3) and the utilization
of multiple imaging sequences facilitates the identification of smaller le
sions, especially those associated with oedema. MRI gives new infor
mation on parenchymal and metabolic disease, 3-dimensional imaging
enables visualization of, for instance, the biliary tree and the liver hilum,
1029
Figure 3.
M RI o f the liver. In
these T1-weighted
images the
anatomy o f the
liver is well dis
played in the
transverse, sagittal
and coronal pro
jections. The por
tal and hepatic
veins are seen as
HVKS 2|
•tt©.E7C<4 VISION dark tubular
structures.
and MR-angiography delineates the blood vessels. Various types of mag

netic and paramagnetic contrast media that increase the signal intensity
of either the lesion or the parenchyma, add significantly to the precision
of MR studies. Drawbacks of MRI include its sensitivity to movement
artefacts, and the rather long duration of study, though with new tech
nology and rapid sequences examination times can be considerably re
duced. MR spectroscopy may become clinically useful in the study of,
for example, metabolic liver disease.
Angiography
Arteriography used to be the most precise method for evaluating liver
disease, but its diagnostic use is now limited to the investigation of cer
tain special problems such as the pre-operative mapping of liver vessels
or the detailed evaluation of certain liver tumours.
Therapeutic angiography is particularly important in the liver as the
organ has a dual blood supply (making embolization a relatively safe
procedure) and interventional procedures are associated with a far lower
morbidity than surgery in a variety of circumstances such as acute arte-
1030
rial bleeding and porto-systemic shunting.

Hepatic venography is valuable in the evaluation o f the Budd-Chiari
syndrome.
Percutaneous transhepatic portography is used for studying the por
tal circulation or for venous sampling of the pancreas. The use of this ap
proach for the embolization of varices is now virtually obsolete except
in the most special circumstances.
Radionuclide imaging
Radionuclide imaging used to be an important method for studying the
liver, particularly focal lesions in the organ, but it has diminished in im
portance mainly because of its poor spatial resolution and non-specificity
in comparison with other methods. Nevertheless, several specialised
agents may be useful for imaging specific pathology, such as radiolabelled
leucocytes for intrahepatic abscess, In-III octreotide for GFP tumours
metastasing to the liver, and 1-123 SAP (serum amyloid P component) for
hepatic amyloidosis. Hepatic haemangioma is a lesion which is charac
teristically associated with low blood flow but high blood volume and
may be diagnosed by dynamic Tc-99m labelled red cell imaging.
Biliary imaging
Proper evaluation of the liver frequently requires imaging of the biliary
tract. This is considered separately in the succeeding section.
NORMAL ANATOMY
The liver is the largest of the parenchymal organs, and weighs apporox-
imately 1500 grams. It is situated in the upper right hypochondrium and
extends from the right flank across the midline. It may reach as far left
as the spleen. Superiorly the liver abuts the diaphragm and in the sagit
tal direction it extends from the ventral to the dorsal abdominal wall. The
liver is divided into a right and left lobe, and for surgical purposes the
border between these, which is not seen on the anatomical liver surface,
extends obliquely from the gallbladder fossa to the vena cava in the plane
of the middle hepatic vein. The caudate lobe is usually considered as a
separate entity and is situated between the inferior vena cava and the por
tal vein at the liver hilum.
1031
Figure 4.
US o f the liver. There is a subcap-
sular lesion 2 cm in diameter
within the liver parenchyma (be
tween arrows). This lesion is well
demarcated from the parenchyma.
The echogenicity o f this entity, a
rounded tumour, is clearly higher
than that o f the surrounding liver
parenchyma. This finding is consis
tent with the diagnosis ofhaeman-
gioma o f the liver.
PATHOLOGICAL CONDITIONS
Benign tumours
The three most important benign tumours of the liver are cavernous hae-
mangioma, adenoma, and focal nodular hyperplasia. Cysts are frequently
seen in the liver.
Haemangioma is the most frequently occurring liver tumour, both in
adults and children, and is an important lesion to consider in the differ
ential diagnosis of malignant tumours. On US a haemangioma is often
seen as a hyper-echogenic localized lesion (Fig. 4). On unenhanced CT
it is seen as a low-attenuation lesion but with intravenous contrast medium
it exhibits a characteristic enhancement from periphery to centre within
a few minutes (Fig. 5), a phenomenon that is particularly evident in large
tumours. On MRI a haemangioma shows a high signal intensity on T2-
weighted images with similar contrast dynamics to those seen on CT.
Fine-needle biopsy of a haemangioma may yield only blood and this find
ing is not specific. The diagnosis is usually made on a combination of at
least two imaging methods but angiography is rarely necessary.
Liver adenomas and focal hyperplasia (Fig. 6) (both of which are re
ported as being more frequent in females), may be isodense or hypodense
on non-enhanced CT, but may show some transient enhancement with
contrast medium.
1032
Figure 5.
Contrast-enhanced CT o f the
liver. An initially low-density
tumour is seen centrally in
the liver (*) (upper left im
age). After contrast injection
sequential scanning over
three minutes shows contrast
medium slowly filling in the
tumour from the periphery to
the centre. This finding is
typical o f a haemangioma.
Figure 6.
MRI o f the liver. A high-sig
nal lesion with a dark centre
is seen anteriorly in the liver
(arrows) on this sagittal, Tl-
weighted image. The finding
is consistent with the diagno
sis o f nodular hyperplasia.
The kidney is seen to the
right, posteriorly.
Cysts of varying sizes are frequently seen in the liver and may be soli
tary or multiple. Multiple cysts in the liver, pancreas and kidneys are a
feature of some specific disorders (e.g. autosomal dominant polycystic
disease, von Hippel-Lindau disease). On US a cyst has characteristic fea
tures, with well-defined sharp borders, echo-free contents and peripheral
echo enhancement. On CT the lesions are well defined, with contents ap
proximating to the density of water and exhibiting no contrast enhance
ment o f either their contents or walls (Fig. 7). Cyst walls may rarely be
1033
Figure 7.
CT o f the liver. A rounded struc
ture is seen which has well de
marcated walls and whose con
tents are o f water density (*). No
contrast enhancement is noted.
These features are typical o f a
liver cyst.
calcified. Hydatid cysts of the liver are common in endemic areas; they
may show a characteristic apearance, especially on CT, with septa and
walls that are frequently calcified (see Chapter 27).
Malignant tumours
Hepatomas or hepatocellular carcinomas are the commonest primary tu
mours of the liver. They occur with varying frequency in different parts
of the world and are commoner in males than females. Cirrhosis and he
patitis В are predisposing factors. They are usually well shown on US,
with both hypo- and hyper-echogenic areas (Fig. 8). On non-enhanced
CT the tumour may be isodense and identified solely by the fact that it
is a space-occuping lesion, but on contrast-enhanced CT the tumour is
characterized by an uneven pattern of contrast enhancement, usually with
areas of diminished density in the (necrotic) centre. There is often evi
dence of portal or hepatic venous invasion. It is important for surgical
planning to delineate the tumour borders and localize the lesion with re
spect to the surgical lobar liver anatomy. This also applies to grading of
the tumour with reference to any extrahepatic spread. In this respect, MRI
may offer some advantage over CT, because of its multiplanar features
(Fig. 9). The tumour may require differentiation from a cholangiocarci-
noma(Fig. 10).
1034
Figure 8.
US o f the liver. Subdiaphragmatically
there is a large 6 cm tumour (between
arrows) which is o f slightly higher
echogenicity than the surrounding
liver parenchyma, and which is well
demarcated from it. These features
are consistent with the diagnosis o f a
hepatoma.
Figure 9.
MRI o f the liver (fat suppression STIR
sequence). Posteriorly, a lobulated tu
mour o f high signal intensity is seen,
with several smaller satellite tumours.
These features are conistent with the
diagnosis o f hepatoma.
Figure 10.
Contrast-enhanced CT o f the liver.
Centrally in the liver there is a large
tumour (arrows) with dark areas o f
central necrosis and mixed attenua
tion in its periphery. In the ventral
part o f the liver a separate small le
sion is seen (arrowhead), suggestive
o f a metastasis. This tumour, how
ever, proved to be a cholangiocarci-
noma.
1035
Figure 11.
US o f the liver. A large tumour o f mixed
echogenicity (between arrows) is seen
which is well demarcated from the liver
parenchyma (L). The tumour proved to be
a metastasis from a breast carcinoma.
Figure 12. CT o f liver metastases. (a) Two large, expanding lesions (arrows) are seen
within the liver. They show mixed attenuation and enhancement, with dark areas o f
necrosis. In addition, two smaller lesions are seen in the lateral segment o f the left
lobe (arrow-heads). These tumours were metastatic deposits from an angioneurosar-
coma. (b) A 2 cm metastasis (arrows) is demonstrated as a lesion with decreased con
trast enhancement in comparison with the surounding liver parenchyma. In this case
the contrast medium was injected directly in the superior mesenteric artery, which is
said to be the most efficient way to demonstrate small foci in the liver on CT. Note that
no contrast medium is seen in the aorta.
The therapeutic embolization of liver tumours by catheter or direct in

jection is a technique in widespread use. Its value has not yet been de
termined with certainty, however, not least because embolization meth
ods are continually evolving - a factor that makes long-term controlled
trials difficult to conduct.
1036
Figure 13.
MRI o f liver metastases. On
this Tl-weighted image two
metastatic lesions (arrows)
are seen, showing varying
signal intensities.
The most frequent malignant tumours in the liver are metastases from
other primary carcinomas. On US metastatic deposits may be seen as
lesions which may be hypo- or hyper-echogenic in comparison to the
surrounding parenchyma, or may show mixed echogenicity (Fig. 11).
Metastatic lesions are usually multiple. On CT metastases are often seen
as hypodense lesions that remain as such after the injection of contrast
medium (Fig. 12). Certain metastases (e.g. hypernephroma) are hyper-
vascular and therefore show increased contrast enhancement. MRI
seems to be the most sensitive method for detecting liver metastases and
the accuracy of the method may be enhanced by the use of magnetic
contrast agents (Fig. 13). CT-portography may also help in the diagno
sis of metastases.
Other focal lesions

Abscesses usually result from systemic infections, but may also result
from a focus of infection elsewhere in the body, or be amoebic in origin.
The abscesses may be solitary or multiple and vary in size and shape. On
US an abscess is well seen, but the findings are non-specific. On CT ab
scesses are hypodense, with contrast enhancement of their peripheral
wall (Fig. 14). On MRI there may be increased signal intensity on T2-
weighted images (Fig. 15), with contrast features similar to those seen
in CT. Fine-needle biopsy is usually necessary to establish the diagno
sis. Percutaneous drainage has become an important alternative to
surgery in the treatment of hepatic abscesses.
Trauma to the abdomen may result in rupture of the liver, with the for
mation of an intraparenchymal and/or subcapsular haematoma. In these
1037
Figure 14.
CT o f the liver. Two typical abscesses
are demonstrated, one showing a thick
abscess wall (large arrow), the other
showing a well demarcated smooth wall
(small arrow).
Figure 15.
M RI o f the liver. On this T2-
weighted fa t suppression STIR-
sequence image multiple foci o f
increased density are seen, the
cause being fungal abscesses o f
the liver. Only the largest foci
were seen on ultrasound or CT,
and this study shows the sensi
tivity o f M RI in detecting small
focal hepatic lesions.
Figure 16.
CT o f liver trauma. Contrast
enhancement brings out the he
patic veins, and CT demon
strates decreased perfusion o f
the right lobe o f the liver, de
marcated by the middle hepatic
vein (arrow). This finding indi
cates that the artery o f the right
hepatic lobe is severed. A trau
matic rift is also seen in the left
lobe in the region o f the falci
form ligament.
1038
Figure 17.
US o f fatty liver. The echogenicity
o f the liver is coarse and clearly
increased in comparison with nor
mal liver (the so-called "bright-
liver”-pattern).
L = liver; К = kidney.
cases the other parenchymal organs have to be studied for traumatic le
sions as well, On US a rupture of haematoma is seen as a hypo-echoic
area. The imaging method of choice in traumatic cases is contrast-en
hanced CT (Fig. 16), which makes it possible to differentiate between
haematoma, other fluid collections (bile) and normal parenchyma. On
MRI a haematoma is seen usually as a lesion with increased signal.
Since many focal liver lesions, with the exception o f cysts, do not show
diagnostically characteristic features on any imaging method, fine-nee-
dle biopsy verification is usually essential to establish the diagnosis. For
some liver disorders a cutting-needle biopsy may be preferable and this
can be obtained with embolization of the track, particularly if there is a
likelihood of haemorrhage (see below).
Parenchymal disease
Fatty degeneration of the liver is fairly common, especially with certain
diseases such as alcoholism, diabetes or chronic infections. On ultra
sound this condition may give increased echogenicity of the liver
parenchyma ("bright liver") (Fig. 17). CT allows direct density mea
surements of the liver, and since fat shows low attenuation this permits
quantitative evaluation of the disease (Fig. 18). The degree of fatty in-
1039
Figure 18. CT o f fatty liver.

The attenuation o f the liver is
markedly reduced, and clearly
less than that o f the spleen, a
feature evident even without
contrast enhancement. Note
that the hepatic veins are visi
ble against the dark liver
parenchyma even without con
trast enhancement. The den
sity o f the liver parenchyma
(R O I1) was measured as
-5, 7 HU, and that o f the
spleen (ROI 2) as 37,5 HU.
Very low and even negative
attenuation values may be
seen on CT o f a fatty liver.
filtration may change rather rapidly, according to the stage of the un
derlying disease. An attenuation of less than 30 HU is a clear indication
of fatty infiltration. The changes may only be segmental or focal. Other
focal lesions such as tumours or metastases, are well seen in a fatty liver,
since they have normal density. A fatty liver is usually larger than a nor
mal liver.
Liver cirrhosis may vary in appearance and depending on its aetiol
ogy the liver may be either smaller or larger than normal. Dynamic CT
may show pathological patterns of perfusion of the liver and spleen,
which may also be seen on colour Doppler US.
Clinical information is also important in the evaluation of parenchy
mal liver disease.
One of the commonest and important interventional techniques is guided
fine-needle biopsy which is most easily performed under US-control (Fig.
19). Needle biopsies are important, since neither focal nor diffuse liver
disease necessarily exhibit diagnostic features on imaging. In some dis
orders a cutting needle biopsy is required and in patients with abnormal
coagulation parameters this is most safely obtained using either the trans
jugular approach or a percutaneous technique with embolization of the
biopsy track after obtaining the specimen.
The drainage of liver abscesses ox: sub-phrenic abscesses is another
important interventional technique that has greatly reduced the need for
1040
Figure 19.
US guidance o f fine needle biopsy. A
percutaneous fine needle biopsy o f a
liver tumour is demonstrated, show
ing the echo from the needle (curved
arrows) within the tumour (between
straight arrows). Normal liver
parenchyma (L) is seen to the left.
surgery in the management of such lesions.

Liver tumours may be treated by embolization or direct ethanol inje-
tion. Both methods are under investigation. Embolization can be partic
ularly useful in the palliative treatment of functioning endocrine metas
tases in the liver. Hepatic bleeding from trauma, biopsy, aneurysm or
other causes is often most effectively treated by embolization. In insti
tutions with the requisite interventional expertise, embolization is the
treatment method of first choice for most types of hepato-biliary haem
orrhage.
There are a number of interventional procedures such as percutaneous
transhepatic portography and percutaneous transhepatic cholangiogra
phy that use the liver as the most suitable access point. Through these
routes a number of interventional procedures may be performed, de
scribed elsewhere in this book. Another important new technique is that
of percutaneous porto-systemic shunting (TIPPS).
1041
The biliary tract
Imaging the gallbladder has changed dramatically in the past two

decades. Peroral cholecystography used to be, and in some
countries still is, the primary method for studying the gallbladder. In re
cent years, however, ultrasonography has almost completely replaced
this technique. Ultrasonography is also important in imaging the biliary
ducts, but a complete assessment still relies on their opacification with
contrast medium.
MODALITIES
Ultrasonograhy
The gallbladder is studied by US with a 3.5-5 mHz transducer. The or
gan is studied in both its longitudinal (Fig. 20) and transverse axes, with
the patient lying supine. Views are also obtained with the patient turned
to the left and upright views are sometimes required. Positional changes
help in the diagnosis of gallstones that move with gravity. The extra-
hepatic biliary ducts are well seen by US, but the intrahepatic ducts are
more difficult to image unless they are dilated. The most distal part of
the common bile duct is not usually seen, because of interference with
the image by gas in the duodenum. The overall diagnostic accuracy of
US of the gallbladder is 90-95% .
Peroral cholecystography
Peroral cholecystography was the primary method for imaging the gall
bladder for over 50 years (since its introduction in 1925), until ultra
sonography largely replaced it in the early 1980's. In some departments,
however, oral cholecystography is still employed (Fig. 21).
In peroral cholecystography the contrast medium is administered by
mouth as tablets, absorbed through the intestinal mucosa, bound to al
bumin in the blood and transported to the liver. From the liver the medium
is excreted into the biliary ducts and concentrated in the gallbladder.
Sodium ipodate and calcium ipodate, however, are concentrated by the
liver and are thus not dependent on the gallbladder's concentrating ca-
1042
Figure 20.
US o f the gallbladder. The
normal gallbladder (gb) is
seen as a cystic structure with
echo-free contents. The walls
o f the gallbladder are smooth.
Normal liver parenchyma (L)
is seen to the left o f the gall
bladder.
Figure 21.
A normal cholecystogram.
(a) In the initial phase the
contrast medium is seen
evenly filling the gallbladder,
the walls o f which are
smooth, (b) After a fatty
meal, the gallbladder has
contracted. Now both the
fundus and the neck o f the
gallbladder, as well as the
cystic duct are filled with
contrast medium and the
common bile duct is demon
strated (arrows).
1043
pacity. When its iodine content exceeds 0.5% the gallbladder is visible
on fluoroscopy and conventional radiographs. The concentration of con
trast medium reaches its maximum 10-15 hours after ingestion and imag
ing usually takes place on the day following ingestion. Some centres ad
vocate a scheme whereby a double dose of contrast medium is ingested
on two consecutive days before the study.
Non-opacification of the gallbladder may indicate gallbladder disease,
such as obstruction of the cystic duct. It may, however, also result from
liver disease or disorders resulting in disturbances in the absorption of
contrast medium from the gut, e.g. diarrhoea. Sometimes the patient may
not even have taken the contrast medium or there may have been a pre
vious cholecystectomy. Gallstones are seen as filling defects in the opaci
fied gallbladder. Most gallstones contain some calcium, and in 15-20%
of cases this is enough for the stones to be seen on a plain radiograph.
The gallbladder is radiographed in multiple projections including some
using external compression. The study is often completed by exposing
a so-called contraction film of the gallbladder 1/2-1 hour after the in
gestion of a fatty meal. This may show the changes of adenomyomato-
sis or cholesterolosis.
The diagnostic accuracy o f cholecystography in diagnosing gall-stones
is 85-90% , i.e. slightly less than that of US though the methods are to
some extent complementary. The use of peroral cholecystography has
undergone a modest revival with the increasing popularity of non-oper
ative methods of treating gallstones.
Cholangiography, biligraphy
Visualization of the extrahepatic biliary ducts may require the intra
venous administration of contrast medium. On intravenous cholangiog
raphy the contrast medium is given intravenously as a slow infusion for
approximately 1/2 hour. The contrast medium is bound to the albumin
in the blood and excreted by the liver into the bile. The concentration of
contrast medium in the biliary tree is usually so low that the ducts can
only be demonstrated by tomography. Some contrast material is also seen
in the gallblader, but since it is immiscible with bile and forms a sepa
rate layer in the organ, the method is unsuitable for the diagnosis of gall
bladder disease or stones. Allergic reactions may still occur on intra
venous cholangiography, and the mortality is not insignificant. The di
agnostic accuracy of the method is only 50-60 % and it should be
1044
employed only when good indications exist and in those cases where
other available methods (US, ERC, PTC, CT) are unhelpful. There has
been some renewed interest in this technique in patients prior to laparo
scopic cholecystectomy.
Percutaneous transhepatic cholangiography

Percutaneous transhepatic cholangiography (PTC) (see Fig. 35) entails
the puncture of an intrahepatic biliary duct, by a percutaneously intro
duced needle. The procedure is performed under US guidance, and is
successful in 95-98% of subjects with dilated ducts and 80% of those
with non-dilated ducts. The biliary ducts are filled with contrast medium
through the needle. The frequency of complications is not insigifnicant,
but depends on the type of needle used. With a Chiba needle it is ap
proximately 2%. Through the needle a guide wire can be negotiated into
the biliary ducts, for the introduction of various catheters or instruments
(see Chapter 8).
Endoscopic retrograde cholangiography

Endoscopic retrograde cholangiography (ERC) (see Fig. 36) entails
cannulation of the papilla of Vater through an endoscope introduced via
the stomach into the duodenum. Contrast medium (low osmolar) is in
jected through the cannula retrogradely into the common bile duct fill
ing the extra- and intrahepatic biliary ducts and the pancreatic duct. The
contrast medium injection is performed under fluoroscopic control.
Overdistension of the biliary tree and especially the pancreatic duct
should be avoided; in the latter case it may cause pancreatitis.
Radiographs are exposed in various projections when the injection is
complete. The study requires an experienced endoscopist and has an
80-90% success rate. Care should be taken not to introduce air into the
biliary tree, since air bubbles may be mistaken for stones; bubbles, how
ever, are always round and move freely with gravity into the uppermost
part of the duct when the patient is moved into an upright position.
Peroperative cholangiography
Peroperative cholangiography is performed in the operating theatre dur
ing operative procedures involving the biliary ducts, and entails the in
jection of contrast medium directly into the exposed biliary ducts through
a needle or cannula. Several injections may be necessary during the study
1045
for maximum diagnostic benefit.

Peroperative cholangiography is performed in order to diagnose or ex
clude the existence of concretions in the biliary tree or to demonstrate a
biliary leak. It is also occasionally used to record biliary tract anatomy.
In many centres it is performed routinely during cholecystectomy. Care
should be taken to avoid the introduction of air bubbles into the biliary
tracts (see section on ERC).
Postoperative cholangiography
Postoperative cholangiography entails the injection of contrast medium
through the T-tube used to decompress the biliary tree following opera
tive procedures. The procedure is usually performed 7-10 days after
cholecystectomy to check for any residual biliary concretions. The con
trast medium should be diluted so that small stones are not obscured. The
procedure is performed under fluoroscopic control and films are exposed
in various projections. Care should be taken to avoid the introduction of
air into the biliary tract, since this may simulate stones (see section on
ERC).
Radionuclide imaging or gammascintigraphy is performed to evalutae
biliary dynamics. The most commonly used agent is 99m Tc-HIDA
which is injected intravenously, where it is bound to albumin and then
excreted through the liver into the bile. The activity over the liver, bil
iary ducts and small intestine is sequentially recorded using a gamma
camera. The study gives information on hepatic function and biliary flow.
It may show reduced flow in, for example, strictures of the biliary tree
or calculus obstruction, non-filling of the gallbladder in obstruction of
the cystic duct, or leakage o f bile from the biliary tree. In normal sub
jects the study takes approximately one hour, but it may take up to 24
hours if the flow of bile is retarded. Radionuclide imaging of the biliary
tree has lost much of its importance with the introduction of other imag
ing methods, such as US, CT and MRI, but may still be useful in special
cases where information on biliary dynamics is important, where direct
visualization of the biliary tree with injected contrast medium is unsuc
cessful, or if the patient is strongly allergic to contrast medium.
1046

The value of MRI has yet to be established in the study of the biliary
ducts but newer techniques that permit so-called MRI-cholangiography
may be valuable in the near future. In gallbladder cancer MRI may be
important in both diagnosis and staging.
Choice of imaging method

Ultrasonography has become the primary imaging technique in the eval
uation of the gallbladder. It has the advantages of being precise, easy and
quick to perform. It gives information on the contents and wall of the or
gan, as well as the surrounding tissues. Stones, cholesterolosis, adeno-
myomatosis, inflammation and tumours are all diagnosed with great pre
cision. Peroral cholecystography is still used in many centres, as being
a relatively easily performed and accurate diagnostic method, especially
in calculus disease. It is still a useful secondary method if the findings
on US are unclear, if there is a discrepancy between the clinical assess
ment and the US findings, or if non-operative treatment of gallstones is
planned. Computed tomography is performed if gallbladder cancer is
suspected.
Ultrasound is also the primary method for studying the intrahepatic
and proximal extrahepatic biliary ducts, giving information on ductal cal
ibre. This is important when studying an icteric patient for example, when
it can distinguish between extrahepatic obstruction and intrahepatic dis
ease. CT gives additional information concerning the biliary tree and sur
rounding structures, PTC or ERCP direct information concerning the bil
iary tree.
NORMAL ANATOMY
The biliary ducts

The intrahepatic biliary ducts from the right and left lobes unite at the
hilum to form the common hepatic duct. This lies to the right of the he
patic artery and ventral to the portal vein. The hepatic duct runs caudally
and medially towards the duodenum. The cystic duct, 3 ^ cm in length,
joins the hepatic duct to form the common bile duct. This is 6-8 cm long
and approximately 6 mm wide. The common bile duct and the portal vein
both lie in the hepatoduodenal ligament. The most distal part of the com
mon bile duct runs in the head of the pancreas, surrounded by pancreatic
1047
tissue, before it joins the pancreatic duct from the right to run into the
duodenum in the major papilla o f Vater.
The gallbladder
The gallbladder lies on the inferior surface of the liver, and its own in
ferior surface is covered by peritoneum. The organ is 7-10 cm long and
3 cm in diameter with a volume of 30-50 ml. The thickness of its wall
is 2-3 mm. The fundus of the gallbladder points ventrally and the neck
runs dorsally into the cystic duct.
Gallbladder anomalies occur, the commonest being a septum, usually
situated in the fundus which partially divides the organ (the "Phrygian
cap"). Very infrequently agenesis occurs resulting in absence of the gall
bladder. Duplication or even triplication of the gallbladder may occur
but these anomalies are very rare.
Gallbladder
Gallstone disease
Stones or concretions frequently occur in the gallbladder. Clinically the
stones do not occur in isolation, but form part of an entity, gallstone dis
ease. Stones occur about twice as frequently in women as in men. The
majority of stones are cholesterol stones and less than 10% are pigment
stones. Approximately 15-20% of calculi contain calcium and can be
seen on a plain radiograph (Fig. 22). US is the primary method for iden
tifying gallstones. A stone is seen as a rounded, echodense structure, with
a typical acoustic shadow behind it (Fig. 23). Sometimes, especially if
the gallblader is small and deformed, only the acoustic shadow is seen,
the stone itself being difficult to visualize. There are a multitude of US
features associated with the presence of gallbladder stones and the accu
racy of detection of stones on US is very high, approximately 95-98%.
In contrast, stones in the extrahepatic bile ducts may be difficult to vi
sualize on US, bowel gas often interfering with interpretation. Oral chole
cystography has traditionally been regarded as one of the most accurate
radiological methods so far as the diagnosis of gallstones is concerned
but its accuracy is only 85-90%. Gallstones are seen in the contrast-filled
gallbladder as dark filling defects (Fig. 24). The drawback with chole-
1048
Figure 22.
Gallstones containing calcium may be
seen on a plain film, without contrast
medium. Here several gallstones are
seen as a row o f white circles on an
abdominal overview roentgenogram.
Figure 23.
US o f a gallstone. The gallbladder
(gb) is seen as a dark, echo-free cystic
structure. It contains a stone (arrow)
giving distal acoustic shadowing (ar
rowheads).
cystography is that a diseased gallbladder does not concentrate contrast

medium, which means that in circumstances in which the gallbladder
wall is inflamed or fibrotic, or the cystic duct obliterated, the organ re-
1049
Figure 24.
Cholecystogram showing multiple
gallstones, which are seen as filling
defects in the contrast-filled gall
bladder.
Figure 25.
Floating gallstones, seen as a layer
o f filling defects in the contrast-
filled gallbladder with the patient
erect.
mains unopacified. Ultrasound is not dependent upon contrast medium

concentration and demonstrates calculi irrespective of the presence of
other gallbladder disorders. Plain film or CT scanning may give some
clues as to the likely composition of stones. Cholesterol stones are usu
ally uncalcified but if calcium is present it often occurs as a ring-like
structure in the stone. In pigment stones the calcium is usually centrally
located. Cholesterol stones may be lighter than the contrast-filled bile
1050
Figure 26.
US o f acute cholecystitis. The gall
bladder (arrows) is filled with
echogenic biliary sludge, and there is
a stone (arrowhead) giving an
acoustic shadow.
and may thus be "floating" on oral cholecystography; they may also form
a layer in the contrast-filled gallbladder, which is seen when a film is ex
posed with the patient in the upright position (Fig. 25). In cholesterol
stones gas-filled fissures may be seen as dark linear strucures - the so-
called Mercedes-Benz sign.
Cholecystitis
Cholecystitis may be acute or chronic. Acute cholecystitis used to be a
diagnosis in which imaging was unhelpful. Peroral cholecystography
could only show that the gallbladder was "non-functioning" as the in
flamed organ does not concentrate oral contrast medium. Fortunately,
the situation is now very different.
Ultrasound has become the primary method for imaging acute chole
cystitis, because the technique demonstrates not only the gallbladder wall
and its contents, but also the adjacent tissues (Fig. 26). On US an in
flamed gallbladder wall appears thicker than normal (over 3 mm) and
with good technique even the various layers of the wall may be identi
fied. Other diseases such as pancreatitis and liver disease, however, may
also cause thickening of the bladder wall. Changes in the surrounding
tissues may include oedema or fluid collections. On US the organ can be
palpated under visual control, and may be tender, the so-called "ultra
sound Murphy's sign". The gallbladder often contains gallstones (pre
sent in 90-95% of cases) or sedimentation of its contents ("sludge"), but
1051
Figure 27.
Porcelain gallbladder. The walls o f the
gallbladder are calcified, and visible on
the plain film without contrast medium;
this phenomenon may be seen as a
sequela to chronic cholecystitis.
Figure 28.
Limey-bile. As a sequel o f chronic chole
cystitis, the gallbladder may contain cal
cified biliary "sludge", which is here visi
ble on a plain film, without the patient
having taken contrast medium.
these are non-specific findings which may occur in the absence of chole
cystitis. Conversely, in so-called acalculous cholecystitis, stones are not
present although the other signs of acute cholecystitis described above
are often present. CT may show the same findings as US and though the
information given by CT is often not as detailed and precise as that given
by ultrasound, any changes present in the surrounding tissues may be
1052
Figure 29.
US o f the gallbladder. The gallbladder
wall is thicker than normal and slightly
uneven. There are several rounded poly
poid structures (arrows) arising from
the bladder wall and protruding into the
bladder lumen. These structures do not
show any acoustic echo. The findings
are compatible with hyperplastic chole-
cystosis.
better shown on CT. A radionu

clide study performed with 99m
Tc-HIDA may show non-activity
over the gallbladder, as a sign of
cystic duct obstruction.
As a sequela to chronic chole
cystitis, the gallbladder wall may
calcify and appear on the plain
film as a so-called ’’porcelain
gallbladder” (Fig. 27). For the
same reason the organ may con
tain calcified ’’sludge’’ which is
also visible on the plain film, i.e.
"limey bile” (Fig. 28).
Hyperplastic cholecystoses
Cholesterolosis and adenomyomatosis belong to a group of disorders
termed the hyperplastic cholecystoses, which share the feature of poly
poid lesions of the gallbladder wall. The term cholesterolosis implies the
presence of polypoid deposits of cholesterol in the bladder mucosa
(’’strawberry gallbladder”). In adenomyomatosis there are epithelial mu
cosal sinuses ("Rokitansky-Aschoff sinuses”) extending between poly
poid formations of localized muscular hypertrophy; these sinuses may
vary greatly in size from the minute to the very large. If the polyps are
bigger than 1 mm, they will show on both ultrasound and peroral chole
cystography as typical lesions protruding from the surface of the wall
into the bladder lumen (Fig. 29). Larger polyps may be difficult to dis
tinguish from stones, but stones usually move with changes in posture
1053
Figure 30.
Gallbladder carcinoma, (a) US o f
the gallbladder. There is an
exophytic growth o f a lobulated tu
mour (*) into the gallbladder (gb),
with infiltration o f the tumour
beyond the gallbladder wall. This
tumour did not move with changes in
posture. These features are sugges
tive o f gallbladder carcinoma, (b)
CT o f the same patient shows the
tumour (arrow) extending into the
gallbladder. Possible tumour infil
tration into the surounding liver
cannot be visualized even on this
contrast-enhanced CT scan.
whereas polyps do not. Furthermore, on US there is no acoustic shadow

behind a polyp.
Gallbladder carcinoma
Gallbladder carcinoma is relatively rare, seen in approximately 0.1 % o f
patients with gallstones. On US a carcinoma may be seen as a space-oc-
cupying lesion in the gallbladder area, as a hypo-echoic mass within the
gallbladder, or as a generalised thickening of the bladder wall (Fig. 30).
It is important to note any extension of the tumour into the surrounding
1054
Figure 31.
Intravenous cholangiography (tomogra
phy) shows dilated extrahepatic biliary
ducts. Distally in the choledochal duct
an obstructing concretion is seen as a
filling defect (arrows).
tissues but this may be difficult to define on US. Peroral cholecystogra

phy is not usually helpful, because of non-visualization of the gallblad
der. CT may show similar changes to ultrasound but usually demonstrates
the extent of the tumour better than the latter technique and should al
ways be obtained in order to assess the potential operability of the lesion.
Biliary duct disease

Gallstones in the extra-hepatic biliary ducts are difficult to evaluate by
US, which has an accuracy of 20-50% in this examination. The biliary
tree is difficult to visualize throughout its length and the common bile
duct in particular may be obscured by bowel contents and gas. A stone
in a normal duct, under 6 mm, may be difficult to discern, whereas a
stone in a dilated duct is easier to see. In non-diagnostic or doubtful cases
contrast media studies such as intravenous cholangiography (Fig. 31),
ERC or PTC should be undertaken. Thin-slice computed tomography
may also be helpful but without oral contrast medium (which may ob
scure a calculus in the lower common bile duct).
Peroperative and postoperative cholangiography is performed to rule
out or diagnose residual stones in the biliary ducts (Fig. 32). Stenosis or
obstruction of the extrahepatic ducts is sometimes seen as a consequence
of trauma occurring during abdominal operations involving the biliary
1055
Figure 32.
(a) Per operative needle cholangiography reveals multiple stones in the extrahepatic
biliary ducts, seen as roundedfilling defects. The needle is marked by arrows.
(b) Postoperative T-tube cholangiography reveals several residual stones in the intra-
and extrahepatic biliary ducts (arrows). The T-tube is marked by arrowheads.
tree, such as a cholecystectomy (Figs. 33, 34). Most obstructing lesions

are, however, tumours (fig. 35), principally carcinoma of the head of the
pancreas. Sclerosing cholangitis causes multiple strictures in both the in-
tra- and extrahepatic ducts (Fig. 36). In Caroli's disease there are ectatic
dilatations of the intrahepatic ducts. A choledochal cyst shows as an area
of dilatation of the distal choledochal duct (Fig. 37). All these changes
are best shown on endoscopic or percutaneous cholangiography.
1056
Figure 33.
Endoscopic retrograde cholangiogra
phy. Contrast medium has been intro
duced in a retrograde fashion through
cannulation o f the papilla o f Vater. The
endoscope is seen in the picture. There is
a post-operative stricture in the hepatic
duct (arrow) and a stone (arrowheads) is
seen as a filling defect in the dilated bil
iary ducts above the stricture.
Figure 34. A patient who had undergone

a previous transduodenal papillotomy,
presented with jaundice and epigastric
pain, (a) Ultrasonogram, showing di
lated intrahepatic biliary ducts, seen as
dark, branching streaks in the liver
parenchyma, (b) Endoscopic retrograde
cholangiography demonstrates dilated
intra- and extrahepatic biliary ducts and
a very tight narrowing o f the distal
sphincter area. At autopsy purulent
cholangitis was diagnosed, the common
bile duct measured 3 cm in diameter and
had a fibrotic narrowing at its distal end,
extending fo r 3 cm above the papilla o f
Vater.
1057
Figure 35. Percutaneous transhepatic Figure 36. ERCP. There are several ar
cholangiography shows narrowing (be eas o f narrowing o f both the intra- and
tween broad arrows) o f the biliary ducts in extrahepatic ducts (arrows), compatible
the area o f the liver hilum and the proximal with sclerosing cholangitis. The patient
hepatic duct The biliary ducts in both the had had ulcerative colitis fo r several
right and the left liver lobes are dilated years.
above the central narrowing (fine arrows).
Note absence offilling o f the gallbladder.
The patient presented with jaundice,
colourless stools and epigastric pain.
Cholangiocarcinoma.
Figure 37.
Peroperative cholangiography. A cystic
dilatation (arrows) o f the most distal seg
ment o f the common bile duct is demon
strated on this left oblique image. The
finding is compatible with a choledocho-
cele or choledochal cyst.
1058
Figure 38. Stenting o f biliary ducts, (a) A short stricture is seen in the liver hilum (ar
row) on an ERCP o f a patient with Klatzkin-tumour. Dilatation o f the proximal intra-
hepatic bile ducts is noted, (b) A stent (arrows) has been introduced via the endoscope
into the biliary duct and through the stricture, the proximal end o f the stent lodging in
the confluence o f the intrahepatic bile ducts above the stricture and its distal end in the
duodenum.
The biliary ducts may be approached in a number of ways; retrogradely
through the papilla of Vater, antegradely by means of percutaneous trans-
hepatic puncture or through the gallbladder.
A sphincterotomy or papillotomy may be performed through an en
doscope, and this facilitates the passage of gallstones from the extra
hepatic ducts into the duodenum; the technique can be used in poor-risk
patients.
1059
Figure 39.
Cholecystostomy. A drainage tube
has been introducedpercutaneously
into the gallbladder. The draining
catheter has slipped out o f the gall
bladder and its tip now lodges in a
fistula from the gallbladder to the
skin.
The transhepatic approach allows the institution of either external or

internal biliary drainage and can also be used for the percutaneous in
troduction of instruments for the dilatation of stenosed biliary ducts.
The same treatment may also be performed via the endoscopic route
(Fig. 38).
The gallbladder can be percutaneously punctured and drained through
a catheter, a technique that is particularly suitable in those cases of acute
cholecystitis where surgery is thought to be inappropriate (Fig. 39).
1060
The pancreas
MODALITIES
The plain radiograph

The plain radiograph is of only limited value in the diagnosis of disor
ders of the pancreas. The pancreas itself is not seen on the plain radi
ograph, because the organ does not normally contain contrast-forming
elements and its surrounding fat planes are inconspicuous. Areas of cal
cification, however, are well seen, and this finding is o f diagnostic value:
characteristic types of calcification may be seen in the pancreatic duct
following chronic pancreatitis, in the walls of calcified pseudocysts or
in the pancreatic parenchyma in hereditary pancreatitis (Fig. 40).
In acute pancreatitis non-specific secondary changes may be seen, e.g.
dilatation of loops of bowel in the upper abdomen or an increase in the
distance between the distended stomach and the transverse colon owing
to the presence of mesenteric oedema. Basal pulmonary infiltrates and
pleural exudates, most commonly left-sided, are frequently seen in acute
pancreatitis, but these findings are also nonspecific. When a large pan
creatic cyst or abscess is present, upward displacement of the dilated
stomach or downward displacement of the transverse colon may be seen.
Gas formation in the pancreas is a pathognomonic sign of a pancreatic
abscess. Absence of the right psoas shadow might suggest the presence
of a retroperitoneal fluid collection.
Duodenography
Enlargement of the head of the pancreas, e.g. from a pancreatic cancer
or cyst, may distort or distend the duodenal loop (Frostberg’s sign, or the
’’inverted 3" sign). This may be seen on a single or double-contrast bar
ium study. The sign is indirect and only seen with marked expansion of
the pancreatic head. Barium duodenography has decreased in importance
with the greater use of cross-sectional imaging techniques such as ultra
sound and CT.
1061
Figure 40.
Calcification o f
the pancreatic
parenchyma
(arrows) seen in
a case o f hered
itary pancreati
tis. The calcifi
cation is visible
on the plain film
and is so exten
sive it defines
the shape o f the
organ.
Ultrasonography
The primary method for studying pancreatic disease is ultrasonography
(US). The pancreas may be visualized by ultrasonography in approxi
mately 85 % of subjects, but in the remainder the organ is partly or wholly
obscured by bowel gas or other bowel contents; this problem is particu
larly evident in acute disease associated with secondary dilatation of gas-
containing bowel loops. The echogenicity of the pancreas is normally
somewhat greater than that of the liver. In most individuals, using good
equipment, the normal pancreatic duct is seen as a narrow streak in the
pancreatic parenchyma and the caudal portion of the common bile duct
is also seen as it enters the head of the pancreas. Important landmarks in
the vicinity of the pancreas include the inferior vena cava, the superior
mesenteric artery and vein, the splenic artery and vein, the hepatic artery
and the portal vein (Fig. 41). It is important to assess the calibre of the
pancreatic and choledochal ducts which are normally 1-3 mm and ap
proximately 5 mm, respectively. Dilated pancreatic ducts indicate either
obstruction or duct ectasia in chronic pancreatitis. Pancreatic tumours
are generally solid lesions and are usually of lower echogenicity than the
surrounding parenchyma. The smallest tumours that can be detected by
US are approximately 1 cm in diameter. Cysts are echofree and show
distal acoustic enhancement. Doppler-US (particularly colour Doppler-
US) is useful to assess the peripancreatic blood vessels which may be in
volved in acute and chronic pancreatitis or by pancreatic neoplasms.
Intra-pancreatic vessels may also be visualized and changes in normal
1062
Figure 41.
Normal pancreas, (a) The pancreas is
seen on ultrasound as a structure o f
moderate echogenicity (arrows); a =
aorta; с = vena cava; * = venous con
fluence. (b-d) CT o f the pancreas
shows the retroperitoneal organ, de
marcated by fat, and extending from
the duodenum (d) on the patient's right
to the spleen (s) on the left. The
amount o f pancreatic parenchyma and
demarcating fa t planes varies with
age, b is a normal adult, с a child, and
d an old person, (e) On MRI (Turbo
Flash) the pancreas is also well
demonstrated.
1063
vascularity may be useful in tumour diagnosis. Ultrasound and CT are

complementary techniques in the diagnosis of pancreatic disease.
Computed tomography
The importance of US in the diagnosis of pancreatic disorders has al
ready been emphasized but CT provides important information that can
not be obtained by US alone and, together, the two techniques are the
most important imaging methods for the organ. The retro-peritoneal fat
that surrounds the pancreas in many patients affords good delineation of
the organ on CT (Fig. 41), even in the presence o f dilated bowel loops
and oedema, circumstances which considerably diminish the diagnostic
efficiency of ultrasound. Image quality may, however, be adversely af
fected by patient movement, e.g. in a restless subject with abdominal
pain. Both cysts and areas o f calcification are imaged with great clarity
and the use of intravenous contrast medium enhances the detection of
pathological changes in many situations. Tumours, for instance, show
slower contrast enhancement than normal pancreatic parenchyma, but
the CT-study has to be performed when the contrast difference between
the tumour and parenchyma is maximal, i.e. within two minutes of a bo
lus injection of contrast medium. Cysts do not enhance with contrast
medium. In addition to the pancreas itself, neighbouring organs are bet
ter seen on CT than US, e.g. the biliary ducts, kidneys, spleen, bowel and
mesentery, and this allows for the precise grading of pancreatic disease
by CT. Opacification of the bowel with oral contrast medium is impor
tant, in order to differentiate between bowel loops and some type of pan
creatic pathology such as tumours or cysts (though not acute pancreati
tis). Fast CT-scanners will further improve the diagnostic capabilities of
computed tomography in the pancreas.
ERCP
At endoscopic retrograde cholangiopancreatography (ERCP) the papilla
of Vater is cannulated under direct visual control through an endoscope
which has been introduced via the oesophagus and stomach into the duo
denum, and water soluble contrast medium is injected into the pancre
atic duct (Fig. 42). The study provides information about the ductal sys
tem, but not about the pancreatic parenchyma. Pancreatitis is a recog
nized complication of the technique which can result from either the
manipulation required for duct catheterization or the action of the con-
1064
Figure 42. Normal en

doscopic retrograde pan
creatogram. The pancre
atic duct o f Wirsung is
seen. The main duct is
filled, but the side bran
ches only minimally. The
diameter o f the duct in
the pancreatic head,
body and tail, respectiv
ely, is indicated in milli
meters, and the diameter
o f the endoscope is also
shown fo r comparison.
trast medium on the pancreas. Care has to be taken, therefore, not to over
fill the ductal system and dilute, non-ionic, contrast medium should be
used. Images of the ductal system are taken in various projections under
fluoroscopic control.
ERCP shows changes such as distortion or obstruction of the main
ducts or their branches as may occur in cancer, or may reveal commu
nications between the ducts and pancreatic cysts. The main value of
ERCP is in the mapping and grading of changes in chronic pancreatitis
and in fully delineating the pancreatic duct before pancreatic resection.
In the evaluation of changes in the head of the pancreas it is also impor
tant to visualize the common bile duct, the distal portion of which tra
verses this region.
Angiography
Angiography used to be the definitive method for the diagnosis of pan
creatic tumours. Since the introduction of US, CT, MRI and ERCP as di
rect imaging methods, however, the role of angiography has been reduced
to the diagnosis and preoperative localization of endocrine tumours and,
occasionally, the provision of further information on the potential oper
ability of a pancreatic cancer in particular cases. Pancreatic angiography
is performed by studies of the coeliac and superior mesenteric arteries,
from which multiple smaller arterial branches supply the pancreas.
Superselective studies of the pancreatic vessels are frequently necessary,
particularly in the search for endocrine tumours and during embolization
procedures (see below under Interventional procedures).
1065
Endocrine tumours are often very vascular and appear as enhancing

structures on angiography which means that the technique can often de
tect lesions too small to be identified on US or CT (0.5-1 cm).
Percutaneous transhepatic portography

Another method for localizing endocrine tumours is the fractionated sam
pling of venous blood through a catheter that is introduced percuta
neously through the liver into the portal system. The vascular anatomy
is displayed by means of percutaneous transhepatic portography (PTP)
and samples are collected from various veins draining the pancreas. The
tumour is localized to that part o f the pancreas showing the highest con
centration of hormone in its draining veins. The accuracy of the tech
nique can be enhanced by the use of arterial and other techniques for
stimulating hormone production and the presence of unsuspected hepatic
metastatic deposits may be revealed by the analysis of simultaneous he
patic vein samples.
Radionuclide white cells, though they do not localise in uncomplicated
pancreatitis, may be useful for diagnosing a pancreatic abscess or an in
fected pseudocyst. Insulinomas expressing somato-static receptors
(about 50%) may be localised with the somatostatic receptor analogue,
In-III pentetreotide (octreotide).

The changes found in pancreatitis and pancreatic tumours are better
demonstrated at present by CT and US than by magnetic resonance imag
ing and MRI is not, therefore, widely used in the diagnosis of pancreatic
diseases; bowel contents and bowel movement, vascular motion and
movements of the patient may all degrade the MRI study. The free choice
of MR imaging planes is, however, an advantage of the technique and
shorter imaging times with fast sequences and the development of new
oral and intravenous contrast agents will certainly ensure continued re
search into the proper role of MRI in pancreatic disease (see Fig. 41).
NORMAL ANATOMY
The pancreas is 12-15 cm long, 3-6 cm wide and 2-4 cm thick, weighs
65-70 g and is situated transversely in the upper part of the retroperi-
1066
toneal space. The organ is surrounded by a layer of fat of varying thick

ness. The head lies adjacent to the duodenal loop to the right of the mid
line, and the uncinate process extends behind the superior mesenteric
vessels. The body runs in a shallow S-shaped loop up to the left, the tail
extending to the hilum of the spleen. The drainage duct o f the exocrine
pancreas, the duct ofWirsung opens together with the choledochal duct
in the major papilla in the middle of the second part of the duodenum.
The secondary duct, the duct o f Santorini, opens into the minor papilla
approximately 2-3 cm above the major papilla. An awareness of the
retroperitoneal location of the pancreas is important to a proper under
standing of the secondary effects of pancreatic diseases.
Anatomical variants of the pancreas include the pancreas divisum,
where the dorsal and ventral parts of the pancreas have not united; pan
creas annulare, where the head of the pancreas encircles, and often
causes narrowing of the duodenum and accessory pancreatic islands.
Acute pancreatitis
The term acute pancreatitis implies primarily inflammation of the organ
itself, but there are often associated secondary inflammatory changes in
the surrounding tissues and organs. The complications of acute pancre
atitis include necrosis of the pancreatic parenchyma, so-called necrotic
or haemorrhagic pancreatitis, and cyst and abscess formation.
Computed tomography, particularly contrast-enhanced CT, has proved
to be o f decisive importance in both the diagnosis of disease and the grad
ing of its severity. The method is valuable for determining the correct
course of management in the individual patient, and is therefore per
formed at an early stage. Other diagnostic methods do not have this de
cisive importance. Since patients with acute pancreatitis are often dehy
drated, proper hydration is essential and intravenous fluids may be nec
essary to avoid contrast-induced renal damage.
The CT examination starts with an un-enhanced study of the upper ab
domen in which the entire area from the dome of the diaphragm to the
pelvic rim is sequentially examined by means of contiguous 5-10 mm
slices. The configuration of the pancreas is noted and an evaluation made
of the organ and its surrounding tissues (e.g. the mesentery), which in
cludes observations concerning the presence of oedema, abscesses, cysts,
1067
Figure 43.
Contrast-enhanced CT o f
acute pancreatitis, (a) The
pancreatic parenchyma (ar
rows) enhances with contrast
material; the pancreas itself is
slightly oedematous and it is
also surrounded by oedema
(e). In the body o f the pancreas
there is a low-density area o f
fo ca l necrosis (*). These fe a
tures are consistent with acute
oedematous non-haemorrhagic
pancreatitis, with preserved
perfusion o f the pancreatic
parenchyma. Note also the low
attenuation o f the liver, indi
cating fa tty degeneration, (b)
M inimal contrast enhancement
in the body o f the pancreas (p),
but no enhancement in the tail.
The pancreas is swollen and
surrounded by oedematous tis
sue (e). This finding is consis
tent with haemorrhagic-
necrotic pancreatitis.
etc. This preliminary study is used to determine the axial section which
demonstrates the pancreas to best advantage and at this level a dynamic
contrast study is performed. This involves the exposure of that slice every
15th second during two minutes after injection of a contrast medium bo
lus. This gives an idea o f the pattern of perfusion of the pancreatic
parenchyma, and allows the distinction to be made between haemor-
rhagic-necrotic pancreatitis, in which contrast-enhancement of part or
all of the pancreatic parenchyma does not occur, and oedematous pan
creatitis in which contrast-enhancement is preserved (Fig. 43). The
severity of pancreatitis can in this way be estimated and graded, and sec
ondary changes and complications evaluated. Oral contrast medium is
not used in CT studies of acute panceatitis so as not to interfere with den
sity measurements of the organ.
Follow-up studies are performed at regular intervals depending upon
the patient's progress.
1068
Figure 44.
US o f acute pancreatitis. The
pancreas (arrows) is swollen
and has a lower echogenicity
than usual (compare with Fig.
41). Ventrally an echo-free
pseudocyst (*), 5 cm in diame
ter, is seen.
The value of ultrasonography in the assessment of acute pancreatitis

is diminished by the gas-filled distended bowel loops that are so often
present in this disease and US is inferior to CT in its ability to provide
comprehensive information on the remainder of the abdomen and the
retroperitoneal space (Fig. 44).
Chronic pancreatitis
Chronic pancreatitis is assessed by means of US, CT and ERCP.
Ultrasound provides information concerning the size and parenchymal
volume of the pancreas, the calibre of the pancreatic duct and the pres
ence of cysts or other abnormal features (Fig. 44). On CT the parenchyma
is displayed with great precision, the pancreatic duct is sometimes seen
and any areas of calcification that may be present are better demonstrated
than on either US or the plain film. Contrast enhancement often improves
the quality of the imaging and allows more accurate distinction between
various entities such as cysts, abscesses, oedema, fluid collections and
adjacent bowel loops (Fig. 45). Knowledge concerning the anatomy of
the ductal system is of importance in grading the changes of chronic pan
creatitis and therefore influences clinical management decisions such as
the choice of therapy and the nature of any operation that may be nec
essary. The ductal anatomy is best seen on ERCP, which is important in
these selected cases. In chronic pancreatitis ductal changes such as di
latation, ectasia, local narrowing and possible communications with
cysts are seen on ERCP (Fig.46), as well as any concretions that may be
1069
Figure 45.
CT o f chronic pancreatitis.
Extensive calcification is seen
in the body and the tail o f the
pancreas (arrows). In the liver
parenchyma and hilum, dilated
bile ducts are seen, caused by
obstructive changes in the
pancreatic head.
Figure 46.
ERCP in a case o f chronic
pancreatitis, showing a dilated
pancreatic duct o f varying cal
ibre, and a local stricture (ar
row). A pseudocyst is seen in
the head o f the pancreas (*).
The distal part o f the common
bile duct (dc) is narrowed and
the proximal duct dilated.
present. The changes are graded on an agreed scale from I to IV.
Pancreatic tumours
When a pancreatic tumour is suspected, the first imaging studies are un
dertaken with ultrasound. A tumour is seen as an area of abnormal
echogenicity which is usually hypoechoic in relation to the surrounding
parenchyma. A careful assessment is made o f the tumour's location, its
possible effect on the pancreatic and/or common bile ducts, its relation
ship to vascular structures and the extent to which it may be invading
neighbouring organs (Fig. 47). Fine-needle biopsy of the tumour can also
be performed under US-guidance. Computed tomography is often per
formed in addition to ultrasound because of the superior anatomical de
tail it affords; the same features are looked for on CT as are described
above for US. Any extension into the surrounding areas is better shown
on CT than US, as are metastatic deposits in, for instance, the regional
lymph nodes (Fig. 48). The CT study should include iv-enhanced se
quences, in order better to delineate the tumour; malignant tumours en-
1070
Figure 47.
US o f the pancreas. A tumour (arrows) is seen on the transverse scans as a region with
lower echogenicity than the surrounding parenchyma, (a) Small intrapancreatic tu
mour, diameter 2 cm. (b) Large tumour, obstructing the pancreatic duct (*). These fe a
tures are consistent with the diagnosis o f carcinoma o f the pancreas.
Figure 48.
Contrast-enhanced CT o f a pancre
atic carcinoma, (a) A low density,
expanding lesion (arrow) is seen in
the head o f the pancreas. The tu
mour displaces the superior mesen
teric vein (small arrow) anteriorly,
while the superior mesenteric
artery is intact, (b) The importance
o f a proper early timing o f the CT
study in relation to the contrast
medium injection is demonstrated.
A non-distorting tumour o f less
than 2 cm (arrow) is demonstrated,
the only criterion for its detection
being its decreased contrast en
hancement in comparison with the
surrounding pancreatic
parenchyma.
1071
Figure 49.
An ERCP in a patient with
carcinoma o f the head o f the
pancreas shows total ob
struction o f the common bile
duct (large arrowhead) and
narrowing o f the pancreatic
duct (small arrowheads),
this is the so-called double
duct sign. The proximal pan
creatic duct is dilated be
cause o f the obstruction.
hance more slowly than normal parenchyma, but this feature is mostly
seen only during the first two minutes after contrast medium injection
(see description of CT technique above). Studies other than US and CT
are usually unnecessary. The smallest tumour that can be detected with
these methods is approximately 1-2 cm in diameter. In doubtful cases
ERCP is performed, where the typical findings o f ductal involvement are
stricture or obstruction with dilatation proximal to the lesion (Fig. 49).
Endocrine tumours have been briefly considered above in the section
on angiography.
Non-neoplastic lesions
Pseudocysts are not infrequently seen, occurring mostly as a complica
tion of pancreatitis. They may or may not have a connection with the
pancreatic duct; in the latter circumstance they may well be infected.
Cysts are well shown on US, CT and MRI and appear as thin-walled,
fluid-filled lesions. Abscesses also frequently arise as a complication of
pancreatitis; they commonly have thick, uneven walls that exhibit con
trast enhancement on CT while the centre has fluid characteristics across
a wide range of viscosity.
Trauma
In abdominal trauma the bowel loops are often distended and computed
tomography (particularly contrast-enhanced CT) is therefore the method
of choice when evaluating traumatic lesions. A disruption of the pan
creas is then seen as a discontinuity in the pancreatic parenchyma.
1072
Peripancreatic changes are also seen, and extravasation o f intravascular

contrast medium may very rarely be visualized in a patient with active
haemorrhage. Under favourable circumstances information on the pan
creas may also be obtained by US and further evaluation may require an
giography.
Interventional techniques in the pancreas consist mainly of biopsy,
drainage and embolization procedures. Fine-needle aspiration biopsy
(FNAB) may be performed under US, CT or ERCP guidance. Guided
fine-needle biopsy has considerably improved the accuracy of diagnosis
with respect to localized abnormalities, so that a specific diagnosis of a
demonstrable lesion can be obtained in most cases. Aspiration of a cyst
allows analysis of its contents, and permits the identification of, for in
stance, complicating infection. Abscesses and cysts may be drained
through a percutaneous catheter or drain. Internal drainage of a pancre
atic pseudocyst into the stomach or bowel is now feasible and may avoid
the need for surgery. This is advantageous to any patient but is particu
larly useful in individuals in whom surgery or general anaesthesia car
ries an increased risk of complications.
Arterial embolization is extremely useful in the management of pan
creatic aneurysms and may be life-saving in cases of acute bleeding.
Aneurysms usually result from chronic pancretitis but may also occur as
a result of iatrogenic vascular drainage during biopsy or surgery.
Haemobilia is usually an indication for arteriography, and when it occurs
in a patient with an appropriate history the presence of a pancreatic
aneurysm should be strongly suspected. If the necessary expertise is avail
able therapeutic embolization is almost always preferable to surgery in the
management of pancreatic lesions that are bleeding or liable to bleed.
1073
The spleen
MODALITIES
Plain radiography
The size o f the spleen may be roughly estimated on the plain film, espe
cially if the organ is enlarged. Calcified lesions such as granulomas or
cyst walls, are well seen.
Ultrasonography
US gives good information on the shape and size of the spleen and on
any pathological changes that may be present. Splenomegaly can be iden
tified and measured. Cysts are seen as well-demarcated echo-free struc
tures. Tumours and metastases have an echogenicity differing from that
of normal splenic parenchyma, being either hypo- or hyper-echogenic.
Lesions as small as 1 cm may be identified, with the exception of diffuse
infiltrates such as lymphoma, which may be difficult to discern on US.
Traumatic changes, such as rupture of the spleen and haemorrhage, are
clearly seen on US, as are infarctions and abscesses.
Computed tomography
The best images of the spleen are obtained by CT, which also gives in
formation on any calcification present, e.g. in granulomas or cyst walls
and allows precise measurement of splenic size. Pathological changes
are seen, as on US, but often with greater clarity, especially after iv. con
trast infusion.

On MRI diffuse infiltrates such as occur, for instance, in lymphoma, may
be seen more clearly than on US and CT, but essentially MRI and CT
are of equal value. The free choice of imaging plane may be one advan
tage offered by MRI.
1074
Localized changes, such as cysts, metastatic deposits, tumours and in
farcts can be shown by radionuclide imaging, though the specificity and
spatial resolution of the technique are inferior to US and CT. Intrasplenic
abscess is difficult to image with radiolabelled leucocytes because the
spleen is a normal site of granulocyte pooling and is therefore very promi
nent in a white cell scan. An abscess may be identified by sequential
imaging, during which an abscess is seen to increase in activity in com
parison with normal splenic tissue which shows a slight fall, or by sub
traction imaging using Tc-99m labelled sulphur colloid.
Images of splenic function may be obtained with autologous radiola
belled blood cells, including heat denatured erythrocytes, platelets, and
leucocytes. Such imaging may be useful for the localization of func
tioning splenunculi and the assessment of the role of the spleen in throm
bocytopenia, particularly ITP.
Angiography
Angiography is not often used for diagnostic purposes (except in acute
bleeding) but may be used as a step in embolizing the spleen or splenic
artery in the treatment of hypersplenism, trauma or aneurysm. Direct
splenoportography, i.e. direct puncture of the spleen and the injection of
contrast medium into the splenic parenchyma through a plastic cannula,
may be performed to map the venous drainage of the spleen in portal hy
pertension. With modem digital subtraction equipment, however, the
requisite information can now almost always be obtained by indirect
splenoportography using the venous phase of a splenic arteriogram and
the direct method is virtually obsolete in advanced centres.
NORMAL ANATOMY
The spleen is located posterolaterally in the left hypochondrium, is 10-12
cm in length and 6-8 cm in width, and weighs 150-200 g. The most com
mon anatomical variant to be seen is an accessory spleen, i.e. one or more
splenunculi that usually lie in the vicinity of the splenic hilum. The size
of the spleen, especially its length, may be estimated on plain radiogra
phy but is best evaluated by US, CT or MRI.
1075
Figure 50.
Splenic infiltrates. (a) On US
several fo c i o f low echogenic
ity (arrows) are seen within
the spleen; these proved to be
infiltrates, (b) Diffuse infil
trates are seen in an enlarged
spleen on this contrast-en-
hancement CT; these were due
to sarcoidosis o f the spleen.
Splenomegaly
US is usually the first imaging modality to be employed in the investi
gation of splenomegaly as the organ size and the structure of the splenic
parenchyma can be assessed. CT or MRI may be useful in certain indi
viduals to characterize the cause of the splenic enlargement.
Infiltrates
Ultrasound and contrast enhanced CT and MRI are all used for the di
agnosis of neoplastic lesions such as lymphoma, metastatic deposits, or,
rarely, primary tumours (Fig. 50). Splenic infarction is seen as a typical,
often wedge-shaped, peripheral lesion (Fig. 51). The different imaging
modalities are complementary to one another, but US is usually the
method of first choice.
1076
Figure 51.
CT o f the spleen, with contrast en
hancement. Dorsally a peripheral
area o f decreased enhancement
(arrows) is seen, representing an
area o f splenic infarction.
Figure 52.
Splenic abscess, (a) On CT an irregular area o f low attenuation is seen (arrows), (b)
An abscess in the spleen has been drained. On this US the draining catheter (curved
arrow) is seen within the abscess (large arrows).
Abscess, infection
With US and contrast-enhanced CT, abscesses are typically seen as lo
calized lesions with thick and contrast-enhancing walls (Fig. 52). Foci
of infection may sometimes be identified by sequential radionuclide
imaging.
1077
Trauma
Splenic rupture is not uncommon in abdominal injury, and is diagnosed
by US and/or contrast-enhanced CT. Parenchymal lesions and intracap-
sular bleeding are seen with equal clarity using either method, but any
changes in the surrounding region, such as may occur with rupture of the
splenic capsule, are better shown on CT. Angiography can be performed
in order to map the vascular anatomy in detail or to embolize if this seems
feasible and appropriate but a decision whether or not to operate can usu
ally be made solely on the basis of US and/or CT. It must be said, how
ever, that most clinicians would base their decision on clinical findings
rather than on CT and US.
Vascular anatomy
The arterial anatomy of the spleen is evaluated by splenic arteriography,
e.g. prior to an embolization. The venous drainage may be demonstra-
teed in certain problem cases, mainly those involving portal thrombosis
and oesophageal varices, by an arterial contrast medium (indirect spleno
portography, best performed using DSA), or by a direct injection into the
splenic parenchyma through a percutaneously-introduced cannula, di
rect splenoportography.
The most important interventional procedures are guided fine-needle
biopsy, the percutaneous drainage of splenic abscesses and embolization
of the splenic artery in bleeding or splenomegaly. Embolization for the
latter indication carries a considerable risk of infection.
1078
Chapter 24
The acute abdomen
David J. Allison, Olle Ekberg and Frans-Thomas Fork
IMAGING STUDIES
Indication
Patients with severe abdominal symptoms including pain, acute onset of
nausea, vomiting and obstruction, should undergo radiological studies
to try and determine the underlying cause (Fig. 1 a). When bowel wall
lesions or obstruction are suspected plain films are often followed by bar
ium studies in order to check bowel patency and transit time (Fig. 1 b).
In cases where the abdominal cavity is involved abdominal CT (Fig. 1 c)
and ultrasound (Fig. 1 d) will follow. CT and transabdominal ultrasound
are usually chosen for the examination of palpable masses, parenchyma
tous organs, retroperitoneal structures, the abdominal walls and the in
guinal regions. Chest studies are often included in patients with upper ab
dominal symptoms and angiography and/or interventional techniques
may be required in patients presenting with gastrointestinal bleeding.
THE ABDOMINAL SURVEY
Technique of examination
No special preparation for the study is necessary but the patients will
commonly already have a gastric tube and a urinary catheter in situ. The
survey, preferably using full-size images includes:
A. vertical beam images with the patient in the supine (Fig. 2), left
(Fig. 3) and right lateral oblique (Fig. 4) positions, including the di
aphragmatic and inguinal regions (Fig. 5), and
1079
Figure 1.
a) АР plain film in a patient with
vomiting, showing gas in the
gastric antrum to the left o f the
vertebral column, in the bulb to
the right o f the vertebral col
umn, in distal loops o f the ileum
and in the left colonic flexure.
b) Follow-through study 90 min
с
utes after the ingestion o f 200
ml o f diluted barium suspen
sion. The distended, proximal
duodenal loop and the gastric
retention indicate a mid-duode-
nal obstruction.
c) Abdominal CT o f the same pa
tient verifies a large duodenal
carcinoma which has almost
obliterated the lumen.
d) Abdominal ultrasound o f the
same tumour prior to a fine nee
dle puncture. The carcinoma is
seen as an hypoechoic mass
lesion.
THE ACUTE ABDOMEN
Figure 2.
Frontal, supine, abdominal film
showing a normal distribution o f
gas and normal haustra in the
large bowel. The ilio-psoas mus
cles (I) and the kidneys (2) are
outlined by fa tty tissue.
Figure 3.
Left oblique vertical beam plain
film o f the left hypochondrium in
a patient with numerous areas o f
pancreatic calcification. The left
ilio-psoas muscle and left kidney
are clearly outlined.
1081
Figure 4.
Right oblique vertical beam plain film o f the
lateral abdominal wall showing fa t between
the abdominal wall muscles (white arrow)
and around the lower border o f the right
lobe o f the liver (arrowheads). Benign rib
calcification is seen underneath the right
breast.
Figure 5.
Frontal pelvic survey in a
patient with a left inguinal
hernia (1) with signs o f
obstruction in a dilated
proximal loop o f ileum with
swollen mucosal folds, often
compared to fingerprints
(2). The urinary bladder
(arrows) is delineated by
fat.
THE ACUTE ABDOMEN
Figure 6. Frontal, horizontal beam plain film in an erect patient with a collection o f
free gas underneath the right hemi-diaphragm. In order to disclose even smaller
amounts o f subphrenic air, a spot film with tight coning should be centred at the di
aphragmatic level
B. horizontal beam images with the patient erect, to demonstrate the sub
phrenic spaces (Fig. 6), or in the right and left decubitus positions, to
demonstrate the paracolic and parahepatic and spaces.
In patients with acute colitis one supine view usually suffices, which can
be enhanced if necessary by minimal air insufflation of the large bowel
(pneumocolon, see below).
Image interpretation
In order to recognize pathology, a knowledge of normal abdominal
anatomy is essential. Areas o f calcification, soft-tissue masses and fluid
collections have to be interpreted with the full knowledge of the patien
t’s history and in close collaboration with the referring clinician.
Fat spaces
As fat is more radiolucent than blood, muscle and solid organs such as
the liver, spleen and kidney, it is depicted as dark grey areas on the ra
diograph. Fat is found along the abdominal wall and ilio-psoas muscles,
in the paracolic spaces (Fig. 4), in the retroperitoneum and in the mesen
tery. It also envelopes the kidneys, urinary blader and rectum, thereby
delineating these structures and the displacement or abolition of these fat
spaces may indicate the presence of pathology.
Gas collections
Gas is seen as dark black areas on the radiograph, and is normally pre
sent in the stomach, large bowel (Fig. 2) and rectum. Gas may also be
1083
found in small bowel loops if the patient is suffering from pain or is un
der mental stress. Deviations from the normal appearances are seen as
abnormally distributed or abnormally large collections of gas either
within the lumen, indicating obstruction (Fig. 5), or outside the bowel as
a result of perforation (Fig. 6).
Normally, there is some saliva and gastric juice, as well as gas in the
stomach and this results in an air-fluid level which is seen on horizontal
beam films lying just underneath the left hemi-diaphragm close to the
midline. Every other air-fluid level found may signify an abnormality -
see below under "obstruction".
Calcification
The chondromatous part o f the ventral thoracic cage may already con
tain areas of calcification in healthy, young adults (Fig. 4). If there is any
doubt an oblique view will disclose the extra-abdominal location of such
calcification.
Intra-abdominal, well-defined, shell-like, benign areas of calcifica
tion may be found along the midline representing calcified lymph nodes
or, lying centrally in the true pelvis, may be seen in the myomatous
uterus.
Punctate calcification may be found in the prostatic gland in elderly
men, or in phleboliths, often symmetrically distributed in the true pelvis.
The latter may be difficult to differentiate from a stone in the ureter; as
a general rule, however, phleboliths are doughnut-like whereas urinary
tract stones are oval in shape and homogeneous. In the elderly a varying
amount o f calcification may be seen in the aorta and in the iliac and
splenic arteries.
Bowel content
Bowel content is recognized by its rich content o f tiny air bubbles. It is
seen as amorphous masses in the right side of the colon and more formed
collections in the left colon and rectum. It has to be differentiated from
an abscess which may have the same feature of multiple, tiny air bub
bles.
The small and large bowel

The diameter of the colon is in general greater than that of the small
bowel which is located in the mid-abdomen and surrounded by the colon.
1084
THE ACUTE ABDOMEN
When the small bowel is air filled it is recognized by its 1-2 mm folds
running spirally from one side to the other (Fig. 1 b), while the large
bowel folds are broken, forming the typical haustra (Fig. 2). The outer
contour of the normal gut is convex.
The parenchymal organs

The liver is seen as an homogeneous soft-tissue structure beneath the
right hemidiaphragm. Its right lower tip stretches down to the iliac crest
and is demarcated by fat (Fig. 4).
In most patients the kidneys are outlined by pararenal fat. The right
kidney is usually located somewhat caudad to the left. The spleen is sit
uated laterally just under the left hemi-diaphragm but is sometimes ob
scured by the stomach and colonic flexure. The normal pancreas, adrenal
and prostate are invisible on the plain film as is the normal uterus, but
calcified myomata are often present. The normal gallbladder is not seen
on plain films whereas the urinary bladder is delineated by fat in the peri
neum and lateral pouches of Retzius (Fig. 5).
PATHOLOGY
Calcification
Calcified stones are radio-opaque, bright grey (on the radiograph), well-
defined and round. Multiple, facetted and multilayered stones may be
found in the gallbladder and the urinary bladder in patients with long
term catheters. Single or multiple stones may be seen in the renal pelvis
and ureters and occasionally in the biliary tree and pancreatic duct.
Benign lesions such as myomata of the uterus, adenomata of the adren
als, organized haematomas, leiomyomas, renal cyst walls and dermoid
may all calcify.
Malignant calcification is a rare entity, usually located in the periph
ery of a hepatoma or centrally in the necrotic parts of a malignancy.
The areas of calcification associated with inflammatory lesions are usu
ally multiple and small and found in the pancreatic gland as a sign of
chronic pancreatitis (Fig. 3). Shell-like calcification may be seen in pa
tients with echinococcosis of the liver.
Vascular calcification occurs in phleboliths, atherosclerotic plaques
and in aneurysms where it commonly has a shell-like appearance (e.g.
splenic artery aneurysms).
1085
Figure 7.
a) Large volume o f ascites obliter
ating the fa t planes around the
kidneys and iliopsoas muscles
and pushing air-containing
bowel loops towards the middle
o f the abdomen, allowing only
barium-filled loops to sink lat
erally.
b) Abdominal ultrasound o f the
same patient revealing free
flu id ventral to the liver seen as
a dark, hypoechoic zone be
tween the liver and the ventral
abdominal wall. The white hy-
perechoic curvilinear line in
the lower part o f the image is
the diaphragm.
Ascites
When the fat planes around the urinary bladder and the rectum are oblit
erated this is often due to the presence of an increased amount of fluid
in the abdominal cavity, seen as a crescentic density in the pelvis (Fig. 7).
Larger volumes of ascites separate the bowel loops and obliterate the fat-
lines in the paracolic gutters, and volumes in excess of 1 litre displace
the air-containing bowel loops centrally in the abdomen while obliterat-
1086
THE ACUTE ABDOMEN
Figure 8.
Abdominal CT in a pa
tient with a perforated
peptic ulcer. Free gas is
seen in the midline (1)
close to the contrast-filled
stomach (2). A minimal
amount o f ascites is seen
around the liver and
spleen (4). Fat is shown
as dark grey areas sur
rounding the kidneys,
large abdominal vessels
and the pancreas behind
the stomach. The gall
bladder (3) is also seen.
ing the fat contours of the kidneys and psoas muscles (Fig. 7 a).
Nowadays, ascites is ruled out by abdominal ultrasound (Fig. 7 b) or
CT (Fig. 8) as these modalities can detect very small quantities of free
fluid.
Pneumoperitoneum
Perforation of a bowel loop allows gas to pass into the abdominal cav
ity. It collects in non-dependent sites, and is best detected on a horizon
tal beam film centred at sites such as the subphrenic space in an erect pa
tient or the uppermost part o f the abdominal cavity in a recumbent one.
In order to improve the image quality coned views are recommended
(Fig. 6). If only a tiny volume of gas has leaked through a perforation
this may only be disclosed on CT (Fig. 8).
Large volumes of gas may be found after open abdominal surgery or
following perforation of the large bowel. In these circumstances the free
gas may be demonstrated even on vertical beam images as it delineates
the gallbladder and the outer, serosal border of the bowel wall, which
will be seen as thin, curved lines (Fig. 9). Postoperatively gas disappears
within two weeks if no complication occurs.
Intra-peritoneal gas may also be seen in patients on peritoneal dialy
sis and following hysterosalpingography and percutaneous endoscopic
or interventional procedures.
1087
Figure 9.
Large amount o f free abdominal
air in a young patient with cae-
cal perforation due to a sigmoid
carcinoma. Widened loops o f
sm all bowel are recognized by
their spiral folds. The bowel
wall is outlined as a white line
by the gas on either side.
Localized gas collections

Although an abscess is a space occupying lesion it is not usually diag
nosed on plain films until it contains gas, either as a collection of small
bubbles or, when these have merged into a large bubble, as an extended
air-fluid level. The latter is commonly seen in the subphrenic space or
the lesser sac (Fig. 10). CT and ultrasound are helpful in distinguishing
a gas-containing abscess from entities having a similar appearance such
as the large bowel contents and retroperitoneal or subcutaneous emphy
sema. Abscess drainage procedures are readily conducted under US or
CT guidance.
Necrosis of the bowel may be revealed by numerous small collections
in the gut wall. This gas may enter the draining mesenteric veins and col
lect intrahepatically in the portal system, a radiographic feature of sinis
ter portent (see below Fig. 32). The presence of intramural gas does not
invariably indicate serious pathology, however, the idiopathic occur
rence of pneumatosis coli seen in the elderly is a reversible condition
(Fig. 11).
1088
Figure 10.
Abscess following a Billroth-1
resection located in the lesser
sac and beneath the diaphragm
(arrows). Secondary pleuritis
with obliteration o f the aorto-
diaphragmatic (1) and lateral
(2) pleural recesses. (When
Gastrografin is given, the anas
tomotic leak is demonstrated.
The air-fluid levels in the ab
scesses are clearly seen.)
Figure 11.
Pneumatosis cystoides coli in
an elderly patient with multiple
air-filled cysts seen as blackfill
ing defects in the barium-filled
lumen.
Figure 12.
Necrotic appendicitis in a
16-year-old boy. A large
soft-tissue mass is seen in the
right lower quadrant repre
senting fluid-containing
bowel loops. The proximal
small bowel is slightly di
lated with short air-fluid lev
els (arrows) and the large
bowel is dilated with long
levels indicating adynamic
(paralytic) ileus.
Figure 13.
Ultrasonography o f the left
lower abdominal quadrant in
a 65-year-old patient with
fever and clinical signs o f
sigmoiditis, disclosing
marked thickening o f the
bowel wall (calipers).
Diverticula can just be dis
cerned to the left o f the im
age.
Inflammatory conditions
Localized inflammation causes limited peritonitis with secondary paraly
sis of neighbouring bowel loops in which fluid and gas collect. Adjacent
fat planes are obliterated owing to oedema. Lateralised peritonitis in young
adults causes sometimes a decompressing contraction of the ipsilateral
psoas muscle and a secondary scoliosis. In patients with localized signs
and symptoms, whether due to possible cholecystitis, pancreatitis, appen
dicitis (Fig. 12), salpingitis or sigmoiditis, CT and ultrasound (Fig. 13)
1090
THE ACUTE ABDOMEN
Figure 14.
Acute cholecystitis with wall
oedema (arrow) and multiple
large stones in the gallblad
der (1) creating a broad
acoustic shadow (2). The
common bile duct is widened
(d) indicating a peripheral
obstruction.
should be considered as the imaging methods of first choice.
Cholecystitis
Nowadays patients with suspected cholecystitis undergo ultrasonogra
phy of the gallbladder and the bile ducts as the primary imaging inves
tigation. In acute cases the bladder is dilated and globular and a rim of
fluid is occasionally seen (Fig. 14). The gallbladder is usually tender to
pressure of the probe, a modem manifestation of Murphy’s sign. Stones
reflect and absorb all the ultrasound energy so creating an acoustic
shadow beyond the stones. In chronic cases a thick gallbladder wall is
also seen.
Gangrenous cholecystitis is caused by gas-producing bacteria; it is
seen as free gas in the gallbladder or as a rim of emphysema in the wall
(Fig. 15).
Pancreatitis
Pancreatitis causes the gland to become swollen (Fig. 16) and its sur
rounding fat planes are obliterated. In severe cases the oedema will spread
into the transverse mesocolon toward the stomach and left kidney.
Secondary peritonitis paralyses the duodenum and the overlying trans
verse colon. The disease may be complicated by the formation of cysts
and abscesses in the lesser sac and sub-phrenic spaces, left sided pleuri-
tis, lung atelectasis and pneumonia. Although ultrasound may be used,
CT is a better choice of imaging modality as these patients are frequently
1091
Figure 15.
Abdominal survey reveal
ing gas in the gallbladder
(star) with wall emphy
sema (arrows).
Figure 16.
Acute pancreatitis with a
swollen pancreatic gland
(I) and partially obliter
ated retroperitoneal fa t
planes. The fascia around
the left kidney is markedly
engorged (arrows) and
flu id can be seen in the
lesser sac (2).
in severe pain resulting in the accumulation o f bowel gas which inter

feres with the ultrasound study.
Chronic pancreatitis may give rise to multiple areas of calcification
(Fig. 3), which are easily detected on CT and ultrasound.
1092
THE ACUTE ABDOMEN
Figure 17.
Ultrasound image in a patient
with an inflamed appendix
(arrows) and a small abscess
(a).
Peritonitis
Generalized peritonitis is accompanied by a purulent exudate which
causes the obliteration of fat planes and a secondary ileus with long air-
fluid levels (Fig. 12).
Appendicitis
Ultrasonography is often helpful in confirming the diagnosis of appen
dicitis in patients in whom the history or clinical presentation is atypi
cal. A normal appendix cannot be seen, whereas a swollen organ may be
identified together with its surrounding oedema (Fig. 17).
Enteritis
Patients with gastro-enteritis and sigmoiditis are not usually examined
radiologically. If studies are undertaken in the former condition, how
ever, they reveal a number of small to medium-sized air fluid levels in
both the small and large bowel; patients with sigmoiditis normally un
dergo investigation only if the disease is complicated by perforation or
obstruction.
Colitis
Both pseudo-membranous colitis and toxic ulcerative colitis may cause an
acute abdomen. The former is drug-induced and caused by toxins and
Clostridium difficile; the latter may give rise to peritonitis. The colon in
both entities is paralysed and the wall is thickened by oedema, seen as poly
poid ’’thumbprint" indentations into the air column of the lumen (Fig. 18).
1093
Figure 18.
Abdominal survey in a patient with
toxic colitis. The transverse colon
(1) is stringlike and "fingerprinted”
with numerous polypoid identa-
tions. Gas is seen in widened ileal
loop (2) and stomach (3).
Patients with toxic colitis, toxic dilatation or megacolon have to be

monitored by repeated examinations until gut motility returns, the fre
quency of the studies being determined by the patient's clinical state. If
the colon dilates or emphysema of the colonic wall appears, there is a
high risk of perforation and immediate colectomy should be considered.
Ulceration
Ulcers in the stomach, pylorus and duodenal bulb may heal with scar for
mation, secondary stenosis, gastric retention and dilatation. In the erect
view, this is seen as a long air-fluid level in the fundus, close to the left
hemi-diaphragm. An ulcer may also be complicated by perforation into
the abdominal cavity and lesser sac. A perforated ulcer is, in fact, the un
derlying pathology in four out of five patients presenting with free ab
dominal gas. If the perforation is rapidly sealed by omentum, only a small
volume of gas may escape, which is hard to detect radiographically un
less CT is used or the perforation itself is outlined by a suitable water-
soluble contrast material such as Gastrografin (Fig. 19).
A dorsal-wall perforation may fill the lesser sac with gastric contents
and induce secondary pancreatitis with its associated complications; the
condition is usually readily demonstrated on CT. A non-perforated ul
cer is nowadays diagnosed and treated endoscopically.
1094
THE ACUTE ABDOMEN
Figure 19.
A patient treated with steroids fo r
psoriatic artritis who suddenly de
veloped severe epigastric pain. Plain
abdominal film s were within normal
limits. A lateral film o f the stomach
shows leakage o f GastrografinR (ar
row) through a perforated duodenal
ulcer (1 = gastric body, 2 = gastric
antrum, 3 = duodenal bulb)
Mechanical bowel obstruction
Bowel obstruction leads to a mechanical or dynamic ileus which may be
intermittent in cases where the obstruction is incomplete. There are a va
riety of causes, including postoperative adhesions and peritoneal bands,
an obstructing bowel tumour, infiltration from a malignancy adjacent to
the bowel, invagination, strangulation, internal or external herniation,
obstruction from ingested material, inflammatory lesions and bleeding
into the bowel wall.
The contents of the bowel distal to the obstructive lesion are usually
evaucated with gas and fluid accumulate proximally. Peristaltic activity
in the proximal bowel is increased in order to overcome the obstruction
and this is manifested on auscultation as a change of pitch in the bowel
sounds. On abdominal survey films the proximal air-filled bowel loops
appear as dark, radiolucent arches. On horizontal-beam films the air-fluid
levels in the respective limbs o f these arches may reach different heights
as a sign of peristaltic activity in the bowel (Fig. 20).
Special considerations
A high mechanical obstruction is a serious condition that can easily be
overlooked. An abdominal survey shows an absence of bowel gas, just
as in the newborn with oesophageal atresia. Vomiting is the dominant
clinical feature.
1095
Figure 20.
Patient with small bowel ileus. Air-fluid
levels are seen at different levels in the
limbs o f dilated small bowel loops.
Multiple air-fluid levels are seen as a
sign o f low small bowel obstruction.
The colon is collapsed. There is a gall
stone in the gallbladder (arrow). The
examination is performed with the p a
tient erect. There is an air-fluid level in
the stomach (*) which is normal. Note
the spiral arrrangement o f bowel folds.
Figure 21.
a) A patient with severe vomiting who
had recently undergone an axillo-
fem oral bypass. The plain abdominal
film shows a stomach distended with
gas in an otherwise gas void ab
domen (apart from small amounts in
the descending colon).
b) The same patient examined in the
left lateral decubitus position with
an horizontal beam. There are air-
fluid levels seen in the gastric fu n
dus, duodenal bulb, and descending
duodenum (arrow), respectively.
(A barium examination o f the stomach showed jejunal obstruction due to bleeding as
a result o f anticoagulant therapy.)
1096
THE ACUTE ABDOMEN
Figure 22.
CT o f the abdomen in a patient
with carcinoma o f the pancreas
and a Roux-en-Yanastomosis.
There is obstruction o f the Y-
loop which is markedly dis
tended (*). Widened intrahep
atic biliary ducts are demon
strated and the wall o f the
abdominal aorta is calcified.
Gastric retention is usually caused by a stenosis secondary to peptic

ulcer disease. Other less common causes are duodenal obstruction due
to intramural bleeding secondary to trauma or anticoagulant therapy. In
patients with duodenal obstruction, however, gas is present in both the
stomach and duodenal bulb (Fig. 21). Another cause of high mechanical
obstruction is invagination of the afferent loop after a Billroth II stom
ach resection (Fig. 22).
Small bowel ileus

Organic obstruction of the small bowel leads to proximal dilatation with
emptying of the bowel (including the large bowel) distal to the site of
the obstruction. The fewer the number of dilated loops seen, the higher
the level of the obstruction. The presence, therefore, of multiple air-fluid
levels in the small bowel indicates a distally located obstruction (Fig.
20).
In long-standing obstruction the small bowel can dilate enormously
and come to resemble the colon. The mucosal pattern, however, i.e. the
folds of Kerkring which traverse the bowel in a spiral fashion, may help
to distinguish between dilated small bowel and colon (Fig. 9).
Large bowel ileus

The more distal the obstruction the more colon is dilated proximally,
while the bowel below the lesion and the rectum are empty (Fig. 23).
Even if the obstruction has lasted for only a few hours the small bowel
may be dilated.
1097
Figure 23.
a) Air-fluid levels are shown in
the dilated ascending, trans
verse and descending colon
in a patient with large bowel
obstruction.
b) Barium study showing com
plete obstruction at the tran
sition between the rectum
and sigmoid colon; the prox
imal colon is distended with
gas (arrow).
c) Ultrasound examination
showing a dilated caecum
and the distal ileum dis
tended with fluid.
Intussusception
Ileocaecal invagination in children does not necessarily produce any ra
diological abnormality. Clinical suspicion of this condition, therefore,
should always lead to a large bowel examination, using either barium or
C 0 2 insufflation (i.e. pneumocolon). With either method the invaginated
small bowel will be delineated by the introduced contrast. The condition
1098
THE ACUTE ABDOMEN
Figure 24.
Ultrasound examination o f
an ileo-ileal invagination
(intussusception) in a child
showing the typical appear
ance o f a "bowel (t) within a
bowel (t)".
b
Figure 25.
a) Gas is seen in the extrahepatic bil
iary tree (arrow) and in the gallblad
der (*) in a patient with gallstone ileus. The small bowel loops are wide (arrow
head) and filled with fluid. The intraluminal gas is outlining the mucosal folds.
b) A fistula (1) from the gallbladder to the duodenum was demonstrated during a bar
ium follow-through in a patient with an entrapped gallstone (2) in the mid-small
bowel.
may also be diagnosed by ultrasound in which its characteristic feature

is an onion-like formation (Fig. 24).
The intussusception may be reduced by increasing the intraluminal
pressure with either barium or C 0 2, at a pressure corresponding to 1.5
m of water, and gentle manipulation of the abdomen. If the patient shows
any signs of ileus, however, the reduction must be performed with ex-
1099
Figure 26.
Strangulation
ileus. An ultra
sound examination
shows fluid in di
lated small bowel
loops (arrows).
treme caution to avoid rupture of a potentially strangulated bowel loop

and many authorities consider this radiological manoeuvre to be con
traindicated in such circumstances.
Gallstone ileus
In patients with chronic cholecystitis a gallstone may erode through a
fistula from the gallbladder to the bowel. Depending on the size of the
stone and the level of the fistulous communication (duodenum, ileum or
right colonic flexure) the stone may get stuck at one of a number of dif
ferent levels, e.g. the bulb, the sigmoid colon, or, as is most often the
case, the distal ileum (Fig. 25). Gas passes spontaneously through the
fistula into the gallbladder and biliary tree and this combination of bil
iary gas and mechanical obstruction is pathognomonic for gallstone ileus.
Strangulation
Depletion of the supply of oxygenated blood to the bowel creates alarm
ing clinical symptoms and the affected bowel loop soon fills with haem-
orrhagic fluid (Fig. 26). On abdominal survey films a rounded mass is
seen together with signs o f obstruction but the true cause is seldomly di
agnosed preoperatively.
Small bowel volvulus

Rotation of the small bowel around its mesentery is a rare entity. Dilated
bowel loops are seen, orientated like a "spiral nebula" in the mid ab
domen (Fig. 27).
1100
THE ACUTE ABDOMEN
Figure 27.
Volvulus o f small bowel around
an adhesion. The appearance
looks like a spiral nebula and this
is caused by progressive gaseous
distension o f the small bowel
which forces it to rotate around
its mesenteric root.
Large bowel volvulus

Colonic volvulus is much commoner than small bowel volvulus. The
cause is an incomplete fixation of the bowel which may thereby form
slings. The most common form of volvulus occurs in the sigmoid and is
seen in debilitated and elderly patients.
Radiologically a gas-filled sigmoid loop is seen which may reach up
to the right upper quadrant. Proximal parts of the large bowel are filled
by air and faeces (Fig. 28). The volvulus may be reduced by the use of
a semi-stiff tube with a smoothly rounded tip and drainage holes. The
tube is introduced during fluoroscopic control and carefully advanced
beyond the torsion into the dilated loop. When gas and foulsmelling fluid
are suddenly expelled from the tube the bowel collapses and the patient
recovers immediately. There is, however, a great tendency for the volvu
lus to recur.
Volvulus of the caecum is seldom complete and often overlooked. The
cause is a mobile caecum in a patient with a distal obstruction. A colonic
carcinoma in the left colon may cause volvulus of the right colon up to
the right flexure. Abdominal survey films show a distended loop of the
bowel, resembling a kidney (Fig. 29), which may be located anywhere
in the abdomen. Gas and faecal materials may still be seen in the distal
1101
Figure 28.
a) Volvulus with marked distension o f
the sigmoid colon up to the right
hemidiaphragm. Moderate dilatation
o f the rest o f the colon.
b) A barium enema shows a twist in the
bowel at the level o f the distal sig
moid.
colon indicating that the torsion is incomplete. All types of colonic volvu
lus are verified by means of a barium enema that reveals a beakshaped
deformity corresponding to the site of torsion (Fig. 29).
Comments
The further evaluation o f a patient with an acute abdomen and abnormal
survey films should always be a matter for consultation between the ra
diologist and the referring clinician. If the patient is to undergo further
1102
THE ACUTE ABDOMEN
Figure 29.
a) There is a long air-fluid level in
the pelvis in a patient with dis
tension o f the caecum (arrows).
b) A barium examination shows a
beak-like deformity o f the proxi
mal ascending colon signifying a
caecal volvulus (arrow).
examinations with ultrasound, CT and/or angiography then any barium

examinations should be postponed.
Patients with a definite diagnosis of mechanical obstruction are very
likely to benefit from CT which often not only confirms the diagnosis but
also establishes the underlying cause such as an abscess or a malignant le
sion. If no definite aetiology is ascertained then an adhesion is likely to be
the cause of the obstruction. Transabdominal ultrasound may also be con
sidered, but this technique is much more operator dependent than CT. The
large amount of gas present in patients with dynamic ileus also contributes
to the difficulties of making an ultrasound diagnosis. Intussusception, how
ever, is usually easy to reveal with ultrasound (Fig. 24).
1103
Figure 30.
a) Chronic ileus in a woman
with advanced ovarian carci
noma that has developed into
a paralytic ileus with long
air-fluid levels.
b) Postoperative paralytic ileus.
A left decubitus view shows a
long flu id level in the colon.
It is normal practice to verify the level and type o f any obstruction with
either a barium follow-through or enema. If the level o f the obstruction
is unclear, a barium enema should always be performed first.
In order to speed up the diagnosis when a follow-through examination
is being performed, GastrografinR may be added to the bariumsulphate
in the proportion 1:4. The radiographic examination should start 15 min
utes after this is ingested and be repeated at regular intervals. When the
1104
THE ACUTE ABDOMEN
Figure 31.
Pseudo-obstruction in a patient
with Parkinson's disease. There
is dilatation o f both large and
small bowel loops.
contrast medium has reached the obstruction, spot films are taken dur
ing fluoroscopy for detailed assessment of the situation.
Paralytic ileus
Adynamic ileus is often seen after abdominal surgery and as a secondary
complication of peritonitis and circulatory insufficiency, but it can also
occur as a sequel to longstanding dynamic ileus (Fig. 30). Intoxication
or glucose and electrolyte imbalance may also cause adynamic ileus.
The abdominal survey films show slightly gas-distended small bowel
loops with long air-fluid levels, signifying lack of bowel activity, i.e. a
"silent abdomen". If there is peritonitis as well, fluid is present in the
peritoneal cavity. Pseudo-obstruction without any known aetiology can
be seen in the elderly (Fig. 31), a condition that is fatal if the bowel is
not decompressed by surgery or colonoscopy.
Ischaemia
Acute bowel ischaemia may be caused by embolism or thrombosis in the
mesenteric vessels, but is more often caused by a low arterial blood flow
without evidence of obstruction. The circulatory insufficiency causes
1105
Figure 32.
a) Gas in the portal vein has a tendency to accumulate in the periphery o f the liver
(arrows) while gas in the biliary tree collects in the hilar region.
b) A plain abdominalfilm shows gangrenous bowel with gas in the rectal wall down to
the anus (arrows).
oedema and bleeding in the bowel wall. Radiologically localized poly

poid swellings of the bowel wall resembling thumbprints are seen. The
ischaemic segment becomes paralysed and fills with fluid, resulting in
an increase in the intraluminal pressure. This may lead to ulceration and
necrosis of the mucosa and gas may pass through the bowel wall into the
splanchnic and portal veins (Fig. 32). This is often fatal as a result of ex
tensive bowel necrosis. The thickened bowel wall is often readily demon
strated on CT and ultrasound, both of which can be used to monitor the
course of the disease.
Abdominal aortic aneurysm

Middle-aged and elderly patients who develop acute abdominal pain and
in whom a palpable pulsatile mass is found in mid-abdomen should be
suspected of having an abdominal aortic aneurysm. The quickest and
easiest way to detect an abdominal aortic aneurysm is by ultrasound and
this shows not only its size but also whether or not blood has dissected
between the intimal and serosal layers of the vessel. CT is, however, the
method of choice as it is a superior method for imaging and subsequently
monitoring both the aneurysm and its potential complications. The dis-
1106
THE ACUTE ABDOMEN
Figure 33.
Rupture o f the left renal artery.
The left kidney (1) is displaced
anteriorly owing to a perirenal
bleed (2). The normal right kid
ney is excreting iodine to the re
nal pelvis.
section is delineated by an intravenous injection of contrast medium as

is the perfusion status and function of the kidneys. The thoracic aorta
should also be examined which, again, is best done with CT. A routine
examination should, therefore, start at the level of the cervical vessels
and end below the aneurysm.
Extrauterine pregnancy (EUP)

In a fertile woman presenting with sudden, severe pain in the lower ab
domen the diagnosis of an extrauterine pregnancy should be suspected.
After the pregnancy has been confirmed by analysing the urine for the
presence of HCG, the patient should undergo an ultrasound examination
in order to detect or exclude the presence of an EUP. If an ectopic preg
nancy is present it can usually be visualized directly as a localized
swelling in the fallopian tube, often accompanied by evidence of bleed
ing into the peritoneal cavity.
Another cause of pain in the lower abdomen of a fertile woman is a
tubo-ovarian abscess, which is easily detected by ultrasound as a fluid-
filled, low-echogenic mass in the true pelvis.
Abdominal trauma
Blunt abdominal trauma may cause bowel wall bleeding (see above), but
can also cause rupture of solid organs and vessels and patients present
ing with a history of such trauma should be examined with CT.
Abdominal survey films may, however, demonstrate enlargement of or
gans or loss of normal contours owing to the infiltration of surrounding
fat planes by ascites, blood, bile and oedema. The patient may also pre
sent with peritonitis. Rupture of a kidney or the urinary bladder can be
detected during intravenous urography as leakage of opacified urine.
1107
Patients who have suffered blunt abdominal trauma to the abdomen

and have symptoms of intra-abdominal injury should undergo CT (Fig.
33). No special preparation is necessary, but a gastric tube will usually
already be in place. Intravenous contrast enhancement is essential but
oral contrast medium is not usually employed in these circumstances. A
tear or area of bleeding in a parenchymatous organ is seen as a low at
tenuation area and the diagnosis of such a lesion is often dependent on
the demonstration of defective enhancement in that particular area.
Bleeding into the general peritoneal cavity can sometimes be seen as a
relatively high attenuation fluid collection in the peritoneal cavity. The
thoracic cavity should always be included in the CT study.
Patients who have suffered penetrating trauma may have damage to
parenchymatous organs and/or perforation of the bowel. Similar lesions
can also be caused by blunt abdominal trauma and should be excluded
by CT.
Gastrointestinal bleeding
Patients who bleed from the gastrointestinal tract often undergo a sub
stantial array of examinations. In a patients with chronic bleeding the
following steps are recommended: fibreoptic-endoscopy of the oesoph
agus stomach and duodenum; colonoscopy, and scintigraphy. If these
studies are negative, barium examinations of the entire gastrointestinal
tract should be performed and angiography may eventually be required.
During ongoing bleeding an emergency angiography should be consid
ered. The examination should be performed with selective catheteriza
tion of the coeliac trunk, superior and inferior mesenteric arteries with
superselective studies as appropriate. The examination is often compli
cated in these severely sick patients. Common bleeding sources in el
derly patients are arteriovenous malformations which are usually seen in
the ileocoecal area. The source of bleeding can be detected either by the
demonstration of leakage of contrast medium into the bowel lumen or
by the identification of a vascular lesion likely to be responsible for it.
Another cause of bleeding is bowel ischaemia, usually seen in the colon.
Bowel ischaemia is frequently caused by a low perfusion pressure that
causes secondary bleeding owing to non-occlusive hypoxia which can
not be detected during angiography. Bleeding from the gastrointestinal
tract is often intermittent and angiography may be required on several
occasions before the correct diagnosis is established. For a more detailed
1108
THE ACUTE ABDOMEN
discussion on gastrointestinal bleeding; see chapter 22.
Ongoing gastrointestinal bleeding may be treated by embolization using
metallic coils, small pieces of spongostan, polyvinyl alcohol and other
agents. Patients may also be treated intravenously by an infusion of va
sopressin.
A patient with an abscess in the peritoneal cavity is often best treated
with a drainage catheter inserted percutaneously under local anaesthesia
using ultrasound or CT guidance.
Ileocolic intussusception and volvulus of the sigmoid colon can also
be resolved using radiological techniques as described earlier.
CONCLUSIONS
The radiological evaluation of an acute abdomen is often difficult and it
is essential for the radiologist to be familiar with the appearances of the
normal abdomen. The assessment of any abnormalities is based on a va
riety of radiological observations including the detection of abnormal
collections of gas or fluid inside or outside the gastrointestinal tract; the
demonstration of calcification, masses, and the enlargement or dis
placement of organs; and the recognitition of any effacement of normal
anatomical structures and contours. Any radiological interpretation
should always be undertaken in the light of a detailed knowledge of the
patient's history and clinical presentation.
1109
Chapter 25
The genitourinary system
Henrik S. Thomsen and Howard M. Pollack
MODALITIES
KUB (Kidney-ureter-bladder survey)

A plain film of the kidneys and bladder is useful for the diagnosis of cal
culi, soft-tissue calcifications and gas. It is an integral part of all con
ventional X-ray examinations of the urinary tract (Fig. 1); it should al
ways be performed prior to contrast medium injection.
Intravenous urography (IVU or IVP)

After the KUB has been taken, contrast medium (e.g. 1 ml per kg body
weight of a 300 mg I/ml solution independent of the kidney function) is
injected into a vein. Within the first 60 seconds up to three exposures
over the kidney are done in order to visualize the renal parenchyma dur
ing the nephrographic phase of the contrast passage (Fig. 2 a). Many ra
diologists make these exposures with tomographic technique (Fig. 2 b).
Another film over the kidney region is taken 5 min. post contrast. If there
are no contraindications (e.g. hydronephrosis, aortic aneurysm, recent
surgery, big abdominal tumor), abdominal compression is applied in or
der to retain the opacified urine in the pelvis and ureter (Fig. 3). Five min.
thereafter additional exposures o f the kidneys including oblique views
are taken. The compression is then removed and a full abdominal expo
sure is obtained. When the bladder is well filled a coned exposure of it
is taken (Fig. 4). Linear tomograms of the kidneys, late radiographs, erect
or prone views, bladder view after voiding are taken as needed.
1111
Figure 1.
KUB covering the majority o f the ab
domen and the pelvic cavity. This is an
indispensable adjunct to intravenous
urography, and one should not attempt
to interpret a urogram without it. The
most common defiency is failure to
demonstrate the upper and lower
reaches o f the urinary tract.
Figure 2.
Nephrographic phase.
a) Nephrogram taken 30 s
after start an intra
venous bolus injection o f
contrast medium. A t this
time there is an obvious
demarcation between
medulla and cortex in
normal kidneys.
b) Nephrotomogram taken
45 s after administration
o f contrast.
1112
THE GENITOURINARY SYSTEM
Figure 3.
Urogram o f the normal upper
urinary tract taken before (a)
and after (b) application o f
abdominal compression. The
calyces are much better visual
ized after the abdominal com
pression has been applied.
Figure 4.
Coned exposure o f the bladder filled
with contrast medium during intra
venous urography.
Figure 5.
Multiple calyces/papillae demonstrated at
intravenous urography. An uncommon
normal variant.
Urography includes standard exposures, but should principally be indi

vidualized. The strengths of urography are 1) rapid overview of the en
tire urinary tract, 2) detailed anatomy of the collecting system, 3) demon
stration of calcifications, 4) it is sensitive for obstruction, and 5) low cost,
whereas the weaknesses are that: 1) it depends on kidney function, 2) it
provides little assessment of parenchymal structure (e.g. cystic vs. solid),
3) it does not show the whole renal contour and may miss masses aris
ing from the anterior or posterior part of kidney, 4) the perinephric space
is not demonstrated, 5) it necessitates the use o f radiation and contrast
medium, and 6) it provides no assessment of glomerular filtration rate.
However, the latter can be determined by drawing a blood sample 3 to
4 hours after the contrast medium injection and measuring the iodine
content in the sample; from this measurement the glomerular filtration
rate can be calculated.
The ability of urography to show detailed calyceal anatomy and the
overlying parenchyma makes it useful for the diagnosis of papillary
necrosis, urothelial neoplasms, sponge kidney, adult polycystic kidney
disease and urogenital tuberculosis. It is able to demonstrate the major
ity of calcifications within the urinary tract, but it is not as sensitive as
CT. Its role in obstruction is debated; a combination of KUB, ultra
1114
sonography and diuresis renography is an alternative, but with acute ob

struction (i.e. colic) the urogram is usually diagnostic. Small mucosal
abnormalities in the pyelocalyceal system and the ureter is best diag
nosed at intravenous urography and it is therefore important for the di
agnosis of early transitional cell carcinoma in the upper urinary tract.
Congenital anomalies such as fusions, rotation anomalies, calyceal vari
ants (Fig. 5) and duplications are well demonstrated by intravenous urog
raphy. In trauma, when the renal injury is thought to be minor, urogra
phy provides a quick and effective screen.
Direct Pyelography
Direct pyelography means direct injection of contrast medium (75-100
mg I/ml) into the upper urinary tract. It may be performed either through
a catheter placed in the ureter during cystoscopy (retrograde) or through
a needle or a nephrostomy tube (antegrade). A meticulous technique (e.g.
sterile conditions, low injection pressure, diluted contrast medium solu
tion with a low viscosity, fluoroscopic surveillance) should always be
employed (Fig. 6). At this examination the visualization of the calyces,
pelvis and ureter is independent of the kidney function in contrast to in
travenous urography. Backflow (extravasation) into the renal
parenchyma and surroundings (pyelosinous backflow, intrarenal back
flow, pyelovenous backflow and pyelolymphatic backflow) should be
avoided through a low injection pressure since backflow not only may
cause complications (e.g. pain, infection) but also obscure the disease.
The examination is excellent for demonstration of 1) small mucosal
abnormalities, 2) diverticula and cavities, 3) urinary leakage, and 4) ob
structing process in the upper urinary tract, when intravenous urography
has not been conclusive. The indications include: 1) non-visualization of
the upper urinary tract on intravenous urography (unless there is an ob
vious cause such as a large tumor, in which case CT would be preferred),
2) an inconclusive or suspicious-appearing segment of the upper urinary
tract which may be better visualized with direct pyelography, 3) unex
plained hematuria in which intravenous urography did not completely
delineate the entire ureter and/or renal pelvic cavity, 4) to differentiate
intrinsic from extrensic ureteral processes, 5) severe contrast material re
action during intravenous urography (the examination may be performed
with gas), 6) as an aid in the diagnosis of renal failure, e.g. renal papil
lary necrosis and 7) possibility of upper urinary tract obstruction (stric-
1115
Figure 6.
Normal antegrade pyelogram demonstrating the
pelvis and the upper part o f the ureter. It is o f ut
most importance not to overdistend the pelvis and
to use no greater than a 10-20 % contrast solu
tion in order to avoid obscuring at both retro
grade and antegrade pyelography.
tore, calculus, papilla), 8) as an aid to

brush biopsy, 9) with endourological pro
cedures (e.g. percutaneous nephrolitho
tomy (PCNL)).
Cystography
Cystography means specific examination
of the bladder with contrast medium. It
can be performed following intravenous
injection of contrast media (in conjunc
tion with intravenous urography) or fol
lowing direct installation of contrast
medium either through a urethral or a
suprapubic catheter. The bladder is exam
ined in several views and exposures are often also taken during voiding
(Fig. 7 a). A post-void film is essential. If vesicoureteric reflux is sus
pected the field of view should include both ureters and kidneys and flu
oroscopic surveillance should be performed both during the filling (low-
pressure) and voiding (high pressure) phase keeping fluoroscopy time to
a minimum. In case of examination for female incontinence the vagina
is marked with barium sulphate, so-called colpocystourethrography.
Cystography is mainly performed for the diagnosis of posttraumatic or
post-operative urinary extravasation, to evaluate certain diverticula and
to look for vesico-ureteral reflux.
Urethrography
Urethrography may be performed antegrade (micturition, voiding) or ret
rograde. Urethrography is an example of an examination which modem
imaging techniques have not yet displaced. In males an obturating can-
ula system or a small balloon catheter is placed with the tip in the fossa
1116
Figure 7. Cystourethrogram in females.

a) Normal cystogram obtained during voiding.
b) Double balloon catheters can be used fo r visualization o f a diverticulum (arrow) in
the fem ale urethra. Contrast medium enters the urethra via a catheter opening be
tween the balloons which occlude the bladder neck and external urethral meatus.
navicularis and water-soluble contrast medium is injected retrogradely

through the urethra and up into the bladder. In females the short urethra
is difficult to examine but special catheters with two balloons (one for
the internal orifice and one for the external orifice) have been developed
(Fig. 7 b). Examination during voiding is best for the posterior urethra,
but nearly always results in inferior visualization of the anterior urethra.
Retrograde studies are excellent for the anterior urethra, but inferior for
the posterior urethra.
Urethrography is used for the diagnosis of urethral strictures, diver
ticula, tumors and in trauma. It may also be helpful in certain postoper
ative conditions.
Hysterosalpingography
Today hysterosalpingography is primarily used in the work-up of female
infertility; previously it was also used for diagnosis of uterine body and
cervical disease. As with urethrography either a cone-tipped obturator is
placed in the external cervical orifice or a tiny balloon catheter inserted
in the uterine cavity. A water-soluble contrast medium is injected slowly
in order to demonstrate that the salpinges are open and that contrast
spreads freely in the peritoneal space (Fig. 8). Exposures are taken after
the patient has been lying on all sides for a few minutes in order to se-
1117
Figure 8.
Normal hysterosalpin-
gogram (HSG). There is
fre e flow through the
salpinges and out into
the peritoneal space.
cure free distribution of the contrast medium in the pelvic cavity of the
peritoneal space.
Angiography
Angiography of the genitourinary system does not differ from the same
examination of other organ systems. A catheter is introduced into the ve
nous or arterial system using Seldinger technique. The tip of the catheter
is placed during fluoroscopic guidance in a vessel leading to or coming
from the region of interest. Injection of vasoconstrictive drugs may be
useful when the veins are examined through retrograde injection but with
the modem digital equipment visualization of the venous tree is often
possible following intraarterial injection of contrast material.
Renal arteriography to diagnose and differentiate renal masses is rarely
performed now due to the advent of ultrasonograhy and especially CT.
Angiography may be performed in the planning of surgery on an anom
aly (e.g. horseshoe kidney) or partial nephrectomy. Other residual indi
cations for renal arteriography includes suspected renal artery stenosis,
vasculitis (e.g. polyarteritis nodosa), aneurysms and arterio-venous fis
tulae. Arteriography is necessary during vascular interventions such as
embolization, stenting and balloon dilatation of the venal vessels.
Ultrasonography
Ultrasonography has gained a central position in genito-urinary imag
ing. It has a diagnostic potential in almost every part of the genito-uri
nary tract and is furthermore easy, cheap and non-invasive. The major
disadvantage is that it is very operator dependent.
1118
Figure 9.
Ultrasonography o f a
normal kidney. The nor
mal parenchyma is echo
poor, whereas the renal
sinus is echo rich. The
поп-dilated renal pelvis
is obscured by the sinus
echoes.
Several special probes have been developed for ultrasonographic ex

amination of the genito-urinary tract. First of all there are the traditional
abdominal transducers, which are useful for examination of the kidneys
(Fig. 9) and the adrenals and overview examination of the pelvic organs.
If the examination with this probe is inadequate one can supplement by
using a transrectal (proximal urethra, prostate), transvaginal (female gen
itals, posterior part of the bladder) or transurethral probe (bladder wall).
Traditional ultrasonography gives information about morphology (e.g.
solid vs. cystic), but not about function. Perfusional data require Doppler
or color Doppler. By flow characteristics and frequency shifts color
Doppler can detect arterial stenosis and demonstrate the vascular nature
of various lesions.
Ultrasonography is superb for guidance in relation to interventional
procedures like nephrostomy, biopsy, and drainage.

CT has assumed an important role in the visualization of the urinary sys
tem. Within a few minutes the entire urinary tract may be visualized in
cluding the surrounding tissue. When doing renal CT one must remem
ber that the iodine concentration in the urine may be high enough to ob
scure small changes e.g. small tumors. Therefore only 10 to 20 ml of a
300 mg I/ml solution should be used when the collecting system is the
main area of interest. For visualization of the renal parenchyma and the
bladder 100 ml of a 300 mg I/ml solution are appropriate. Modem CT-
scanners are fast and sometimes too fast for human physiology. The en-
1119
Figure 10.
CT o f normal kidneys
before (a) and after (b)
intravenous administra
tion o f contrast medium.
tire urinary tract may be examined before the excreted contrast material
has reached the renal pelvis (approx. 1 1/2 min. after the contrast medium
has reached the renal artery) (Fig. 10). Therefore the timing of the scans
should be tailored to the specific purpose of the examination. Dynamic
CT with rapid scans through the same slice or spiral CT after bolus con
trast administration is sometimes used to study vascularity more pre
cisely.
CT is excellent in detecting and differentiating renal masses and in
staging renal malignancies. It is very sensitive in identifying calcifica
tions, even non opaque stones. It surpasses the efficiency of ultrasonog
raphy in identifying perinephric, peri-ureteral and pelvic processes sec
ondarily affecting the urinary tract. CT is the method o f choice for eval
uating renal injuries thought to be clinically severe (or if the initial
1120
Figure 11.
MRI o f normal kidney.
a) Coronal Tl-weighted image
showing good demarcation be
tween cortex and medulla.
b) Axial Tl-weighted image.
c) Coronal T2-weighted image
showing that the kidney
parenchyma is signal intense.
1121
urogram is abnormal). It is the best modality to demonstrate the normal

adrenal glands in detail and it has become the mainstay in diagnosing
and differentiating adrenal pathology.
Magnetic Resonance Imaging (MRI)

The role of MR in the imaging of the urinary tract is not completely es
tablished whereas it has assumed a very important role in the imaging of
the genital organs. Principally the examination is performed in the same
way as it is performed of other regions of interest (Fig. 11). Special coils
(endovaginal and endorectal) are available for pelvic uroradiologic imag
ing. When paramagnetic contrast media containing gadolinium are used
one should remember that high concentration results in overshooting
(T2-effect) producing low rather than high signal on T1-weighted im
ages. As with CT the dose of contrast medium should be adjusted ac
cording to the purpose of the examination. High (1.5 T), mid (0.5 T) and
low (0.1 T) field units are suitable for genitourinary imaging. A role for
MR spectroscopy of the urogenital organs has not been shown, whereas
MR angiography within the next years may replace X-ray angiography.
Pelvic imaging (bladder, prostate, uterus and genital organs) are for the
time being the major area for MRI within the genitourinary system. It
seems very useful for local staging of various types of cancers; prelim
inary indications are that it may surpass the sensitivity of CT in detect
ing enhancement of small lesions. At present its use in the kidney is usu
ally reserved for cases which cannot be solved whit CT and US, when
iodinated contrast media is contraindicated, and for vascular lesions.
Nuclear Medicine
Nuclear medical examinations give functional information about the
genitourinary system, especially about the kidneys and the adrenals (Fig.
12). Their role in imaging of the lower urinary tract and genital organs
is limited. In contrast to conventional X-ray the ionizing radiation is in
ternal and generated by radionuclides, which emit radiation that is de
tected by a gamma camera or Single Photon Emission Computer
Tomography (SPECT). Many radiopharmaceuticals are available for ex
amination of the genitourinary tract. The most frequently used are: 99mTc
MAG3, 99mTc DTPA, 131I-Hippuran, 123I-Hippuran, 99mTc DMSA, 99mTc
Glucoheptonate, 57Cr-EDTA. The latter is used for in-vitro determina
tion of the glomerular filtration rate. The rate at which 99mTc DTPA and
1122
Figure 12.
Renography (a: Histogram
b: Scintigram) o f normal
kidneys performed with
99mTc MAG3. Normal his
togram values:
Time to peak <3,5 min.; Split
function within the normal
range 43-57 %; and Residual
activity at 20 min. < 22 %.
m mm
X-ray and MR contrast media are cleared from the plasma, can also be
used. DTP A is nearly exclusively filtered by the glomeruli, whereas hip-
puran and MAG3 are both filtered by the glomeruli and excreted by the
tubular cells. DMSA and glucoheptonate accumulate in the functioning
1123
Figure 13.
Cortex
Coronal section o f the
kidney showing the re
lationship o f the cor
tex, the medulla, and
Renal pelvis
the renal collecting
system.
Ureter
tubular cells and are excellent for renal scintigraphy. MAG3, DTP A and
hippuran are used for renography and interventional renography. With
all 6 radiopharmaceuticals the function of each individual kidney can be
determined. Nuclear medical imaging is an indispensable complement
to all the more morphologic imaging modalities since it provides infor
mation about renal function/perfusion and particularly about renal out
flow obstruction (diuresis renography), renal artery stenosis (captopril
renography), split functions, scar detection, and renal transplant moni
toring. Scintigraphy is useful for diagnosis o f urinary leakage, and iso
tope cystography is an alternative to conventional cystography for the
diagnosis of vesico-ureteral reflux. Special radiopharmaceuticals are
available for both cortical (131I cholesterol) and medullary (131I or 123I
MIBG) adrenal imaging.
KIDNEY AND URINARY TRACT
Anatomy
Kidney
The kidneys (Fig. 13) are located in the retroperitoneum and measure ap
proximately 12 cm (height), 6 cm (width) and 4-5 cm (depth). The re
nal surfaces are usually smooth, but fetal lobulation may persist for life.
The kidneys move with respiration; the cranio-caudal excursion may be
as much as 10 cm. The renal pelvis is normally within the confines of
the kidney, but it may also be extrarenal. The size of the pelvis depends
in part on the state of hydration. At ultrasonography the parenchyma is
echopoor whereas the renal pelvis and the surrounding sinus tissue
(mostly fat) is echorich. The arcuate vessels when seen mark the loca
1124
Figure 14.
Relations o f a transplant
kidney. The graft artery
may also be anastomosed
end to end to the internal
iliac artery.
Figure 15.
Enhanced CT o f a normal
renal transplant in the
right iliac fossa.
tion of the cortico-medullary junction. At CT it is not possible to distin

guish between cortex and medulla on unenhanced exposures, whereas
on images taken during the first 60 seconds after the contrast medium
has reached the kidney there is a clear demarcation between medulla and
cortex; during the excretion phase the attenuation of the two areas is again
the same. On T2-weighted MRI the renal parenchyma is bright whereas
the medulla has lower signal intensity than the cortex on unenhanced T 1-
weighted images.
The transplanted kidney

The transplanted kidney does not differ from the kidney in situ with one
exception: the location. Normally the graft artery is anastomosed end-
to-end to the internal iliac artery or end-to-side to the external iliac artery
(Fig. 14). The graft vein is anastomosed to the external iliac vein. It is
placed in either the right or left iliac fossa just beneath the skin. Often
only the upper two-third is covered by peritoneum. Its location just be
neath the skin makes the allograft quite suitable for ultrasonographic ex
amination whereas the underlying iliac bones are an obstacle to good
urographic visualization. The location just under the skin makes is pos-
1125
sible to differentiate between medulla and cortex at ultrasonography; the

medulla is slightly less echogenic than the cortex. Its presentation at CT
and MRI is similar to that of kidneys in situ (Fig. 15).
Ureter
The ureters course along the psoasmuscles from the renal pelvis, pass
over the common iliac vessels, and enter the bladder deep in the bony
pelvis dorsolaterally. Visualization of the normal ureter requires in the
majority of patients intraluminal contrast.
Bladder
The urinary bladder is best examined when it is full, at which time it fills
the anterior part of the pelvis. The top of a filled bladder may extend into
the abdomen. Normally the bladder contains between 200 and 500 ml.
The bladder wall is thicker in men than women and decreases from 2 cm
to 2 mm during filling. In males the bladder is located ventral to the an
terior wall of the rectum with the seminal vesicles posterior. The outlet
o f the bladder (e.g. neck) is separated from the membranous urethra by
the prostate. In females the uterus and vagina are located behind and un
derneath the bladder and the urethra, whereas the salpinges and the
ovaries are located supero-laterally to the empty bladder. The upper one-
third of the bladder is intraperitoneal.
Urethra
The male urethra (Fig. 16) consists of four parts: pars prostatica in which
the ejaculatory ducts empty on either side of the posteriorly located veru-
montanum; pars membranacea, the shortest part, is the part of the ure
thra, which transverses the urogenital diaphragm, and is followed by pars
bulbosa and pars pendula. Taken together the prostatic and membrane
ous parts are defined as the posterior urethra while the bulbous and pen
dular portions are known as the anterior urethra.
The female urethra is 2 to 3 cm in length and is located anterior to the
vagina. It is surrounded by the internal and the external sphincter.
Physiology
The kidney has several functions including excretion o f metabolic prod
ucts and foreign substances ("waste products"), regulation of body fluid
osmolality and volume, regulation of electrolyte balance, regulation o f
1126
Figure 16.
Diagram o f the male
urethra and genitals.
Seminal vesicle
Rectum
Figure 17.
DCT
The nephron. The
kidney is divided into
cortex, medulla and Afferent
arteriole
papilla. The blood
enters the glomerulus Efferent
(G) through the arteriole
afferent arteriole and C ortex
leaves fo r the vasa
recta (VR) through
the efferent arteriole.
The filtered compo
nent passes through
PCT (proximal con M edulla
voluted tubule), PST
(proximal straight
tubule), tDL (thin
descending limb o f
the loop o f Henle),
tAL (thin ascending Papilla
limb o f the loop o f
Henle), TAL (thick
ascending limb o f the
loop o f Henle), DCT
(distal convoluted tubule), CCD (cortical collecting duct), MCD (medullary collecting
duct), PCD (papillary collecting duct) and out into the calyx.
acid-base balance, and production and secretion of hormones. The kid

ney forms concentrated urine as a mechanism for relieving the body of
waste materials (Fig. 17). This is accomplished by filtration of the blood
at the glomerulus, resulting in a protein-free ultrafiltrate of plasma. The
kidneys are perfused by one-fourth of the cardiac output, resulting in a
renal blood flow of 1,250 ml per min. The glomerular filtrate averages
125 ml per min., which then through reabsorption of water is reduced to
1127
the normal urine output o f about 1 ml per min. Approximately two-thirds

o f the ultrafiltrate volume is reabsorbed by the proximal tubule by a
process linked to the active secretion of hydrogen ions and the active re
absorption of sodium, glucose, amino acids, and other solutes ("obliga
tory" reabsorption). Isotonicity of the fluid in the proximal tubule with
the plasma is maintained as the cells of the proximal tubule are freely
permeable to water. The counter-current multiplier system of the loop of
Henle then acts to create a high solute concentration in the medulla by ac
tive transport of sodium out of the ascending limb o f the loop, resulting
in a high osmotic gradient between the medulla and the collecting ducts
descending through it. The cells in the descending limb have a high per
meability for water, whereas the cells in the ascending limb are imper
meable to water. The gradient, in conjunction with antidiuretic hormone
secreted by the posterior lobe of the pituitary, allows water to diffuse from
the collecting ducts into the medulla and results in a concentrated - so-
called mature - urine. From the collecting ducts the final 15% of water
absorption is achieved ("facultative" reabsorption). Body acid-base bal
ance is maintained by the ability of the kidney to secrete hydrogen by
the formation of titrable acid and excretion of ammonium and its ability
to reabsorb bicarbonate selectively in exchange for hydrogen. The kid
ney is also instrumental in erythropoiesis, being the chief site of either
the activation or production of erythropoietin. It also produces renin and
1,25-dihydroxyvitamin D3. Parathyroid hormone also acts on the distal
tubule to conserve calcium.
After formation by the kidney, urine is delivered to the bladder by the
collecting system and ureter. The calyces function independently and
asynchronously in transmitting urine to the renal pelvis. While the loca
tion of a pacemaker for coordinated peristalsis is not precisely known, it
is felt that the first propagating wave begins in response to urine dis
tending the renal pelvis, although in some kidneys the activity can orig
inate in the upper infundibulum. This wave then passes down the ureter
in a coordinated fashion via an electrical impulse that passes through
connecting smooth muscle cells in the ureteral wall. As one segment of
the ureter contracts to propel the urine bolus caudad, another immedi
ately below relaxes to accept the bolus, this sequence repeating until the
bolus reaches the bladder into which it is expelled as a jet (Fig. 18).
Peristaltic waves are inhibited as pressure in the bladder rises and by
ureteral distension.
1128
Figure 18.
CT o f the bladder demon
strating a je t (arrow) o f con
trast medium entering the
bladder from the ureter (ar
rowhead).
The micturition reflex arc is parasympathetic and derived from the sec
ond through fourth sacral cord segments. The external sphincter has a
somatic innervation. Receptors in the bladder wall initiate the micturi
tion reflex via afferent fibers in the arc in response to bladder distention.
This voiding reflex can then be inhibited or facilitated by activity origi
nating in the cerebral cortex and extending down the spinal cord to the
sacral level. During voiding, the bladder detrusor contracts and actively
funnels the bladder neck; the sphincters surrounding the membranous
urethra then relax, allowing complete expulsion of the bladder content.
Between voiding, the intravesical pressure normally remains at a low
level because of the reflex arc by the inhibitory effect of the central ner
vous system as well as the elastic properties of the bladder smooth mus
cle. Urinary continence is maintained by the internal and intrinsic sphinc
ters combined.
Pathology
Prerenal pathology
The kidneys are commonly affected by disorders of the aorta, renal ar
teries, and renal veins. Hypertension is a frequent concomitant of renal
artery disease - both as a cause and as an effect. Disorders that affect the
renal artery and its major branches include atherosclerosis, fibromuscu-
1129
Figure 19.
Arteriosclerosis.
Arteriogram demonstrating
arteriosclerosis in the
lower abdominal aorta and
a stenosis (arrow) o f the
left renal artery close to the
aorta.
Figure 20.
Fibromuscular dysplasia.
Arteriogram demonstrating
several narrowings in the
right renal artery o f a
young woman.
lar hyperplasia, arteritis, neurofibromatosis, aneurysms, arteriovenous

malformations, embolic disease, and thrombosis.
Renal artery stenosis

In atherosclerosis deposition of lipid material on the intimal surface
leads to a secondary reaction within the intima. Arteriosclerosis is pri
1130
marily a problem of the elderly (Fig. 19). Fibromuscular hyperplasia is

term that encompasses several disorders characterized by multiple fi
brosing lesions in main and segmental vessels. It typically occurs in
young females (Fig. 20). Among the protean manifestations of neurofi
bromatosis are renal artery stenosis and renovascular hypertension. Two
characteristic lesions are seen in patients with neurofibromatosis: 1)
stenosis of one or both renal arteries, and 2) unilateral or bilateral
aneurysms in the renal artery or its branches. The aorta and renal arter
ies may be involved in inflammatory processes that result in marked nar
rowing. One such disorder, Takayasu's arteritis, occurs most frequently
in young females.
Hypertension
Hypertension is reported to affect from 7% to 20% of the adult popula
tion. An exact prevalence is, however, unknown, mainly because of dif
ferences in the study populations and the diagnostic criteria. Among the
rare secondary causes of hypertension renovascular disorder is the most
frequent. The prevalence depends not only on the source of the study
population but also on the definition of hypertension in that population
and on its severity. The prevalence of renovascular hypertension in a hy
pertensive population with diastolic pressure between 90 and 104 mmHg
is probably less than 1%, whereas in a population with a diastolic pres
sure above 125 mmHg the prevalence is reported to about 30%. With
such a low prevalence in the largest group of patients, screening of all
hypertensive patients for renovascular hypertension with either scintig
raphy, intravenous urography, or digital angiography is not advisable
owing to the low number o f true positives, the cost and the unacceptably
high false-positive rate. Before the patient is referred for an imaging ex
amination, some selection must take place. Patients with a diastolic pres
sure above 110 mm Hg, young patients, those with a sudden rise in blood
pressure independent of age, and patients with a poor response to ther
apy should be examined further. The captopril-enalpril renogram appears
to be the most cost-effective procedure for screening those patients.
Understanding the effects of angiotensin-converting enzyme inhibition
on the kidney distal to a stenosis and appreciating the potential effect of
sodium balance or antihypertensive medications are crucial in anticipat
ing the putative changes in the radionuclide studies of the renovascular
bed following angiotensin-converting enzyme inhibition (Fig. 21).
1131
A. Normal Figure 21.

Glomerulus
The effect o f angiotensin converting
Afferent areteriole afferent areteriole enzyme inhibition on glomerular p er
fusion and filtration rate in renal
artery stenoses.
Normally, renin secretion is

stimulated by extracellular fluid
B. Renal Artery Stenosis
volume contraction, reduced
pressure in the baroreceptor o f
the afferent arteriole, dimin
ished sodium delivery to the
macula densa, and influence o f
cathecholamines or prostaglan
dins. A negative feed back loop
also exists such that angiotensin
C. Renal Artery Stenosis plus Captopril II,
of renin. Renovascular hyper
tension appears to be dependent
on renin secretion from the jux
taglomerular apparatus from the
underperfused stenotic kidney
and is partially maintained by
participation of the contralateral
kidney, which demonstrates an
abnormal pressure-natriuresis relationship in which a new set-point of
sodium homeostasis is attained at a higher level of arterial pressure.
Angiotensin-converting enzyme inhibition acts to interrupt the renin-an-
giotensin-aldosterone system pathway by preventing the conversion of
the decapeptide angiotensin I to the octapeptide angiotensin II such that
both the vasoconstrictor-hemodynamic and aldosterone-stimulating ef
fects of angiotensin II are blocked. Hence, angiotensin-converting en
zyme inhibition acts as a pharmacological probe for investigating the
role of angiotensin II in the pathophysiology of renovascular hyperten
sion. In addition, the converting enzyme also serves to degrade va-
sodilatory prostaglandins and bradykinins, such that enzyme inhibition
may result in the enhancement of the tissue levels of these vasodilatory
substances. The rationale for captopril- and enalpril-stimulated radionu-
1132
Figure 22. Captopril scintigraphy.

a) Without captopril.
b) With captopril. Captopril abolishes the uptake o f 99mTc DMSA in the right kid
ney (arrowheads) (PA-image) causing so-called medical nephrectomy. Subsequent
angiography showed a stenosis o f the right renal artery.
elide studies is that the angiotensin-converting enzyme inhibitor removes

the angiotensin II-dependent efferent arteriolar resistance, which results
in a reduction in transcapillary forces and, therefore, reduces renal func
tion in the kidney distal to stenosis. When renal perfusion is reduced, as
seen in patients with renal artery stenosis, the transcapillary pressures
that maintain the forces to drive glomerular filtration are sustained by a
preferential increase in efferent arteriolar resistance. The increased ef
ferent arteriolar resistance is maintained via angiotensin II. Captopril and
enalpril act to block the formation of angiotensin II and consequently re
move postglomerular forces maintaining filtration; thus, the glomerular
filtration rate of the affected kidney decreases. The decrement in indi
vidual kidney function may then be noninvasively assessed using con
ventional radionuclide studies (Fig. 22). The hippuran renogram after
captopril or enalpril has been reported to be highly predictive of the blood
pressure response to angioplasty or reconstructive surgery with a sensi
tivity of 96% and specificity of 95%. In the 1970’s intravenous urogra
phy and simple renography were popular for screening a hypertensive
patient, but these modalities are no longer used due to poor sensitivity
and specificity. Doppler ultrasonography demonstrating hemodynamic
changes may be useful in very experienced hands, but as a routine ex
amination the sensitivity and specificity are less than that for captopril-
enalpril renography. In some places central vein renin assay is used for
the diagnosis of renal artery stenosis. The role of MR angiography is
1133
Figure 23.
Wedge-shaped photon defi
cient area in the left kidney
due to an infarct demon
strated during 99mTc
DMSA scintigram.
promising, but unsettled regarding screening. A major drawback is the

expense. Conventional or digital radiographic angiography is still needed
for definitive demonstration of the lesion. However, it should be kept in
mind that only after correction of the stenosis is achieved and the blood
pressure has become normal, can the diagnosis of renovascular hyper
tension be made with certainty.
E m b o li and thrombi
Emboli or in situ thrombosis can result in acute obstruction of the renal
artery or its branches. Failure to restore renal blood flow within a few
hours after renal artery occlusion usually results in infarction and loss o f
function. Intravenous urography and nuclear medicine will show absent
function or delayed function if the obstruction is incomplete (Fig. 23).
A rim-like nephrogram ("cortical rim-sign") may be seen on enhanced
CT or angiography due to collateral circulation. However the cortical
rim sign may also be seen in renal vein obstruction, acute tubular necro
sis (vasomotor nephropathy) and cortical necrosis. Ultrasonography is
often normal in the acute stage; in the ensuing days the size decreases
and the kidney becomes more echogenic. Both Doppler ultrasonography
and angiography (Fig. 24) will show absence o f flow.
Renal artery aneurysm

Renal artery aneurysm may impress the renal pelvis and mimic a para-
pelvic cyst on intravenous urography and ultrasonography. Color
1134
Figure 24.
Multiple infarcts in a transplanted
kidney shown at arteriography.
Estimated original outline o f the graft
( ------- )■
Doppler ultrasonography, enhanced CT and angiography will confirm

the diagnosis.
R enal arteriovenous fistu la

A renal arteriovenous fistula may be congenital (arteriovenous mal
formation) or acquired. Causes of the latter include rupture of a renal
artery aneurysm, blunt trauma, penetrating injuries (e.g. renal biopsy).
The typical presenting sign are a bruit, hypertension, hematuria, and
signs of high output congestive heart failure. Intravenous urography
and ultrasonography are rarely helpful, although pyeloureteral "notch
ing" from collaterals is sometimes noted on the urogram. Dynamic CT,
nuclear medical angiography (first passage scintigraphy) and Doppler
ultrasonography may be diagnostic. Selective renal arteriography is de
finitive and demonstrates early venous filling with dilatation of each
feeding artery and draining vein. Embolization may be attempted at the
time of angiography. MRI will demonstrate signal void on both T1-and
T2-weighted spin-echo images due to flowing blood, but MRA is much
more sensitive and graphic, and the vascular images can be projected
1135
in any plane as well as in 3D.
R en a l vein throm bosis

The patient with acute renal vein thrombosis typically presents with
flank pain, hematuria, fever, and proteinuria. Signs of the nephrotic
syndrome may appear in the subacute phase. Renal enlargement is de
tected by many imaging studies. Whether there is opacification at in
travenous urography and accumulation o f radioactivity on scintigrams
depends on the degree of obstruction and the extent of collateral ve
nous circulation, which is usually better in the left kidney. Intravenous
urography and direct pyelography may show notching of the ureter by
periureteric collaterals. CT may demonstrate a thrombus in the renal
vein and/or inferior vena cava and perinephric venous engagement
("cobwebbing"). Ultrasonography will show nephromegaly and de
creased echogenicity due to edema. Renal arteriography demonstrates
prolongation of arterial and capillary flow, stretched vessels, a de
creased nephrogram, and non-visualization o f the renal vein. Clot vi
sualization with renal phlebography is superior, but invasive proce
dures are no longer called for in renal vein thrombosis unless throm
bolysis is attempted, which is unusual. At present, MRA is probably
the most sensitive, accurate and best test, but lack of availability is a
major drawback.
Renal pathology
A nom alies
Renal agenesis is often an incidental radiological finding. A major clue
is the characteristic compensatory hypertrophy of the contralateral kid
ney. If this is lacking one should search for an ectopic kidney. A nonvi
sualizing kidney on urography caused by renal agenesis can be confirmed
by ultrasound or CT. Ultrasonography can evaluate the renal fossae, but
CT is more effective in evaluating the lower abdomen for a small ectopic
kidney (Fig. 25). Renal anomalies, especially agenesis, are associated
with a significant incidence of seminal vesicle anomalies, and in the fe
male, with utero-vaginal anomalies. This should be kept in mind during
ultrasonographic examination.
Fusion anomalies of the kidney are often asymptomatic. Intravenous
urography will show the abnormal axis of fusion and delineate the ureters
1136
Figure 25.
Normal sized ectopic
kidney above os
sacrum. The kidney is
also rotated.
Figure 26.
Intravenous urography demonstrat
ing crossed renal ectopy. The "left"
kidney is located below the right
kidney.
(Figs. 26 and 27). Horseshoe kidneys are recognized on ultrasonography

by the extension across the spine. CT, MRI and scintigraphy readily iden
tify both horseshoe kidneys and renal ectopy. Very graphic visualization
is produced by arteriography (Fig. 28).
In renal dysplasia there is no kidney parenchyma, usually just a col
lection of cysts. Renal dysplasia is nonfunctional and thus not seen by
urography or scintigraphy. Calicification in cyst walls is sometimes rec
ognized on KUB, however. CT can identify the variation of renal dys
plasia that does not display multicystic changes as a small mass of tis-
1137
sue in the renal fossa. Ultrasonography will show absence of a normal

kidney and will identify a typical multicystic dysplastic kidney. There is
no renal pelvis, but there may be a rudimentary ureter.
Figure 27.
A horseshoe kidney is easily
demonstrated at intravenous
urography. The renal axes inter
sect inferiorly.
Figure 28.
A horseshoe kidney is well
outlined at digital subtraction
angiography.
1138
Figure 29.
Simple renal cyst.
Ultrasonography reveals an ane-
choic cyst with dense echoes in
the posterior wall. There is
acoustic enhancement deep to the
lesion.
Cysts
Simple cysts are the most common renal mass. They have been detected
more readily since the advent of ultrasound and CT, and may be found
in more than 50% of patients over the age of 50 years. The ultrasound
criteria for a benign cyst include the absence of internal echoes, smooth,
sharply defined walls and acoustic enhancement beyond the posterior
wall proportional to the fluid content (Fig. 29). Refraction lines at the
edges o f the cyst are typical, as is the absence of flow on color Doppler
ultrasonography. The CT criteria for a benign cyst include homogenous
attenuation value near the density of water, imperceptible cyst wall,
smooth interface with renal parenchyma, and lack of enhancement fol
lowing intravenous contrast injection (Fig. 30). When these criteria are
met, the diagnosis of a simple cyst is accurate in 93% - 98% of cases.
In those cases not meeting the strict criteria for ultrasound or CT, nee
dle aspiration or enhanced MRI should be considered to establish the fi
nal diagnosis (Fig. 31). MRI is extremely sensitive to vascularity and has
detected small occult tumors in the wall of renal cysts. Unlike CT, it is
not unusual to visualize cyst walls with MRI. Scintigrams obtained with
a renal parenchymal agent such as 99mTc-glucoheptonate or 99mTc-dirner-
captosuccinic acid demonstrate an area of absent activity that persists
through the dynamic (blood pool) and static (parenchymal) phases.
1139
Figure 30.
Simple renal cyst in a left kid
ney demonstrated at en
hanced CT. Homogenous
low-attenuating process,
which does not enhance after
administration o f intravenous
contrast (apparent unsharp
ness at cyst-kidney interface
is due to volume averaging).
Bleeding into a cysts produces a "hemorrhagic cyst" which may be dif

ficult to differentiate from a renal carcinoma on imaging studies, although
it is usually possible to do so.
A d u lt polycystic kidney disease

In adult polycystic kidney disease, which is inherited as an autosomal
dominant condition, the cysts may occur anywhere along the nephron.
Approximately 90% of patients have a positive family history. Cysts may
be diagnosed by imaging from approximately the age of 20 years, while
they are still asymptomatic. Ultrasonography demonstrating multiple
cysts in a patient with positive family history is diagnostic. The patients
often present with symptoms like pain, urinary tract infection, hematuria
and hypertension most commonly in the fourth or fifth decade, although,
rarely the cysts may be obvious at birth. The median age for end stage
renal failure is in the late fifth decade. Cysts are easily detected by ul
trasonography, CT and MRI using the criteria for cysts. Intravenous
urography demonstrates enlarged kidneys with smooth or irregular con
tours (Fig. 32) and multiple radiolucensies on nephrotomography
("swiss-cheese"). The pyelocalyceal system is usually splayed and de
formed by the multiple cysts. Bleeding into cysts occurs very often and
are best diagnosed by MRI demonstrating cysts containing hemorrhagic
fluid with mixed signal intensity and a fluid-level on both T1-weighted
and T2-weighted sequences. Fine curvilinear calcifications - probably a
residual of intracystic bleeding - can be diagnosed at CT (sometimes on
KUB) and they do not signal malignancy (Fig. 33). The frequency and
1140
Figure 31.
Simple renal cysts demonstrated
at MRI. The patient had one
cyst in each kidney.
a) T1-weighted image.
b) T2-weighted image. MRI
clearly delineates renal cysts.
On TI-weighted images the
content is signal poor often
with a clearly delineated
wall, whereas on T2-
weighted images it is signal
intensive, sometimes with
edge enhancement.
Figure 32.
Adult autosomal dominant polycys
tic kidney disease demonstrated at
intravenous urography. Both kid
neys are enlarged with irregular
contours. The pyelocalyceal sys
tems are splayed and deformed.
1141
Figure 33.
Adult autosomal dominant
polycystic kidney with m ul
tiple parenchymal calcifi
cations on unenhanced
CT. The patient is on re
placement therapy due to
end-stage renal failure.
number of calcifications increases with age. As many as 40-80% of all

patients with adult polycystic kidney disease have hepatic cysts. In many
cases the liver cysts may be larger and more numerous than the renal
cysts. Also the frequency of detectable hepatic cysts increases with age
of the patients. After the start of replacement therapy (dialysis or trans
plantation) the size of the polycystic kidneys decreases.
M edullary sponge kidney

Medullary sponge kidney (’’tubular ectasia”) is a sporadic disorder of de
velopmental origin. The collecting ducts (Bellini) in the distal renal pyra
mids and papillae become dilated; small cysts which usually communi
cate with the collecting ducts and in which calculi frequently form, are
occasionally seen in the medulla in the more severe cases. Medullary
sponge kidney is usually bilateral but may be unilateral and/or segmen
tal. It is often an incidental finding in intravenous urography. Plain films
show clusters of small calculi in the distribution of the papillae or medulla.
Intravenous urography is diagnostic and shows linear dilated collecting
tubules (’’streaks" or "brush" appearances), some of which contain calculi
(Fig. 34). Neither ultrasonography, CT nor MRI add anything.
A cquired cystic disease

Acquired cystic disease refers to cystic formation in the cortex and
medulla in patients with end-stage renal failure treated with intermittent
hemodialysis. It is most frequently seen in patients with glomeru
lonephritis and the cysts often disappear when the patient receives a func-
1142
Figure 34 .
Medullary sponge kidney
(tubular ectasia).
a) Nephrogram.
b) Excretory phase.
Intravenous urography
shows multiple distinct col
lections o f contrast material
in dilated papillary collect
ing ducts ("brush effect”)
and punctuate calcifications
in the same locations.
Figure 35. Acquired cystic

disease. Enhanced Tl-
weighted MRI demonstrating
solid lesion (arrow) anteriorly
in the left kidney due an ery-
thropoetin producing tumor.
The parenchyma is signal
poor; compare it with the im-
age o f a normal kidney ob
tained with the same TRJTE
sequence shown in Fig. 11.
1143
Figure 36.
Renal variants (pseudotumors),
which may simulate a tumor.
lobation hump
Prominent Suprahilar
column of Bertin "bump"
tioning graft. Ultrasonography shows haphazardly dispersed small cysts,

usually less than 3 cm in size, some with hemorrhage or calcification.
The kidneys demonstrate increased echogenicity which is presumably
due to the underlying renal parenchymal disease and may become very
large. CT and MRI show small cysts scattered throughout the cortex
and medulla. Contrast enhances non-cystic tissue on both CT and MRI
(Fig. 35). Patients with acquired renal cystic disease are at risk for the
development of renal cell carcinoma.
Pseudotum or
One of the most common space-occupying lesions in the kidney is the
hypertrophied column o f Bertin, which is an infolding or double thick
ness of healthy renal cortex, most characteristically separating the supe
rior from middle pole calices. Other so-called pseudotumors include the
prominence of the lateral renal margin secondary to the splenic impres
sion ("dromedary hump”) and the hilar lip, which often occurs superior
to the hilus, secondary to focal hypertrophied parenchyma (Fig. 36).
Focal parenchymal hypertrophy adjacent to an area of scarring from pre
vious inflammation is another cause for a pseudotumor. The diagnosis
1144
Figure 37.
Angiomyolipoma. CT without
(upper row) and with (lower
row) intravenous contrast
medium applied and bone set
tings (left column) and soft tis
sue setting (right column) o f
window and level. The an
giomyolipoma (arrows) had
attenuation values similar to
that o f fat. At ultrasonography
it was hyperechoic.
is well established with renal scintigraphy showing normal accumula

tion of the tubular cell seeking 99mTc DMSA. CT and especially MRI can
also be used for the diagnosis in indeterminate cases, whereas ultra
sonography is usually of limited value.
Adenom a
Renal adenomas are slow-growing, solid parenchymal epithelial tumors
that originate in mature tubular cells and are thought to be pre-malig-
nant. Cystic areas and calcifications can occur. Lesions less than 3 cm
are usually benign, but the final classification is based on histology and
clinical behavior rather than on size.
Angiomyolipom a
Angiomyolipomas (hamartomas) contain varying amounts of smooth
muscle, blood vessels and mature fat cells. Demonstration of fat by CT
(Fig. 37) (negative attenuation values [-15 or lower]) or MRI (fat sup
pression sequence) within the tumor is nearly pathognomonic of it an an
giomyolipoma, although there have been a few cases of fat-containing
renal cell carcinoma. On the other hand some angiomyolipomas contain
undetectable amounts of fat or have the fat masked by hemorrhage and
are therefore not diagnosed until after removal. Sonography is non-spe
cific and reveals a hyperechoic mass. Surgery is unneccesary in the vast
majority of the cases.
1145
Figure 38.
Oncocytoma (arrowheads)
in the left kidney at en
hanced CT. Centrally a
scar (arrow) was found.
The findings are only sug
gestive o f oncocytoma.
Oncocytoma
Oncocytomas are epithelial neoplasms believed to originate from the
proximal collecting tubules. These tumors are characteristically benign,
but due to their solid nature can not be definitely categorized as benign
prior to surgery. A central scar demonstrated at ultrasonography, CT (Fig.
38) or MRI is suggestive of, but not pathognomonic. Because a renal cell
carcinoma may mimic an oncocytoma completely, conservative surgery
(i.e. partial nephrectomy) is rarely justified.
R en a l cell carcinoma
Renal cell carcinomas occur most commonly in the sixth decade and are
often detected incidentally. Depending on the initial imaging study further
evaluation by at least one other study is usually required. Symptoms, when
present, are usually non specific; e.g. hematuria, flank pain and a palpable
tumor may occur in adult polycystic kidney disease as well as in renal cell
carcinoma. Intravenous urography typically shows renal enlargement with
a well-circumscribed or occasionally irregular mass. Five% - ten% will
show calcification, which if central or diffuse is extremely suspicious. The
kidney is often rotated on its axis and/or displaced (Fig. 39). Tomograms
obtained during the nephrogram phase show a lucent or inhomogenous
mass whose interface with the adjacent renal parenchyma may be smooth
or irregular. When the mass extends beyond the renal contour a thick or
irregular wall can sometimes be discerned. CT, MRI and ultrasonogra
phy can all be used in establishing the nature of a renal mass more pre
cisely. Demonstration of a solid mass is indicative of a renal cell carci
noma until another diagnosis has been proven. CT is excellent for both
1146
Figure 39.
Renal cell carcinoma in the
upper pole o f the right
kidney. The collecting
system is displaced and the
upper pole is occupied by a
mass.
Figure 40.
Renal cell carcinoma.
a) Tumor in the latero-
posterior part o f the left
kidney.
b) Tumor in the anterior
part o f the right kidney
slightly dislocating the
liver. Both the contrast-
enhancing wall and the
inhomogenous enhance
ment o f the lesion exclude
the possibility o f a simple
cyst. a
1147
Figure 41.
Recurrent renal cell carci
noma. The process (arrows) in
the left renal bed does not en
hance and its appearance is
not reminiscent o f any normal
abdominal structure.
Figure 42.
Renal cell carcinoma. Mixed
hyper- and hypoechoic mass
(arrows) in the upper pole.
diagnosis and staging. The CT criteria for renal malignancy include het
erogeneous tissue with an attenuation value near to that of renal
parenchyma, contrast enhancement, irregular interface with surrounding
parenchyma, and areas of calcification (Fig. 40). Secondary spread to re
gional lymph nodes and extension into the renal vein are clear signs of
a malignant tumor. At most institutions CT is used as the primary modal
ity to stage renal carcinoma prior to treatment because of its diagnostic
accuracy, and its ability to detect local extension, regional lymph node
involvement, and distant metastases as well as to evaluate the contralat
eral kidney. CT is also best for evaluating the renal bed for recurrent tu
mor (Fig. 41). Ultrasonography can also be used for the diagnosis of a
solid mass (i.e. sound absorption) and thereby exclude the presence of a
cyst. Common ultrasonographic patterns are a hyperechoic somewhat at-
1148
Figure 43.
Renal cell carcinoma in the
lower pole o f the right kidney
at MRI. Tl-weighted image af
ter application o f intravenous
contrast - gadodiamide
(Omniscan). There is central
necroses.
tenuating mass (Fig. 42) and a complex mass containing echo-poor, rel
atively transsonic areas that represent foci of liquefaction necrosis.
Ultrasonography may also be used for excluding a tumor in the opposite
kidney and extension into the perinephric space. MRI demonstrates an
inhomogenous, enhancing mass. The Tl-weighted and T2-weighted sig
nals vary with the composition of the tumor (Fig. 43). MRI appears to
be the most sensitive and most accurate method of diagnosis in renal cell
carcinoma and detecting venous extension. However, because of its ex
pense, lack of universal availability and because CT and ultrasonogra
phy are also very accurate, it is usually reserved for special situations,
i.e. patients with very complicated lesions, or those who can not receive
iodinated contrast medium. Renal angiography is seldom necessary any
more for diagnosis.
Lym phom a
Imaging techniques demonstrate renal involvement in approximately
one-third of patients with systemic lymphoma. Renal lymphoma can pre
sent as a mass, as multiple, unilateral or bilateral masses, as diffuse in
filtration with renal enlargement or as infiltration into the sinus or the
perinephric space. Retroperitoneal adenopathy is nearly always present.
Leukemic and myelomatous infiltration causes renal enlargement.
M etastases
Metastases to the kidney are usually associated with primary neoplasms
of the lung, breast, stomach, cervix, colon, and pancreas. Differentiation
1149
from a primary renal malignancy is sometimes suggested by the infil

trative, poorly defined pattern of metastases or bilaterality, but in gen
eral this differentiation is unreliable, and needle biopsy is required for
diagnosis.
Infection
Acute pyelonephritis is usually caused by bacteruria resident in the gas
trointestinal and genital tracts. Underlying systemic diseases and condi
tions of altered host resistance predispose to renal infection. Imaging
studies are unnecessary in most adult patients with typical clinical signs
who respond to medical therapy. If an imaging examination is indicated,
ultrasonography is often preferred at the initial imaging procedure be
cause of its ability to demonstrate calculi, hydronephrosis, intrarenal or
perinephric abscesses. Subtle parenchymal changes associated with in
fection, as well as extrarenal spread, are more consistently demonstrated
by CT than by ultrasonography and include patchy area of underperfu
sion, small, dense nephrographic foci and perinephric edema. 99mTc-glu-
coheptonate or 99mTc dimercaptosuccinic acid scintigraphy is also use
ful, because localized infections appear as focal defects, often before they
can be seen with CT or ultrasonography. Hydronephrosis and ureteral
obstruction is demonstrated on delayed images.
Emphysematous pyelonephritis is a very serious condition which is
due to extensive necrosis and gas formation caused by gram-negative or
ganisms. Gas in the renal parenchyma (and sometimes in the perinephric
space and in the pyelocalyceal system) may be seen on plain film or CT.
Ultrasonography show increased echogenicity with blurred acoustic
shadowing due to reverberations of sound in the gas medium. Intrarenal
gas is readily seen on CT scans.
Severe pyelonephritis, if inadequately treated or unresponsive to an
tibiotics may lead to the formation of a chronic occult infection or a re
nal abscess. Intravenous urographic findings include obliteration of the
ipsilateral psoas stripe, diffuse enlargement or a focal mass, and defor
mity of the pyelocalyceal system. Ultrasonographically, a renal abscess
appears as hypoechoic or anechoic mass with fluid-fluid (or fluid-debris)
level and distal acoustic enhancement. The wall may appear as an
echogenic rim. Unenhanced CT scans show low attenuation within the
abscess cavity. The wall enhances, but the center does not. The findings
at MRI are similar. Pus is signal intensive on T1-weighted and T2-
1150
Figure 44.
Bilateral reflux nephropathy. IVU lO m in
Clubbed calyces with overly 77 12 0 8 jj#
ing reduction o f parenchyma

in a 17 year old female with
increasing serum-creatinine
and hypertension.
T c -9 9 m DMSA R IG H T
LEFT OBLIQUE BACK RIGHT OBLIQUE
Figure 45. Right-sided reflux nephropathy. 99mTc DMSA scintigraphy is more sensi
tive than intravenous urography fo r depicting scars or active parenchymal disease
since it only mirrors active tubular cells. Oblique views are o f great importance fo r the
detection o f small scars.
weighted images. A perinephric abscess has similar imaging features,

but its location is extrarenal.
Chronic pyelonephritis is an interstitial, nonsuppurative nephritis. The
inflammatory process originates in the medulla from retrograde ascent
or in the cortex from antegrade or blood-borne infection and involves the
pyramids, the cortex, or both, producing cortical scars and calyceal de
formities. It rarely occurs in patients with a normal urinary tract. It may
be due to vesico-ureteral reflux (reflux nephropathy - a residual of in-
trarenal reflux in infancy), obstruction, sickle cell disease and analgesics.
Urographic findings include unilateral or bilateral small kidneys. In re
flux nephropathy calyceal clubbing, and adjacent cortical scarring is
found (Fig. 44). Intravenous urography often underestimates the extent
of renal scarring compared to renal scintigraphy (Fig. 45). In obstructive
ll5l
nephropathy the whole kidney is involved. Ultrasonography shows fo

cal parenchymal atrophy and areas of fibrosis. CT demonstrates scarring
with irregular renal margins.
Xanthogranulomatous pyelonephritis is a complication of chronic in
flammation that is believed to represent an inadequate acute inflamma
tory response in an obstructed, infected, and ischemic kidney. The renal
parenchyma is replaced by yellow tumor-like masses containing lipid
laden histiocytes. In the diffuse form plain films commonly demonstrate
a radiopaque staghom calculus in an enlarged kidney. Intravenous uro
graphy shows an absent or decreased nephrogram and absent, decreased
and/or delayed opacfication of the pyelocalyceal system. Ultrasono
graphy demonstrates renal enlargement with parenchymal replacement
by multiple anechoic or hypoechoic masses surrounding the pyeloca
lyceal system, which usually contains stones. Pyonephrosis may be pre
sent. CT shows an enlarged kidney with a contracted renal pelvis which
usually contains a staghom calculus and replacement of renal sinus fat
by fibrosis. The parenchyma is replaced by low-attenuation masses rep
resenting xanthoma, cavities, and dilated calyces. Extrarenal extension
into the perinephric and paranephric spaces, psoas muscle, and adjacent
viscera is commonly present. In about 10 to 20% of cases xanthogranu
lomatous pyelonephritis is segmental. A proteus organism is usually
found in the urine.
Renal tuberculosis is usually secondary to hematogenous spread from
a pulmonary focus. Although gross morphologic changes are typically
more severe in one kidney, microscopic lesions are invariably present in
both. Progressive disease is associated with tuberculoma formation and
antegrade destruction of the medulla, pyramids, and papillae with cavi
ties. Healing of these lesions is accompanied by interstitial fibrosis,
parenchymal calcification, cortical scarring, stricturing of infundibula
and calyces, and hydronephrosis. Extrarenal extension (e.g. perinephric
or psoas abscess and fistulas to small intestine or colon) is not uncom
mon. The findings on plain films, intravenous urography and pyelogra
phy reflect the bilateral, but asymmetric distribution of active renal in
fection and sequelae of healing (Fig. 46). These include absent, decreased
or delayed excretion of contrast material, localized caliectasies with mi
nor irregularity of the calyces, papillary necrosis with irregular or moth-
eaten calyces and occasional filling of adjacent medullary parenchymal
abscesses, amputation of the tips of calyces and infundibula, hy-
1152
Figure 46.
Tuberculosis. Retrograde
pyelography was performed
since no contrast medium was
excreted during intravenous
urography. Typical changes
with medullary-papillary
cavitation, moth-eaten
calyces and pipe stem ureter.
dronephrosis, a parenchymal mass or abscess that does not communi

cate with pyelocalyceal system, cortical scarring, linear, ring and/or
amorphous parenchymal calcifications, and autonephrectomy resulting
in an enlarged reniform sac filled with caseous material or an atrophic
fibrotic calcified kidney. Imaging modalities other than intravenous urog
raphy and retrograde pyelography are non-specific in renal tuberculosis.
Depending on the stage of the disease, the findings on ultrasonography
and CT resemble those of papillary necrosis and xanthogranulomatous
pyelonephritis. Involvement of the ureter bladder and/or internal geni
talia is quite common in patients with renal tuberculosis. Alternating
strictures and dilatation may give the ureter a ’’corkscrew" or "beaded"
appearance. More extensive infiltration can produce a rigid "pipe stem"
ureter (Fig. 46).
P apillary necrosis
Papillary necrosis is believed to be due to localized ischemia. It is espe
cially frequent in diabetes mellitus and analgesic abusers. Less common
associations include hypotension, renal vein thrombosis, obstruction,
sickle cell disease, and sickle cell trait. Intravenous urography remains
the best imaging modality for demonstrating the various stages of pap-
1153
Figure 47.
Renal papillary necrosis due to
analgesic abuse. Irregular calyces
with central contrast defects
(= necrotic papillae) and backflow
o f contrast into the collecting
tubules (pyelotubular backflow).
A necrotic papilla obstructs outflow
from the renal pelvis.
Figure 48.
Nephrocalcinosis secondary to Alport's disease.
Chronic calcifications outlining the contracted
kidneys.
illary necrosis. The findings include de

creased opacification of the affected ca
lyces, contrast material surrounding the
separated necrotic papilla - central separa
tion produces a ring sign while marginal
separation produces a claw sign - , a single
contrast-filled cavity within a papilla, a con
vex irregular calyx which becomes a
"blunt" calyx with healing, hydronephrosis
due to obstruction of the ureter by necrotic
tissue or a calculus, punctuate or ring-
shaped papillary calcification due to calci
fication of one or more necrotic papillae.
Because of its relatively poor spatial reso
lution, ultrasonography is generally not di
agnostic in the early stages of papillary
necrosis. The resolution of CT and MRI is
1154
not great enough to show papillary changes, but retrograde pyelography

can provide this information (Fig. 47), if the urogram is indeterminate.
Nephrocalcinosis
Nephrocalcinosis is a form of metastatic or dystrophic calcification in
the renal parenchyma. It can be secondary to hypercalcemic and hyper-
calcuric states, hyperoxaluria, medullary sponge kidney cortical necro
sis, adult polycystic kidney disease chronic nephrosclerosis and chronic
glomerulonephritis (Fig. 48). CT is the best modality to diagnose tiny
calcifications, whereas more gross calcifications may be seen on plain
films. Calcifications within or close to the genito-urinary tract may have
many causes (Fig. 49).
M edical disease
The kidney is involved in numerous pathologic conditions. Some like lu
pus erythromatosus are systemic, while others like glomerulonephritis
are localized to the kidney. The so-called "medical” diseases of the kid
ney involve primarily the renal parenchyma as distinct from the collect
ing system and tend to be bilateral. The kidneys may be enlarged, nor
mal in size, or small. Since many of these diseases resemble each other
radiologically the role of imaging in patients with such renal disease
and/or renal failure is not to make a specific histological diagnosis, but
Costochondral calcification
Adrenal calcification
Splenic granulomata
Renal artery calcification Caliceal stone
Stone in caliceal diverticulum
Staghom calculus
Cortical nephrocalcinosis
Medullary nephrocalcinosis
Calcification in renal tumor Calcification in wall o f renal cyst
Calcified mesenteric nodes Aortic aneurism
Ureteral stone
Diac artery calcification
Appendicolith
Phleboliths
Calcified uterine fibroid
Calcified vasa
Bladder stones
Prostadc calculi
Figure 49. Etiology o f calcifications within or close to the genito-urinary tract on

KUB.
1155
Figure 50.
End-stage renal failure.
Ultrasonogram demonstrating a
small contracted kidney (ar
rows) with high echogenicity
and loss o f corticomedullary
boundary.
to exclude surgical renal disease, namely, obstruction. A renal biopsy

may in most cases be needed to establish a definitive diagnosis. The med
ical diseases include vasomotor nephropathy (formerly termed acute
tubular necrosis), cortical necrosis, glomerulonephritis, Goodpastures
syndrome, periarteritis nodosa, sclerodermia, Wegener’s granulomato
sis, systemic lupus erythromatosus, acquired immune deficiency syn
drome (AIDS), diabetes mellitus, sickle cell disease, amyloidosis, mul
tiple myeloma, hemophilia, and radiation nephritis. Every patient in re
nal failure should have a screening ultrasonography. Because
ultrasonography of the kidney is independent of renal function, hy
dronephrosis can be excluded. However, up to 25% of patients with hy
dronephrosis do not have underlying obstruction, and approximately 4%
of patients with obstruction do not develop hydronephrosis due to a low
glomerular filtration rate. Diuresis renography can not be used confirm
or exclude the occurrence of obstruction in patients with a glomerular
filtration below 10-15 ml/min x 1.73m2. The normal renal cortex is less
echogenic than the liver or spleen. Most parenchymal disease are char
acterized sonographically by increased cortical echogenicity with gen
eral preservation of corticomedullary boundaries, but these may be lost
in severe cases (Fig. 50). Iodinated contrast media (urography, CT, an
giography) should be avoided in patients with diminished renal function,
since contrast agents may further depress the renal function. MRI may
be helpful in the future, but it is too soon to be sure. Periarteritis nodosa
is an exception for the limited use of imaging in medical diseases. Renal
1156
Figure 51.
1311 hippuran renography o f
renal transplants. The 5 min.
images as well as the his
togram show good uptake in
and excretion from the graft
in the right side, whereas
there is only a very slow up
take in the left sided graft.
The latter is undergoing
chronic rejection, whereas
the one in the right side has
recently been transplanted.
angiography demonstrates microaneuryms and irregular arteries and ar

eas of decreased perfusion distal to occluded vessels.
Transplantation
Renal transplantation has been a routine procedure at many institutions
for three decades. The failing allograft can present a complex and con
fusing diagnostic problem. The clinical presentation of fever and ten
derness of the renal graft is non-specific. Initially one will exclude any
overt mechanical problem such as hydronephrosis, urinoma, lymphocele
etc. that can be remedied by imaging-guided intervention or surgery.
However, these complications cause less that 5% of graft dysfunction.
This is the reason why most attention is directed to the interplay of the
intersti-tial processes causing the decrease in renal function, and why ra
dionuclide studies, which can quantify perfusion and function, have as
sumed an important role in the management of renal transplants (Fig.
51). The most commonly adopted procedures are perfusion studies and
renography. Nuclear medical examinations can with high certainty ex
clude pathology and should be the primary imaging tool for monitoring
post-operative renal transplants. Ultrasonography can yield an anatomic
record of the renal allograft, but except for Doppler imaging, no con
clusions can be drawn about any aspect of renal function. Duplex and
1157
color Doppler imaging permit simultaneous evaluation of vascular flow

from the main renal artery through the arcuate arteries. All other imaging
is supplementary to nuclear medical examinations and ultrasonography in
renal transplants. CT offer a significant anatomic imaging value because
it can demonstrate the kidney and perinephric anatomy whereas ultra
sonography cannot because of technical factors such as bowel loops, sur
gical sutures, osseous structures and so forth. MRI in evaluation of the al
lograft for parenchymal disease is an area of current interest. Only time
will show whether it is valuable, but preliminary studies have indicated
that MRI is able to give both information about perfusion and function, as
does nuclear medical examinations, as well as very fine anatomic details.
Traum a
The kidney is the most frequently injured organ in blunt abdominal
trauma. The choice of imaging depends on the patient's clinical condi
tion, the severity of trauma and the possibility of multiple involvement.
In a patient who presents with hematuria following relatively minor flank
trauma it is appropriate to begin with an intravenous urography. In a mod
erately or severely injured patient - whenever possible - contrast-en
hanced CT should be the initial imaging procedure, since it depicts the
extent of renal and perinephric injury and may demonstrate injuries of
other abdominal viscera. Ultrasonography is not helpful in the acute sit
uation and only causes the appropriate examination and treatment of a
traumatized patient to be delayed. The usefulness of ultrasonography is
limited because it is often impossible to perform properly due to the
trauma (pain, ileus, wounds et c.). In the most severe injuries there may
not be time for any pre-operative imaging.
Intravenous urography will demonstrate whether there are one or two
functioning kidneys. A renal contusion or intrarenal hemorrhage appears
as a localized decrease in intensity of the nephrogram or as an intrarenal
mass with splaying of the collecting system. Extravasation of opacified
urine indicates a lacerated collecting system, which is often associated
with a serious parenchymal injury (but does not always mean surgery).
It must be kept in mind that asymmetric opacification can be due to pre
existing disease. If the patients is in shock at time of injection, the kid
neys may not opacify or there may be a persistent nephrogram without
opacification of the collecting system. In a patient who has sustained rel
atively mild trauma and is clinically stable, further imaging is usually
1158
Figure 52.
Posttraumatic renal
hematoma involving on the
right kidney (probably sub-
capsular). Upper level: No
contrast has been adminis
tered. Lower level: After intra
venous contrast medium ad
ministration. The attenuation
value o f the hematoma (ar
rows) is higher than o f the re
nal parenchyma before admin
istration o f contrast medium
but lower after contrast was
given.
unnecessary if the intravenous urography is normal. On the other hand,

abnormal intravenous urogram may warrant further evaluation by means
of CT. Intrarenal and extrarenal hematomas (Fig. 52), disruption of the
renal parenchyma, perfusion defect and extravasation of contrast laden
urine or blood into the perinephric and paranephric spaces are readily
demonstrated by CT. Leakage of urine implies laceration of the collect
ing system and/or renal parenchyma, which often is self-limited, but
sometimes requires stenting or even open surgery. A locally decreased
or striated nephrogram indicates local contusion. In some patients with
renal pedicle injuries, only a rim of cortical tissue is opacified. This in
dicates occlusion of the renal artery and perfusion through collaterals.
Postrenal pathology
Duplication of the renal collecting system is the most common urologi
cal anomaly and easily diagnosed on urography when renal function of
both the upper and lower segments is preserved. When complete, reflux
into the lower collecting system commonly occurs, and an ectopic ureter
with or without associated ureterocele often obstructs the upper collect
ing system. Obstructed duplication may be suspected on the urogram
when there is downward displacement of the lower calyces and an in
sufficient number of them, the so-called ’’drooping lily" sign. Ultrasound
is a good method to demonstrate the dilated upper collecting segment,
which is seen as a cystic structure just superomedial to the normal renal
parenchyma, but ultrasound can not determine whether there is obstruc
tion. For this purpose diuresis renography may be used to distinguish be-
1159
Figure 53.
Ureteroceles. Mild dilatation o f
both distal ureters with bulbous
protrusion into the bladder. The
lucent rim surrounding the
ureteroceles is mucosa elevated
by the intravesical portion o f the
dilated ureters.
tween obstructive and non-obstructive dilatation, if there is sufficient

function in the ectopic segment. Duplication of the contralateral collect
ing system is a helpful sign, since renal duplication is bilateral in 15% of
the cases, and partial duplication is even more frequent.
A simple or non-ectopic ureterocele (Fig. 53) is usually associated
with a non-duplicated ureter. On intravenous urography a so-called co
bra-head deformity representing the dilated distal ureter surrounded by
a uniformly thin rim of lucent epithelium is seen. Simple ureteroceles
are also easily demonstrated by ultrasonography and CT.
U rothelial tumors
Most urothelial neoplasms are malignant. Transitional cell carcinoma,
the most common, occurs most often in older men. Squamous cell car
cinoma and mucinous adenocarcinoma are much less common. The var
ious imaging techniques (intravenous urography, pyelography (Figs.
54-55), contrast-enhanced CT (Fig. 55), MRI and ultrasonography (Fig.
56)) demonstrate an irregular filling defect in the renal pelvis, often as
sociated with obstructive hydronephrosis or mucosal irregularity. Severe
hydronephrosis or infiltration of the parenchyma by tumor commonly re
sults in nonvisualization on intravenous urography or contrast-enhanced
1160
Figure 54.
Small pelvic tumor (arrowheads)
demonstrated during retrograde pyel
ography.
Figure 55.
Large pelvic tumor demonstrated by
retrograde pyelography (a) with the
patient positioned at various angles
and by CT (b).
1161
Figure 56.
Pelvic tumor (arrows).
Ultrasonography shows an echo-
poor mass within the echo-rich
pelvis.
Figure 57.
Urothelial tumor in the lower ureter at
retrograde pyelography.
CT. Retrograde pyelography is

needed in most renal pelvic or ca
lyceal filling defects to better
characterize the lesion and to ob
tain tissue by means of brush
biopsy.The appearance of
ureteral tumors is similar to that
of upper tract urothelial neo
plasms (Fig. 57).
Infection
Pyelitis and ureteritis are
chronic inflammations of the
uroepithelium and suburoepithe-
lium, often resulting in cysts.
Intravenous urography shows
multiple round eccentric fillings
defects related to the pyeloca-
1162
Figure 58.
Ureteritis cystica. Intravenous
urography reveals multiple
round filling defects in the pelvis
and upper part o f the ureter.
lyceal system or the ureteral wall (Fig. 58).

Pyonephrosis (purulent material in the obstructed pyelocalyceal sys
tem) is usually secondary to an underlying congenital anomaly, stricture
or calculus, which in turn leads to hydronephrosis, urine stasis and in
fection. Plain films may show an enlarged renal outline, an opaque cal
culus, or an abnormal gas collection. Intravenous urography typically
shows a decreased or absent nephrogram and poor visualization of the
pyelocalyceal system; because of the poor diagnostic yield, this study is
generally omitted, when pyonephrosis is suggested. Retrograde pyelog
raphy shows blunted, irregular calyces sometimes with evidence of pap
illary necrosis. Filling defects representing necrotic tissue or purulent
material can sometimes be seen in the pyelocalyceal system and ureter.
Ultrasonography typically shows a dilated pyelocalyceal system con
taining echogenic fluid and/or a shifting fluid-debris level. Radiopaque
and non-radiopaque calculi can often be identified. Failure to visualize
the proximal ureter suggests that there is an obstruction of the uretero-
pelvic junction. CT shows multiple coalescing low-attenuation, urine-
filled spaces containing fluid-debris or contrast-debris. CT can detect
even minimally opaque calculi. Perinephric extension of the inflamma
tory process is more reliably detected by CT than by other imaging
modalities. MRI does not seem to add anything. Changes of xan
thogranulomatous pyelonephritis can be superimposed on long-standing
pyeonephrosis.
1163
Figure 59.
Pouch stone (arrow) form ed
around a metal suture. Foreign
bodies (e.g. metal sutures which
are not covered with mucosa)
within the urinary tract may act as
a nidus around which calculi can
be formed.
Figure 60.
Staghorn stone in the left renal col
lecting system (arrows) and in the
lower left ureter (arrowheads) with
hydronephrosis in the right kidney
due to a small stone, which can not
be seen on this urogram. The uro
gram was taken 3 hours after
administration o f the contrast
medium. No excretion o f contrast
medium is seen on the left side.
1164
Figure 61.
Nephrotomogram demonstrating a cal
culus (arrows) in the renal pelvis. It was
not seen on the plain film. The kidney
has also a dromedary hump.
Figure 62. Large stone in the left renal pelvis on KUB (a) and after administration o f
intravenous contrast medium (b). The stone does not totally obstruct the outflow from
the renal pelvis. The contrast medium partly obscures the stone.
Calculi
It is estimated that 2-3% of the population develop urinary calculi. Men
are affected twice as often as women. Approximately 10% of stones are
caused by an identifiable metabolic abnormality such as hyperparathy
roidism, but most are idiopathic. Chronic infections and/or foreign bod
ies (Fig. 59) can also cause stones. The incidence of calculi is unusually
1165
Figure 63.
Renal pelvic calculi (ar
rows).
a: Large staghorn calcu
lus.
b: Small pelvic calculus.
A t ultrasonography cal
culi are highly
echogenic and show
sharp acoustical show
ing.
high in certain geographic regions. The clinical significance of urinary

calculi lies in the accompanying symptoms and sequelae. Increased in
traluminal pressure in the collecting system secondary to a calculus
causes pain and can result in perforation of a calyceal fornix with leak
age of urine and/or contrast material into the renal sinus and perinephric
soft tissues. This so-called pyelosinous backflow is usually self-limited
if the urine is sterile. Approximately 90% of upper urinary tract calculi
are radiopaque and therefore potentially visible on plain films (Fig. 60).
Tomography may be helpful in visualizing poorly opaque stones (Fig.
61). The factors that determine whether or not calculi will be detected
are respiratory motion, overlying gas and feces, size and position of the
calculus and technical quality of the film. On intravenous urography, an
opaque calculus may be more, less or equally opaque as the surrounding
opacified urine (Fig. 62). When obstruction is present, the collecting sys
tem proximal to the calculus is dilated. If there is a filling defect in the
pyelocalyceal system and no opaque calculus is seen on the plain film,
1166
Figure 64.
Stricture in the lower ureter follow
ing ureteroscopy demonstrated at
intravenous urography. Such stric
tures may be found months after a
patient has undergone
ureteroscopy.
blood clot or neoplasm must be considered as a differential diagnosis.

Ultrasonography can be helpful, but is highly operator-dependent and
some patients have minimal obstruction. The combination of KUB and
ultrasonography works very well when dilatation is present, but the mid
dle third of the ureter can be a problem. Ultrasonography is indicated in
patients in whom intravenous urography fails to demonstrate the col
lecting system and in patients with markedly impaired renal function. A
renal calculus appears sonographically as an echogenic focus with sharp
acoustical shadowing (Fig. 63). CT is extremely sensitive in detecting
calculi, but is usually reserved for patients in whom the diagnosis is in
doubt. On CT, calculi usually exhibit very high attenuation values. The
complications of calculus disease such as hydronephrosis and retroperi
toneal pathology are clearly depicted by CT. MRI does not give further
information.
Obstruction
Obstruction to antegrade flow of urine may occur at any level from the
renal collecting tubules to the distal urethra (Fig. 64). The urographic
manifestations of acute obstruction are normal or enlarged kidneys, an
obstructive nephrogram (Fig. 65), mild to moderate dilatation of the pye
localyceal system which may be visualized best on delayed films, and
1167
Figure 65.
Obstructive nephrogram on the left side
due a ureteral calculus. The renal
parenchyma on the left is still opacified
by contrast medium, whereas it has al
ready been excreted on the right side.
pyelosinous backflow secondary to small fomiceal ruptures of the ca

lyces. The classic urographic sign of long-standing obstructive hy
dronephrosis is a dilated collecting system. Other characteristic uro
graphic findings include the crescent sign, a thin curvilinearopaque line,
which represents reoriented, dilated tubules that are arranged parallel to
the calyceal surface rather that perpendicular to it; a negative pyelogram,
representing a dilated pyelocalyceal system filled with unopacified urine
seen against a background of opacified parenchyma; the rim sign, a thin
rim of opacified parenchyma seen during the parenchymal phase, often
seen in patients with marked parenchymal atrophy secondary to long
standing severe obstruction; layering of contrast medium in the erect po
sition, a consequence of lost peristalsis, and total absence of excretion.
The worst cases will result in renal atrophy. The quality of the nephro
gram and opacification of the collecting system vary with the degree of
residual functional impairment. Intravenous urography is also excellent
for evaluating the results of corrective surgery for pyeloureteral ob
struction (Fig. 66). Because ultrasonographic visualization of the col
lecting structures is independent of renal function, hydronephrosis is
readily demonstrated by ultrasonography (Fig. 67) even when there is no
1168
Figure 66.
Urogram before (a) and after (b)
Anderson Hynes pyeloplasty fo r
uretero-pelvic junction obstruc
tion. After surgery the renal
pelvis is much smaller and the
form o f the calyces has nearly
normalized.
1169
Figure 67.
Hydronephrosis.
Ultrasonography shows a di
lated, fluid-filled (echo poor)
collecting system.
Figure 68.
Hydronephrosis due to
ureteral calculus. Immediately
after administration o f con
trast medium there is poor
parenchymal opacification
(a - right kidney), whereas 24
hours after the administration
both opacification o f the
parenchyma and the pelvis
(b - right kidney) may be
found. The slight excretion on
the left side 24 hours later is
probably due to reabsorption
o f contrast medium through
pyelosinous reflux on the right.
visualization on intravenous urography. It should be remembered that

ultrasonography can be normal in patients with acute obstruction in
whom dilatation of the collecting has not yet occurred. A full collecting
system from overhydration can be mistaken for hydronephrosis. Ureteral
jets will be diminished or absent. While CT readily demonstrates hy-
1170
Figure 69.
Hydronephrosis due to cervical
carcinoma. Sagittal Tl-weighted
image after administration o f con
trast shows the ureter (arrows) as
a dilated, elongated, low signal
intensity column.
Figure 70.
Diuresis renogram.
a) Classic diuresis renogram
Furosemide
responses when the
Dilated obstructed
frusemide is injected 20
min. after the radiopharma
ceutical. The response (bot
tom left) is equivocal. In
such cases it may be an ad
vantage to repeat the study
and inject the frusemide 15
min. before the radiophar
maceutical
b) Diagram showing conver
sion o f equivocal (F +20)
washout to obstructive or
non-obstructive patterns on
F - 15 diuresis renograms.
1171
Figure 71 a, b.
No obstruction at diuresis
1
renoscintigraphy. There is a good
ф response to the Lasix injection on

both sides. Lasix was injected 20
min. (arrow) after 99mTc MAG3.
ф 1
dronephrosis, it is usually obtained to determine the etiology and extent

of pathology rather than as a screening examination (Fig. 68). CT clearly
depicts retroperitoneal lesions, a frequent cause of ureteral obstruction.
Hydronephrosis is also well demonstrated on both T1 and T2-weighted
MRI. The dilated collecting system appears as a cluster of communicat
ing low-intensity structures within the renal parenchyma, which has a
more intense signal on T1 -weighted images and the ureter is seen as a
dilated, elongated, low signal intensity column (Fig. 69). While retroperi
toneal pathology is readily detected by MRI, calcium-containing calculi
are very low signal and may go undetected against a T1-weighted back
ground. With a T2-weighted pulse sequence where urine is bright, stones
may, however, stand out very clearly. While intravenous urography pro
vides more precise morphologic information, nuclear medicine has a
number of important advantages in the management of the patient with
1172
Figure 72 a, b.
Obstruction at diuresis renoscintig
raphy. There is absence o f response
to Lasix on both sides. Also in this
case Lasix was injected 20 min.
(arrow) after 99mTc MAGy
urinary obstruction. It can give information about whether the hy

dronephrosis is obstructive or non-obstructive. It is especially useful in
patients with possible stenosis of the ureteropelvic junction. In equivo
cal cases, the use of furosemide (Lasix) either before or during the ex
amination ("diuresis" renography) can help to clarify many cases (Figs.
70-72).
Retroperitoneal fibrosis
Although the cause of retroperitoneal fibrosis is uncertain, it is a known
complication in patients taking methysergide and has been alleged to be
related to several other drugs (such as 13-blockers). Occasionally a spe
cific cause can be identified e.g. an aortic aneurysm with perianeurysmal
fibrosis or a retroperitoneal tumor with a marked desmoplastic reaction.
Retroperitoneal fibrosis usually occurs between L5 and S2 and generally
1173
Figure 73.
CT in a patient with retroperi
toneal fibrosis reveals a dense
soft tissue attenuation mass
surrounding the aorta. This
mass extended from L2 to L5.
involves both ureters at this level. The intravenous urogram demonstrates

varying degrees of ureteral obstruction and typically shows medial de
viation of one or both ureters. In periureteral fibrosis the fibrotic reac
tion is limited to the periureteral tissues and the affected ureter may not
be deviated. The fibrotic mass can be demonstrated by CT (Fig. 73), MRI
and ultrasonography.
Traum a
The ureters are well protected in the retroperitoneal paraspinal region
and are seldom traumatized in blunt abdominal trauma. On the other
hand, partial or complete disruption of the ureter can result from pene
trating injuries such as knife or bullet wounds. Iatrogenic injuries can re
sult from instrumentation or surgery. Provided adequate renal function
is preserved, intravenous urography may demonstrate narrowing or dis
ruption of the ureter; if renal function is diminished, direct pyelography
may be needed to evaluate adequately the injured segment. CT, ultra
sonography and MRI give information about the surroundings.
Pathology of the lower urinary tract

Hematuria can be a sign of many urinary tract diseases (Fig. 74). How
ever, it may also occur in the absence of demonstrable disease ("essen
tial hematuria"). Terminal or initial hematuria points towards disease in
the bladder trigone and/or urethra, whereas uniform (total) hematuria is
more indicative of disease in the upper urinary tract or the rest of the
bladder. Erythrocytcylinduria is found in medical renal disease e.g.
glomerulonephritis. Patients with mixed hematuria should probably un
dergo cystoscopy, but beyond this the need for imaging and if so what
1174
Figure 74.
Various causes o f hema
turia. Treatment with anti
coagulants can also cause
hematuria.
type of examination is often debated. Hitherto intravenous urography has

been the most frequently performed examination in those cases, but there
is a clear tendency that ultrasonography is now preferred in many coun
tries as the initial examination. While ultrasonography may detect renal
parenchymal tumors earlier than urography, it is important to remember
that urography is more sensitive in detecting tumors of the renal pelvis
and ureter.
Diverticula
Diverticula are acquired (usually) or congenital (rarely) outpoutchings
of the bladder wall. They may range from very small to so large that they
press on other pelvic organs. The wall of a diverticulum is often smooth
in contrast to the irregular trabeculated bladder wall. Approximately one-
fourth of all diverticula contain calculi and in approximately 3 % a ma
lignant tumor may be present. Two important investigations for the di
agnosis of diverticula are ultrasonography which demonstrates an
echopoor out-poutching (Fig. 75), and cystography, which quantifies the
degree of diverticular emptying. As with unenhanced CT and MRI it is
important to demonstrate the neck of the diverticulum in order to avoid
the wrong diagnosis of a perivesical fluid collection. At intravenous urog-
1175
Figure 75.
Bladder diverticulum. It is o f utmost
importance to demonstrate the neck
o f the diverticulum in order to dis
tinguish it from a fluid collection
with no connection to the bladder.
Figure 76.
Trabeculated bladder with divertic
ula. Due to outflow obstruction
(BPH) a spiral metallic prosthesis
has been inserted in the prostatic
urethra. There are also metal clips
outside the genito-urinary tract
(large bowel anastomosis from pre
vious sigmoid resection).
raphy (Fig. 76), enhanced CT (Fig. 77) and enhanced MRI, contrast
medium is found in the outpouching confirming the presence of a diver
ticulum. Intravenous urography often overlooks non-filling diverticulae
or those located on the anterior bladder wall, but cystography will demon
strate them. Frequently the pelvic ureter will be medially displaced.
Urethral diverticula occur most frequently in females. They may be so
large that they elevate the bladder base, giving the impression of a "fe
male prostate". The primary examination is voiding urethrography, but
sometimes ultrasonography during micturition has been reported to be
successful.
1176
Figure 77.
Bladder diverticula filled with
contrast medium. Urothelial
cancer in the upper left part o f
the bladder.
Tear-drop bladder
At intravenous urography a so-called tear-drop or pear-shaped bladder
is sometimes seen. This special configuration o f the bladder is due to
compression from extravesical processes. The possible causes can be re
vealed at ultrasonography, CT and MRI and include hematoma, abscess,
urinoma, hypertrophy of the iliopsoas muscle, lymphoma, tumor, fibro
sis, bilateral iliac aneurysms, occlusion of the vena cava and pelvic lipo
matosis.
Urachus
Urachal remnants can be seen in all degrees ranging from a tiny elonga
tion of the anterior upper contour of the bladder to a fistula extending to
the umbilicus. A tumor may arise in the residual tissue. CT is the best
modality to demonstrate a urachal tumor since it very often contains very
gracile calcifications anterosuperiorly to the bladder.
Infection
In simple cystitis no changes are found with the various imaging modal
ities, but in severe cystitis one can find a slightly diminished bladder ca
pacity with a thick bladder wall and mucosal edema at ultrasonography,
CT and MRI and sometimes on intravenous urography. In chronic cys
titis the bladder shrinks and the wall thickens. Bilharzia causes chronic
cystitis and mucosal edema as well as thickening of the distal ureter in
cluding the vesicoureteral orifices. With time thin linear calcifications
may develop in the bladder ureters and even renal pelves. Calcifications
may also be due to tuberculosis, but most frequently these are found in
the seminal vesicles seminalis, and ampullae of the vasa deferentia.
1177
Figure 78.
Bladder stone.
Ultrasonography shows an
echorich process in the upper
part o f the bladder with
acoustic shadowing.
C alculi
Bladder calculi are indicative of residual urine since they very rarely de
velop in a bladder which can be completely emptied. Some stones (e.g.
uric acid) do not contain calcium and together with very small calcium
containing stones they may be overlooked at conventional roentgenog
raphy, but they can be seen at ultrasonography (Fig. 78) and CT.
N eurogenic bladder
Residual urine including maximal bladder volume is easily determined
by ultrasonography. Residual urine can also be measured at nuclear med
icine. The main cause o f incomplete bladder emptying is bladder outlet
obstruction, but neurogenic diseases often cause residual urine, which is
also a consequence of vesicoureteral reflux. Urodynamic evaluation and
cystography are complementary examinations in the evaluation of pa
tients with neurogenic diseases and are often performed simultaneously
(video urodynamics). Cystography gives information about the bladder
neck and vesicoureteral reflux.
Trauma
In connection with trauma lesions may involve the bladder and the male
urethra. Rupture of bladder and the urethra in a patient who is not se
verely injured is properly diagnosed by cystography (Fig. 79) and ure
thrography, respectively, showing contrast outside the natural lumen. In
case of a multitraumatized patient CT should be performed as the primary
examination since it gives information about the surroundings (Fig. 80)
and the relations to bones. While intraperitoneal bladder rupture should
be operated promptly, a conservative attitude toward the management of
extraperitoneal bladder rupture is sometimes justified. Disruptions of the
1178
Figure 79.
Extraperitoneal bladder rupture.
Cystography shows bladder rupture
secondary to a pelvic fracture.
Figure 80.
Extraperitoneal bladder rup
ture. Contrast medium
around the bladder 10 hours
after intravenous urography,
which showed only slight el
evation o f the bladder. A
fracture o f the symphysis
was obvious on one o f the
subsequent sections. It was
impossible to perform ultra
sonography adequately due
to pain.
posterior urethra are usually managed by initial cystostomy and delayed

second stage repair in order to reduce the incidence and severity of late
complications like stricture and impotence.
Bladder hernia
Bladder hernia, which occurs most commonly in the inguino-scrotal area,
is diagnosed equally well by all modalities. Therefore the least expen
sive modality - ultrasonography - should be used as the primary modal
ity. Sometimes it may be necessary to perform cystography to demon
strate the outline of the hernia to the surgeon. In the 1970's colpocys-
tourethrography was frequently performed in females with incontinence
1179
Figure 81.
Artificial sphincter. A plain film
should be taken both during inflated
and deflated phase. I f the fluid con
tains contrast medium, the integrity
o f system may be studied.
Figure 82.
Urethral stricture verified by ure
thrography.
and/or genital hernia for diagnosis and planning of treatment. Its value
was severely questioned in the 1980's but now the examination is re
served for rare cases of recurrent incontinence.
Artificial sphincters
Plain radiographs are excellent for control of the placement and eval
uation of mechanical malfunctioning artificial sphincters (Fig. 81) and
other prostheses. Urethrography may be necessary if intraurethral erosion
is suspected. Diagnosis of fluid accumulation including infection and ab
scesses around the artificial material requires ultrasonography and/or CT.
1180
Urethral stricture
Stricture (stenosis) of the urethra, urethral trauma and urethral tumors
are the urethral diseases most frequently investigated radiologically.
Strictures occurs almost exclusively in males, are readily diagnosed by
urethrography demonstrating luminal narrowing (Fig. 82), and in adults,
are nearly always acquired (e.g. infection, post-cystoscopy lesion,
trauma, catheter). Urethrography should be performed in patients in
whom urethral fistulas are suspected. Problems with urethral catheteri
zation (except for BPH) are also an indication for urethrography. Most
urethral neoplasms occur in the anterior urethra of the male and are usu
ally imposed on long standing strictures. Squamous cell carcinoma is by
far the most common type. Urethral tumors are much less common in
women, are not related to a stricture, and can be o f any cell type.
Figure 83.
Bladder tumor.
Ultrasonography may detect
tumors as small as 10 mm (a).
Normally the echogenicity o f
bladder tumors is moderate
(b). On (b) one can also see a
balloon catheter (b) and por
tions o f a hypertrophic
prostate (p).
1181
Figure 84.
Bladder tumor at vesicoureteral
junction (lower part) causing
hydronephrosis (upper part).
Tum or
Ninety percent of all bladder tumors arise in transitional epithelium.
Cystoscopy with biopsy is the most sensitive method of detecting blad
der tumors, but imaging must be done for staging. Ultrasonography, CT
and MRI each have their advantages. Ultrasonography can also recog
nize some bladder tumors, but it often overlooks low grade papillo
matosis, very small tumors (< 10 mm), and tumors in trabecular blad
ders. At abdominal or transrectal ultrasonography localized thickening
and/or protrusion in the bladder lumen is found (Fig. 83). The echogenic
ity of bladder tumors is moderate. It is very important that before an ul
trasonographic examination the bladder be well filled, because a folding
of the wall should not be interpreted as a tumor. It is often difficult to
differentiate between small to moderate sized bladder tumors and tra-
1182
Figure 85.
Bladder tumor. There is
a filling defect arising
from the right bladder
wall.
с
Figure 86. Bladder tumor.
a. Sagittal Tl-weighted image demonstrating a tumor in the bladder base.
b. Same as (a) after administration o f gadodiamide. Only slight increase in signal
intensity o f the tumor.
с: T2-weighted image o f a signalpoor tumor at the ureterovesical junction causing di
latation o f the ureter (different patient than a and b).
1183
beculation of the wall. In some institutions transurethral ultrasonogra

phy is still used, since it gives a clearer image of the tumor and may
demonstrate invasion. However, transurethral ultrasonography requires
anesthesia and cystoscopy and is thus invasive. In patients in whom two
to three consecutive cystoscopic controls have revealed no recurrence o f
bladder carcinoma, abdominal ultrasonography of a well filled bladder
has proved to be sufficient both from disease controlling and economi
cal aspects. Ultrasonography of bladder tumors should always include
examination of the kidneys (Fig. 84). The role o f intravenous urography
in the work-up of bladder carcinomas is limited to control of the upper
urinary tract, especially the ureters. It has been shown in comparative
studies that intravenous urography overlooks approximately one-third of
all bladder tumors (Fig. 85). In contrast to both CT and ultrasonography
it is not possible with intravenous urography to distinguish between ad
herent blood clots, non radiopaque calculi and bladder tumors. Overlying
gas may sometimes be confused with an intravesical lesion on intra
venous urography, but not with ultrasonography, CT or MRI. MRI is ex
cellent for evaluation of the rare urethral tumors. The main indication for
CT (Fig. 77) is not the diagnosis of bladder tumor or degree of bladder
wall invasion, but diagnosis of extravesical spread e.g. iliac nodes and
extension outside the bladder wall. MRI and clinical staging are com
plementary for staging urinary bladder cancer; in superficial tumors, clin
ical staging, including deep transurethral biopsy, is the best technique.
For invasive tumors, MRI is the best technique (Fig. 86). In the deter
mination of local tumor growth and the detection of bone marrow infil
tration MRI is superior to CT. For the detection of lymph node involve
ment, CT and MRI are equal. A limitation of all staging procedures is
the determination of extent of tumor growth within the muscle layer of
the bladder wall (differentiation between stages T2 and T3a). It seems
likely with endorectal coils or phased-array multicoils and paramagnetic
contrast media MRI may soon be able to solve the problem of differen
tiating stage T2 from stage T3 tumors. A limitation of MRI is its diffi
culty in differentiating between tumor and acute edema resulting from
transurethral resection or biopsy. Even with endorectal coils and intra
venous contrast medium it remains impossible to differentiate the two
stages. Therefore, staging of urinary bladder cancer should start with
MRI, followed by clinical staging.
1184
Figure 87.
Ileal urinary conduit. Diagram
demonstrating a bladder substi
tute (conduit) made from part o f
ileum and anastomosed to the
ureters (Bricker procedure).
Figure 88.
"Pouchography " ("loopography ")
demonstrating leakage (arrows)
at the anastomoses between the
ileal loop and the urethra.
Enteric neo-bladder
In cases of muscular invasion (but without extravesical spread) or of con
genital or acquired atrophic bladders, total cystectomy is often per
formed. A bladder replacement is made by parts of the bowel. There are
several types of "bowel bladders" each with their advantages and disad
vantages (Fig. 87). The radiologist is involved in postoperative control
1185
Figure 89.
Renal artery stenoses before (a)
and immediately after (b) percuta
neous transluminal renal angio
plasty.
of these urinary reservoirs or conduits. Evaluation for urinary leakage in

the first days after surgery and later on determination of capacity, stenoses
or reflux are some of the indications for imaging. Cystography ("pou-
chography", "loopography", etc.) is the appropriately primary imaging
modality in these cases (Fig. 88).
Intervention
Angiographic interventions
Percutaneous Transluminal Renal Angioplasty (PTRA)

Since the first report of renal artery percutaneous angioplasty in 1978 the
method has rapidly become accepted as the treatment of choice for most
patients with renovascular hypertension. Transluminal angioplasty is sim
ply designed to enlarge the lumen of a stenotic artery (Fig. 89). Since
atheromatous material is not compressible, it must be fractured and pushed
1186
Figure 90. Stenosis o f arterial anastomosis o f transplant before (a) and months after
(b) percutaneous transluminal angioplasty. The dilatation improved the flow (and
function) considerably.
off the intima of the renal artery. The arterial media is also split and the
adventitia is stretched beyond its elastic recoil. The atheromatous plaque
is forced into the medial portion of the artery. The adventitia remains in
tact, the media heals by fibrosis, and there is reendotheliazation over the
tears in the intima. A similar process of controlled injury also occurs with
nonatherosclerotic stenosis (Fig. 90). The intima is disrupted and the le
sions are split or stretched beyond their point of elastic recoil. The over
all technical success rate for percutaneous transluminal renal angioplasty
is generally reported as 80-90%. Obviously the number, type, location
and experience of the radiologist contribute significantly to the success
or failure of the procedure. Complications of renal artery percutaneous
transluminal angioplasty may be considered as general complications
such as adverse contrast medium reaction or problems at the puncture
site, or specific to percutaneous transluminal renal artery, such as a rup
ture, dissection, embolus, or thrombosis of the renal artery.
Embolization
Percutaneous transcatheter embolization of the renal artery or of the vesi
cal branches of the internal iliac artery is used in a variety of situations.
It may be used in cases where renal ablation without surgery is desired
or where arrest of bleeding from the kidney or the bladder is needed.
Embolization is also effective for treatment of arteriovenous fistulas and
1187
Figure 91.
Percutaneous stone dislodgement
from the mid ureter to the renal
pelvis with a balloon catheter. In
the pelvis ESWL was applied.
aneurysms. Much less commonly percutaneous transcatheter thrombo

lysis can be performed for arterial or venous thrombosis, but the usual
treatment for these conditions is medical (anticoagulants, etc.).
Vein sampling
Selective renal vein sampling provides a method of measuring the renin
level being secreted by each kidney.
Non-angiographic interventions
Nephrostomy
Percutaneous nephrostomy is the single most valuable interventional tech
nique in uroradiology. It relieves obstruction of the urinary tract and provides
access to the collecting system for a variety of diagnostic and therapeutic pro
cedures. The indications include: 1) Reliefof obstruction (preserve renal func
tion, treatment of infection, relieve pain), 2) Urinary diversion (heal leak or
fistula), 3) Diagnostic study (antegrade pyelography, Whitaker test, biopsy
or brushing for biopsy), 4) Removal of solid material (stone (Fig. 91), foreign
body), 5) Access for ureteral intervention (stricture dilation, stenting, ureteral
occlusion), 6) Infusion of chemolytic agents, and 7) Access for nephroscopy.
The procedure may be guided with fluoroscopy, ultrasonography (Fig. 92) or
CT; the combination of ultrasonography (guidance) and fluoroscopy (control
incl. placement) is the best. Either trocar technique or the Seldinger technique
may be used. With some experience and adequate equipment the success
1188
Figure 92.
Percutaneous nephrostomy.
Under continuous real-time
ultrasonographic guidance a
posterior calyx is punctured
using either a trocar or
Seldinger technique. The tip o f
the needle is easily seen (ar
row).
Figure 93. Steps in percutaneous stent placement. After access to the renal collecting
system is gained through a nephrostomy, which has been in place fo r one to two weeks
a straight guide wire is passed through the region o f ureteral obstruction and into the
bladder. After dilatation a double-pigtail catheter is straightened and passed over the
guide wire. The pigtail catheter is advanced by a pusher until one end is in the bladder
and the other in the renal pelvis. When the guide wire is removed from the catheter,
the pigtail catheter acquires its desired shape. A nephrostomy catheter is left in the
pelvic cavity until it has been documented that the stent functions properly.
rate is above 95%. The most common complications are related to bleed
ing, urine extravasation and infection.
Balloon dilatation and stenosing

With the nephrostomy catheter providing access to the collecting system
interventional procedures can be performed in the ureter. This direct ap
proach avoids problems associated with transversing the urethra, blad
der, and ureterovesical junction. Ureteral stents may be placed to bypass
obstruction (Fig. 93), to heal a ureteral leak or fistula, or to prevent stric-
1189
ture formation. In patients in whom a stricture has already occurred an

gioplasty balloon catheters may be used to dilate the stricture. Balloon
dilatation of urethral strictures via the direct route is now a routine pro
cedure at many institutions. Complications o f ureteral or urethral stric
ture dilation are rare. The most untoward event is perforation of the ureter
or urethra. However, these usually heal without sequelae. Because seri
ous complications are so unlikely, percutaneous stricture dilatation is of
ten undertaken as the initial procedure. If it fails, surgery is not com
promised. During the recent years special urethral stents (endoprothesis)
have been developed for both acquired urethral strictures and prostatic
obstruction (Fig. 76). They are inserted using either fluoroscopic or en
doscopic guidance.
Drainage
Both renal and non-renal retroperitoneal abscesses are particularly well
suited to percutaneous drainage. They can usually be approached poste
riorly during guidance with CT or ultrasonography such that peritoneum,
bowel, and other organs are not transversed. In most patients percuta
neous drainage results in cure and surgery can be avoided. The response
to percutaneous abscess drainage is seen within the first 24 to 48 hours.
The complications of percutaneous abscess drainage include bleeding,
spread of infection into a previously uninfected space, and exacerbating
bacteremia or sepsis during manipulation.
Biopsy
Percutaneous biopsy has become a common radiological procedure.
Using a variety of imaging modalities cutting needles provide tissue for
histological evaluation. Aspiration needles provide material for cy-
topathology and may be used to diagnose the primary tumor, but they
are commonly used to confirm the presence of metastases when the pri
mary tumor has been diagnosed previously. Fine needle histology biop
sies can also be obtained. They are used to diagnose the occurrence of a
primary tumor. Gross needle biopsy (18-20G) is used primarily for re
nal biopsy in patients suspect of having a medical renal disease in order
to obtain enough tissue for immunological diagnosis. The most common
complication of biopsy is bleeding. In about 60% of patients undergo
ing medical renal biopsy perinephric bleeding occurs, but it is rarely nec
essary to treat (transfusion, surgery) it. Arteriovenous fistulas occur in
1190
many patients but in nearly all patients they close within the next days.
If persistent, they can be embolized. Tumor seeding can not be excluded,
but it occurs rarely.
Ureteral occlusion
In patients with urinary leakage, which does not stop following urinary
diversion, ureteral occlusion can be performed either by inserting a bal
loon in the ureter or injecting embolizing drugs.
MALE GENITAL ORGANS
Anatomy
The normal prostate is formed like a pyramid with the widest part, the
base, which lies adjacent to the bladder, measuring approximately 4.5
cm in diameter. The apex lies adjacent to the membranous urethra (Fig.
16). The prostate is approximately 3.5 cm in length and weighs approx
imately 20 gram in healthy young men. At both ultrasonography and
MRI one can distinguish between the central gland, which consists of
the histological central and transition zones, and a peripheral zone. This
distinction is of great importance, since hypertrophy mainly originates
in the transition zone, which is the area around urethra above the veru-
montanum, whereas malignant tumors are most frequently found the pe
ripheral zone. Prostatitis can originate in any part of the prostate.
The normal testis measures approximately 4-5 x 3 x 2.5 cm and has
at both ultrasonography and MRI an homogenous structure. An inho-
mogeneous structure indicates occurrence of disease.
The penis consists of three cavernous bodies, a corpus spongiosum
which surrounds the urethra, and paired corpora cavernosa which lie dor
sal to the urethra (Fig. 16). The penis receives its blood supply from the
internal pudendal branch of the internal iliac artery.
Pathology
Diseases in the prostate occur frequently. For the most part, however,
the spectrum of diseases is limited to infection, hyperplasia and cancer.
Today prostate cancer is the most frequent cancer among males in North
America and parts of Europe.
1191
Figure 94.
Urethral obstruction due to BPH demon
strated at urethrography. Note the nar
rowed elongated prostatic urethra.
Prostatitis and abscess

Prostatitis is a clinical diagnosis; imaging is irrelevant. If an abscess is
suspected a transrectal ultrasonogram should be done. At ultrasonogra
phy a relatively echopoor area - often surrounded by an echogenic rim
- is seen. Needle aspiration and drainage can be carried out concurrently.
Prostatic abscesses can also be imaged by MRI and CT. At MRI a sig
nal intense area is seen on T2-weighted images. At CT a low attenuat
ing area is seen; after contrast "rim" enhancement may be seen.
Benign prostate hyperplasia

Benign prostate hyperplasia (BPH) does not in itself require any imag
ing examination. It is often found at examinations performed for other
reasons. On plain abdominal radiographs bladder stones and/or a full
bladder may be seen and after injection of contrast medium an elevated
bladder with a smooth floor may be found; sometimes there is dilatation
of the upper urinary tract. In case of median-lobe (Albarrans) BPH a fill
ing defect in the bladder is seen. These changes are nonspecific and may
also be seen in prostate cancer. The size of the prostate can not be de
termined at urography. The volume of BPH can be determined at MRI,
1192
Figure 95.
Prostate cancer.
a: Hypoechoic process on
transrectal ultrasonogra-
phy.
b: Ultrasonography is an ex
cellent method for biospy
guidance.
1 CM/DIV
CT and transrectal ultrasonography, however. At the latter examination

discrete centrally localized nodules with varying echogenicity are found
in BPH. On T1-weighted MRI a heterogeneous prostate with discrete
nodules or a homogenous gland are found; T2-weighted MRI shows cen
trally localized nodules with varying signal intensity and a bright pe
ripheral zone. At CT a homogenous enlarged gland with smooth demar
cation is found. The elongated prostatic urethra can be appreciated at ure
thrography (Fig. 94).
Prostate cancer
Diagnostic imaging in prostate cancer includes primary diagnosis and
staging, but not screening. For the first purpose transrectal ultrasonog
raphy is suitable as the primary examination, since it may demonstrate
a hypoechoic area in the peripheral zone. However, hypoechoic
processes may also represent benign nodules and invasive rectal cancer.
Therefore, a biopsy must be taken from any suspicious hypoechoic area
(Fig. 95). In case of a normal transrectal ultrasonography prostate can
1193
Figure 96.
Low-signal prostate cancer
(arrow) in the left side o f the
peripheral zone. T2-weighted
image obtained with whole
body coil.
SE-210MgL^i
:L I h k T & O m ]
Figure 97.
Prostate cancer in the right
side. The cancer breaks
through the fibrous capsule
so it is a stage С cancer (ar
row). T2-weighted image ob
tained with an endorectal
coil.
cer can not be excluded. If the clinical suspicion of prostate cancer is

high, e.g. elevated PSA, the next step should be random biopsies or MRI.
On T2-weighted images signal poor areas may be seen in the otherwise
signal rich peripheral zone (Fig. 96). However, similar signal changes
may also be seen in BPH and prostatitis; the diagnostic problem is great
est if the disease is present in the signal poorer central zone. The advan
tage of MRI is its ability to scan in multiple planes. With an endorectal
coil it is possible to demonstrate invasion of the fibrous capsule and
hereby discriminate between stage В and С (Fig. 97). Correct staging is
of major importance for the choice of treatment: e.g. radical prostatec
tomy (stage B) and radiation/chemotherapy (stage C). Regarding pe
ripheral soft tissue metastases the capabilities o f MRI are similar to those
of CT. Bone metastases should primarily be diagnosed at bone scintig
raphy followed by confirming conventional X-rays or CT of the region
with increased accumulation of radioactivity. MRI can be helpful in
equivocal cases, but sometimes bone biopsy must be done (Fig. 98).
1194
Figure 98.
"Super” bone scan demon
strating symmetrical in
creased uptake o f the radio
pharmaceutical with diffusely
metastatic disease due to
prostatic cancer. It is signifi
cant that the kidneys are not
seen due to extensive skeletal
deposition o f the radionu
clide.
Scrotal enlargement
Despite the fact that the scrotal contents including the testes can easily
be examined manually it may be difficult to determine the character and
cause of scrotal enlargement. The most important diagnoses are epi
didymitis, orchitis, abscess, hydrocele, spermatocele, varicocele (Fig.
99), testicular tumor, torsion and testicular rupture. Ultrasonography
with a 7 MHz probe is valuable in most cases, since it can distinguish
between solid and cystic lesions and determine whether the lesion is in-
tra- and extra testicular. In case of epididymitis an enlarged epididymis,
which is more echo rich than the normal epidydimis, containing small
cystic areas is found. In case of orchitis the testis is uniformly enlarged
with either an unchanged or slightly diminished echopattem. The ultra
sonographic signs of a scrotal abscess are similar to those of abscesses
in other organs. Testicular cancer breaks the homogenous echopattem of
the normal testis; more or less well demarcated areas are found in the
diseased testes (Fig. 100). There is no relation between the echopattem
including demarcation and the various cancers, although presence of
amourphous calcification should raise the possibility of teratoma.
Approximately one-half of the testicular cancers are seminomas; the re
maining cancers are embryonal cell carcinoma, teratoma, and teratosar-
coma and choriocarcinoma. In older men lymphoma is the most com
mon tumor. In case of diffuse infiltrating cancer the ultrasonographic
findings are nonspecific, but diffusely enlarged, hypoechoic (and pain-
1195
Figure 99.
Hydrocele (arrow), spematocele (arrowhead)
and varicocele (open arrows) at scrotal ultra
sonography.
Figure 100.
Testis cancer.
Ultrasonography demonstrat
ing echo poor tumor in the
right testis. Normal left testis.
less) testes are suspect of infiltrating cancer. T2-weighted MRI is ad

vantages for the diagnosis of testicular tumors. A low signal intensity fo
cus is the usual finding (Fig. 101). In contrast to ultrasonography MRI
can sometimes differentiate between seminoma, non-seminoma and
leukemic infiltration. Testicular cancer usually spreads by the lymphatic
system, which together with the venous blood passes directly toward the
renal hilum on the left and the aorto-caval interspace on the right. CT
and MRI are equally good for the diagnosis of metastatic nodes.
At both ultrasonography and MRI cystic areas are found in case of oc
currence of the various fluid collections: hydrocele, spermatocele and
varicocele.
1196
Figure 101.
Testis cancer. Signal poor process
in the left testis, whereas the right
testis has a high homogenous signal
on this T2-weighted image.
Testicular trauma
An echopoor area may be found by ultrasonography in a patient having
been subjected to a testicular trauma. This finding may to due testicular
bleeding and a hematoma in the surrounding tissues. MRI may be able
to demonstrate the rupture of the tunica albuginea.
Testicular torsion
Doppler ultrasonography is the most appropriate examination to perform
when testicular torsion is suspected. Demonstration of blood flow in the
mediastinum testis nearly always rules out testicular torsion, since the
torsion most frequently takes place in the spermate cord just proximal to
this level. Alternatively MRI or scintigraphy may be performed; the lat
ter will show a photon deficient area at the site of the torsed testes.
Impotence
In impotence of organic origin Doppler ultrasonography may be useful
for obtaining information about the arterial blood flow to the penis. If an
abnormally low blood flow is found, selective arteriography of the in
ternal pudendal arteries before and after papaverine are indicated to
1197
Figure 102.
Normal fem ale genitals. Sagittal T2-
weighted image demonstrating a normal
cervix with a central high signal intensive
stripe (the canal) surrounded by low sig
nal intensity due to fibrous tissue. The
uterine body has also a zonal structure
with a high signal centrally (endo
metrium), a thick outer myometrial zone
with an intermediate signal intensity, and
a narrow inner zone with low signal
intensity.
demonstrate stenosis or occlusion as a cause of impotence. If caver-

nosometry is indicative o f insufficient venous occlusion during erection,
cavemosography may useful for determining the site of massive venous
leaks. Cavemosography can also be used for demonstration of traumatic
penile rupture.
Intervention
Imaging guided intervention is limited to biopsy of the prostate - mainly
guided by ultrasonography (Fig. 95), dilatation/embolization of penile
arteries/veins in patients with impotence or priaprism and embolization
of varicoceles.
FEMALE GENITAL ORGANS
Anatomy
The uterine cervix is only partially available for visual inspection.
Transvaginal ultrasonography can show the border between the cervix
and the parametria. On T2-weighted MR images of the cervix two to
three zones are often seen (Fig. 102); it has for the major part a low sig
nal intensity because of its high fibrous structure. The cervical canal con
taining mucus and epithelial glands is seen as a central high signal in
tensive stripe. On Tl-weighted images the structure is homogenous and
it is possible to demarcate it from its surroundings.
1198
Figure 103.
Ovaries. Abdominal and
transvaginal ultrasonography
o f a normal ovary.
Transvaginal ultrasonogra
phy gives more details.
The size of the uterus depends on the hormonal state of the female. At
ultrasonography its echogenicity is homogenous with an echo rich cen
terline (the endometrium). On T2-weighted images the uterine body has
a typical zonal structure (Fig. 102). The central high signal intensity area
represents the endometrium. The myometrium has two different zones:
a thick outer zone with an intermediate signal intensity and a narrow in
ner zone with a low signal intensity, called a junctional zone. On T l-
weighted images the uterus has a homogenous medium signal intensity
structure and the outer surface is more clearly demarcated from the sur
roundings than on T2-weighted images. The uterus is often located an-
terior-superiorly to the vagina, but it may be even more anteflexed. It
may also be retroflexed or retroverted.
Visualization of normal salpinges requires direct injection of contrast
media. (Fig. 8). Sometimes the isthmic part is seen in the uterine cornua
at ultrasonography and MRI.
The ovaries may be located anywhere in the pelvic part of the abdomen.
Their size depends on the hormonal cycle. Following external hormonal
stimulation they may become very large. At ultrasonography (Fig. 103)
performed late in the menstrual cycle echo poor areas (follicles) are seen
in the ovaries, which already are somewhat hypoechoic. It is often diffi
cult to see normal ovaries at abdominal ultrasonography, whereas at trans
vaginal ultrasonography is often possible to identify one or two non-en-
larged ovaries. MRI is able to demonstrate normal ovaries in most women
of reproductive age. They appear as slightly heterogeneous masses, and
they are well delineated on axial, sagittal and coronal images. On T l-
weighted images they have a low to medium signal intensity difficult to
distinguish from the surrounding bowel loops; on T2-weighted images
they are often indistinguishable from the surrounding fat.
1199
Figure 104.
Cervical cancer.
a) Transverse T2-weighted image
demonstrating tumor invasion
into the right parametrium (ar
row).
b) T2-weighted image demonstrat
ing that the cervical tumor ex
tends into the uterine body,
where three leiomyomas (arrow
heads) were also present.
Pathology
Transvaginal ultrasonography has become an important supplement to
the traditional gynecological examination of the uterus and its adnexae.
Structures larger than 6 cm may be overlooked at transvaginal ultra
sonography. Therefore both transvaginal and transabdominal ultra
sonography should always be performed.
Cervix
Correct staging of cervical cancer is of utmost importance because it is
decisive for the choice of treatment. A patient with stage lb cancer (con
fined to cervix) can undergo surgery, whereas a patient with stage Ila is
better treated with radiotherapy. Radiotherapy of a recently operated re-
1200
Figure 105.
Multiple cervical ovula nabothi in a
patient with stage I endometrial
cancer o f the uterine body.
Figure 106.
Bicornuate uterus. T2-weighted im
age showing two areas with high
signal intensity.
loil: Sm all_8ody
S 1500/40
gion results often in complications. Neither ultrasonography nor CT have

proved to be better than manual palpation during general anesthesia for
staging, whereas MRI seems to be more accurate than manual examina
tion. In some patients T2-weighted images give a good outline of the
cancer whereas in other patients contrast enhanced images are necessary
to delineate the cancer (Fig. 104). MRI can also be used for demonstra
tion of ovula nabothi, a kind of retention cyst, (Fig. 105), which occur
more frequently with increasing age.
Uterus
Uterine anomalies have been reported to be best delineated on MR-im-
ages (Fig. 106). They can best be evaluated with a combination of T2-
weighted axial and sagittal images. The diagnostic capability of MRI
1201
Figure 108.
Endometrial cancer stage II. Total disappearance o f the zonal structure and occur
rence o f necroses.
a) T2-weighted image.
b) Tl-weighted image after administration o f gadodiam ide.
seems to be better than ultrasonography regarding size and number o f

uterine leiomyomas (Fig. 104 b); CT can only show calcifications and
prominent changes on the surface of the uterus (Fig. 107). T2-weighted
MRI is optimal for the diagnosis of submucosal and intramural lesions,
since the contrast between the leiomyoma and the myometrium or en
dometrium is high. Tl-weighted images are needed for determining the
extent of subserosal leiomyomas. Neither ultrasonography nor MRI are
able to distinguish between benign cystic leiomyoma and leiomyosar
coma. Adenomyosis produces diffuse and smooth uterine enlargement,
which can be seen on both ultrasonography, CT and MRI. At MRI the
junctional zone is thickened. Changes in the endometrial echopattem are
indicative of endometrial cancer. At MRI endometrial carcinoma has a
1202
Figure 109. KAS Hetlev Univ.of Copot hogen

^ PICKER NORDSTAR
Benign ovarian tumor. T l- а Л л 1 MERTT
weighted image after adminis
tration o f gadodiamide. Large,
thin walled, low signal inten
sity process behind the uterine
body. No solid component was
demonstrated.
Figure 110.
Malignant ovarian tumor. T l-
weighted image after adminis
tration o f gadodiamide. Solid
mass (arrows) whose signal
intensity increased after appli
cation o f contrast medium and
a major cystic part which had
a moderate signal intensity
unchanged after administra
tion o f contrast medium.
higher signal intensity than that of the myometrium and cervix. The over
all accuracy of MRI for stage I and II is higher than that for clinical ex
amination and CT. The use of MR-contrast medium improves the accu
racy of staging (Figs. 105, 108). As regards stage III and IV MRI is not
more accurate than CT. MRI seems also to be useful to control the ef
fect of chemotherapy. With the use of MRI (and CT) intravenous urog
raphy and bowel X-ray for indirect demonstration of invasion are no
longer indicated.
Ovaries
A torsed ovary can be diagnosed with Doppler ultrasonography demon
strating absence of blood flow in the ovary. Ovarian tumors - even the
malignant ones - are often asymptomatic for a long time. Normally it is
possible by ultrasonography to measure the size of the ovaries (the larger,
the higher the risk for malignancy) and determine whether the process
is solid and/or cystic. The flow pattern determined by color Doppler can
give some indications about whether the mass is benign or malignant.
The MRI appearance of ovarian tumors (Figs. 109, 110) can vary con
1203
Figure 111.
Recurrent ovarian tumor (ar
row) close to the enhancing
uterus.
Figure 112.
Peritoneal carcinomatosis.
Tl-weighted image after ad
ministration o f gadodiamide
demonstrating high signal
intensity tissue around the
bowel (arrow) and ascites
(arrowhead). The bladder is
displaced to the right.
siderably. Primary MRI criteria indicating a malignant lesion are 1) size

greater than 4 cm, 2) solid mass or large solid component, 3) wall thick
ness greater than 3 mm, 4) septa greater than 3 mm thick and/or pres
ence of vegetations or nodularity, and 5) necrosis. Ancillary criteria are
1) involvement of pelvic organs or sidewall, 2) peritoneal, mesenteric,
or omental disease, 3) ascites, and 4) adenopathy. A lesion can be clas
sified malignant when at least two of the primary criteria are present and
benign when either none or of the criteria are present. Ovarian tumors
are still in many centers not biopsied due to the risk of peritoneal seed
ing. CT can be used for diagnosis of recurrence (Fig. I l l ) but a normal
CT does not exclude recurrence. The ability of MRI with and without
intravenous contrast to detect recurrence (Fig. 112) makes it is possible
to obviate the need for second look operations in up to 75% of the pa
tients.
1204
Figure 113.
Tubo-ovarial abscess.
Ultrasonography shows an
echo poor septated process
close to the uterus (U).
Figure 114.
Endometriosis. T2-weighted
image showing signal intensive
and signal poor cystic
processes.
Adnexa
In the adnexae fluid collections, hematomas, abscesses (Fig. 113) and
endometriosis (Fig. 114) may occur. Transvaginal ultrasonography is ex
cellent for the diagnosis (mainly echopoor areas) and treatment of the
three first diseases. Abscesses from bowel diverticula and inflammatory
bowel diseases may be difficult to differentiate ultrasonographically
from diseases in the adnexae. In case of an uncertain ultrasonography
primarily MRI and secondarily CT should be performed. At MRI in
fected cystic masses have longer Tl and T2 relaxation times than hem
orrhage. On T2-weighted images they have a high signal, but their ap
pearance can vary considerably. Endometriosis presents various types of
lesions. Large endometrial cysts or endometriomas have very variable
features. They undergo cyclic bleeding during the menstrual cycles.
Neither ultrasonography nor MRI can exclude the occurrence of en
dometriosis, but the sensitivity of MRI is higher than that of ultra-
1205
Figure 115.
Extra pulmonary small cell cancer
occupying the pelvis and displacing
a normal cervix and uterine body
cranial T2-weighted image. The
anatomy is well demonstrated on this
sagittal image.
Figure 116.
Hydrosalpinx.
Hysterosalpingography demonstrat
ing a closed and dilated right am-
pullary end.
sonography.
In rares cases tumors like extrapulmonary small cell cancer and sar
comas may arise from the connecting tissue. MRI is superior compared
to both CT and ultrasonography in the work-up of these rare malignan
cies (Fig. 115).
Infertility
For evaluation of infertility primarily ultrasonography and secondarily
MRI should be performed to exclude anomalies and cystic ovaries. The
next step is hysterosalpingography, which can demonstrate congenital
anomalies, processes in the uterine cavity and postinflammatory changes
of the salpinges and the peritoneal cavity. A typical finding is bilateral
sactosalpinx (hydrosalpinx) (Fig. 116), in which case the ampulary ends
1206
Figure 117. Anatomic relations o f the adrenal glands and arterial supply.
are closed and dilated; sometimes minor adhesions may be broken dur
ing the examination.
Intervention
Biopsy and diagnostic puncture are performed under imaging guidance.
Included is also oocyte aspiration for in-vitro insemination. It should be
remembered that transvaginal punctures nearly always are very painful.
Selective catheterization of the salpinges can be performed through the
uterine cavity. Thereby, some occlusions of the isthmic part of the salp
inges can be reopened. The technical success rate is between 80 and 90%
and the pregnancy rates are around 30%. Also balloon dilatation of
stenotic portions of the salpinges is possible.
ADRENALS
Anatomy
Along with kidneys, the adrenal glands lie within the perinephric space
(Fig. 117). In most patients, there is sufficient perinephric fat so they are
easily seen on CT. The right adrenal glands lies anteromedial to the up
per pole of right kidney and immediately posterior to the inferior vena
cava. The left gland is anteromedial to the upper pole of the left kidney
and posterior to portions of the splenic vein and artery. The right adrenal
gland consistently extends above the upper pole of the kidney while the
left is more often at the level of the left upper pole and extends to the re
nal hilus. Both adrenal glands have an inverted Y configuration with the
tail of the Y pointing anteromedially. The adrenal glands weigh only
1207
about 5 g each and vary from 3 to 6 mm in width. The small size makes
it difficult to distinguish between a normal or an atrophic or hypoplastic
configuration.
The best imaging modality for the study of the adrenal glands is in
most instances CT. In medullary disease scintigraphy is very useful es
pecially for localization of aberrant tissue along the sympathetic chain
in the retroperitoneum. It should be remembered that ultrasonography
can not exclude adrenal pathology; it can only confirm its presence. MRI
is also excellent for adrenal imaging and offers unique advantages (see
below).
Pathology
Adrenal diseases are often divided into two major groups: functional (hy
per and hypo) and non-functional diseases. Since adrenal hormones can
be readily measured, there is seldom doubt as to which category a pa
tient belongs.
Functional adrenal diseases

The adrenocortical functional diseases include Cushing's Syndrome,
Conn's Syndrome, Adrenogenital Syndromes, Virilizing Syndromes,
Feminizing Syndromes, and Adrenal Insufficiency. Paroxysmal hyper
tension is the classical functional disorder produced by overactivity of
the adrenal medulla.
Cushing's syndrome
Cushing's syndrome is the manifestation o f excess glucocorticoids.
These steroids may come from either exogenous or endogenous sources.
Endogenous Cushing's syndrome is due to overproduction of cortisol by
the adrenal cortex. This can be due to an autonomous adrenal tumor, be
nign or malignant, or due to adrenal hyperplasia from unregulated ACTH
production. The most common etiology of Cushing's syndrome is bilat
eral adrenal hyperplasia, which accounts for approximately 70% of
cases. A few of these patients have macronodules, which can be demon
strated by CT. These macronodules measure less than 3 cm and may be
less than 1 cm in diameter. Macronodular hyperplasia is due to an ACTH-
secreting pituitary microadenoma in the majority of cases. A benign but
autonomous adrenal cortical adenoma is the etiology of 20% of cases of
endogenous Cushing's syndrome, and a primary adrenal cortical carci-
1208
Figure 118.
Adrenal tumor (aldos-
teronoma). Ultrasonography
demonstrates a small echo
poor tumor cranially to the
right kidney in a patient with
Conn's syndrome.
noma is responsible for about 10% of cases.
Conn's syndrome
Conn's syndrome, or primary aldosteronism, is the result of excess al
dosterone produced by the adrenal glands. As with Cushing's syndrome,
it may be caused by either adrenal hyperplasia or a primary adrenal tu
mor. A benign but unregulated aldosterone secreting adenoma is the most
common etiology of primary aldosteronism, being responsible for almost
80% of cases, while hyperplasia is responsible for nearly all of the re
mainder (Fig. 118). Cortical carcinoma accounts for less than 1% of
cases. Aldosteronism also occurs in patients with renovascular hyper
tension. However, this form of secondary aldosteronism is distinguished
from primary aldosteronism by measuring the serum renin which is low
in Conn's syndrome.
Adrenogenital syndromes
Adrenogenital syndromes are the result of an inborn error in the adrenal
enzyme which blocks or impairs the synthesis of cortisol or aldosterone
and are manifest at birth. Androgen-producing (virilizing) tumors are
rare, may be benign or malignant, and occur in either males or females
at any age. Feminizing tumors are even less frequent.
Addison's disease
Adrenal insufficiency may result from inadequate stimulation by ACTH
(secondary) or may be due to tissue destruction of the adrenal glands
(primary). Primary adrenal insufficiency, or Addison's disease, occurs
only after at least 90% of the adrenal cortex has been destroyed.
1209
Figure 119.
Adrenal metastases from lung
tumor. Large process cranial
to the kidney with mixed
echogenicity. Biopsy showed
metastases from lung tumor.
Figure 120.
Adrenal cortical carcinoma
displacing the right kidney
centrally. Mixed enhance
ment after administration o f
contrast medium indicating
central necrosis.
Idiopathic adrenal atrophy is the most common cause and is most likely
an autoimmune disorder. Destruction can also be due to granulomatous
disease, usually tuberculosis. However, other causes such as infarction,
amyloidosis, hemochromatosis, hemorrhage, or destruction by histo
plasmosis, blastomycosis, disseminated fungal infection, lymphoma,
and metastatic tumor are possibilities. The radiographic manifestations
of adrenal insufficiency depend on the cause of adrenal dysfunction.
Calcifications caused by tuberculosis or histoplasmosis made be seen on
plain abdominal radiographs, but the most useful examination is CT,
since it not only demonstrate calcifications but also the size and shape
of the adrenal glands.
Im aging in hypo- and hyperfunctioning adrenal cortical disease

Unless there is calcification or fat in the adrenal the plain radiograph and
intravenous urography are usually unrewarding in patients with hyper-
or hypofunctioning adrenal cortical disease. However, the urogram can
1210
be very sensitive in distinguishing between a renal and an extrarenal

mass. Although the normal adrenal gland may be difficult to image with
ultrasonography, tumors larger than 2 cm can often be detected (Fig.
118). The right adrenal gland is usually easier to study because the liver
provides a good acoustic window. Ultrasonography has two major uses
in patients with hyper- or hypofunction: to distinguish large tumors (Fig.
119) from other organs due to the availability of the multiplanar imag
ing and to differentiate a small homogenous adenoma from an adrenal
cyst. The single most valuable modality for the adrenal glands is CT (Fig.
120). The perinephric fat present in most patients allows the adrenal gland
to be clearly displayed and tumors as small as 5 mm in diameter can be
identified. Intravenous contrast is not usually needed but may be used to
distinguish an adrenal mass from the upper pole of the kidney. For most
patients with hyper- or hypofunction of the adrenal cortex, MRI does not
provide additional information after a CT examination. Cortical imag
ing agents e.g. 13lI-19-iodocholesterol have been developed that can lo
calize hyperfunctioning adrenal cortical tumors, particularly in patients
with Cushing's syndrome. However, the success of CT in localizing these
adrenal tumors made this examination redundant.
Pheochromocytoma
Pheochromocytomas are tumors comprised o f chromaffin cells and are
usually located in the adrenal medulla. Extraadrenal pheochromo-cy-
toma (paragangliomas) may lie anywhere between the base of the brain
and the epididymis but usually lie along the symphatic chain in the
retroperitoneum. They are rare tumors and account for less than 1% of
patients with systemic hypertension. Classically the hypertension is
paroxysmal, but it may be sustained and of any magnitude.
Approximately 13% of all pheochromoctymas are malignant.
Pheochromocytomas may be associated with other endocrine tumors or
with von Hippel-Lindau syndrome and neurofibromatosis. The multiple
endocrine neoplasia (MEN) syndrome, Type 2 A, includes medullary car
cinoma of the thyroid and parathyroid hyperplasia as well as pheochro
mocytoma. The MEN syndrome, Type 2B, is comprised of pheochro
mocytoma, medullary carcinoma of the thyroid, and the mucocutaneous
manifestations of mucosal neuromas, intestinal ganglioneuromatosis,
and a marfanoid habitus. The majority of patients with MEN 2A or 2B
syndromes have pheochromocytomas that are bilateral and almost al-
1211
Figure 121.
Malignant phaeochromocytoma.
1231 MIBG scintigraphy.
a) Normal
b) Large process at the site o f
the right adrenal gland.
c) Lung metastases taking up the
radiopharmaceutical.
d) Metastases behind the blad
der.
ways intraadrenal. All manifestations of the syndrome may not occur at

the same time. These syndromes are inherited in an autosomal dominant
fashion. About 10% o f pheochromocytomas are multiple.
As with tumors of the adrenal cortex, CT is the primary localizing ex
amination. Most intraadrenal pheochromocytomas are detected, the sen
sitivity being around 95%. Pheochromocytomas are both identified and
characterized by MRI. Tl-weighted sequences are used to identify the
mass while the high signal intensity seen on T2-weighted images helps
to characterize it as a pheochromocytoma. This intense T2-weighted sig
nal helps to distinguish a pheochromocytoma from an adrenal adenoma.
The analogue of guanethidine - MIBG - is taken up by adrenergic tis
sue. Labeled with a radionuclide it can localize pheochromocytomas.13ll
is the most frequently used isotope, but 123I has a better detection effi
ciency and dosimetry. The overall accuracy of MRI, CT and scintigra
phy seems to be the same, but scintigraphy has some advantages. With
a single injection of the radiopharmaceutical the whole body can be
scanned. This is particularly helpful for ectopic or multiple tumors or in
the detection of metastatic deposits (Fig. 121). Ultrasonography may be
used to localize an intraadrenal pheochromocytoma, but may also iden
tify ectopic tumors lying in the paraaortic area. Pheochromocytomas tend
to be more echogenic than normal adrenal tissue. All patients with
1212
Figure 122.
Incidentaloma. Small low at
tenuating process in the left
adrenal gland found inciden
tally in an asymptomatic p a
tient. This probably represents
an adenoma.
pheochromocytoma should have either an MIBG scan or MRI prior to

surgery to rule out accessory lesions.
Non-functional adrenal diseases

The non-functional adrenal diseases include adenoma, carcinoma,
myelolipoma, hemorrhage, cysts, hemangioma, metastases, and lym
phoma.
Adenoma
Benign, nonhyperfunctioning adrenal adenomas are commonly encoun
tered on abdominal CT examinations (Fig. 122). Typically it is a well-
defined, rounded, homogenous mass; calcification, central necrosis or
hemorrhage occur rarely. MRI may be used to distinguish the adenomas
from metastases since metastases typically has a higher signal on T2-
weighted images. Most adenomas contain lipid and can be identified my
MRI fat-detection technique. Large adenomas can be detected by ultra
sonography, which then is useful to distinguishing solid tumors from
cysts. Sometimes smaller lesions can be found especially if associated
with endocrinopathy.
Carcinoma
Primary adrenal cortical carcinoma in an uncommon malignancy with a
median age at presentation in the fifth decade. The typical CT-appear-
ance is a large mass with central areas of low attenuation representing
tumor necrosis (Fig. 120). Often calcifications are seen. Evidence o f he
patic or regional lymph node metastases as well as venous extension are
1213
Figure 123.
Adrenal cortical carcinoma. T l-
weighted image demonstrating a
moderately signal intensive process
cranial to the right kidney.
well detected by CT. A high signal on T2-weighted MRI supports the

malignant diagnosis. The tumors are low or moderate signal on T l-
weighted images (Fig. 123). At ultrasonography a suprarenal mass is
found; smaller lesions are often homogeneous, whereas larger lesion are
inhomogenous representing necrosis and/or hemorrhage. Renal dis
placement without calyceal distortion at intravenous urography is in
dicative of a suprarenal mass.
Myelolipoma
A myelolipoma is a hamartoma comprised of mature adipose cells and
hematopoetic tissue. CT is the most definitive radiographic examination.
A fatty adrenal mass is virtually diagnostic of a myelolipoma. MRI does
not add anything. Ultrasonography will show a highly echogenic mass.
Small islands of calcium or even bone formation are sometimes present.
Hemorrhage
Adrenal hemorrhage may be spontaneous, traumatic, or related to anti
coagulation. Spontaneous hemorrhage often occurs in patients with sep
ticemia, hypertension, renal vein thrombosis, or adrenal pathology such
as a tumor. Again CT is the most reliable method of diagnosis. Initially
the hematoma has a high attenuation. Follow-up studies usually show re
sorption of the hematoma and a gradual decrease in density to near wa
ter. Also MRI appearance will reflect the evolution from acute to chronic
stages with hemoglobin breakdown; initially high signal at both Tl - and
T2-weighted sequences. If detected, the echogenicity at ultrasonography
1214
varies with the state o f hematoma.
Cysts
Adrenal cysts are uncommon and their detection does not differ from di
agnosis of cysts in other organs. Some adrenal cysts are probably the
residua of old hemorrhage ("pseudocysts”).
Hemangioma
Adrenal hemangioma is a rare tumor of the adrenal cortex and does not
differ from hemangiomas of other organs. The CT-appearance depends
on tumor morphology. Typically, a large mass with a thick irregular wall
and hypodense center is seen. Ultrasound demonstrates a complex mass
and may reveal cystic areas.
Metastases
The adrenal glands are a common site of metastatic disease. Of patients
with an epithelial malignancy 27% will have adrenal metastases with
time. Figures for patients with breast cancer and lung cancer are 54%
and 36%, respectively. The radiographic appearance of adrenal metas
tases is unspecific. They may be small, unilateral or bilateral. A metas
tases is a solid mass on ultrasound, and when less than 3 cm in diame
ter, is usually homogenous, whereas in larger lesions central necrosis and
hemorrhage may occur. CT features suggesting malignancy includes a
large size (> 3 cm), poorly defined margins, invasion of adjacent struc
tures, inhomogenous attenuation, and a thick irregular enhancing rim.
Evidence of widespread metastatic disease makes the diagnosis easier.
MRI demonstrating a high signal on the T2-weighted images is also help
ful. However, the definitive method is still percutaneous aspiration
biopsy.
Lymphoma
Involvement of the adrenal gland by malignant lymphoma is more com
mon with non-Hodgkin lymphoma than Hodgkin's disease. The adrenal
glands are seldom an isolated site of disease, although other involvement
may be distant. Adrenal lymphoma can be diagnosed by ultrasound, CT
and MRI. On US, lymphoma appears as a well-defined, relatively
echogenic homogeneous tissue mass. However, CT provides the best
morphologic delineation. The adrenal glands are enlarged with either a
1215
rounded mass or more symmetric enlargement, preserving the basic glan

dular configuration.
Intervention
The most frequent interventional procedure on the adrenals is percuta-
neoues aspiration biopsy. Cyst aspiration is rarely performed. The most
worrisome complication is precipitation of a hypertensive crises by a
pheochromocytoma.
The arterial supply to the adrenal glands comes from many feeding ar
teries. In contrast each adrenal gland is drained by a single vein. This
fact make the adrenal glands suitable for venous sampling.
1216
Chapter 26
Obstetric imaging
Con Metreweli
There is no doubt that in the last twenty years obstetric diagnosis has
been dominated by ultrasound. It is such an essential tool for the obste
trician that apart from a few centres, obstetric ultrasound is mostly out
of the hands of radiologists. Obstetricians and gynaecologists have been,
and are, leading the way with ultrasound applications and development.
One has only to look at transvaginal US (TVUS), colour flow imaging
(CFI) and pulsed doppler and 3D imaging to realise that in its obstetric
applications US is being pushed to its limits.
There is a danger that obstetricians, having so much satisfaction and
control with US, will miss out on the latest upcoming developments es
pecially as there are few radiologists interested in obstetric imaging. For
this reason, this chapter is biased towards a radiologist's point of view
rather than an obstetrician's in the hope that radiologists currently min
imally involved will rekindle their interest in this field.
MODALITIES
The imaging technologies that may be used in obstetric practice are:
Ultrasound (US)
Transvaginal ultrasound (TVUS)
Colour Flow Imaging (CFI)
Conventional Radiography (X-ray)
Computed Digital Radiography (CDR)
Computed Tomography ICT)
Ultrasound (US)
Sometimes termed conventional, or transabdominal, ultrasound is the
most widely available and most used imaging technique in obstetrics. It
1217
is safe, provides images and measurements essential to obstetric prac

tice and generally only requires the inconvenience of a full bladder tech
nique for adequate visualisation of the lower uterus.
Transvaginal ultrasound (TVUS)

Also known as endovaginal or endolumenal US, it by-passes the need
for a full bladder. Being closer to the uterus and ovaries enables higher
frequency transducers and therefore higher resolution images to be ob
tained.
It is indispensible in the firsttrimester and its problems, and in assisted
reproduction (IVF and GIFT). In this field it plays an important role in
gynaecological interventional imaging, particularly ovum pickup, and
the relatively new technique of coelomocentesis which may replace
chorionic villous biopsy. In the third trimester it can be useful in diffi
cult cases of susepcted placenta praevia.
Virtually, all manufacturers supply an appropriately constructed probe
that works from the standard transabdominal US units. The use of a pro
tective condom on the probe is mandatory. The probe can be introduced
by the sonographer or the patient herself, the latter allaying anxiety and
embarrassment.
The patient’s position can either be in a supine frog-leg on a flat bed,
or lithothomy, or even decubitus depending on the preferences of the op
erator.
Colour Flow Imaging (CFI)

CFI is based most commonly on the colour doppler imaging principle
(CDI) or colour velocity imaging principle (CVI).
Colour Doppler has given rise to anxieties regarding insonation power
levels and possible hazard to the developing fetus. Most manufacturers
have built-in safety features that will set the Doppler to lower levels when
obstetric examinations are activated. No harm has even been demon
strated in actual practice. Colour velocity imaging does not generate the
same anxieties and therefore has a theoretical safety advantage.
Computed digital radiography (CDR)

CDR uses the enhancing qualities of digitized images and computers and
substantially reduces the dose of ionizing radiation to mother and fetus.
It would therefore be ideal for chest x-ray in pregnancy and for pelvime
1218
OBSTETRIC IMAGING
try, when MRI is unavailable.

Despite the generally high radiation doses produced by CT a significant
dose reduction can be obtained in CT pelvimetry using the CT scout film
function which is essentially a digitally enhanced computed radiograph.
CT is more widely available than CDR apparatus.

MRI in obstetrics is still in its very early phase. There are three major
factors to be considered: availability and cost, unsureness of obstetri
cians and anxiety regarding potential hazards.
Although MRI does not involve ionizing radiation, potential hazards
may arise from the use of such unnaturally powerful static and time vari
able magnetic fields required in MRI. An increased rate of ocular ab
normalities in a susceptible mouse strain has been demonstrated.
Therefore, in early pregnancy the use of MRI must be carefully consid
ered.
In later pregnancy, hazard may still arise from the excessive temper
ature rise caused by the heat deposition as a result of the changing ra
diofrequency fields.
The Department of Health in the United Kingdom has laid down guide
lines regarding patient exposure. They suggest that there should be a
lower level below which exposure may be considered to be safe and an
upper level which present knowledge suggests should not be exceeded.
Their recommendations suggest that the first level is no greater than 2
W/kg averaged over 15 minutes. This should ensure a rise of less than
0.5°C for the mother and a temperature no greater than 38°C for the fe
tus. The ambient temperature should be kept below 22°C and adequate
air flow for cooling are required. In exceptional circumstances these
guidelines may need to be disregarded.
Different sequences used in MRI not only produce images with dif
ferent appearances and ease of identification of structures but also dif
ferent levels of heat deposition. Furthermore, equipment design may af
fect heat deposition for the same apparent sequence. Therefore, each unit
should be assessed for its own heat deposition as the same assumptions
cannot be made for different designs.
1219
The role of MRI in obstetrics has so far been in examining disorders

in the maternal brain, liver and adrenals in conditions such as: eclamp
sia, acute fatty liver o f pregnancy and phaeochromocytoma. It can re
place radiography, CDR and CT in pelvimetry. It is finding increasing
use in diagnosis of fetal malformation but at present only as a technique
supplementary to prior US.
APPLICATIONS
Diagnostic imaging in pregnancy fulfills two major requirements. The
first and numerically most frequent is in screening and monitoring the
pregnancy and the second is in assisting in diagnosing the complications
of pregnancy.
Screening and monitoring the progress of pregnancy

Ultrasound is without doubt the technique of choice in this aspect of ob
stetrics. It has naturally evolved into three relatively distinct areas of ap
plication with differing degrees of involvement of radiologists:
1. Routine antenatal screening
2. Fetal morphology and abnormality
3. Fetal well-being
Routine antenatal screening

This screening is most commonly carried out by radiographers, techni
cians and midwives, and usually consists of establishing fetal number,
measurements to confirm or establish gestational age, placental site lo
calisations and varying degrees of fetal morphology check, depending
on the skill and experience of the operator.
The measurements usually carried out are Crown Rump Length (CRL),
Biparietal Diameter (BPD), Abdominal Circumference (AC), and Femur
Length (FL). These are too well known to need further elaboration. But
there are many others: Amniotic Fluid Index (AFI) which is becoming
increasingly popular for documentation of amniotic fluid volume;
Occipito Frontal Diameter (OFD), Head Circumference (HC), which
may be used when the BPD is not measurable, and when the head shows
unusually marked degrees of dolichocephaly or brachycephaly; Trans
verse Cerebellar Diameter (TCD), which is also useful for gestational
age estimation and is independent of head shape. Virtually, anything
measurable in the fetus has been measured, but many of these measure
1220
OBSTETRIC IMAGING
ments have specific rather than general usage.

The use of routine antenatal screening has recently been critizised as
being ineffective in reducing adverse perinatal outcome and adding un
necessary cost to antenatal care. However, the conclusions of these in
vestigations do no more than support the general principle of the law of
diminishing returns. In any selected low risk population the chances of
abnormal findings are diminished and the cost of finding them will be
high. However, one cannot extend these obvious conclusions to the
whole obstetric population which includes high risk and uncertain risk
mothers. For instance, one of the major functions of routine screening is
to establish gestational age (GA). Without having an accurate GA how
could you identify postmaturity, premature labour or premature rupture
of membranes if you do not know what time to call "maturity”? How
could you monitor intrauterine growth retardation? Furthermore, could
you interpret the results of laboratory data such as AFP and HCG with
sufficient accuracy?
Up to 30% of pregnant women may not be accurate in their reported
LMP because of irregular cycle, first trimester spotting, breast feeding,
oral contraception or just plain fecklessness. Fundal height may be con
fused by multiple pregnancy, obesity or fibromyomas.
A CRL below 35 mm or a BPD between 12-18 weeks has a 90% ac
curacy predicting GA compared with 70% based on menstrual age.
Combined measurements are even more accurate.
To suggest that one can practice modem obstetrics without the use of
routine US is to recommend a return to the dark ages!
Ideally, all pregnancies should have routine screens at least twice. First
at 18 weeks to establish GA and exclude major anomalies and the sec
ond at 32 weeks for fetal growth and placental site. Pregnancies with
identifiable risk factors may need more.
Fetal abnormality
The demonstration of fetal abnormality involves radiologists, as well as
radiographers and obstetricians. Radiologists should be able to contribute
significantly in this field with their experience in imaging and anatomy
and with MRI looming on the horizon as a powerful supplementary tech
nique for the fetus. However, as diagnosis of fetal abnormality is gener
ally less useful towards the end of pregnancy there has been great pres
sure to make the diagnoses earlier. This is not surprising, as all major
1221
congenital malformations originate in the embryonic period (six to ten

weeks) with the exception of the external genitalia which take up to 14
weeks to achieve fetal maturity. There is increasing effort to make the
diagnosis can be made as early as the first trimester. In this use a TVUS
is essential to visualize the embryonic and early fetal anatomy. This has
been given much impetus in the assisted reproduction programmes and
can be put to good use in early threatened abortion.
Fetal well-being
The majority of findings in routine antenatal US tend to show the end re
sult, of what has happened to the fetus in its intrauterine environment up
to that point of time. The aim of fetal well-being studies is more to pre
dict what is likely to happen in the future o f that pregnancy based on
mainly physiological parameters. Such studies of fetal physiology in
volve the considerable use of Doppler wave form studies, and available
time. As radiology is a shortage speciality and this territory appears to
be the prerogative of the obstetrician it will not be mentioned further
here.
Complications of pregnancy
The complications of pregnancy that are most likely to require the ser
vices of the radiologist, and the techniques that may be potentially use
ful, are:
- Threatened abortion (US, TVUS, CFI)

- Ectopic pregnancy (US, TVUS, CFI)
- Trophoblastic disorders (US, TVUS, CFI)
- Fetal abnormality (US, TVUS, CFI, MRI)
- Placenta praevia (US, TVUS, CFI, MRI)
- Pelvis mass discovered
during pregnancy (US, TVUS, CFI, MRI)
- Deep vein thrombosis (US, CFI)
- Eclampsia (MRI)
Threatened abortion
The radiologist may be requested to investigate PV bleeding with or with
out pain in early pregnancy. The common causes will be pseudomen
struation with a viable pregnancy, ectopic and molar pregnancy (see be-
1222
OBSTETRIC IMAGING
Figure 1.
A 3D US o f a living em
bryo within its gestation
sac next to an aborting
twin (asterisk). The umbi-
cal cord (arrowhead),
limb buds (small arrows)
and yolk sac (large ar
rows) o f the living twin
are clearly visible.
low) aborting twin (Fig. 1), missed abortion, and incomplete abortion.
Crucial to the management of such cases is the necessity to demon
strate a living embryo or fetus in a healthy gestation sac. This is achieved
by demonstration of what is usually termed fetal heart motion (strictly
speaking, it should be embroynal heart motion). If this can be demon
strated the chances of a successful ongoing pregnancy will be between
90-97%. It is usually clearly visible and there is no need for M-mode
scan or Doppler other than for documentary proof.
Signs that the gestation has failed are:

- an irregular shaped sac
- poor decidual reaction with poor delineation between decidua capsu-
laris and parietalis giving a "thin-walled" sac appearance
- a low position of the sac (just above the internal os)
- no embryo visible in a sac of mean diameter in excess of 25 mm
- no heart activity in an embryo with a CRL greater than 5 mm (ca. 6.5
weeks)
- no embryonic body activity with a CRL greater than 15 mm (ca. 8
weeks)
- no embryo within a gestation sac containing a yolk sac of 5 mm
Ectopic pregnancy
The presence of an ectopic pregnancy can now be very confidently es
tablished even without the necessity to measure serum HCG although
this is still a useful adjunct.
1223
Transabdominal US is no longer considered to be sufficient. The best

results are obtained with TVUS and CFI.
The signs to seek are:

— empty uterine cavity
— up to 14% may show a decidual cyst deep in the endometrium not
reaching the endometrial interface
— blood in the uterine cavity may be mistaken for a sac, but it will not
contain either an embryo or yolk sac
- differential blood flow demonstrable between the uterine blood ves
sels in the two cornua. This is difficult to quantify by Doppler wave
forms but relatively easy to see
- a cystic mass in the adnexae surrounded by a hypervascular ring, de
scribed as being a "ring of fire" on CFI. Unusually, the mass may not
be cystic. The waveform of the vessels in the ring is the characteris
tic low impedance, pregnancy type, flow.
- the cyst may contain a recognizable embryo and in about 10% even
a demonstrable heart beat if the embryo's CRL measures beyond 10
mm (7 weeks)
If there is still doubt, measure the serum HCG. If the HCG level exceeds
1,800 MIU per ml there should be an intrauterine sac visible with TVUS.
Go back and recheck. If still negative a follow-up of HCG and TVUS
must be performed. Copious blood in the cul de sac is a late sign! If doubt
still remains, the gynaecologist/obstetrician will get fed up and do a la
paroscopy!
Early diagnosis of ectopic pregnancy allows for non-surgical interven
tional treatment with TVUS guided direct injection of Methotrexate into
the ectopic sac.
Trophoblastic disorders: hydatidiform mole and choriocarcinoma

The diagnosis of hydatidiform mole is easy with conventional ultra
sound. The presence of a fetus or fetal parts suggests the possibility of a
partial mole. The fetus will show congenital malformations and kary
otyping is often triploid. These moles are always benign.
The imaging diagnostic problem arises with the complete moles. These
have a 46XX karyotype and about 20% progress to choriocarcinoma.
When the uterus has been evacuated but the HCG fails to return to nor-
1224
OBSTETRIC IMAGING
mal in 12 weeks or still remains high or begins to rise again, and if there
is a persistent corpus luteum cyst, TVUS and CFI is again essential to
seek the site of remaining trophoblast. A chest x-ray is necessary to ex
clude lung metastases.
The conventional gray scale image may appear to be normal or only
mildly abnormal but CFI invariably reveals a wealth of unsuspected ves
sels indicating the presence and location of persistent trophoblast/chori-
ocarcinoma.
Fetal abnormality
There are now excellent reference texts concerned with fetal abnormal
ity and virtually half of the subject matter in obstetric ultrasound texts is
devoted to this subject. It would be impossible to do justice to the sub
ject in just a few pages, but some general observations and comments
are pertinent.
1. The diagnosis o f fetal anomaly is dificult and considerable expertise

is required.
The German protocol in which suspected fetal anomalies have to be sent
to specialist centres is an excellent model.
2. Karyotyping facilities are an essential complementary feature fo r fe

tal anomaly diagnosis.
Karyotyping is a boon for the problem of the suspected abnormal fetus
in which only soft signs can be demonstrated. Any ultrasound service
without this back up is incomplete.
3. The frequency o f abnormalities within any particular ethnic or racial

group is subject to variation.
For instance, urinary tract anomalies are relatively rare in the Chinese,
common in Europeans and very common in the Middle Eastern races.
Spina bifida is also relatively rare among Chinese but common in
Europeans. But Down’s syndrome and anencephaly appear to be fairly
steady in all races.
1225
Figure 2.
Acrania. Free floating
brain is seen above a mi-
croopthalmia (arrow).
4. Significance offinding a fetal abnormality

When a fetal abnormality is discovered one must carefully categorise it.
Is it:
a) Incompatible with fetal survival?
Example: the majority of fetuses with severe cystic hygroma die in utero.
Early diagnosis will not make a major difference to the outcome. It may
enable an earlier termination and alert to possible risks in subsequent
pregnancies.
b) Incompatible with survival post neonatal or early infant age.
Example: renal agenesis, bilateral multicystic kidneys, hypoplastic left
heart, acrania (Fig. 2), trisomy 18, hydranencephaly, lethal dwarfism.
Early diagnosis will enable early termination and avoid considerable
parental distress and distress of the medical staff who would otherwise
be left to care for the doomed baby.
c) Compatible with extrauterine life but incompatible with an indepen
dent existence?
Example: microcephaly, spina bifida, Down's syndrome. Early diagno
sis is essential to make an informed decision regarding possible termi
nation.
d) Compatible with a normal independent life following repair of the ab
normality?
Examples: posterior urethral valve with well preserved kidneys, pelvi-
ureteric junction obstruction, choledochal cyst (Fig. 3 a, b), cleft lip,
mesoblastic nephroma.
Prenatal diagnosis is beneficial because the parents and clinicians can
be forewarned and appropriate treatment can be planned ahead, includ
1226
OBSTETRIC IMAGING
Figure 3.
a) Transverse scan o f a fe
tal abdomen (19 weeks
GA) with a choledochal
cyst (arrow).
b) Longitudinal scan show
ing the sinus venosus an
terior (arrowhead) and
IVC posterior (arrow) to
the choledochal cyst.
ing transfer to a specialist centre if considered necessary. The discovery

of urinary tract abnormalities at this stage may prevent children pre
senting in later life in an irreversibly damaged state.
e) Compatible with normal life as the abnormalilty is self-limiting and
not essential?
Examples: ovarian cyst, fetal adrenal haemorrhage, multicystic kidney.
Following diagnosis, the parents require reassurance and perhaps fol
low-up as in the case of the multicystic kidney, where there may be a
25% chance of developing a pelviureteric junction obstruction on the
contralateral side.
f) Compatible with a normal life despite a permanent deformity such as
achondroplasia?
g) The last group is those in whom the echographically suspected diag

nosis is uncertain.
Not diagnosing or missing abnormalities of groups a), b), e) and f) will
not alter the long term outcome even though it could affect the quality
of care provided. Missing group d) lesions may delay necessary correc
tive treatment. Missing group c) abnormalities is the most serious error
- committing the unfortunate family to decades of unhappiness in the
majority of such cases. In group g) there is scope for further delineation
if karyotyping and MRI are available.
5. Ultrasound alone has not achieved as high a degree of sensitivity as

might be hopedfor.
It is reasonably good at identifying the more gross abnormalities (60-90
%) but may miss the more subtle ones, either when these are solitary or
when they make up essential parts of a syndrome where the abnormali
ties may not be functionally related. For instance, a choledochal cyst is
a solitary abnormality, but posterior urethral valve may produce func
tionally related bladder hypertrophy, hydroureter and hydronephrosis.
The inexperienced examiner may then miss the bladder changes and re
port only hydronephrosis. Spina bifida is accompanied by a Chiari II mal
formation but this may be difficult to demonstrate with US. In conditions
such as Zellweger's syndrome, the brain abnormality or the renal abnor
mality may be identified alone and the lack o f appreciation of the other
leads to a failure of accurate diagnosis.
In some conditions signs are ’’soft" apart from some disagreement of
measurements such as head circumferences vs. abdominal circumference
in Trisomy 18, in which there otherwise may be little else to see. It may
be that 3D US will enable better visualization of these soft signs. The
well known paediatric diagnostic category of "funny looking kid” could
well become "funny looking fetus" in the future (Fig. 4). In adult and
paediatric medicine one has a whole armamenterium of investigations.
With fetal medicine these have been limited until karyotyping and MRI
became available.
MRI of fetal abnormality presents unique problems. In addition to the
thermal problems already alluded to, fetal motion requires fetal paraly
sis. The most commonly used technique currently is ultrasound guided
umbilical vein injection of pancuronium bromide. But this is a technique
not without significant hazard of fetal demise! Rapid imaging techniques,
1228
OBSTETRIC IMAGING
Figure 4.
3D US o f a fetal face.
such as echo planar sequences suffer from a relativley limited spatial res
olution and therefore may not be suitable for some organs. Because of
the rapid rise times and high gradients heat deposition will be high but
this can be balanced by the shorter scan time. Transmitted maternal aor
tic pulsation can be minimised by placing the mother in a decubitus po
sition. The fetal brain has a high water content providing some further
constraints to MRI diagnosis, especially as there has been a greater in
terest in the fetal brain than other parts.
The reported experience does appear to be clustered into the last
trimester and is invariably supplementary to an echographically dis
closed abnormality. In some of these cases there were doubts and diffi
culties (consistent with group g) above). There is generally reasonable
agreement between MRI and US but in certain cases MRI does add fur
ther information of clinical value, and is likely to become an important
supplementary technique.
6. Nonspecific signs o f fetal abnormality

In this section attention is drawn to some non-specific signs that should
alert to the possibility of a significant fetal abnormality.
Nuchal translucency in the first trimester

A unilocular cystic collection over the fetal posterior neck and upper
back containing an estimated volume of fluid greater than 3 mm3 has an
approximated 30% chance of having an abnormal karyotype. A multi-
1229
loculated or multitrabeculated nuchal cystic hygroma with a midline sep

tum has similar chance of abnormal karyotype but also a 20% chance o f
having another abnormality but normal karyotype.
Nuchal thickening disappears as the embryo matures into fetalhood,
but remains as a soft sign in a small number of Down's syndrome babies,
and progresses to full blown cystic hygroma in many cases of Turner's
syndrome (46X0).
Choroid plexus cysts (CPC)

These are mentioned because there is still confusion and controversy re
garding their presence. Undoubtedly, in late pregnancy persistence o f
CPC is strongly associated with trisomy 18. However, in early pregnancy
CPCs are relatively common and unless a careful scan reveals another
abnormality they are highly likely to be benign. Therefore, it is not nec
essary to karyotype all fetuses found to have CPC in early pregnancy,
and one would consider it is also not necessary if additional abnormali
ties are found. However, it will still be very useful in borderline cases.
Single umbilical artery (SUA)

The umbilical cord is easy to visualize. There is a high association with
fetal anomaly which may be found in between 15-48% of all cases with
SUA.
Amniotic fluid abnormalities: polyhydramnios and oligohydramnios

In the second and third trimesters of pregnancy amniotic fluid is pre
dominantly fetal urine. The prerequisites for fetal urine production are
good renal artery perfusion, functioning normally formed kidneys (or at
least one kidney), and a competent urinary tract allowing normal expul
sion of urine.
Production of amniotic fluid (fetal urine) has to be balanced by its re
duction which requires competent fetal swallowing and propulsion
through stomach and doudenum into small bowel where the fluid can be
reabsorbed and homeostasis maintained via the placenta.
This balance can be upset by any abnormalities of the urinary tract,
cardiovascular system or upper gastrointestinal tract, or any generalized
abnormalities that make the fetus "sick" and indirectly affect the above,
e.g. most causes of fetal hydrops and diabetes mellitus.
1230
OBSTETRIC IMAGING
The presence of an adequate quantity of amniotic fluid is essential for

fetal lung and musculoskeletal development. Therefore, the observation
of abnormal quantities of amniotic fluid is an excellent non-specific sign
that there may be underlying fetal abnormalities or fetal sickness.
Abnormalities are present in between 30-60% of polyhydroamnios and
about 40% of oligohydramios. However, these figures are somewhat
meaningless as there has not been a rigid standard adhered to in classi
fying poly- and oligohydramnios.
Measurement of the amniotic fluid index (AFI) has emerged as a sim
ple popular and reproducible technique of estimating amniotic fluid. The
AFI is obtained by dividing the uterus into four quadrants, measuring the
vertical deepest pocket in that quadrant and summing the four measure
ments. Currently values above 25 are taken to indicate the presence of
polyhydramnios and values below 5 are taken to indicate oligohy
dramios.
One anticipates that with future universal use of technique we will be
able to have a better measure of the relative risks of abnormality with a
given amniotic fluid index at a specific gestational age.
Placenta praevia
Placenta praevia occurs in about 0.5% of all pregnancies. US is already
very accurate in determining placental site and the presence of placenta
praevia and is therefore the technique of first choice.
The conept of placental migration and possible confusion caused by
an overfilled or underfilled bladder are well known but there are about 5%
pregnancies in which it may be difficult to establish placental location
relative to the external os with confidence. These are: the obese mother,
posterior location of placenta and intervening fetal head, vasa praevia,
and the rare but potentially fatal placenta accreta and percreta.
In these situations further investigation prior to delivery are now avail
able. The most easily available would be TVUS.
The probe is introduced gently with on-screen guidance to avoid im
pacting the cervix. The uterus is examined from positions in the vaginal
fomices. With the addition of CFI it is easy to identify placenta cover
ing the internal os, and marginal vessels covering the os. Obliteration of
the placental myometrial line and high flow venous lakes within the pla
centa suggest placenta accreta.
1231
Figure 5.
Transverse scan o f an
early viable pregnancy
with a large complex
mass with thick septae
behind the uterus.
Claims have also been made for the value of MRI in such situations,
but as yet there has not been any study comparing the value of TVUS
and CFI with MRI.
On cost and availability it would seem that US, TVUS and CFI is suf
ficient.
Discovery o f parauterine mass during pregnancy

A parauterine mass may be discovered during pregnancy by palpation
but more frequently it is revealed during careful routine antenatal ultra
sonography (Fig. 5). "Careful" indicates that the pelvis has been scanned
properly and that the routine study was not tunnel-visioned onto mea
suring the BPD and little else!
The differential diagnosis includes uterine fibromyoma, functional
luteal cysts, endometrial chocolate cysts, cystic teratomas, and ovarian
malignancy.
It is the last diagnosis which is most feared and for which radiologists
will be recruited to test their powers of clairvoyance. The five year
survival rate of stage I ovarian carcinoma is 60-90% but for stage IV
0-4% , and therefore early diagnosis is crucial. Early diagnosis of ovar
ian cancer is usually incidental such as discovery in pregnancy during
antenatal US or caesarean section.
The use of serum tumor markers, such as CA125, may be limited as
these are also raised during pregnancy and with endometriosis.
Ovarian tumors may be found in 1/2000 to 1/600 pregnancies. The com
monest tumor reported is benign cystic teratoma. Malignancy, fortunately,
is realatively rare constituting up to 5% of the ovarian masses found.
1232
OBSTETRIC IMAGING
Surgical removal is recommended in all cases. It will not only remove

possible malignancy but also lessen the chance of torsion (about 25%)
and haemorrhage. Supportive progestational therapy reduces the subse
quent abortion rate form 85% to 10%.
Radiologists have used US, TVUS and MRI with success in demon
strating the presence and origin of the lesion although it is often difficult
to distinguish an endometrial from an ovarian cyst. The diagnosis of ma
lignant potential is more difficult.
CFI has been used successfully to identify tumor neovascularity which
can then be interrogated with pulsed Doppler. Tumors show character
istic low impedence waveform. This holds true for the non-pregnant
woman. Unfortunately, it is not clear whether this also applies in preg
nancy as the characteristic of pelvic vascular flow during pregnancy also
shows low impedence and it may be that any low impedence vascular
changes discovered in an ovarian mass are purely the effect of pregnancy.
The conventional wisdom still holds that pure cysts are more likely to
be benign and any solid components raise the risk level of possible ma
lignancy and indicate need for surgery.
Deep vein thrombosis (DVT)

Suspicion of DVT can be easily allayed or confirmed by the use of US
and CFI without need for radiological contrast venography. Worries re
garding irradiation of the fetus are removed and pregnant women can be
examined at a lower threshold of clinical suspicion.
Eclampsia
MRI has not only provided another non-ionising radiation type of imag
ing diagnosis, but has its own unique information to reveal. In obstetrics
this has been very true in studies of eclampsia and preeclampsia.
Pregnancy induced hypertension can result in headache, confusion,
raised intracranial pressure and coma, visual loss and paralysis from cere
bral hemorrhage with long term morbidity. Early diagnosis and appro
priate treatment is essential in these previously healthy women.
Women with preeclampsia may show hyperintense signals on T2-
weighted images in the deep cerebral white matter. Those with eclamp
sia show increased signal at grey matter junctions, cortical oedema and
haemorrhage especially in the region of the posterior cerebral circula
tion.
1233
Current MRI is more sensitive than CT in demonstrating abnormali

ties in eclamptic women who have had seizures but still does not show
abnormality in all studies. As newer more sensitive sequences become
available one can anticipate that MRI will be more sensitive and may be
come a screening tool for mothers at risk. It may be that the "at risk" cri
teria will be altered as mothers without all the accepted signs such as
oedema and proteinuria may still develop cerebral problems.
The severe vasospasm that accompanies eclampsia is demonstrable by
magnetic resonance angiography. This information is similar to that ob
tained by more invasive modalities such as angiography or radionuclide
studies using SPECT.
In addition to eclamptic changes, MRI has shown physiological
changes of the pituitary during pregnancy consisting of hyperintensity
on Tl-weighted images, upward bowing and increase in size to 10 mm
vertical height which shold not be confused with pathology.
Pathological conditions of the pituitary such as pituitary haemorrhage
and tumors have also been reported as here other intracranial patholo
gies: intracranial aneurysm, venous thrombosis and venous angiomas.
PELVIMETRY
Conventional standing lateral pelvimetry means a very high radiation
dose with increased risk of subsequent malignancy in the fetus. However,
it is still thought to be of value in cases where trial of labour for breech
presentation is being considered or cephalopelvic disproportion is sus
pected.
Pelvimetry can be obtained with digital radiography or CT with a de
sirable dose reduction, or with MRI. With CT, both sagittal and AP views
can be obtained (Fig. 6 a, b). Dose reductions are typically around 10%
of conventional radiography with fast film screen combinations.
However, accuracy can only be achieved with protocols for the most
ideal window and level settings and proper trraining in interpretation.
This should be done by the radiologist. Obstetricians not being used to
CT often misplace the calipers.
Pelvimetry using MRI should observe the heat related hazards men
tioned previously, but when available MRI is now the method of choice.
Fetal movement does not blur the landmarks and therefore there is no
need for fetal sedation (Fig. 7).
1234
OBSTETRIC IMAGING
Figure 6.
CT pelvimetry
a) Lateral view showing outlet measure
ment
b) AP view fo r maximum transverse diam
eter o f the inlet
In order to obtain the best visualization of pelvic landmarks and keep

to safe limits the use of a proton density, sequences in the sagittal pro
jection is recommended, with single echo or GE axial projections, if nec
essary. The specific absorption rate (head deposited) should be obtained
and recorded in the obstetric notes.
1235
Figure 7.
M RI pelvimetry with ЛР inlet
and outlet measurements.
1236
Chapter 27
Tropical diseases
Philip E.S. Palmer,

with Stanley P. Bohrer, Carlos Bruguera, Xing-Rong Chen,
Mahmoud R. Elmeligi, Hassen A. Gharbi, S.B. Lagundoye,
M.W. Wachira
Articles are frequently published in reputable radiological journals de

scribing diseases such as Echinococcosis (Hydatid disease) as ’’rare", or
expressing surprise that a worm (Ascaris) has been demonstrated in the
common bile duct by ultrasonography. Case reports show that plain ra
diography will demonstrate "unusual" calcification in the bladder of a
patient with schistosomiasis.
The truth is very different, because about 40 million people suffer from
hydatids, at least one quarter of the world's people harbour ascaris, 200
million or more have schistosomiasis and untold millions have a bewil
dering variety of "tropical diseases". Very few tropical diseases are rare.
Which is why this chapter is important, even if the title is not really
accurate: most of the diseases described in this chapter are not confined
to the tropics, but will be seen all over the world in immigrants or brought
home by travellers. Some have adapted and now flourish in distinctly
nontropical climates, presenting in ways which differ from the same dis
ease in the tropics. Nevertheless, it is in the tropics that these diseases
occur most frequently. Individually and together they are the most nu
merous of all afflictions which cause ill health in people of all ages.
It is very important to remember that the natural history of these dis
eases will vary, depending on whether there is an acute onset in the trav
eller who has never previously been exposed, or a recurrent chronic in
fection which is almost part of the normal life of someone who lives in
the tropics. It is equally important to be aware of their geographical dis
tribution. Chaga’s disease, for example, occurs only in the central and
southern parts of the Americas, and will not occur in patients who do not
1237
live there, or who have never visited that part of the world. When re
viewing the diagnostic images of someone who has visited or lived in
the tropics, it is essential to know not only where they come from, but
also how long they were there. Most o f the tropical diseases are due to
infections or parasites and there is a variable delay before they become
clinically obvious. The pattern also depends on the stage of the disease
and the general health of the patient.
The radiologist should have as much information as possible about the
results of the laboratory tests for the individual patient, particularly in
travellers who have returned home after visiting the tropics. There are
too many specific diagnostic tests for each infection for them all to be
included here, but there is one which is useful for screening when a par
asitic infection is suspected. In the acute stage, the invasion or multipli
cation of so many parasites often causes a marked peripheral
eosinophilia. Any patient with a strange infection or an unusual abnor
mality on a radiograph or ultrasound scan, who has just been to the trop
ics and who has a raised eosinophil count, is not likely to have one of the
more commonM western diseases". Unfortunately, this is not absolute and
the differential cell count may be normal. As is necessary for every di
agnostic interpretation, the whole clinical picture must be taken into ac
count. What also makes it more difficult is that many patients who live
or have lived in the tropics will suffer from multiple diseases. Parasitic
infection may almost be a normal state, and the illness which brings them
to their doctor may be added onto, or be an acute exacerbation superim
posed on several other less obvious infections. And, to complicate the
diagnosis even further, laboratory findings may be misleading, because
normal levels are not the same in every part of the world, while high im
munological titres may indicate a past infection not relevant to the pre
sent illness.
If the patients bring images with them, extract as much information
from them as possible, even if the quality is not ideal. Imaging facilities
vary enormously throughout the world, but there is usually some useful
information even in a poor film or scan. Do not put poor quality images
aside as unhelpful: compare them with the current findings. You and your
patient may need all the help you can get!
In a global textbook such as this, it is not possible to provide a detailed
account of the epidemiology, and life history of the many tropical dis
eases, nor can they all be included. Some have no radiological interest,
1238
TROPICAL DISEASES
others can only be mentioned briefly. When in doubt, or curious, refer

to a more comprehensive tropical radiology text. This chapter describes
only the most common findings in the most common diseases, not their
many possible permutations.
AMOEBIASIS
Infection with the pathogenic protozoan, Entamoeba histolytica, occurs
worldwide and at all ages. Once known as amoebic dysentery, almost
any part of the body can be infected, including the skin and the lungs. In
some patients the colon and liver escape or show no clinical evidence of
infection. A normal gastrointestinal tract certainly does not exclude
amoebiasis. There are numerous strains ofE. histolytica, which are non-
pathogenic and others which are found as commensals. Amoebiasis may
be non-invasive. Infection is acquired through contaminated food or
drink, and is particularly prevalent where sanitation is poor. It is proba
ble that flies and other insects also spread the disease.
There is a wide spectrum of clinical presentation. An amoebic infec
tion may cause either severe, acute illness or chronic ill health. Many pa
tients have a history of diarrhoea, but in contrast some patients are con
stipated. Acute amoebic dysentery presents with frequent loose, blood
stained stools, colic, tenesmus and in many cases, severe systemic illness.
Chronic amoebic dysentery may cause ill health, yet the colonic symp
toms may not be striking. Pain is usual in the right lower abdomen, and
the liver may become enlarged and tender. Children may present with
intussusception, adults with intestinal obstruction. Some patients will
complain of cough and have symptoms of pneumonia with a pleural ef
fusion, but no symptoms referable to the bowel.
Amoebiasis of the bowel

The most frequent sites of infection are the caecum, ascending and sig
moid colon. The amoebae burrow below the mucosa, and ulceration fol
lows. Occasionally, the infection spreads outwards, through the muscle
layer to the peritoneum. The earliest imaging abnormality is usually
found in the caecum and right colon. There is local oedema and the bowel
becomes less mobile: with a barium enema, the bowel mucosa appears
hazy and spiculated, because of the oedema and ulceration. There may
be areas of spasm and irritability, but as the oedema increases, the bowel
wall is thickened and becomes rigid. The caecum becomes very distorted
1239
a) An amoebic infection distorting the caecum and causing mild ileocecal obstruction.
There is a "skip” area o f colitis at the splenic flexure and probably another in the
descending colon. (Nigeria)
b) Amoebiasis causing constriction in the proximal transverse colon and at the ileo-
coecal junction (Amoeboma). There are areas o f ulcerating colitis just below the
splenic flexure and ju st above the sigmoid colon. (Nigeria)
c) Severe and extensive amoebic colitis, with spasm o f the descending and sigmoid
colon. There is shortening and ulceration o f the caecum and ascending colon: the
terminal ileum is dilated. (Nigeria)
d) Late stage o f amoebic colitis. The colon has become smooth, with decreased haus-
tration, particularly the rectum and sigmoid. (Nigeria)
1240
TROPICAL DISEASES
and there is usually reflux into the terminal ileum. There may be in
flammatory pseudopolyps (Fig. 1 a). Ultrasound will show the thicken
ing of the wall of the right colon and as the diseases progresses, there
will be a pericaecal mass. It is important to examine carefully the whole
colon, because amoebic bowel infections often occur at several differ
ent sites, with intervening normal areas of bowel (Fig. 1 a). Only in
Crohn's disease, tuberculosis and lymphoma are similar multiple sites
likely. When the infection is acute and severe (fulminating amoebic col
itis), the colon may be very dilated, resembling the toxic megacolon
which is seen in ulcerative colitis: perforation or haemorrhage may oc
cur. Fortunately, ulcerative colitis is rare in many parts of the world,
which helps the differential diagnosis, but careful mucosal biopsy is nec
essary if surgery is considered. In less severe cases, there can be coarse
mucosal thickening throughout the length of the colon, with pericolic ex
tension due to fistulae. Involvement of the small bowel, or extension to
the bladder or skin, can occur but is uncommon. In the later stages the
caecum becomes contracted, often with shortening of the ascending
colon. Fibrosis during healing can result in a smooth, narrow, rigid colon
(Fig. Id).
Amoeboma
Amoebic infection can cause an amoeboma, which is a localised hyper
plastic granulomatous reaction, usually in the colon, but sometimes in
the ileum (Fig. 1 b). This causes a large mass with central stenosis which
closely resembles a carcinoma. Again, geography is important, because
cancer of the colon is rare in many parts of the world and an amoeboma
is often the more common cause of such a tumour. However, amoeboma
are also geographically variable, being common in some regions and rare
in others. Diagnostically, the demonstration of another area of colitis
elsewhere in the bowel makes an amoebic infection more likely than a
tumour. Unfortunately, neither ultrasound nor any other form of imag
ing can reliably distinguish between a carcinoma and an amoeboma; rec
tal biopsy followed by a short period of antiamoebic treatment may pre
vent unnecessary surgery (which can be dangerous with any severe amoe
bic infection).
Infants and children are not spared any of these varieties of amoebia-
sis, and, in addition, intussusception may be caused by the rigidity or
swelling of a segment of amoebic bowel. Reduction by any form of in-
1241
temal pressure must be carried out with extreme caution.
Amoebiasis of the liver

Amoebic abscesses occur in any part of the liver. Patients do not always
have a history of diarrhoea or other evidence of amoebiasis and there
may be no amoebae in the stool or on rectal mucosal biopsy. Amoebic
infection may not even be suspected clinically, because liver involve
ment may not present for many years after exposure, and the patient may
never have been to the tropics. A recurrent fever, pain or local tender
ness in the right upper quadrant of the abdomen, or an elevated diaphragm
on a chest x-ray, sometimes with a pleural effusion, may be indications
of an amoebic abscess (Fig. 3 a). However, a clinically normal liver does
not exclude a hepatic abscess. The majority of liver abscesses are reli
ably demonstrated by ultrasound, CT or MRI (Fig. 2). Radionuclide scan
ning is less sensitive until the abscesses are large. Angiography may show
a "blush" around the abscess, but is not a very helpful procedure: a tu
mour or an other infection may be similar.
The ultrasound appearance of amoebic hepatitis varies with the stage
of the infection. At first, before there is abscess formation, there will be
hypo- or anechoic areas, most often in the right lobe of the liver. The
borders are vague and ill-defined, but the general shape is round or oval,
varying from 1-20 cm in size. Some have marked back-wall enhance
ment. While similar areas may be found in any infection, a subcapsular
lesion is more likely to be amoebic than pyogenic, and if amoebic, most
patients will have more than one hepatic lesion.
In the later stages, as liquefaction develops centrally, thick-walled,
roughly circular absceses can be recognized with ultrasound (Fig. 2 b).
Many have internal debris, and most are surrounded by hypoechoic
oedema or hyperechoic compressed liver parenchyma. High dose con
trast infusion or contrast angiography will show these changes as a non
specific halo "blush" around the abscesses (Fig. 2a).
In the early stages of an amoebic infection, the lesions may be isoe-
choic and not demonstrated with ultrasound. Repeat scanning is essen
tial, because the abscesses change quite quickly and will become obvi
ous as the infection progresses. The images shown by CT and MRI will
follow a similar sequence of changes (Fig. 2 c, d, e), but have no imag
ing advantage over ultrasound, except in the transitory phase when the
lesions are isoechoic. Even then, a few hours is all that is required be-
1242
TROPICAL DISEASES
Figure 2.
Amoebic liver abscess.
a) I f ultrasound or other scanning is not
available, a liver abscess can be
demonstrated by intravenous high
dose contrast infusion, with tomogra
phy. This large amoebic abscess
shows a well marked peripheral, hy-
pervascular inflammatory rim.
(Kenya)
b) A liver abscess shown by ultrasound.
(Kenya)
c) A CT scan o f an amoebic abscess at an early stage, with poor edge definition
(arrowheads). (Pakistan)
d) The abscess becomes more clearly shown (arrows). (Pakistan)
e) Amoebic abscesses in both lobes o f the liver. (Pakistan)
1243
Figure 3.
Amoebiasis in the chest.
a) An amoebic hepatic abscess causing a raised right diaphragm with pleural effusion
and right lower lobe oedema and infection. (Kenya)
b) An amoebic hepatic abscess causing a subphrenic abscess, elevation o f the right di
aphragm, right pleural effusion and lower lobe oedema. (Egypt)
c) A large right amoebic empyema with raised right diaphragm and right lower lobe
consolidation, all due to an amoebic abscess in the liver. (Nigeria)
fore there will be positive results with ultrasound. After treatment the
abscess may heal completely over a period of months, or may leave a
scar which may calcify eventually. If untreated or unresponsive (or sub
ject to trauma) the abscess may rupture into the biliary tract or peri
toneum, pericardium or chest. It is extremely difficult to distinguish be
tween amoebic and pyogenic abscesses in the liver with any form of
imaging. The early lesions may suggest hepatoma or even hepatitis or
haematoma. Aspiration may be necessary, or the result of specific treat-
1244
TROPICAL DISEASES
ment assessed before a pyogenic abscess or infected hepatic cyst can be

excluded.
Amoebiasis of the chest

An amoebic liver abscess may be associated with a pleural effusion or
empyema on either side of the chest, and there may be lower lobe pneu
monia. Amoebic abscesses may rupture into the pericardium, particu
larly from the left lobe of the liver, or may also rupture into the pleura
or lung (Fig. 3). The contents may then be coughed up, a dramatic and
rather unpleasant event, which produces thick, pink, stained sputum in
stead of ordinary sputum. A ”collar-stud” abscess penetrating through
the diaphragm may result in a true amoebic pneumonia, but more often
the lung reaction is a result of static pulmonary oedema because of the
immobile diaphragm, with secondary pyogenic infection.
It is also important to remember that an amoebic lung abscess can oc
cur even without evidence of liver or bowel infection. If communicating
with the bronchus, there can be a fluid level in the abscess. Such lung
abscesses are usually thick-walled, but cannot be distinguished radio-
logically from a pyogenic abscess or even some cases of tuberculosis.
When pulmonary amoebiasis is suspected, careful ultrasound of the liver
may show a clinically unexpected hepatic abscess. Even if the liver is
normal, the possiblity of an amoebic infection must be considered when
ever there is a lung abscess which fails to respond to standard treatment.
Amoebiasis of other sites

Amoebic infections can occur in the brain and skin. Cutaneous amoebi
asis can be a primary infection, but is usually an extension of an intesti
nal or hepatic source. Skin involvement around the anus is particularly
common: ultrasound should be used to exclude a perirectal abscess.
Except around the terminal ileum, where involvement may occur when
there is a caecal infection, amoebiasis seldom affects the small bowel.
This is helpful when trying to differentiate between amoebiasis, tuber
culosis and Crohn’s disease.
Whereever it may occur, a high level of suspicion is essential for the
diagnosis of an amoebic infection. A chest radiograph which shows an
elevated diaphragm on one side, with or without a pleural effusion, a
large, tender liver with abnormal ultrasonography, bowel obstruction
from a ’’tumour” with areas of colitis elsewhere, intussusception in small
1245
children, or a perianal fistula can all be the presenting evidence of amoe-

biasis. But of course, patients of any age may still appear with classical
amoebic dysentery and ultrasound may show a normal liver. Amoebiasis
can be very confusing!
SCHISTOSOMIASIS (BILHARZIA)
This infection with one or more of four different species of parasitic blood
flukes (trematodes) is one of the most common and widespread diseases
suffered by humanity. The life cycle o f the fluke requires warm water
and a specific snail, so the disease is only acquired in the tropics. If
brought back by travellers into colder climates, further spread of the in
fection is unlikely. Schistosomiasis is endemic in many tropical coun
tries: at least 200 million persons are infected, together with other pri
mates and many mammals. How much cross-infection occurs between
human and other species is debatable.
The life cycle is of clinical significance, and complex. Infection may
occur without the patient being aware that it has happened. It starts with
an infected snail, which, together with the schistosome sporocyst can tol
erate several dry weeks. The snail is normally in water which must never
fall below 15° C, and should be placid, stagnant or slow moving. Any fresh
water in the tropics, natural or artificial, may be part of the life-cycle.
Under the stimulus of sunlight, the snails release larval cercaria, which
penetrate the bather’s skin, unrecognized except perhaps for irritation and
erythema which may last for a few days - the "swimmer's itch". Often
this is thought to be "sunburn". Then the larvae take a 10-21 day mi
gration by way of the lymphatics and thoracic duct, the heart and the
lungs until the portal system is reached and maturation starts. Copulation
occurs only in the liver, where a pair of flukes may live 15-20 years or
more. The adults do not multiply in man but do not waste their time: de
pending on the species, one pair may produce from 300 to 3000 eggs per
day. These are swept away to their predestined site, e.g. for S. haemato
bium, the walls of the urinary bladder and ureters. This selective distri
bution explains the clinico-pathological disease patterns for each type of
schistosomiasis.
The flukes are strictly intravenous parasites and cause no clinical dis
eases while alive (if one can ignore all those ova). Dead worms embolize
and cause a granulomatous reaction. No organ escapes. Granulomas are
also caused by the ova. Most ova die and calcify, which is why organs
1246
TROPICAL DISEASES
appear to be calcified, for example a calcified bladder. Some ova cause

an acute allergic reaction: the whole series of events is very dependent
on many host factors, from re-infection rates, diet, and even differences
in the schistosomes. As a result, what happens in one country or region
and group of people may not happen elsewhere.
If the ova are not caught, to become granulomas, they leave the host
after ulcerating through the wall of the intestine or urinary tract, (de
pending on the species). This is another complex reaction. In fresh wa
ter the ova hatch and release miracidia which infect the host snail, thus
starting the cycle again.
There are many varieties of schistosomes, but only four which are par
ticularly important in man.
S. haematobium occurs throughout Africa and in Arabia, South West
Asia, and around the Mediterranean. The urinary tract and the portal sys
tem are mainly affected, but the lungs and colon do not escape, and the
central nervous system may occasionally be involved.
S. mansoni is also prevalent throughout Africa, particularly in the
north, in Arabia, and in the north of South America. It mainly affects the
colon, the portal system and the lungs, very rarely the central nervous
system.
S. japonicum is found mostly in Asia; in China and Japan, the Philip
pines, and other Pacific islands. It primarily affects the colon and small
intestine, the portal system and the lungs, rarely the central nervous sys
tem.
The fourth variety, S. intercalatum, is much less common and occurs
only in equatorial Africa, particularly Zaire, and affects the digestive tract
and the portal system. There is one other, S. mekongi, clinically similar
to S. japonicum, but found only in the Mekong river basin.
There is considerable variation in the distribution of the four main vari
eties with overlap causing combined infections. Re-infection is common.
The clinical diagnosis is confirmed microscopically by recognising the
characteristic ova, and by serological and skin tests. None indicate the
severity or extent of the disease, and many remain positive after suc
cessful treatment. Rectal biopsy may be necessary, because other labo
ratory examinations (e.g. of urine) may be unreliable. The clinical symp
toms are very variable, and may be acute or chronic, mild or severe. As
the disease becomes chronic, there will be the clinical results of portal
cirrhosis, such as oesophageal varices and chronic rectal bleeding (see
1247
Figure 4.
Acute schistosomiasis: the
Katayama stage. There are in
creased interstitial and vascular
markings in both lungs and mild hi
lar lymphadenopathy. (China)
below), together with bowel or urinary tract complications.
The Katayama syndrome

All varieties of schistosomiasis start with a similar reaction, known as
’’Katayama disease”. Patients who have been previously exposed to
schistosomes do not develop this syndrome, but those who have never
had schistosomiasis, and who have been exposed to infected water within
the previous 3-9 weeks, may present with a ”flu-like” illness. They al
most always complain of a fever and persistent cough. Questioning may
elucidate the recent history of skin irritation after swimming in fresh wa
ter (in the tropics). Patients often complain of headache, and rarely may
have meningeal and neurological symptoms. However, the majority will
be diagnosed clinically as having flu or bronchitis, except that almost
every patient will have a raised eosinophil peripheral count (20-60%).
The chest radiograph will show faintly increased vascular markings
throughout both lungs, with mild hilar and mediastinal lymphadenopa
thy (Fig. 4). All the findings are very non-specific. If a correct diagnosis
is made and treatment given at this stage, a few patients may then have
an acute allergic reaction to the dead larvae. Later, there may be calcifi
cation of the resulting granulomas, but in the vast majority the illness
improves after a few weeks even without treatment. The chest x-ray
clears and the original cause of the infection may have been overlooked.
What happens next will depend on the type of schistosome.
1248
TROPICAL DISEASES
a b
Figure 5. S.haematobium
a) The bladder is full, the ureters show strictures and dilatation.
b) After micturition the bladder is empty but strictures in the lower ureters cause
ureteric dilatation and delayed emptying. (Nigeria)
S. haematobium
Schistosomiasis haematobium mainly involves the urinary tract.
Haematuria may be the first clinical indication, apart from tiredness and
generalized ill health. All the early imaging findings are in the urinary
tract. Plain radiography at this stage is not helpful, and ultrasound is very
dependent on the skill of the observer. A contrast urogram may show
persistent filling of the lower segment of the ureters (Fig. 5). Careful ul
trasound scanning may show thickening and nodularity of the ureteric
walls. Next, the lower ureteric segment becomes dilated, due to con
striction within the bladder wall. These early changes, although mini
mal, are important because they can still be reversed by treatment.
In the next stage the lower ureters are shown by contrast urography or
ultrasound to be nodular, beaded or irregularly dilated. As these changes
progress, the dilatation may affect the whole ureter or be segmental, usu
ally most marked at 2-5 cm above the bladder. Multiple strictures and
dilatations then develop, always bilateral but seldom symmetrical (Fig.
6 a). At this stage, fine ureteric calcification may be seen radiographi-
cally and on ultrasound (Fig. 6 b). Later, these calcified areas coalesce
1249
Figure 6.
S. haematobium
a) Markedly dilated ureters with lower
third strictures. There is calcification
in the walls o f the bladder. (Nigeria)
b) This heavily calcified bladder has
contracted completely (arrowheads).
There is also calcification in the
ureters (arrows). (No contrast has
been used.) (Nigeria)
and the ureters appear "calcified", even along their full length.
The bladder changes progress in a similar way. First, on contrast cys
tography, there is "haziness" in the bladder outline, due to submucosal
oedema, then multiple small flat papillomas can be seen. Ultrasound will
demonstrate the early thickening of the bladder wall, then the papillomas
and the calcifications. Changes in the upper urinary tract only develop as
the ureteric obstruction increases. If there are renal abnormalities found
during what is thought to be the early stage of schistosomiasis, renal tu
berculosis must be excluded. Tuberculosis seldom causes calcification in
the ureter. After treatment for a tumour there may be a small localized
area of calcification in the bladder, a very different apperance.
1250
TROPICAL DISEASES
Figure 7. S. haematobium
a) A contrast cystogram showing reflux
up both ureters, which are stenosed d
and dilated irregularly. (Nigeria)
b) A contrast urogram in the late stages o f schistosomiasis. There is bilateral hy
dronephrosis and hydroureter, with irregular strictures in the lower thirds o f the
ureters. (Egypt)
c) A large bladder calculus and a slightly smaller calculus in the lower end o f the left
ureter. There is the same calcification in the bladder wall. (Egypt)
d) A contrast urogram showing a large malignant tumour in the bladder, displacing
the contrast to the left. The bladder walls are calcified, the ureters are dilated and
stenosed, and there is delayed emptying. (Nigeria)
1251
If schistostomiasis is untreated, the ureteric obstruction and nodular

changes will increase, there may be marked cystitis and patchy ureteric
and bladder calcification visible radiographically. On ultrasound, the
bladder walls will be thickened and may be so heavily calcified that they
appear solid. However, because the calcification is in the ova which lie
in the submucosa, in the early stages this does not alter the ability of the
bladder to distend or empty(Fig. 5 a, b; Fig. 6 b). CT will show similar
calcified ova in the perirectal and periureteric tissues, but this has no clin
ical significance, and there is no indication for this examination.
Treatment may result in improvement and the calcification may be less
visible as the ova are excreted. Eventually, the ureters become unalter
ably fibrosed, stenosed and/or dilated, there is reflux from the bladder,
and the end-result is kidney infection with severe hydronephrosis (Fig.
7 a, b). However, as already noted, if there is evidence of kidney in
volvement early in the patient’s illness, tuberculosis is much more likely
than schistosomiasis, which is not primarily a renal disease.
Because of the repeated urinary infection, bladder calculi and occa
sionally ureteric calculi may be found (Fig. 7 c, d). There is close epi
demiological association between chronic S. haematobium infection and
carcinoma of the bladder, so any localized thickening of the bladder wall,
or a mass within the bladder, should cause suspicion of malignancy. This
should lead to cystoscopy and biopsy to establish the diagnosis, unless
ultrasound has shown definite tumour invasion of the bladder wall.
Ultrasound, because there is no ionising radiation, has an important
role in the diagnosis and management of schistosomiasis. For S. haema
tobium infections, ultrasound can be used in epidemiological surveys
(recording the results with the WHO protocol) and to assess the effects
of treatment. Particularly, the state of the ureters and bladder, and later,
the degree of hydronephrosis can be observed. The eventual fibrotic (hy
perechoic) changes in the kidney will indicate that the renal damage is
irreversible.
However, it must be stressed that in the early stages of schistosomia
sis, both experience and high quality ultrasound images are essential if
the assessment is to be reliable. A negative ultrasound scan does not ex
clude early schistosomiasis (nor does a normal contrast urogram) and at
no stage can ultrasound alone assess renal function.
CT and MR can demonstrate almost all the pathological changes, but
for practical purposes ultrasound is as efficient, less expensive, available
1252
TROPICAL DISEASES
in the field and without any hazard.

S. haematobium rarely can affect the colon and central nervous sys
tem, but is almost always associated with urinary tract infection.
Figure 8.
S. mansoni
a) Multiple mucosal polyps in the
descending and sigmoid colon
(barium enema). (Egypt)
b) Severe sigmoid polyposis coa
lescing into a mass (barium en
ema) (Egypt)
1253
S. Mansoni
The earliest findings are in the colon, starting with oedema and mucosal
ulceration, followed by loss of haustration. These changes can be demon
strated with a barium enema or ultrasound, and if untreated will progress
to multiple mucosal polyps, usually in the rectum, sigmoid or descend
ing colon (Fig. 8). The polyps are very fragile, on a short stalk, bleed eas
ily, and may cause intussusception or obstruction. Where there is com
bined infection with S. haematobium and S. mansoni, polyps are even
more common. Severe schistosomiasis can cause extensive colonic ul
ceration leading eventually to pericolic inflammation, with strictures. A
solitary bilharzioma, resembling an amoeboma, may occur in either the
large or small bowel. In teenage patients particularly, there can be se
vere enteritis. S. Mansoni infection does not seem to be associated with
an increased risk of cancer, except perhaps in the rectum. As the infec
tion continues, calcification may be seen, particularly around the rectum,
but often in multiple areas throughout the length of the colon. It is asymp
tomatic and usually of no significance. As occurs in the bladder, the cal
cification is in ova rather than in fibrotic scars. Neither in the bowel or
the bladder does the extent of calcification indicate the severity or ac
tivity of infection. The end-result of the S. mansoni infection can be a
smooth colon, very similar to the end-result of ulcerative colitis and caus
ing similar clinical disabilities.
S. mansoni can occasionally affect the small bowel, and even the blad
der. In the duodenum there can be quite marked oedema, and the symp
toms may resemble peptic ulceration.
S. Japonicum
S. japonicum can be an acute or chronic infection which mainly affects
the small bowel, but also the descending and sigmoid colon, and the rec
tum. These are the parts of the gut with venous drainage into the inferior
mesenteric vein. The ova cause wide-spread submucosal granulomas.
On ultrasound, and particularly contrast radiography, there is oedema of
the bowel with a cobble-stone appearance of the mucosa (Fig. 9).
Eventually, the bowel mucosa will become coarse and irregular, partic
ularly in the upper small bowel. There may be areas of dilatation and de
creased motility with excess mucus. A retroperitoneal inflammatory
granuloma has been reported (and can also occur in S. haematobium). S.
japonicum has also been known to cause intestinal polyps.
1254
TROPICAL DISEASES
Figure 9.
S. japonicum
a) Oedema o f the duodenal loop
(barium meal) (China)
b) Early colitis, especially in the
descending colon (barium
enema). (China)
a
The lungs in
schistosomiasis
The pulmonary radiographic
findings vary with the type of
schistosome, although in the
stage of acute infection all
can cause the Katayama syn
drome if the patient has never
previously had schistosomia
sis (see above). The end-re-
sult of this first stage is al
ways a normal chest radio
graph.
In 5. haematobium infec-
tion the majority of chest ra
diographs will be normal, in
spite of the fact that histolo
gical sections will show mul
tiple ova in about 50% of all cases. A few elderly patients may develop
generalised, symmetrical interstitial fibrosis, which histologically is due
to numerous peribronchial ova and associated diffuse fibrosis. Emp
hysema and clinical cor pulmonale are uncommon, but may develop later
in a few patients.
1255
Figure 10.
S. mansoni
Aneurysmal dilatation o f the main
pulmonary arteries and pulmonary
conus: there is decreased peripheral
lung vasculature. (Egypt)
In S. mansoni infection the lung changes are more important. The ova
may embolize and penetrate the pulmonary arterioles, causing a localised
inflammatory reaction. Some cause distinct bilharziomas, but in the ma
jority of patients the arterioles narrow and many are obliterated. This
causes pulmonary artery hypertension. Radiographically the main pul
monary arteries become prominent, but seldom symmetrically. The pe
ripheral vascular markings decrease, particularly at the lung bases.
Because there may be ova damaging the pulmonary artery walls, the main
pulmonary arteries may become aneurysmal, especially the main pul
monary trunk (Fig. 10). Apart from this excessive and asymmetrical di
latation, there is nothing to distinguish the radiographic changes due to
schistosomiasis from other causes of pulmonary fibrosis and hyperten
sion. It is unlikely that the calcified granulomas would be mistaken for
miliary tuberculosis, varicella pneumonia or histoplasmosis.
The liver in schistosomiasis

Although the changes in the urinary tract and bowel which result from
schistosomiasis are both clinically and radiologically important, it is the
damage which the organisms do to the liver which is more likely to be
fatal in the majority of cases.
All schistosomes cause severe liver damage. The ova obstruct and pen
etrate the small portal veins, and the surrounding inflammatory reaction
causes periportal fibrosis, resulting in presinusoidal blockage and portal
hypertension. This occurs long before there is damage to liver function.
1256
TROPICAL DISEASES
Figure 11.
S. mansoni
a) Ultrasound. Typical appearance
o f hepatic periportal fibrosis
(arrowheads). (Nigeria)
b) Atrophy o f the right lobe o f the
liver and periportal fibrosis
(Brazil; Courtesy o f Professor G.
Cerri)
Clinically, the liver and spleen enlarge in the early stages. The portal
pressure rises, but ascites does not immediately develop and hae-
matemesis is unlikely. It is not until later, as the fibrosis increases, that
varices develop: a collateral circulation is opened, and there is ascites
with all the clinical sequelae. (Fig. 13 a)
Schistosomal cirrhosis is readily recognized on ultrasound and CT:
both show the periportal fibrosis. The earliest stages seen on ultrasound
are diffuse, scattered echogenic areas, usually either rounded, in sheets
or in bands (Fig. 11 a). Characteristically, there are faint, central sonolu
cent areas. The portal tract is thickened by fibrosis, and it is common to
find atrophy of the right lobe of the liver, with associated hypertrophy of
the left lobe (Fig. 11 b and Fig. 12 d). There is a standard WHO proto
col to grade the degree of periportal fibrosis, which should be used to as
sess progress and for epidemiological surveys.
Figure 12. CT scanning o f S. japonicuma

a) Subcapsular and interlobular calcification in the liver. (China)
b) Interstitial calcification in the liver (arrows). (China)
c) Calcification in the wall o f the portal vein and splenic vein. (China)
d) Atrophy o f the right lobe o f the liver with enlargement o f the left and caudate lobes.
(China)
As the cirrhosis progresses, the portal, splenic and mesenteric veins

are always dilated, the splenic veins particularly. Doppler ultrasound
does not show any reduced flow velocity in the portal system. The he
patic artery is reduced in diameter, the hepatic veins are unchanged. Both
ultrasound and CT images during the early stages might be mistaken for
metastases, but the schistosomal changes are more uniformly distributed.
As the fibrosis increases, the spleen enlarges. It usually retains a homo
geneous pattern, unless there are siderotic nodules causing a more nodu
lar ultrasound appearance. CT can demonstrate calcification in the liver
capsule, and less commonly in the portal, splenic and mesenteric veins
(Fig. 12). There are seldom any biliary polyps, but there can be thicken
ing of the wall of the gallbladder and there may be fibrosis eventually.
There is close correlation between the ultrasound findings and the de
gree of portal hypertension. Oesophageal and gastric varices result in
1258
TROPICAL DISEASES
Figure 13. The results o f schistosomal

cirrhosis, leading to portal hypertension
and collateral circulation.
a). A barium swallow shows extensive с
oesophageal varices. (Egypt)
b). Early selective angiography showing an enlarged spleen with dilated splenic and
portal veins. (Egypt)
c). Later stage o f angiography, confirming the markedly dilated splenic and portal
system, with collaterals and varices (arrow) at the gastric cardia. (Egypt)
haemorrhage as the many collaterals develop. Angiography may be nec

essary if surgery is contemplated (Fig. 13), but ultrasound, including
Doppler flow studies, is helpful in monitoring treatment and to exclude
other causes of portal hypertension.
Schistosomiasis is a widespread, slow, chronic disease which is pre
ventable and easily curable in the early stages. If allowed to progress, or
if re-infection occurs continuously, there will be irreversible changes in
the urinary tract, the bowel, the lungs and, most importantly, the liver.
Death seldom occurs in the early stages, but in many parts of the world
every one is so familiar with the symptoms that their significance is ig
nored. In all types of schistosomiasis there is considerable morbidity and
mortality in the later stages.
1259
HYDATID DISEASE - ECHINOCOCCOSIS

This is a very ancient disease, known to the Greeks and described
throughout the historical literature of medicine. Hydatid cysts are per
haps more often seen in temperate climates than in the tropics, and par
ticularly where there are sheep and dogs. In the most common variety,
due to E. granulosus, the primary hosts are carnivorous, e.g the dog, while
herbivora, e.g. sheep, cattle and pigs (swine) serve as intermediate hosts.
In the less common infection, with E. multilocularis, the wolf, fox, cat
and dog are the principal hosts and reindeer, moose and rodents are the
intermediate carriers. There are other species which are pathogenic for
humans: E. vogeli, found in central and tropical South America, and E.
oligarthrus, which is of questionable pathogenecity. Their clinical and
imaging presentation is similar to that of E. granulosus. Humans are ac
cidental intermediate hosts for all species. The parasite is a tiny tape worm
only 3-6 mm in length, but it may occur in hundreds or thousands, par
ticularly in the small intestine of dogs. Man becomes infected by close
contact with dogs or by ingesting food, water or soil which has been con
taminated by faeces. Children and agricultural workers are the most likely
to be infected, but uncooked food may also transmit the parasite.
When the ova have been ingested by the intermediate host, the walls
of the ova are destroyed and the larvae escape, to migrate through the
mesenteric venules and lymphatics. The majority are filtered out by the
liver, but some will pass through to the right side of the heart and then
to the lungs. As a result, the liver and lungs are the organs most com
monly infected, but larvae also may lodge anywhere in the body, in
cluding soft tissues and bone. When the larva is lodged in any tissue, it
develops within seven days into a tiny cyst, (or, if£. multilocularis, mul
tiple cysts) which steadily grows over a period of years at an average rate
of about 1-3 cm annually. Cysts grow more quickly in lungs than in the
liver, even more slowly in bones. The cysts may remain clinically silent
for many years, depending very much on the anatomical site. Each
hydatid cyst has two walls (the ecto-cyst and the germinal membrane,
the endo-cyst). A third wall, the pericyst is formed as the cyst grows,
causes an inflammatory reaction and compresses the surrounding host
tissue. Within the cyst are hydatid fluid and brood capsules (scolices),
which can be seen radiographically and with ultrasound as ’’sand” at the
bottom of the cyst.
1260
Figure 14.
Ultrasound o f
hydatid cysts.
(Tunisia)
a) Uncomplicated
cyst. Stage I.
(Liver)
b) Uncomplicated
cyst with hydatid
sand. Stage I-U.
(Liver)
c) Multivesicular
cyst in right kid
ney. Stage III.
d) Heterogenous hy
datid cyst, a solid
mass. Stage IV.
(Liver)
e) The pathogno
monic appear
ance o f mem
branes within the
cyst. (Liver)
f) Heavily calcified
old hydatid cyst.
Stage V. (Liver)
The two major species of hydatid infection are E. granulosus (uniloc

ular) and E. multilocularis (multilocular or alveolar). The latter is more
serious and much less easily cured, but fortunately, less prevalent. For
both types of infection, symptoms are usually the result of the pressure
caused as the cysts enlarge, so that the clinical presentation may be cough,
hemoptysis abdominal pain or mass, a large liver, jaundice, ascites,
headache, bone pain or fracture. Many hydatid cysts are a chance find
ing on a chest radiograph or abdominal scan. Epidemiological surveys
with ultrasound have been effective in high risk populations.
Occasionally, internal rupture of the cyst, usually following trauma, may
cause an acute illness.
Hydatid disease of the liver (E. granulosus)

Most hydatid cysts in the liver cause no symptoms for a long time. They
are usually multiple and the majority are in the right lobe of the liver.
The cysts may rupture spontaneously into the biliary tract, into the peri
toneal cavity or upwards into the chest, including the pericardium. Cysts
will not be demonstrated in the liver on plain radiographs until there is
some peripheral calcification, which usually occurs after 5-10 years.
With ultrasound, CT or MR, they are commonly demonstrated as sim
ple, well-defined cysts in which the hydatid sand can usually be seen.
However, the scanning appearances depend on the maturity and health
of the cyst, so that five different stages may be recognized in the liver
and elsewhere in the abdomen: the stages are similar when cysts are seen
in chest radiographs (Fig. 14).
Stage I. A cyst with clear fluid. Ultrasound shows either a small
punched-out space without clear walls or an anechoic cyst with back wall
enhancement. The cyst fluid is clearly defined. The cyst walls vary in
thickness, and segments of localised thickening are a helpful diagnostic
sign of hydatid disease. Most cysts are round, unless situated at the pe
riphery of the liver (or spleen) where the cyst may follow the parietal
outline. The diameter of the cyst may be from 1 cm to 20 cm.
Stage II. The fluid contents remain clearly defined but the cyst is less
well rounded, perhaps because of lowered intracystic pressure. Sections
of the cyst wall may have separated, either bulging just outside or into
the cyst or floating freely within it. A floating membrane is another im
portant diagnostic sign.
1262
TROPICAL DISEASES
Stage III. The fluid is now divided by septa, which are often quite thick
and result in oval or rounded spaces within the well- defined surround
ing cyst. There will be enhanced back wall echoes, and there may be so
many septa that there is a coarse net appearance. Whenever the cyst mem
branes are detached, the internal spaces are less well rounded.
Stage IV. A well-defined cyst is not seen. Instead, there is a roughly
rounded mass with an irregular outline. There are three different ultra
sound patterns:
(a)Hypoechoic, with some internal irregular echoes. This indicates an
infected, multiseptate cyst.
(b) Hyperechoic. A solid "mass" without back wall shadowing.
(c) An intermediate, mixed pattern, about half hypoechoic but with nodu
lar hyperechoic clusters.
The stage IV patterns are not always easily recognised as being due to
hydatid disease. It is important to search carefully for the linear or band-
pattem of the surrounding membranes, for the hyperechoic contour, per
haps with some acoustic shadowing, and for fluid in intra- or extracys-
tic spaces. Another characteristic appearance is variation of the echoes
in different areas within the mass. But perhaps most helpful in diagno
sis is the finding of another hepatic, or extrahepatic cyst at a different
stage. Hydatid cysts (of E. granulosus) are seldom solitary and all are
not likely to be at the same stage of development.
Stage V. A thick-walled, unusually hyperechoic cyst, causing a well-
defined, cone-shaped acoustic shadow. Cysts vary so much in size that
while small cysts may be imaged completely, very large cysts may only
be seen in part, usually the arching image from the thick front wall. The
full outline must be scanned.
In older, or damaged ( E. granulosus) cysts, hyperechoic calcification
may be seen within the cyst walls. When calcification is heavy, it may
indicate severe damage or even death of the cyst. Separation of the in
ternal germinal layer occurs within 48 hours of the appropriate medical
treatment, but may also be seen as a result of injury, usually from indi
rect trauma to the liver or other organs. With scanning it is possible to
recognize the cysts at an early stage, and show that there are multiple
cysts at different stages of development in most patients. Although the
accurate diagnosis of hydatid disease is easy when there are multiple typ
ical cysts, it is sometimes difficult to differentiate a solitary cyst from a
hepatoma. In some parts of the world hepatomas are common and also
1263
Figure 15. CT o f hydatid cyst.

a) Typical multiseptate hydatid cyst in the liver. (Tunisia)
b) Large hydatid liver cyst with membranes separated to give the "double wall"
appearance. Stage II. (China)
c) Multiple hydatid cysts o f the liver and spleen o f different sizes. (Tunisia; courtesy o f
Professor M. Ben Cheikh)
d) Old, thick-walled hydatid cyst in the liver. Stage V. (Tunisia; courtesy o f Professor
M. Ben Cheikh)
e) Multiple cysts in the peritoneum following rupture o f a hepatic hydatid cyst. (China)
f) Partially calcified hydatid cyst with detached membranes and increased density
after oral drug therapy. (Tunisia)
1264
TROPICAL DISEASES
Figure 16. Hydatid cysts in the lungs.

a) A large hydatid cyst in the right
lower lobe, which has ruptured into
a bronchus and now contains air
and fluid, on which the membrane
can be seen. There is a right
pleural effusion. (Tunisia; courtesy
o f Professor J. Daghfous)
b) A largefluid-filled hydatid cyst in the e
left lung, with air between the mem
branes: the "crescent sign" (arrows). (Tunisia; courtesy o f Professor J. Daghfous)
c) Two (perhaps more) hydatid cysts in the lungs o f a 4-year-old boy. (Tunisia)
d) Multiple hydatid cysts (eight or more) in the lungs and mediastinum. Some are fu ll
offluid, others have ruptured into the bronchi. (Tunisia; courtesy o f Professor J.
Daghfous)
e) A large hydatid cyst close to the right side o f the mediastinum. (China)
1265
present as large irregular echogenic masses with well-defined margins.

Other hepatomas are more homogeneous and may resemble a metastasis.
When infected, a hydatid cyst cannot be distinguished from an abscess or
a hematoma and the correct diagnosis cannot be made unless there are other
recogniseable hydatid cysts elsewhere, or well-defined septa can be recog
nised within the cyst.
There are some differences between the ultrasound and the CT findings,
although the same 5 stages can be seen (Fig. 15). In particular, CT may
not demonstrate the walls of the cyst so clearly, unless the surrounding
liver is contrast-enhanced. Most cyst walls do not enhance, but a few may
and show higher attenuation. CT will show clearly the daughter cysts
within the main (mother) cyst. They are usually at the cyst periphery,
smaller and with lower attenuation. When dislodged, the daughter cysts
float freely within the mother cyst, changing position when the patient
moves. This is a useful diagnostic sign and, if there is any doubt, it is worth
scanning the patient in different positions to demonstrate this movement.
CT can clearly demonstrate partial separation of the cyst membranes,
causing a "double wall”, or show the ribbon appearance of a separated
germinal membrane. When curled or shrunken, a membrane may be
shown floating on the fluid contents of the cyst, described as the ap
pearance of a water-lily on a pond. (This is an equally important sign
when seen on an erect chest radiograph.) The floating membrane is an
other diagnostic finding, which is unlikely to be mimicked by any other
condition.
On MRI the signal intensity of hydatid cysts is the same as any other
similar cyst, except that the rim is of lower intensity on both T1 and T2
weighted images.
Hydatid disease in the lungs

A chest radiograph is always required when a hydatid cyst is suspected
in the liver or peritoneal cavity (Figs. 16, 17). Most lung cysts are clin
ically silent and present as well-defined circular densities in any part of
the lung or mediastinum. Pulmonary hydatid cysts are very seldom cal
cified. As already noted, some cysts have an internal fluid level, and the
membranes and daughter cysts may be seen floating within the cyst, one
of the few pathognomonic signs in radiology. If the outer membrane is
broken, there may be a thin layer of air between the inner and outer walls.
If all the fluid has been coughed up, the cyst may resemble a thin-walled
1266
TROPICAL DISEASES
Figure 17.
a) CT scan o f multiple pulmonary hy
datid cysts. (Tunisia)
b) CT scan o f a partly collapsed me
diastinal hydatid cyst. The folded
membranes are clearly shown.
(Tunisia; courtesy o f Professor M.
Ben Cheikh)
tuberculous cavity. When secondarily infected, the appearance is the

same as any lung abscess. When entirely filled with fluid, or pus, the cyst
can resemble a solid tumour. However, hydatid cysts are seldom soli
tary, nor are they usually at the same stage of development. Nevertheless,
there may be so many cysts in the lungs that they resemble metastases.
Rupture of the cyst into the pericardium or pleural cavity can be a dra
matic event, and the patient may be severely ill (Fig. 17). Care should
be used to avoid spillage when aspirating a pulmonary cyst.
Skeletal hydatid disease (E. granulosus)

The recognition of hydatid disease in any bone requires a high level of
suspicion, unless the patient is known to have cysts elsewhere or comes
from an endemic area. Confusion with any other osteomyelitis is the
usual error, but a tumour may also be suspected (Fig. 18).
In the long bones, hydatid cysts first appear as ill-defined, thin-walled
radiolucent areas, usually near the epiphyseal end of the bone. They are
1267
Figure 18.
a) Posterior mediastinal hydatid cyst, af
fecting the vertebral body and trans
verse process. (Tunisia)
b) Destruction o f the right side o f the
pelvis and the right fem ur by hydatid
disease. (Tunisia)
c) CT scan o f a hydatid cyst in the gluteal
muscles. (Tunisia; courtesy o f
Professor M. Ben Cheikh)
often multi-loculated, without a sharp line of demarcation. Later, well-

defined cystic areas will develop, the shape affected by the position
within the bone. CT is helpful because it can provide better definition,
especially when the cyst is in the vertebrae. The cyst may penetrate
through the cortex and periosteum, producing a localised abscess. If there
is a periosteal reaction, this is unlikely to be due to the hydatid disease
alone and almost always indicates superimposed infection. Hydatid cysts
may involve any o f the long bones, the pelvis, skull, or spine. Particularly
in the pelvis it is difficult to differentiate the multilocular alveolar cysts
from bone tumours (see below). With any variety of hydatid disease, the
destruction may become very extensive. It may be mistaken for
myeloma, metastatic disease, primary bone tumours, fibrous dysplasia,
other bone cysts, as well as tuberculosis or other osteomyelitis. A chest
radiograph and a liver scan are essential. Aspiration is not without mi
nor risk of a mild allergic reaction if any of the cyst contents are spilled,
but can be safely performed.
1268
TROPICAL DISEASES
Figure 19.
Cerebral hydatid cysts. CT scan.
(Tunisia)
(Previous surgery with relapse)
Hydatid disease in other locations (E. granulosus)

Hydatid cysts can develop in the spleen, pancreas, kidneys, or the peri
toneal cavity, as well as in other parts of the body. In the brain they may
present clinically in the same way as any other space-occupying lesion
(Fig. 19). The walls of some cysts will calcify and be clearly visible on
plain radiography, a very helpful diagnostic sign. However, CT or MRI
are essential to establish the location and number of cysts within the skull
because many cannot be seen on plain radiographs. Hydatid cysts are
avascular and do not blush on cerebral angiography.
Alveolar hydatid disease (E. multilocularis)

The alveolar type o f disease (£. multilocularis) is less common than E.
granulosus and is most often seen in colder climates, e.g. North America,
Central and North Eastern Europe, Russia, Siberia, Australasia.
Although it also causes a chronic granulomatous reaction, there are many
smaller cysts (like a bunch of grapes) and the whole process is more de
structive and much less easily cured than E. granulosus. Clinically, E.
multilocularis infections differ from E. granulosus only because of lo
cal multiplicity and a more malignant course. Alveolar hydatidosis is
usually chronic, afebrile, and almost always fatal if aggressive therapy
1269
Figure 20.
Alveolar (E. multilocularis)
hydatid cyst o f the liver, with fine
punctate calcification and
multiple small cysts. (China)
is not available. In some ways the clinical progress may resemble that
caused by E. granulosus, for example, by rupture through the diaphragm
from the liver with resulting pleural and pulmonary disease. But in most
cases the imaging appearances of E. multilocularis infections are differ
ent and the clinical course more persistent, almost malignant in failure
to respond, in recurrrence and in outcome.
Alveolar hydatid disease produces a mass-like infiltrating lesion with
out well-defined borders in almost all organs or tissues, including bone.
Alveolar hydatid disease o f the liver

In the liver (or kidney) it may be possible to demonstrate multiple small
calcifications in the hydatid mass on plain radiography: they are usually
clustered and characteristic (Fig. 20). But scanning is much more reli
able. On CT in the early stages, there are low density masses, without
any cystic appearance, and there is no contrast enhancement. Any calci
fication is nodular or amorphous, quite unlike the ring or linear calcifi
cation of E. granulosus.
MRI of early alveolar echinococcosis is a little less effective than CT
in establishing the exact diagnosis, because such small masses, less than
2 cm, may not be clearly demonstrated and microcalcification will not
be seen. However, the larger masses caused by the multiple, clustered
cysts and surrounding fibrosis are easily recognised with a low signal ra
tio on T1 and T2 weighted images. (Occasionally there may be a higher
signal on T2-images.) Indeed, the T2 weighted MR-images usually show
the outline and extension into the liver and surrounding tissues more ac
curately than is seen with CT. When there is central necrosis, the gen
eral pattern, of cysts surrounded by an irregular boundry with a low sig-
1270
TROPICAL DISEASES
nal intensity, is easily recognised by MRI.

Similarly, the ultrasound appearance of alveolar hydatid disease of the
liver is that of a non-specific pseudotumour, a mass of variable size and
shape. Ultrasound may show cystic areas and internal calcification, quite
unlike the peripheral calcification of E. granulosus. The pressure of the
echinococcal mass may cause dilatation of the biliary tract (better seen
with ultrasound and CT than MRI) or narrowing of the portal or hepatic
veins, even of the inferior vena cava.
Differentiation of alveolar hydatid disease from malignancy in the liver
(or indeed in kidney, bone or elsewhere) can be very difficult and biopsy
is necessary to confirm the diagnosis, especially when the punctate cal
cification is seen. Unlike E. granulosus infections, there are seldom mul
tiple sites involved.
Alveolar hydatid infection of bone is a very difficult diagnostic prob
lem. The natural course of the disease is very unpredictable and may vary
from rapid local spread, to chronic, slowly invasive destruction.
Sometimes diagnostic imaging is a better way to watch progress and as
sess the whole situation than clinical impression.
Interventional procedures in hydatid disease

Intervention may be requested in either form of hydatid disease, but par
ticularly for the more common E. granulosus, when biopsy or cyst aspi
ration is required or systemic therapy has failed. Therapeutic success has
followed ultrasound guided aspiration, utilising various drugs (e.g. hy
pertonic sodium chloride, alcohol) injected after removal of all or part
of the cyst contents. Some advocate irrigation of the cyst before injec
tion, others find this unnecessary. In the past, aspiration was regarded
with anxiety, mainly from fear that spillage would cause severe ana
phylactic shock or metastatic spread. In the recent series reported, there
have not yet been any complications. Modem equipment and techniques
seem to have made it safe, except for an occasional, moderate, brief al
lergic reaction with fever, which is easily controlled medically. There is
no contraindication to repeated aspirations. The success of aspiration and
the results do depend on the location of the cysts, e.g. intraperitoneal
cysts respond more quickly than hepatic. Progress can be assessed with
ultrasound, showing decrease in size, change in shape, less posterior wall
enhancement and increased echogenicity (or increased CT density).
1271
CHAGAS' DISEASE:
AMERICAN TRYPANOSOMIASIS
This infection, due to Trypanosoma cruzi, is confined to the Americas,
from Texas to Argentina, and is particularly common in rural areas of
Brazil, Argentina, Uruguay, Chile and Venezuela. Children and young
adults are most often infected, because the trypanosome is transmitted
by reduviid or triatomine bugs, which bite at night. These bugs com
monly live in the mud or adobe walls of huts or stables, and in homes
which have cracked walls through which they can enter. At least one
hundred and fifty animal species carry the organisms, but particularly
domestic dogs and cats, pigs, monkeys, opossums and armadillos. The
clinical infection can be acute, subacute or chronic. It starts from the orig
inal bite as the trypanosomes spread through the lymphatics to the lymph
nodes (7-14 days) and then into the blood stream 5 days later. T. cruzi
multiplies within the host cell and the disease is extremely difficult to
diagnose and treat: almost any part of the body may be affected, but par
ticularly smooth and striated muscle, glial and nerve cells. The try
panosomes may be found in the blood for the first 6 weeks o f the acute
stage, but not thereafter. The characteristic lesion is a Chagoma, a fi
brotic encapsulated focus which can develop at the site of inoculation or
elsewhere. It is particularly important in the heart and central nervous
system.
Apart from the acute and chronic phases, there is an uncommon sub
acute form affecting the heart, in which there are large numbers of the
parasites in the peripheral blood and in the cardiac tissues. It is likely that
there is also a latent phase, because millions of people in the endemic ar
eas are known to have been infected yet do not show clinical signs of the
disease. Careful electrocardiography and oesophageal motility studies
suggest that although the disease is clinically silent, it is still active and
capable of further progression.
The heart in Chaga’s disease

T. cruzi infection results in a multi-focal myocarditis, causing cardiac
enlargement and decreased cardiac pulsation. The findings on imaging
are indistinguishable from any other myocarditis (Fig. 21). The acute
stage usually resolves within a few weeks and goes on to a latent phase
(which can occur without any previous clinical illness). Eventually, there
may be progressive heart failure, but in some patients there is acute bi ven-
1272
TROPICAL DISEASES
Figure 21.
Chaga's cardiomyopathy, MRI. The
Tl-weighted, postgadolinium en
hanced image shows patchy areas of
inflammation in the cardiac muscle.
(Brazil)
tricular failure, causing dramatic and sudden death in an apparently

healthy individual.
The gastrointestinal tract in Chaga’s disease

The oesophagus and colon are the other organs particularly affected in
the chronic stage. In both the result is motor dysfunction and eventually
denervation, causing decompensation and dilatation, and, eventually,
stasis. After a phase in which there is abnormal contraction and incoor
dination, the oesophagus becomes enormously dilated and can be rec
ognized on plain radiographs of the chest, or on contrast studies. There
is often a large residual food content, because of the lack of propulsive
peristalsis (Fig. 22).
The stomach and small intestine may be involved, resulting in megas
tomach or megaduodenum, but megacolon is more common. There will
be chronic constipation, the bowel emptying incompletely and irregu
larly at intervals of days or even months. There is often impaction and
obstruction due to desiccation of the bowel contents. As the bowel be
comes more atonic and dilated, there may be sigmoid volvulus. Barium
or other contrast enemas will show an enormously dilated large bowel
with poor ability to empty (Fig. 23). The mucosa may be abnormal be
cause of the retained contents. In a few cases there may be some parts of
the colon where denervation is not complete and short segments remain
comparatively normal.
In the later stages of Chaga’s disease, the imaging diagnosis is not dif
ficult. There are few diseases which cause such huge megacolon and
1273
a, b
Figure 22.
The changes in the oesophagus in
Chaga 's disease. (Brazil)
a) An erect contrast barium swallow
shows a normal oesophagus with
normal peristalsis.
b) When supine, the same patient has
tertiary oesophageal contractions.
c) In the intermediate stage, the
oesophagus is dilated, the gastro-
oesophageal region is narowed.
This resembles achalasia.
d) In the advanced stage, the
oesophagus is elongated and
grossly dilated, with a flu id level
and retainedfood.
mega-oesophagus. The retained liquid and food may obscure the devel
opment of oesophageal carcinoma (Fig. 24), which may infiltrate the wall
and allows rupture of the contents into the mediastinum, leading to ab
scess formation. Although the abnormalities on chest radiographs or me-
1274
TROPICAL DISEASES
Figure 23.
Chaga's disease, (barium enema).
Megacolon with dilatation and gross
elongation. The sigmoid colon reaches
into the upper abdomen. Obstruction
due to volvulus is very likely to occur
at this stage.
b
Figure 24. Chaga’s disease
a) An air-contrast examination shows a small tumour
in the mid third o f the oesophagus. It is essential to
empty as much o f the contents o f a mega-oesopha
gus as possible, before doing the contrast examina
tion.
b) The CT scan o f the same patient confirms the thick
ening o f the oesophageal wall and that the tumour
has not spread into the mediastinum.
(Allfigures o f Chaga's disease - courtesy o f Professor
a G. Cerri, Brazil).
1275
diastinal scanning may be obvious, clinically the leakage may be sur

prisingly silent. The cardiac enlargement does not have specific charac
teristics. The problem with Chagas' disease, particularly for the patient,
is that it remains silent for many years. Patients whit asymtomatic
megaoesophagus may present only cough and then a chest radiography
is usually indicated. Widening of the upper mediastinum, especially on
the right, may be seen, but only if the patient had a recent meal. The lat
eral view will show anterior displacement o f the trachea as responsible
for the “irritating” cough and very seldom the “regurgitation” coughing.
TROPICAL BOWEL INFESTATIONS AND

INFECTIONS
A wide variety of parasites cause gastrointestinal disease. Many are clin
ically unrecognized until their later stages, and in some societies their
effects are regarded by the patient as a normal fact of life. Other infec
tions present acutely, without any preceding chronic symptomatology.
Almost all the clinically important intestinal parasites occur worldwide
and the number of patients infected is almost incomprehensible. Parasitic
infection should be considered as one of the causes of chronic ill health
in any patient living in or coming from the tropics, or indeed, from any
area where there is malnutrition or substandard living conditions. The
clinical presentation may vary from an irritating chronic cough to acute
intestinal obstruction: no age is exempt, but children are particularly af
flicted.
Ascariasis
The Nematode round worm, Ascaris lumbricoides, (alone or occasion
ally together with A. suum) probably infects 25% of the world's popula
tion, but in the tropics the infection rate may be as high as 90% in some
populations. This is not surprising, because during a busy period o f 6-12
months, one (very) fertile female worm can produce up to 200 000 ova
every day! This bounty is acquired by humanity from contaminated food,
water and soil, and re-infection is common. The worm is most frequently
found in patients aged from 1-15 years and no intermediate host is
needed. Clinically there may be no symptoms, or there may be ill health,
vague abdominal pain, colic or acute obstruction. In children, ascaris are
one of the commonest causes of jaundice.
1276
TROPICAL DISEASES
Figure 25. Ascariasis

a) Multiple worms in the right lower abdomen o f a child, outlined by gas and fa e
cal content in the bowel. (Nigeria)
b) Ultrasound scan o f ascaris in the cystic duct and the gallbladder, which is di
lated. (Brazil; courtesy o f Professor J. Cerri)
c, d) Worms shown during gastrointestinal barium studies. Most o f the worms have in
gested barium, (c = Pakistan; d = China)
In the acute stage there may be fever, cough, even haemoptysis or

chronic recurrent "bronchitis”, symptoms for which the possibility of a
worm infection is not even considered unless a high peripheral eos-
inophilia provides a clue to the correct diagnosis. Curing a cough with an
antihelmintic always surprises clinicians! A chest radiograph may be very
non-specific, but in a few patients there may be transient, ill-defined, soft
1277
and asymmetrical densities around the larvae as they pass through the
lungs. Some may progress to bronchopneumonia, and if an adult worm
has been regurgitated and inhaled, there may be atelectasis or lobar pneu
monia.
The worms may be visible on a plain radiograph of the abdomen, seen
as a coiled, hazy indistinct "ball of wool" when the worms are outlined
by bowel gas (Fig. 25 a). But ultrasound is more accurate. The body of
the worm shows as two hyperechoechoic lines on either side of a hy-
perechoechoic space when seen on a longitudinal scan relative to the
worm. If scanned transversally, there will be a round, hyperechoechoic
center (the worm's alimentary canal) surrounded by a hyperechoechoic
ring (the worm's body). This is the characteristic "target sign", and may
also be seen in the biliary tract (Fig. 25 b). Ascaris is the only intestinal
worm which ingests barium and it does this most reliably after the pa
tient (and the worm) has fasted overnight (Fig. 25 c, d). There will be
then be one or more white lines (the worm's alimentary canal) within the
stomach or small bowel, perhaps surrounded by a clear space on either
side (the negative shadow of the worm's body) within the barium col
umn. There may be excess intestinal secretions: worms are irritating.
Most of the Ascaris inhabit the small bowel and their movements can
be monitored by ultrasound or barium studies. A few will be in the stom
ach or duodenum, but the majority will be in the lower ileum, with some
in the caecum and colon (Fig. 26). Ascaris is a common cause of in
testinal obstruction in children in any region where infestation is more
than usually prevalent. The level of the obstruction is usually ileocaecal,
especially if the child has been given an anthelmintic which has caused
a mass of dead worms. Ultrasound is a rapid way to demonstrate the tan
gled, obstructing bodies. In many parts of the world an erect plain radi
ograph of the abdomen of a child which shows multiple small bowel fluid
levels is recognised as yet another complication of ascaris infections.
The worms may have to be removed surgically, which is yet another good
reason to be a radiologist!
Ascaris is the commonest cause of jaundice in children in Africa, Asia
and South America. Ultrasound will demonstrate the worm within the
biliary tract, either as a target sign or a linear shadow. If in the cystic
duct, it will probably cause obstruction. The worm can, of course, also
be seen by CT or intravenous cholangiography. Cholecystitis and hepatic
abscesses can be caused by worms and ascaris have been found in sub-
1278
TROPICAL DISEASES
Figure 26. Ascariasis

a) Worms in the lower ileum and a fe w in
the duodenum and jejunum. The bowel
is mildly dilated and oedematous. The
worms have not ingested much barium.
(Nigeria)
b) The alimentary tract o f a long worm
containing barium. There are excess se
cretions in the upper small intestine.
(China)
phrenic abscesses, or, occasionally, in the peritoneal cavity. Even if the

worm is in the biliary tract, oral therapy will probably be successful.
Strongyloidiasis
Infection with S. stercoralis is particularly significant in any patient who
is immunosuppressed. In others, the infection is usually asymptomatic
or, at the worst, causes mild peptic ulcer symptoms or occasional colic.
Strongyloides are more common in adults than in children, and infection
occurs through the skin, usually the foot. As with many other worms,
there are early chest symptoms (cough) and a peripheral eosinophilia.
Although imaging is not the way to recognise strongyloidiasis, radiolo
gists should be aware of the parasite’s effects and complications.
In the early stages of S. stercoralis infections, contrast studies of the
alimentary tract, using microfine, non-flocculating barium, will show
mucosal oedema from the pylorus to the upper jejunum, sometimes also
in the stomach. Barium passes rapidly and the bowel is apparently in
flamed and irritable. The appearance may be indistinguishable from
sprue.
In the later stages, the bowel becomes fibrosed and more rigid, peri
stalsis is absent: the mucosa is atrophied: ulceration occurs and the ap-
1279
Figure 27.
Strongyloidiasis.
Distended, gas-filled loops o f small
bowel due to strongyloides. (Nigeria)
pearence may incorrectly suggest obstruction (Fig. 27). The colon may
be involved and in patients with severe immunosuppression (e.g. as in
AIDS) very severe colitis may occur, leading eventually to sepsis and
death. Barium contrast studies of the large bowel at this stage show se
vere ulcerating colitis with sinus formation.
Giardiasis
This is yet another alimentary parasite which should be known to radi
ologists, although it is not their responsibility to make the diagnosis.
Giardia lamblia are ingested through contaminated food and especially
water, and have been found throughout the world, wherever there are
water reservoirs. Most patients are unaware of their infection, others have
vague abdominal symptoms with intermittent diarrhoea and malabsorp
tion. It must be remembered that having Giardia lamblia in the alimen
tary trace does not mean that this is the cause of the patients symptoms;
other diseases must be excluded.
1280
TROPICAL DISEASES
When barium is used for contrast studies of the gastrointestinal tract,

it should always be microfine and nonflocculating. Using this for patients
with giardiasis, barium studies of the duodenum and jejunum will show
mucosal thickening, marked spasm and distortion: there may be rapid
transit of barium, with segmentation and increased intraluminal fluid.
Sprue may be suspected. It is seldom that giardia infection spreads be
low the jejunum, except when the patient is immunosuppressed or suf
fers from dysgammaglobulinaemia, when there will be a nodular pattern
in the small intestine due to hypertrophy of the Peyer's patches.
It is only because Giardia is much more localized to the upper small
bowel that this infection may be distinguished from strongyloidiasis by
barium studies.
Hookworm (ancylostomiasis).
"Hookworm" is an infection with a nematode worm, usually
Ancylostoma duodenale or Necator americanus, or both. (A. ceylanicum
can also be pathogenic for man.) The worms enter the body through the
feet and spread through the lymphatics and blood to the lungs and even
tually down the oesophagus to the jejunum. Although the origin has been
known for nearly a century, millions of people are still infected and it is
a common cause of chronic anaemia in many tropical countries. Some
patients will be symptom-free, others will have severe infections and a
marked peripheral eosinophilia. It is essential to differentiate between
hookworm infection and hookworm disease, between the mild and the
severe. At the onset of infection, and while the worm is migrating and
developing, the clinical complaints are pruritis and erythema: the
"ground itch" of barefoot people. Within 3-14 days there may be a cough
and low fever, but the chest radiograph will be normal. There can then
be a long latent period, particularly if the host is otherwise healthy. But
in the malnourished or otherwise unhealthy, there may be mild gastric
symptoms, and if the parasite load is heavy, anaemia and further mal
nutrition result.
In chronic infection, causing anaemia, a chest radiograph may show
cardiomegaly. A barium contrast study will show a normal gastroin
testinal tract in many patients, but in others there will be a deficiency or
malabsorption pattern. There is a marked geographical variation in the
reported imaging abnormalities, possibly due to association with a vari
ety of other parasites. Hookworms have been known to occur in tissues
1281
Figure 28.
Helminthoma.
A large mass arising from the medial
wall o f the caecum (barium enema).
(Zimbabwe)
outside the bowel, but for all practical purposes ancylostomiasis is a small
bowel infection.
Helminthoma
Almost any parasite can migrate into the bowel wall, yet this happens
surprisingly seldom. When it does occur, there is an inflammatory, gran
ulomatous reaction forming a tumour, the helminthoma. The intestinal
parasites which most commonly infiltrate are nematodes, and one in par
ticular, oesophagostomum. Ascaris and ancylostoma rarely also cause
the same reaction. There is a different result when a parasite perforates
completely through the bowel wall, causing a localized peritoneal ab
scess, compared with the granulomatous reaction which occurs first
within the wall itself and then subsequently perforates. Clinically, when
this occurs, most patients will be suspected of having appendicitis or per
haps intussusception or perforated diverticulum. The correct diagnosis
of helminthoma is very seldom made before surgery (and not always
even at surgery). With a barium enema or ultrasound scan, a mass can
be demonstrated in the wall of the bowel, often eccentric, and sometimes
leaving the lumen open (Fig. 28). Very seldom is the whole internal di
ameter of the bowel affected, although it may be narrowed due to pres-
1282
TROPICAL DISEASES
sure. The mucosa appears intact and the mass is often surprisingly well-
defined. Helminthomata occur most commonly in the caecal area, less
often in the sigmoid and only occasionally elsewhere in the bowel.
Clinically or radiologically the mass might appear to be an inflammatory
abscess or a bowel tumour. A radiologist will only make the correct di
agnosis if he or she has a very high index of suspicion and a great deal
of good luck! Usually the diagnosis is made by the histopathologist, who
may be as surprised as everyone else.
Other intestinal parasites

Two other parasites should be mentioned. The nematode Capillaria
philippinensis was first described in humans in 1963 and occurs almost
exclusively in the Philippines. It causes a severe protein loosing en
teropathy. The radiological appearances are those of malabsorption; pa
tients with severe infections can be acutely ill and die quite rapidly: those
who survive are liable to have several relapses.
Trichuriasis is often clinically silent and is not a "radiological" dis
ease, but the worms may be found if a contrast enema is carried out for
some other reason. A double contrast barium enema can demonstrate the
tiny whipworm, Trichuris trichiura (30-50 mm) throughout the whole
length of the colon, accompanied by a granulomatous mucosal pattern,
with excess mucus. The actual radiolucent lines of the "whips" may be
seen and it is possible to differentiate the male from the female, although
this is not really helpful information. Judging by their numbers, the
worms manage to do this very well on their own.
Liver flukes: clonorchiasis

In East Asia, from Indochina to Japan, infection with the liver fluke
Clonorchis sinensis occurs quite commonly: it is one of the risks of eat
ing raw fish. The end-result may be severe cholangiohepatitis with the
bile ducts becoming dilated and thickened, most severely in the left lobe
of the liver. The process begins in a few segmental ducts and then spreads
until almost the whole intrahepatic biliary tract is elongated, tortuous,
and dilated, often partially filled with debris (Fig. 29). Eventually, the
extrahepatic ducts become involved. If the patient is jaundiced, this sug
gests that there is added infection, calculus formation, or even pancre
atitis.
1283
Figure 29.
Clonoarchiasis.
A T-tube retrograde cholangiogram
showing the dilated, saccular biliary
tract, filled with debris. (Korea)
Most patients with clonorchiasis will eventually develop calculi

around debris in the bile ducts and gallbladder, together with an E . coli
or Typhi cholangitis. There may be liver abscesses and eventually severe
hepatobiliary damage and cirrhosis. Cholangiocarcinoma occurs quite
frequently in chronic cases.
Ultrasound and CT of the liver demonstrate the grossly dilated and
thickened biliary tract, with ducts which may be as much as 2 cm in di
ameter. Transhepatic cholangiography confirms the diagnosis and will
often show the small calculi and biliary sand. Occasionally, the actual
flukes may be visible as small curved translucencies, but they may be
difficult to distinguish amongst the debris. The ducts become very
irregular, due not only to infection but to adenomatous hyperplasia of
the mucosa. Stricture formation can occur and the resulting hepatic ab
scesses must be distinguished from the malignant disease which may
ocur concurrently.
Typhoid, parathyphoid and salmonella infections

These enteric fevers are still a major health problem in many parts of the
world, particularly where a hot climate contributes to rapid dehydration.
They are spread by ingesting contaminated water and food, occasionally
1284
TROPICAL DISEASES
Figure 30.
AP (a) and lateral (b)
views o f the dense chronic
bone reaction due to
typhoid osteomyelitis.
There is a central
sequestrum. (Pakistan)
by direct cross infec

tion. Clinically these
"dysenterys" can be
misleading, starting
with fever, headache,
geneal malaise and ab
dominal pain. Typhoid
produces a high fever
and bradycardia, fol
lowed by delirium and
stupor.
For the radiologist,
the principle finding in
typhoid is grossly dis
tended small bowel
due to paralytic ileus.
Fluid levels on an erect
abdominal radiograph
are uncommon. Per
foration occurs in
many typhoid patients,
usually at the end of
the third week of in
fection, but in some
countries perforation occurs earlier, even during the first week. After per
foration there is often a large amount of free intraperitoneal gas, and the
distended bowel wall is outlined between the intestinal gas and the in
traperitoneal gas. There is almost always peritonitis also. There is little
indication for any contrast examination during the acute infection. When
chronic, both typhoid and salmonella infections can cause segmentation
1285
Figure 31.
Lymphogranuloma.
Barium enema. Note the smooth
tapering rectum o f lymphogranuloma
venereum (small arrows). There is a
perirectal abscess (arrowheads).
(China)
and hypomotility of the small bowel.

Typhoid and salmonella also infect bone, and salmonella osteitis is es
pecially common in infants and young children with sickle cell anaemia.
This osteomyelitis progresses more slowly and with less acute symptoms
when compared with pyogenic infections (Fig. 30). Biopsy may be nec
essary to make the correct diagnosis, especially in the spine. There is sel
dom a paravertebral abscess.
Lymphogranuloma venereum
Appropriately, the last gastrointestinal disease to be considered is lym
phogranuloma venereum, affecting the rectum and lower colon. It is
caused by Chlamydia trachomatis and, except in rare cases involves only
the rectosigmoid, the lower colon, the genital tract, the surrounding tis
sues and regional lymph nodes. Clinical proctocolitis and suppurating
lymphadenopathy are common. The infection is acquired by sexual con
tact: transmission by any other route is very uncommon.
Ultrasound will show the thickening of the rectal wall and the sur
rounding oedema and inflammatory reactions. A barium enema will
show spasm, narrowing of the rectum and lower colon, and then loss o f
the normal colonic pattern (Fig. 31). Eventually, there will be loss o f
haustration, multiple fistulae, perirectal abscesses and sinuses. The dis
1286
TROPICAL DISEASES
ease progresses to fibrosis and stricture formation and may involve the
last 25 cm of the large bowel. In women, rectovaginal fistulae may de
velop. The differential diagnosis will include mycotic infection, amoe
biasis and tuberculosis (because of the fistulae formation), but in prac
tice there is usually little doubt about the correct diagnosis.
TROPICAL PULMONARY DISEASE

Patients in or from the tropics can also get "ordinary" infections. They
suffer from pneumonia, lung abscesses, bronchiectasis and particularly
tuberculosis as do patients from many other parts of the world. However,
if malnourished, immunosuppressed or suffering from malaria or other
parasitic infections, their pulmonary diseases may be more severe than
is usual in the western world. Measles (rubella), chicken-pox (varicella)
and whooping cough (pertussis) can be severe illnesses with accompa
nying pneumonia. The pulmonary changes of amoebiasis, ascariasis, fi-
lariasis and other parasitic infections have already been noted, but there
are other specific pulmonary infections which need to be considered (see
below, page 1301 for tropical eosinophilic lung).
Paragonimiasis
This is the result of an infection with one or other lung flukes of the genus
paragonimus, usually P. westermani. (There are 15 other species of
paragonimus, which can infect man.) The infection is found throughout
the tropics but particularly in Asia, and is usually mistaken for tubercu
losis. Paragonimiasis is acquired by eating raw or inadequately cooked
crabs, crayfish, and occasionally from eating animals which also enjoy
fresh water crabs. The life cycle is similar to that of schistosomiasis, and
includes warm water snails, but there is no direct infection of man.
Clinically, the majority of patients, even with heavy infections, are not
ill. The minority will complain about chest pain, chronic cough and
chocolate-coloured sputum, while remaining remarkably well in general
health. At this stage the sputum often contains multiple recognizable eggs
of P. westermani.
Apart from the lungs, cerebral involvement is not uncommon and
causes convulsions, fever, headache or other neurological symptoms.
Some species prefer the central nervous system and the lungs may re
main clear, but this is in less than 20% of the patients.
1287
Figure 32. Paragonomiasis.

a) Bilateral interstitial and basal consolidation in a patient with paragonomiasis.
(China)
b) Tomography o f the right upper chest showing the nodular and fibrotic pattern o f
paragonomiasis. This is indistinguishable from tuberculosis. (China)
Chest radiographs in the acute stage show a predominantly exudative

basal pneumonia, sometimes with pleural effusion. The lungs clear af
ter a few weeks, leaving either small nodules or cysts, which are the most
characteristic findings (at this stage there will be mature worms in the
pulmonary parenchyma) (Fig. 32). This pulmonary pattern may persist
for years without causing clinical ill health. Most of the cysts are in the
periphery of the mid lung or at the lung bases, but they can occur in the
upper part of the lungs. A pneumothorax is not uncommon. The cysts
are from 0 .5 -4 cm in diameter and change constantly, with varying pat
terns of surrounding reaction. Hilar adenopathy is very uncommon.
These ring-shadows may be seen in 80% or more of patients and can be
recognized on plain radiographs or CT. In some cases, the tortuous bur
rows through which the worm moves may be recognized, close to the
cysts. When the parasite dies, there is a fibrotic reaction and the cyst dis
appears, leaving a residual density with surrounding fibrosis. Even these
fibrotic lesions may disappear. It should be noted that in some patients,
1288
TROPICAL DISEASES
treatment of the infection causes a hypersensitive reaction, with transient

fluffy densities throughout the lungs. This may incorrectly suggest that
the patient’s condition is worsening.
Cerebral paragonimiasis results in elevated intracranial pressure: the
multiple cerebral cysts may calcify and may occasionally be seen on plain
skull radiographs, but are more easily recognized on CT or MR. With
scanning, the cysts may be seen before they have calcified, and are al
most always multiple and bilateral. For some unknown reason, involve
ment of the frontal lobes and cerebellum is uncommon. Some patients
develop one larger cyst or even a cerebral abscess. About 80% of the pa
tients with a cerebral infection will have lung infection also. The cysts
of paragonimiasis may be mistaken for those of cysticercosis, in which
the cysts are smaller, discrete and fewer in number.
P. Westermani may be found in the abdomen or elsewhere in the body
and be recognized with ultrasound or CT scanning. A plastic peritoneal
reaction may occur, causing intestinal obstruction. The cysts may cal
cify in the soft tissues and in the liver.
Melioidosis
Infection with the gram negative bacillus, Pseudomonas pseudomallei,
is known as melioidosis. While occurring most commonly in South East
Asia, cases have been reported from many other parts of the world, usu
ally in visitors returning from Asia. The exact method of infection is un
known, but may be due to contaminated dust or soil, perhaps from in
sect bites.
Clinically, the disease may be asymptomatic or subclinical. It is eas
ily mistaken for tuberculosis or other fungal infection, both clinically and
radiologically. Those with clinical symptoms may present with an acute
illness with a high temperature. Others, who have a less acute infection,
present with haemoptyses and a low fever or, less commonly, as a chronic
extrapulmonary infection.
The radiological appearance of the chest suggests tuberculosis. In the
acute variety, there will be multiple irregular nodular densities which
may coalesce or cavitate. There may be lobar pneumonia, or both ap
pearances may be seen simultaneously in different parts of the lungs.
When the infection is less acute, there can be lobar consolidation and
cavity formation (Fig. 33). In both forms, acute and subacute, pleural in
volvement and hilar adenopathy are uncommon. In those without clini-
1289
Figure 33.
Melioidosis.
a) Bilateralfluffy nodules
throughout both lungs.
(Vietnam)
b) Two thin-walled cavities
(tomogram). (Vietnam)
cal symptoms, tuberculosis

a is the usual diagnosis be
cause of upper lobe infection
and cavity formation.
The extrapulmonary infec
tions produce subcutaneous
or muscle abscesses with si
nuses, osteomyelitis, septic
arthritis, and even abscesses
in the spleen, brain, kidneys
and liver. Bone infection
cannot be easily distin
guished from any other type
of osteomyelitis, and the soft
tissue abscesses are very
non-specific.
CARDIAC DISEASE
Acquired valvular disease is
still by far the commonest
cause of cardiac pathology in
the tropics and essential hypertension is widespread. However, there are
several cardiac diseases which are specific to the tropical countries: it is
not possible to describe all of them in detail here, but they must be dis
tinguished from many of the common, nontropical cardiac problems.
Cardiomegaly
An enlarged heart in South America may be due to Chaga's disease, but
in Africa cardiomegaly may be due to idiopathic endomyocardial fibro
sis, which can be predominantly right- or leftsided. Alternatively, idio-
1290
TROPICAL DISEASES
Figure 34.
A large heart with a left ventricu
lar, partially calcified aneurysm.
On contrast angiography the
aneurysm did not fill properly,
probably due to a thrombus.
(Nigeria)
pathic cardiomegaly can occur as an acute or chronic disorder of un

known aetiology. A different problem is the subvalvular aneurysms
which can occur below the aortic and mitral valves. They can be single
or multiple and are also of unknown aetiology. Such aneurysms are of
ten a chance radiological or echocardiographic finding, or even first rec-
ogised at autopsy. On an erect frontal chest radiograph, the large heart
may have a significant bulge, usually on the left cardiac border, perhaps
only clearly seen on an oblique or overpenetrated film: there may seem
to be a double cardiac contour (Fig. 34). Calcification can occur in the
aneurysms. The distorted cardiac outline can be mistaken for a pericar
dial cyst or for rupture of the sinus of Valsalva. Careful echocardiogra
phy will usually confirm the diagnosis, but if surgery is to follow, an
giocardiography or cardiac MRI may be required.
AORTIC DISEASE
Idiopathic arteritis (Takayasu’s disease, or aortic arch arteritis) is un
usually common in the tropics but follows the patterns recognised else
where. It occurs most frequently in young children and young women,
is rare over the age of 30, and may affect any part of the aorta: these fac
tors make a syphilitic aneurysm an unlikely alternative diagnosis. Aortic
arteritis is commonly associated with hypertension and can clinically
present as an unexpected cerebrovascular accident in a young person.
Alternatively, renal failure, obscure abdominal pain or cardiac failure in
a young female are other presentations. The anatomical distribution of
the vascular disease will dictate the clinical symptoms. The arteritis can
1291
Figure 35. Idiopathic arteritis.

a) Upper mediastinum, (AP chest) showing
partially calcified aneurysms o f the right
subclavian artery and descending thoracic
aorta. (Nigeria)
b) A pulsatile swelling on the right side o f the
neck o f a patient, with increased blood
pressure. The angiogram shows the right
common carotid aneurysm, with reduced
carotidflow beyond it. (Nigeria)
c) Abdominal angiogram: the same patient as
Fig. 35 b. The mid-abdominal aorta is ir
regular with stenosis o f left renal artery.
The left kidney is small. (Nigeria)
d) Retrograde aortogram (when passing the
catheter from above, it was not possible to
get below the level o f 9-1 Oth thoracic verte
brae). There is coarctation of the upper
abdominal aorta, with a large collat
eral circulation. (Courtesy o f
Professor Komolafe, Ilorin, Nigeria)
1292
TROPICAL DISEASES
be multifocal and cause segments of stenosis or dilatation. It is progres

sive and can cause complications by narrowing major branches, e.g. a
renal or carotid artery. Sudden rupture of the aorta can occur.
Echocardiography and Doppler ultrasound can monitor the major ves
sels, but it is also necessary to image the aortic arch and thoracic aorta.
If surgery is considered, angiography to demonstrate the whole length
of the aorta and the origins of the major branches is essential (Fig. 35).
SKELETAL AND SOFT TISSUE DISEASE
Osteomyelitis
There is a wide variety of osteomyelitis found throughout the tropics and
bone infection is probably more common than in many temperate cli
mates. Osteomyelitis due to typhoid and salmonella should also be con
sidered, especially in patients with sickle cell disease. The use of ultra
sound in the early diagnosis of any acute bone infection is important in
children. Needle aspiration guided by ultrasound will not only decom
press the abscess, but allow identification of the organism and accurate
antibiotic therapy. Healing will be quicker and the skeletal deformity will
be less. Tuberculosis can affect the skeleton in a wide variety of ways,
resembling an acute osteomyelitis, a cyst in a long bone, an acute or
chronic arthritis, a severe periosteal reaction, or a destructive lesion.
Think of tuberculosis in any tropical bone disease, but remember typhoid,
klebsiella and syphilis also: then worry about more common organisms!
Tropical ulcer
A tropical ulcer is an acute specific, localised necrosis of skin and soft
tissues, followed by a chronic ulcer involving the entire skin and subcu
taneous tissues. It usually occurs in the front of the lower leg or on the
foot. The acute organism is Bacillusfusiformis , with secondary infection
inevitably following. Tropical ulcer must not be confused with the sores
due to cutaneous Leishmaniasis. After the acute phase, the surrounding
oedema and granulation tissue persist, and in many patients the ulcer
spreads to involve the deep fascia, the tendons and the underlying bone.
When this occurs there is a characteristic radiological change, almost al
ways first in the tibia but involving the fibula also. A localized periosteal
reaction, usually fusiform and linear but sometimes with spiculation, de
velops under the soft tissue ulcer (Fig. 36). This eventually results in a
1293
с
Figure 36. Tropical ulcer.
Four different patterns o f bone reaction beneath tropical
ulcers.
a) A laminated periosteal reaction on the tibia. (Nigeria)
b) An “osteoma ” on the anterior edge o f the tibia.
(Nigeria)
c) AP and lateral views o f a large tibial “osteoma ”.
(Nigeria)
d) A very irregular hypertrophic postero-lateral “os
teoma ” on the fibula, with minimal cortical thickening
on the tibia. (Kenya).
All these reactions are smooth and there are no changes
which might suggest malignancy.
1294
TROPICAL DISEASES
thick sclerotic layer of bone, which may be as much as 2.5 cm in thick

ness and resembles (and has been called) an ivory osteoma. At this stage
the original layered periosteal reaction will have disappeared. The reac
tion can spread around the whole bone, above and below the site of the
soft tissue ulcer. It varies in width and length, and may be followed by
superficial sequestration in a localized area. There is loss of the overly
ing soft tissue, with underlying osteoporosis, followed by expansion of
the medullary cavity, with considerable remodelling into a cancellous
osteoma. This residual deformity may have to be removed surgically be
fore the ulcer can be properly treated. Secondary infection of the ulcer
with further bone reaction can occur.
The tissues around tropical ulcers may undergo malignant change, but
usually after a period of some years. There will then be soft tissue and
Figure 37. Malignant tropical ulcer.

a) Ulceration in the upper third o f the lower leg with bone destruction. (Nigeria)
b) More advanced ulceration in the lower half o f the leg with destruction o f more than
two thirds o f the tibia. (Nigeria)
1295
Figure 38. Ainhum.

a) The typical soft tissue band around the fifth toe, constricting the middle and proxi
mal phalanges. (Nigeria)
b) A much less common, but similar appearance in the hand. The distal h a lf o f the
middle finger has been auto-amputated and there is another tight band constricting
the middle phalanx o f the index finger. (Nigeria)
bony destruction which spreads, involves the cortex and the medullary
cavity and may lead to pathological fracture (Fig. 37). Systemic tumour
dissemination and metastatic spread is possible, but is not common. The
whole chronic destructive process can be prevented if the initial skin
wound is thoroughly washed with soap and water and kept clean.
Ainhum
This is an unusual afflication of one or more toes, usually in middle-aged
black men who are otherwise healthy. A constricting, sometimes painful
groove develops around the base of the toe which can lead to autoam
putation. It can occur, but is much less common in the fingers. The aeti
ology is unknown. The fifth toes, often bilaterally, are the most com
monly affected, but other phalanges may be involved. Clinically, the dis
ease is obvious, easy to diagnose, and appears trivial. However, it can
be painful and crippling. The radiological changes are similarly charac
teristic (Fig. 38). The fibrous groove around the toe can be seen in the
soft tissues and there will be underlying localized osteoporosis, usually
1296
TROPICAL DISEASES
of the proximal phalanx. The cortex becomes absorbed and the affected
phalanx is concentricaly thinned and asymmetrically tapered. If there is
infection, there may be a small cortical reaction. Eventually, there is an
gulation of the digit, a pathological fracture which can be very painful,
and autoamputation. Fortunately, treatment is seldom necessary, but
surgery may be helpful to ease the pain or the lymphoedema which re
sults from the tight constriction.
It is important for the radiologist to distinguish this benign process
from leprosy. It is unusual for leprosy to affect only one bone and very
seldom in leprosy is the only clinical abnormality in one toe, or even one
toe of each foot. Unlike leprosy, there is no sensory loss in ainhum, no
other soft tissue abnormality and very seldom any ulceration or infection.
It is, clinically and radiologically very easy to recognise and there are very
few complications. There is no indication for complex investigations to
exclude some other disease. Ainhum is an entity in its own right.
Leprosy
This bacillary infection has been feared for centuries and there are still
several million lepers in the world, with 650,000 new patients every year.
It is a chronic and destructive infection due to M. leprae with many unan
swered questions. As with many of the other tropical diseases, there can
only be a brief summary here, but if suspected, reference to a more com
prehensive description is strongly recommended.
Many of the clinical results of leprosy are in the soft tissues, and for the
radiologist it is the effects of soft tissue infection, distorsion and dener
vation which are of importance. However, one result is absolutely diag
nostic. Calcification of nerves occurs in leprosy and in no other condi
tion. It may be linear, along the nerve, sometimes in flakes, or oval cal
cification may be the end-result of a perineural abscess. Contrast injection
along the nerve sheeth has been suggested, to localise the calcification,
but a clinical diagnosis of leprosy should be much easier! Except in the
skeleton (particularly the extremities) there are no other significant imag
ing findings. Leprosy granulomas do occur in the liver, spleen and in many
other organs, but are not reliably identifiable by any imaging method.
When primary bone changes in leprosy are recognised, they are
medullary and destructive, with only a little bone response until healing
occurs. The digits are the most frequently affected, showing localised
osteoporosis, honeycombing and concentric bone absorption. There can
1297
be well-defined cystic lesions (from which M. leprae can be aspirated),

but these are not necessarily related to the soft tissue changes.
Microfractures are common, but heal with treatment, as do the cysts.
A periosteal reaction occurs in about one third of all leprosy patients,
usually painless except in a minority who have severe pain and tender
ness. The tibia and ulna are common sites. During the “lepra” stage bone
destruction can be severe, usually in the vascular parts o f bone.
The soft tissue changes are ulceration, atrophy and fibrosis, all modi
fied by infection. There is often underlying osteoporosis, particularly dur
ing the "lepra" stage. Almost all the other skeletal changes in leprosy re
sult from neurological and vascular deficits, which are superimposed on
the changes caused by motor and sensory paralysis. Added complica
tions are the soft tissue infection and ulceration, and sometimes sec
ondary bone infection as well. To these must be added the results of
trauma, often repeated, to limbs which have damaged sensory apprecia
tion and poor motor control. This prolonged and sad sequence can be
summarised:
- Localised osteoporosis
- Periosteal and subperiosteal reaction. Infection and sequestration
- Absorption of bone and formation o f new bone, a combination of is
chaemia and soft tissue contraction
- Fractures of the distal metatarsal shafts and absorption of the
metatarsal heads (characteristic)
- Contraction of the soft tissues and bone absorption with resulting ap
parent gaps on the radiograph between the remaining bones
- Secondary bone infection, especially related to soft tissue ulceration,
which is common and persistent
- Neurotrophic changes in the joints, usually in the small joints of the
hands and feet, with subluxation. This is added to the ischaemic
changes and hastened by weightbearing on the feet and hands (sticks
and crutches will be needed eventually) when there is no protective
sensation.
The end-results are major destructive bone loss with disorganised joints,
most obviously in the digits and later in the tarsus, less often in the car
pus (Fig. 39). Similar destructive changes can be seen in the nasal bones
and occasionally elsewhere.
1298
TROPICAL DISEASES
Figure 39.
Leprosy.
a, b) The destructive
process o f lepro
sy in the foot and
the hands. (India)
It must be re-emphasised that the diagnosis of leprosy is almost always

made clinically. The task of the radiologist is to assess the damage which
results. Reconstruction is often undertaken and requires cooperation be
tween all concerned. There are special radiographic positioning tech
niques to aid this process.
Filariasis
Many different filaria infect millions of people around the world.
Amongst them, the most important are Wuchereria bancrofti, Brugia
malayi and B. timori. These filaria cause elephantiasis. Loa loa causes
"calabar swellings" and Onchocerca volvulus causes onchocerciasis or
"river blindness". Each have a distinctive geographical distribution, but
together infect millions of people. All are transmitted by insect bites.
The limbs of patients who have gross clinical elephantiasis do not have
very specific radiological changes. There is loss of the soft tissue fat lines.
1299
Figure 40. Filariasis.

a) Multiple circular calcified nymphs
o f armillifer armillatus seen
throughout the liver and spleen (an
upper abdominalfilm taken during
contrast urography). (Nigeria)
b) Abdominal ultrasound showing sim
ilar calcified nymphs o f armillifer
armillatus. (Nigeria; courtesy o f Dr.
Marinho)
c) The faintly calcified line which re
sults from calcification o f the dead
filaria, Loa Loa, in the soft tissues
o f the hand. (Nigeria)
The underlying limb bones may show marked periosteal and cortical
thickening, which results from the soft tissue changes and is not an ef
fect of the filaria on the bones. Contrast urography will show dilated re
nal lymphatics in patients with lymphuria. Lymphangiography is tech
nically very difficult and only useful to exclude congenital lymphoedema
(which is often unilateral).
Not all elephantiasis is due to filariasis. Any lymphatic obstruction,
e.g. due to tuberculosis, Kaposi's sarcoma, or L.G.V., may be responsi
ble. To make the differential diagnosis more difficult, filarial elephanti
asis can be unilateral.
1300
TROPICAL DISEASES
Figure 41.
Tropical eosinophilia.
Soft bilateral fluffy nodules
throughout the lungs. There
was a 67 % peripheral
eosinophilia, which suggested
the correct diagnosis:
filariasis. (Nigeria)
Porocephalosis
Porocephalosis results from tongue worm infection, usually Armillifer
armillatus or Porocephalus crotali. There are few clinical symptoms.
The A. armillatus are acquired by eating snakes, or drinking water used
by snakes.
Many of these small parasites calcify and may be recognized as fine
strands of calcification in the soft tissue (Fig. 40). They are then dead,
but the filaria cannot be accurately identified. The fine calcified remnants
must be distinguished from cysticercosis (usually oval and more nu
merous) and porocephalosis (multiple, crescentic or horseshoe calcifi
cations in the abdomen or chest, but seldom elsewhere). (See also guinea
worm page 63).
TROPICAL EOSINOPHILIC LUNG

All filaria, but most commonly Brugia malayi, may cause radiological
changes in the lungs. Clinically, there is almost always a high peripheral
eosinophilia, often a dry cough and shortness of breath. Chest radi
ographs will show multiple small nodules throughout both lungs, indis
tinct in outline and seldom more than 5 mm in size (Fig. 41). Sometimes
there are diffuse homogeneous patches of increased density, which are
very difficult to define. These pulmonary abnormalities change fre
quently, even in a few days, and this is a useful diagnostic finding. The
1301
localised densities change in shape and in position and disappear with

appropriate treatment. The problem is the differential diagnosis: schis
tosomiasis, ascariasis, paragonimiasis, and even strongyloidiasis will
have to be excluded. Miliary tuberculosis may be a very similar picture,
but there is seldom the rapid change in appearance. Most cases o f tu
berculosis will show hilar lymphadenopathy, and there is not likely to
be peripheral eosinophilia.
In a few cases, pulmonary filariasis may leave coarse, localised resid
ual interstitial fibrosis.
DIROFILARIASIS
The dog heart worm, D. immitis, can infect man. Pulmonary infarction
may result. The worm usually presents radiologically as a small solitary
dense lesion on a chest radiograph which may eventually cavitate. The
differential diagnosis will include carcinoma, mycotic (fungus) infection
and tuberculosis. Accurate diagnosis from a chest radiograph is not
possible.
GUINEA WORM INFECTION (DRACUNCULIASIS)

Infection with D. medinensis results from drinking water infected with
the larvae which have been ingested by a minute crustacean (cyclops) or
water fleas. It is therefore most common in rural areas and where there
is poor sanitation. The worm burrows into the deep connective tissues
after fertilization. The female guinea worm migrates to areas most likely
to come into contact with water, such as the lower leg and the lower part
of the body, and the larvae then develop. This may take more than a year.
The female worm may reach 30 cm or more in length (the smaller male
worm probably dies after copulation). Clinically, a blister or ulcer de
velop on the skin, showing where the guinea worm will shead its larvae
into the water to complete the cycle. Just prior to release, the patient may
be quite ill, with vomiting, diarrhoea, pruritus and giddiness. Later, af
ter sheading the larvae, the guinea worm dies and the resulting foreign
body and granulation tissue may calcify. Radiologically, this results in
a long string-like calcification, which may be coiled or remain stretched
along the leg, across the tissues of the abdomen or the chest, or deeper
within the peritoneum (Fig. 42). Guinea worms, alive or dead, can be lo
calised by ultrasound and are easily seen on plain radiography when cal
cified. Arthritis may occur if the worm is near a joint, or abscesses may
1302
TROPICAL DISEASES
Figure 42. Guinea worm.

a) A curled, partially calcified guinea worm within a soft tissue abscess o f the lower
leg. (Nigeria)
b) Several long, and other curled calcified guinea worms in the thigh and scrotum.
(Nigeria)
develop anywhere the worm is in the tissues.
TROPICAL SPLENOMEGALY
Enlargement of the spleens of those who live in the tropics can be due
to many causes, particularly malaria and leishmaniasis. In many patients
the exact cause remains unknown. There are no characteristic imaging
1303
findings either radiographically or with ultrasound, apart from the large

homogeneous spleen. Since the spleen is very large and firm, distorsion
of the left kidney can occur, with flattening of the upper pole in particu
lar. The enlarged spleen emergas from the protective abdominal rib-cage,
becoming easily ruptured with minor abdominal trauma.
MALARIA
Malaria is a very significant cause of morbidity and mortality. At least
one million people of all ages die o f malaria every year. For the radiol
ogist, the only significant imaging abnormality in the patient with malaria
(apart from the large spleen) is the fortunately uncommon development
of severe bilateral pulmonary oedema. This has no radiological charac
teristics to differentiate it from pulmonary oedema of any other aetiol
ogy. It is important to be aware that this pulmonary oedema is an intrin
sic complication of severe malaria and does not have to be the result of
fluid overload or any other therapy. It is very difficult to treat and can be
fatal. Generalised oedema may be the result of malarial nephropathy/
glomerulonephritis. There are no distinguishing features on imaging.
In infants, cerebral malaria can cause cerebral oedema and suture di
astasis (separation) might be mistaken for an intracranial tumour, espe
cially when the child lapses into a coma.
The splenomegaly of malaria can be gross, but the ultrasound appear
ance remains homogeneous. Pressure distortion and displacement of the
left kidney can occur.
TAENIASIS (TAPEWORM). CYSTICERCOSIS.

Many people are infected with tapeworms, particularly by the beef tape
worm, T. saginata, or the pork tapeworm, T. solium. Cysticercosis is an
infection with the larval stage of the pork tape worm (originally named
cysticercus cellulosae, before it was known to be the larval form of T.
solium). Infection of man by the corresponding larval stage of the beef
tape worm is not known.
Taeniasis
Tapeworms occur throughout the world. Human infection results from
eating undercooked, or raw, infected meat. There may be no clinical ill
ness or abdominal discomfort, but loss of weight and diarrhoea may oc
cur. There may be a 10% eosinophilia. Multiple tape worms can cause
1304
TROPICAL DISEASES
intestinal obstruction. Worms have caused appendicitis.

Taenia saginata is very seldom recognised radiologically or by ultra
sound: there may be a long radiolucent line within a column of barium
in the lower jejunum and ileum. The adult worm may be extremely long,
up to 10 m or more, and in extreme cases it is so long that it is seen as a
translucent line in the colon as well as in the small bowel. The worm
does not absorb barium (it has no alimentary canal).
T. solium has not been identified by imaging.
Cysticercosis
As occurs with so many other parasites, cysticercosis results from swal
lowing infected food or water. Occasionally, autoinfection in a patient
who has a resident tape worm may occur. Except in the brain (or the eye)
the cysticercus becomes surrounded by a fibrous capsule, but may re
main alive for some years. When it dies the cellular reaction may even
tually calcify, usually after about 3 years. Living and dead may occur to
gether. In skeletal muscles, the dead cysts cause few symptoms, but heart
block has been recorded in the cardiac conducting tissue. In the central
nervous system the scarring may cause epilepsy, and occasionally severe
encephalitis and death. If the cerebral ventricular system is blocked, there
may be raised intracranial pressure and the clinical symptoms may sug
gest a cerebral tumour.
The first calcified cysts were recognised radiologiccally in the 1890s,
long before the adult worm. Radiographically the calcified cysticercus
is oval or linear and from 4 to 10 mm in length: larger cysts have been
reported. The oval cysts lie with their long axis in the line of the muscle
(Fig. 43 a). They may be very numerous, particularly in the legs and back,
and may be a chance finding seen in the thoracic muscles on a routine
chest radiograph. If cysticercosis is suspected, soft tissue radiographs of
the upper legs should be obtained. The appearance of the cysts is so char
acteristic, and in many patients there are so many cysts that the differ
ential diagnosis is straightforward. No other soft tissue calcification re
sembles this or is present in such large numbers.
In the brain, it is rarely possible to see the calcified cyst on a plain ra
diograph of the skull. In fact, plain skull radiographs are not likely to be
a useful examination in this disease. Soft tissue radiographs of the thighs
will provide more confirmation if cysticercosis is suspected as the cause
of seizures. However, on CT not only the calcified cysticercus but the
1305
Figure 43.
Cysticercosis.
a) The typical oval calcification o f
cysticercosis lying in the thigh
muscles. (Nigeria)
b,c) CT scans o f calcified cysticerci,
lying periventricularly, but in
this patient not causing any other
lesions (post contrast). (Egypt)
1306
TROPICAL DISEASES
multiple cerebral cysts can be visualized in the cortex and the walls of
the ventricles (Fig. 43 b). MR will demonstrate the cysts, but not the cal
cification. The cysts are thin-walled and contain clear fluid and free float
ing scolices. Some cysts may be quite large, so that the ventricular sys
tem is blocked with resulting internal hydrocephalus. Complete obliter
ation of the aqueduct can occur, but is uncommon. In some cases there
will be basal arachnoiditis. Very rarely, there is erosion of the skull by
the underlying cyst.
Similarly, spinal cysticercosis can be recognized by CT or MR. The
cysts may be intradural or extramedullary, are of different sizes, but usu
ally spherical. They may fragment or become irregular and there may be
associated arachnoiditis. Complete spinal canal obstruction can occur,
but is uncommon. If CT or MR are not available, myelography will
demonstrate intradural and extramedullary filling defects of different
sizes, or irregularity of the contrast column and in some cases partial or
complete obstruction. Plain radiographs of the spine do not demonstrate
the cysticercus.
(Figures number 28,29, 33 a, b, 39 a, b, come from the "Radiology of
Tropical Diseases" by Palmer, P.E.S. and Reeder M.M., Springer,
Heidelberg, 2nd edition. In press.)
1307
Chapter 28
Radiology in AIDS
Marie-France Beilin, Philippe Grenier and

Nadine Martin-Duverneuil
More than 12 years have passed since the initial publications docu
menting the onset of the acquired immunodeficiency syndrome (AIDS)
epidemic, caused by a retrovirus, the human immunodeficiency virus
(HIV). By November 1993, AIDS had been diagnosed in more than
750,000 patients worldwide, with reported mortality of over 50%. It is
estimated that the number of HIV positive people througout the world is
between 5 and 7 million. From the outset, a wide variety of systemic
manifestations, both neoplastic and non-neoplastic, have been noted in
patients with AIDS. The manifestations that have benefitted most from
imaging modalities are those involving the central nervous system, tho
rax and abdomen.
NERVOUS SYSTEM MANIFESTATIONS
Cerebral pathology
The occurrence of AIDS has made cerebral infection a routine problem.
Diagnostic difficulties are related to the multiplicity of pathology that oc
curs in association with cerebral HIV infection, often treatable oppor
tunistic infections arise as a consequence of the immunodeficiency and
simultaneously, tumours, especially primary CNS lymphomas, develop
with increased frequency. Neuroimaging techniques (CT and/or MR
scans) have a triple role: detection, diagnosis and monitoring under treat
ment. MRI is the most sensitive procedure, providing more precise eval
uation of not only infra- but also supratentorial lesions, detection of the
white matter and meningeal lesions, which are invisible or highly un
derestimated with CT, and better detection of hemorrhagic lesions.
Furthermore, because of the underlying immunodeficiency, with poor
1309
Figure 1.
Toxoplasmosis.
Post-contrast CT scan. Ring-en
hanced lesions in the right basal
ganglia and the left frontal lobe
with a large mass effect and p e
ripheral oedema.
Figure 2.
Toxoplasmosis.
Post-contrast CT scan. A very
large, single, ring-enhanced
parieto-occipital lesion with a
large mass effect and peripheral
oedema.
host-defense mechanisms, contrast-medium enhancement is often poor.

Enhancement is better detected with MRI because of its high contrast
sensitivity; with CT, a delayed scan may detect enhancement related to
dye diffusion which is more intense about an hour after contrast injec
tion. Doubling the dose of injected contrast medium has also been pro
posed to improve scan sensitivity, but the poor renal function frequently
1310
RADIOLOGY IN AIDS
Figure 3.
Toxoplasmosis.
Axial gadolinium-enhanced
Tl MR-image. Punctiform
nodular enhanced lesion is
clearly seen at the left frontal
corticomedullary junction.
Note the ventricular enlarge
ment.
associated with HIV infection limits this possibility.
Parenchymatous lesions
These lesions can be subdivided schematically into cerebral masses and
white matter lesions.
Cerebral masses
Cerebral masses, which have as a common denominator contrast en
hancement, are represented predominantly by opportunistic infections
and primary CNS lymphoma. The radiological findings are often quite
suggestive of the diagnosis, but the lesions may resemble one another
quite closely. Therefore, disease monitoring of the lesion during an an
titoxoplasma treatment test may confirm the diagnosis and should be un
dertaken before stereotaxic biopsy is considered.
In France, haematogeneously spread toxoplasmosis is the most com
mon opportunistic infection. Its characteristic appearance (Fig. 1) con
sists of multiple, bilateral, infra- and supratentorial lesions, which are
most frequently found at the corticomedullary junction and in the basal
ganglia. Single lesions (Fig. 2) are less common but can be observed
even with MR. The diagnosis of toxoplasmosis is based on the appear
ance of the lesions, but their site and response to anti-toxoplasma treat
ment is also very important. The lesions may appear as nodular (Fig. 3)
(toxoplasmic granulomas) or ring-like (Figures 1, 2) (toxoplasmic ab
1311
scesses) areas, surrounded by extensive oedema with a mass effect seen

even in small-sized lesions. On CT scans, the lesions are iso- or hypo
dense. On MR-images, the sharply-defined lesions appear as Tl hypo
and T2 hyperintense areas with the more hypointense center of the ring
like lesions corresponding to the central necrosis. Most lesions are fo-
cally enhanced (Figs. 1-3). Contrast uptake, which can be absent or
doubtful on CT scans, is more frequently observed on MR images, but
non-enhanced lesions can be seen on MR, which probably reflects the
extent of immunodeficiency. Haemorrhagic areas, usually o f small-size
are not rare; they are best detected on MR; they occur frequently after
effective anti-toxoplasmia treatment, and thus are strongly suggestive of
toxoplasmosis (in the absence of steroid treatment which can induce he
morrhagic necrosis within lymphomatous lesions).
Under anti-toxoplasma treatment, the other criteria of therapeutic ef
ficacy include; the diminution of the volume and/or the number o f le
sions; the lesions can remain unchanged, but oedema and the mass ef
fect can be reduced (without associated steroid treatment). In the absence
of these findings, in the case of an initial atypical clinical presentation,
if the lesions do not increase in size within 8-10 days a priori, this rep
resents a criterion in favour of the diagnosis of toxoplasmosis and the ef
ficacy of the treatment.
Primary cerebral non-Hodgkin's lymphoma (Fig. 4) is common, usu
ally immunoblastic or lymphoblastic В type. It occurs in 2-5% of cases.
Early diagnosis enables the rapid initiation of radiotherapy with signifi
cant improvement in survival despite the poor overall prognosis.
Lymphoma can be unifocal but, in more than 50% of the cases, lesions
are multiple and their sizes vary. The masses have been described as be
ing predominantly located supratentorially within the basal ganglia or
cortex; in contrast to toxoplasmosis, the deep white matter may also be
affected. Locations within the corpus callosum and caudate nucleus are
also characteristic. These tumours are highly infiltrative with only mod
erate edema and mass effect. On non-contrast-enhanced CT they are usu
ally heterogeneous, iso- or hypodense; on MR, their appearance is hy
pointense as compared to the normal brain on Tl, iso- or hyperintense
on T2 sequences. In the absence of steroid treatment haemorrhagic stig
mata are not demonstrated. Following intravenous contrast medium ad
ministration, moderate or marked enhancement is evident; it can be ho
mogeneous, but ring-enhancing patterns (well-delineated, quite similar
1312
RADIOLOGY IN AIDS
Figure 4.
Primary lymphoma.
Post-contrast CT scan. Large
homogeneously enhanced
periventricular mass with mild
peripheral oedema and mass
effect.
to toxoplasmosis) have been observed, sometimes with a more typical

irregular serpiginous enhancement. Lymphomas characteristically ex
hibit a thick irregular periventricular enhancement; the alternative diag
nosis is CMV encephalitis.
Cryptococcal disease (Cryptococcus neoformans) is very frequently
associated with AIDS, most often presenting as cryptococcal meningi
tis. Cryptococcomas can also develop, but CT is often non-contributory
to the diagnosis because of the weakness of the inflammatory reaction.
These lesions are most likely to be seen on MR, they are often small, lo
cated in the basal ganglia or cortex, exhibit minimal oedema and mass
effect and are uniquely homogeneously, but minimally, enhanced.
Other aetiologies of cerebral masses are more rarely diagnosed.
Cerebral candidiasis (Candida albicans) occurs much more frequently
in the United States. CT and MR findings are similar to those described
above for toxoplasmosis. Nocardial brain infection (Nocardia aster-
oides) is reported to show multiloculated, cystic lesions that exhibit ring
enhancement with contrast. Tuberculosis is not rare, and may character
istically manifest itself as meningitis. As in non-immuno compromised
patients, tuberculomas can develop, detected as nodular or ring-enhanced
masses with an appearance similar to that of toxoplasmic abscesses.
Tuberculous "cerebritis" displays an ill-defined T1 hypointense and T2
1313
Figure 5.
HIV encephalitis.
Plain CT scan. Bilateral and
symmetric diffuse hypodensity
in the periventricular white
matter without any mass effect.
hyperintense pattern in both cortex and white matter; post-contrast stud

ies show a diffuse, irregular gyral-like enhancement.
White matter lesions

HIV encephalitis and viral infections are the most common white mat
ter abnormalities. Their prognosis is very poor, but their neuroimaging
patterns must be recognised to enable differentiation from the other more
treatable lesions.
MR is the best neuroimaging technique for evaluation of gliosis and
demyelination foci due to HIV infection; the most frequently reported
abnormality on CT is cerebral atrophy, rarely white matter hypodense
abnormalities are observed (Fig. 5); early cerebral atrophy is considered
to be a poor prognostic element. Progressive subacute HIV encephali
tis■,early in its evolution, appears on MR as small-sized T2 hyperintense
areas that, as time passes, progressively coalesce becoming larger with
ill-defined margins within the periventricular white matter. The diffuse
T2 hyperintense white matter zones seen in the HIV leukoencephalopa-
thy are bilateral and symmetric and spare the arcuate fibers. In both cases,
no hyposignal is detected on T1 sequences, and the absence of a mass
effect and lack of contrast enhancement are constant.
1314
RADIOLOGY IN AIDS
Progressive multifocal leukoencephalopathy (PML) (Papova JC virus)

remains fatal. On MR, the areas of demyelination, with oedema, appear
as asymmetrical, uni- or bilateral, Tl hypointense and T2 hyperintense
areas. They are predominantly in the parieto-occipital regions, usually
extending, with sharp margins, to the inferface between gray and white
matter. They reach the paracentral regions without any mass effect or
gadolinium enhancement. CT reveals hypodense lesions, but their extent
is underestimated and subtle enhancement cannot be eliminated; in such
cases, MR remains essential.
Cytomegalovirus infection (CMV), initially thought to be the causal
agent of AIDS, induces encephalitis, demyelination and neuronal lesions
that are rarely detected by CT; when they are, scans show hypodense ill-
defined non-enhanced areas. On MR, nodular hyperintense areas located
in the basal ganglia and cortex with white matter lesions, are highly sug
gestive of CMV when they are associated with the characteristic
subependymal lesions.
Vascular lesions
Vascular lesions can be of embolic origin (endocarditis), vasculitis (tu
berculosis, aspergillosis, CMV, candidiasis) can have ischaemic (vas
cular narrowing or occlusion) or hemorrhagic (infectious aneurysms or
haemorrhagic infarcts) presentations.
Subependymal and leptomeningeal lesions

Subependymal lesions are rare and are essentially due to CMV necro
tizing ventriculoencephalitis. On CT, as on MR, the ventricular inter
faces are finely underlined with a characteristically enhanced border.
When the lesions extend into the parenchyma, differentiation from lym
phoma can become difficult and a stereotaxic biopsy may be necessary.
Although meningitis is frequently diagnosed based on clinical exam
ination (HIV, CMV, toxoplasmosis, Candidiasis, Coccidioidomycosis,
Histoplastomosis, Listeriosis ...), diffuse meningeal enhancement is
rarely detected even on MR scans. In addition, tuberculous meningitis
can display a more characteristic pattern as an intensely thickened basal
cisternal meningeal enhancement. Cryptococcal meningitis is character
ized by the presence of small cystic collections of cryptococcal organ
isms in the perivascular (Virchow-Robin) spaces which display focal
non-enhanced areas of increased T2 and decreased T 1 signals in the basal
1315
Figure 6.
Lymphoma.
Axial Tl MR image at the T4
level. Extensive spinal cord
compression (arrows) with ad
jacent corporeal erosion (ar
rowheads).
ganglia regions. Lastly, meningeal lesions can be observed with primary

lymphoma or more often with distant localizations of systemic malignant
lymphoma.
Spinal pathology
Neuroimaging (particularly MRI) is essentially devoted to the detection
of extradural compression of the spinal cord or its nerve roots by, for ex
ample, lymphoma (Fig. 6), immunoblastic sarcoma, plasmocytoma,
metastases and more rarely, spondylodiscitis (candidiasis, tuberculosis).
The clinically, frequently observed HIV myelopathy and polyneu
ropathies do not lend themselves to radiological diagnosis (non-specific
hyperintense medullary signal, rarely thickened nerve roots).
THORACIC MANIFESTATIONS
Thoracic manifestations of AIDS can be divided into infectious and non-
infectious entities, the latter including neoplastic and non-neoplastic dis
eases. The type of pulmonary manifestations seen in AIDS has evolved
considerably; this is partly due to improvement in therapy, such as the
widespread use of prophylaxis for Pneumocystis carinii pneumonia
(PCP), while infection due to Mycobacterium tuberculosis has been ris
ing at an epidemic rate, and the number of patients with Kaposi's sar
coma (KS) has been decreasing continuously.
1316
RADIOLOGY IN AIDS
Figure 7.
Cystic PCP. Radiographic
CT correlation.
a) Posteroanterior chest ra
diograph shows the pres
ence o f diffuse pulmonary
infiltration, predominantly
distributed in upper and
middle lung zones, associ
ated with subtle, bilateral
thin-walled cysts in the up
per lobes.
b) CT scans made through
the carina at the same
time as (a), shows that nu
merous cysts o f various
sizes and wall thickness
are seen bilaterally in the
upper lobes that are infil
trated with nodular and
ground glass opacities.
Subtle bilateral pneumoth
orax is also seen.
Infectious diseases
Pneumocystis carinii pneumonia (PCP)

PCP is the most common pulmonary infection in patients with AIDS.
This infection occurs at least once during the course of the disease in ap
proximately 60% of AIDS patients, and nearly one-quarter of these ini
tial episodes is fatal. In addition, the likelihood of severe recurrent in
fection occurs in between 20 and 40% of all cases. Radiographically,
PCP appears as peripheral interstitial infiltrates that may progress within
a few days to diffuse consolidation involving the entire lung. Atypical
patterns, including focal parenchymal lesions, cavitary nodules, hilar
and/or mediastinal adenopathy, pleural effusions and even a miliary pat
tern, occur in 5 % of the patients. They should prompt consideration of
possible coexisting infections.
1317
Figure 8.
M. Tuberculosis.
Posteroanterior radiograph shows
consolidation in the upper part o f the
left upper lobe containing several
cavities. This pattern is consistent
with mycobacterium or bacterial in
fections.
An increasing number of patients also developing cystic lung disease

demonstrated radiographically by the presence of air-filled cysts or pneu
matoceles predominantly located in the upper lobes. The etiology of both
these signs has not been firmly established, but there is a clear associa
tion between the presence of cystic abnormalities and the development
of pneumothorax (Fig. 7). Calcified lymphadenopathy is increasingly
common and seems to be related to prophylaxis with aerosol delivered
pentamidine. Finally, in 10% of the cases, the chest radiograph will ap
pear normal in patients with proven PCP. Although the radiograph re
mains the radiological standard of diagnosis, CT can show ground-glass
densities even when the chest film has been interpreted as being normal.
In addition, CT may show unexpected bronchial dilatation as well as cys
tic lung disease.
Mycobacterial infection
Infection with Mycobacterium tuberculosis occurs in about 10% of cases
and its incidence is increasing every year. The radiologic appearance of
tuberculosis reflects the degree of impairment of the immune system.
When the deficiency is subtle, tuberculosis is usually indistinguishable
from that which occurs in non-HIV-infected patients, with upper lobe
cavitary infiltrates (Fig. 8). The more advanced the immunodeficiency
is, the more suggestive of primary disease the radiographic pattern is, in-
1318
RADIOLOGY IN AIDS
eluding adenopathy, effusion and diffuse infiltrates without evidence of

cavitation. At this stage, the presence o f extensive low-density medi
astinal and hilar lymphadenopathy on contrast-enhanced CT scans is
highly suggestive o f the diagnosis of tuberculosis or fungal infection.
Pulmonary disease is relatively uncommon in patients infected with
M. avium-intracellulare and usually occurs late in the course of HIV in
fection. The radiographic abnormalities include intrathoracic adenopa
thy, pulmonary infiltrates, nodules and a miliary pattern. Other atypical
mycobacteria may cause pulmonary infection in AIDS is M. kansasii.
Bacterial infections
The incidence of bacterial infections in AIDS patients has risen sharply.
It is currently estimated that 5-30% of AIDS patients develop bacterial
pneumonia during the course of their disease.
In pyogenic infections, the radiograph typically shows lobar consoli
dation, nodules and focal infiltrates with or without an associated pleural
effusion. However, some cases present with a predominant interstitial
infiltrate which is indistinguishable radiographically from that usually
associated with PCP infection. A prompt diagnosis of bacterial infection
is necessary because most patients respond to routine antibiotic therapy.
In some cases, CT can be of value by revealing foci of cavitation or necro
sis, as well as documenting the presence of unsuspected loculated pleural
effusions or bronchiectatic foci.
Fungal diseases
Fungal infections are uncommon, occurring in less than 5 % of AIDS pa
tients. They include infections with Cryptococcus neoformans,
Histoplasma capsulatum, Coccidioides immitis, Candida albicans and
Aspergillus.
C. neoformans is the most common cause of fungal pulmonary infec
tion in patients with AIDS. Chest radiographs may show a wide range
of abnormalities but, in most patients, films are either normal or show
focal parenchymal disease. In histoplasmosis, the chest radiograph is nor
mal or shows disseminated nodular disease. In patients with coccid
ioidomycosis, films usually reveal a diffuse interstitial infiltrate often as
sociated with thin-walled cavities. Aspergillus is rarely the cause of pri
mary infection, however, secondary aspergillosis of cavities has been
noted in association with PCP.
1319
Figure 9.
KS.
a) Posteroanterior radiograph
shows bilateral perihilar in
filtrates predominantly dis
tributed in middle and lower
lung zones.
b) CT scan through the lower
lobes shows a typical pattern
o f tumours extending along
perivascular and peri
bronchial pathways from the
hila into the lung associated
with a few, small, poorly de
fined peripheral nodules.
Non infectious diseases
Kaposi's sarcoma (KS)

Almost all cases of KS in AIDS patients have been documented to oc
cur in homosexual or bisexual men. It has been postulated that its de
velopment may be dependent upon an as yet undiscovered cofactor and
may not be directly due to HIV infection, per se. Pulmonary involve
ment occurs in approximately 20% of the patients with AIDS-associated
KS, and it is almost always preceeded by cutaneous or visceral involve
ment. The radiograph shows bilateral infiltrates associated with charac
teristic poorly delineated nodules. Pleural effusions occur in up to one-
third of the patients and are typically serosanguineous. Lymphadenopathy
develops in nearly 10% of cases and tends to be a late manifestation of
KS. As diffuse interstitial infiltrates are non-specific and may be sec-
1320
RADIOLOGY IN AIDS
ondary to either KS or other entities, especially opportunistic infections,

both CT and radionuclide imaging may be useful. On CT scans, the pul
monary involvement due to KS is seen as poorly defined peribronchial
and perivascular densities, typically emerging from the hilum, associ
ated with subpleural nodules and pleural effusions (Fig. 9). This highly
characteristic distribution of the disease allows a presumptive diagnosis
of parenchymal involvement in selected cases. Sometimes, CT scans
show a pattern more consistent with lymphangitic carcinomatosis, prob
ably reflecting involvement of central nodes. Since gallium rarely accu
mulates in KS patients, in those with KS and a coexisting opportunistic
infection, gallium-67 scans may indicate the optimal site for biopsy or
lavage. Bronchial erythematous plaques seen during bronchoscopy
should be considered pathognomonic. The diagnosis can also be made
based on a bronchial biopsy. Because chemotherapy can achieve short
term palliation, bronchoscopy, bronchoalveolar lavage and scans should
be performed in an attempt to diagnose KS.
Lymphocytic interstitial pneumonitis (LIP)

LIP occurs in patients with AIDS and is considered a disease indicator
when confirmed histologically in children under 13 years of age or if
documented in HIV-positive adults. The cause of LIP is unknown and
could possibly be an indirect immune response to pulmonary infection
by HIV. Radiographically, LIP is seen as fine and coarse diffuse, non
specific reticular or reticulonodular opacities with or without superim
posed patchy foci of airspace consolidation. These findings are typically
indistinguishable from those of other opportunistic infections.
Adenopathy and pleural effusions are usually absent. Diagnosis requires
an open lung biopsy. As in non AIDS patients, progression to lymphoma
is unusual.
AIDS-related lymphoma (ARL)

The incidence of ARL is clearly increasing. These tumours have a ten
dency to be highly aggressive, displaying poorly differentiated histologic
subtypes associated with a poor prognosis. In most cases, AIDS is at an
advanced state at the time of ARL diagnosis. The tumours are primarily
extranodal in distribution and thoracic sites are relatively less common
than those in the central nervous system, gastrointestinal tract, liver,
spleen and bone marrow. ARL usually manifests itself as either solitary
1321
or multiple well-defined pulmonary masses, or as a focal parenchymal

infiltrate, often in association with pleural effusions and frequently with
out mediastinal or hilar disease. These findings are non specific and may
also be seen in patients with fungal infection or other tumours, includ
ing KS or solid tumors. The definitive diagnosis usually requires histo
logic confirmation.
Diagnosis and role of imaging

AIDS patients suspected of having pulmonary disease usually undergo
fibreoptic bronchoscopy, particularly when a non-infectious etiology is
suspected. Bronchoscopic investigation includes bronchoalveolar lavage
sometimes in conjunction with transbronchial biopsy. In some cases, the
initial bronchoscopic findings are non-diagnostic and further monitoring
is required, including the patient's clinical status and radiologic findings.
Gallium scintigraphy can be indicated to determine if active disease is
present. In the case of clinical or radiological deterioration, patients
should undergo a repeat bronchoscopy. Patients with focal lung disease
may benefit from thoracic needle biopsy. The role of open lung biopsy
is more controversial. However, surgery may be indicated specifically
for patients in whom no diagnosis has been established. CT can help to:
a/ identify occult pulmonary disease including areas of ground-glass
opacity in early PCP as well as occult tuberculous infection; Ы differ
entiate PCP from KS and lymphoma; с/ identify the low-density lym-
phadenopathy in patients with tuberculosis; d/ guide transthoracic nee
dle biopsy.
ABDOMINAL MANIFESTATIONS
Abdominal manifestations of AIDS are numerous and include
parenchymal, lymph node and primary gastrointestinal and urinary tract
disorders. Abdominal symptoms are frequent and affect up to 90% of
patients with AIDS or AIDS-related complex (ARC). Multiple infections
are the rule in AIDS and may be associated with lymphoma and/or
Kaposi's sarcoma (KS). Moreover, AIDS patients can also be affected
by protozoan and bacterial infections, such as tuberculosis, related to
sexual promiscuity and low socioeconomic status. Multiple sites of in
fections are involved in 64% of patients. Clinical symptoms and physi
cal findings alone rarely suggest a specific etiology. The role o f imaging
methods is to identify the target-organ as well as the extent of pathologic
1322
RADIOLOGY IN AIDS
involvement, to suggest a specific diagnosis and to facilitate percuta

neous needle biopsy for a precise diagnosis.
AIDS-related complex (ARC)

Patients with ARC generally present with weight loss, fever, malaise, di
arrhoea, and generalized lymphadenopathy. Ultrasonography (US) and
CT findings include mild splenomegaly and clusters of mesenteric and
retroperitoneal lymph nodes less than 1.5 cm in diameter. Percutaneous
needle biopsy is warranted only when lymph nodes measure 2 cm or
more in diameter, because such enlarged nodes are rarely the result of
reactive hyperplasia but are generally the sign of infection or neoplastic
disease.
Malignant lymphomas
An increased incidence of all lymphomas is observed in AIDS patients,
especially non-Hodgkin's lymphoma (NHL) of the small noncleaved cell
type, immunoblastic sarcoma and Hodgkin's disease of the high-grade
mixed-cellularity type. Moreover, the Center for Disease Control rec
ognizes undifferentiated lymphomas as a criterion for AIDS. The ma
jority of AIDS-related lymphomas (ARL) have aggressive histologic
subtypes and are diagnosed at advanced stages, generally stage III or IV.
They carry a poor prognosis, the median survival time for patients on
chemotherapy being 5.5 months. AIDS patients with systemic NHL have
an abnormally large number of Epstein-Barr virus-infected В cells.
Symptoms at the time of presentation are often nonspecific and include
weight loss, fever, night sweats, diffuse abdominal pain and malaise.
Only 4% of patients have demonstrable peripheral adenopathy.
Moreover, 74-95% of AIDS patients have involvement of extranodal
sites and the majority of patients have multiorgan involvement.
Intrahepatic involvement is a stricking feature of ARLs, when com
pared to non-immunocompromised patients. Its incidence is between 9%
and 26%, compared with 4-6% in patients without AIDS. US and CT
are equally valuable in diagnosing multiple small nodular areas of macro
scopic involvement. The typical findings include hypoechoic nodules on
US, and hypodense, homogeneous and well-defined nodules on CT (Fig.
10). However, the nodules can occasionally be hyperechoic with a tar
get appearance on US, and peripheral enhancement on CT. Diffuse in
filtration is less frequent and is associated with homogeneous he-
1323
Figure 10.
AIDS-related lymphoma.
Abdominal contrast-enhanced
CT scan shows bilateral renal
enlargement with low-density
lymphomatous renal masses
associated with two focal he
patic lesions (arrows).
patomegaly. Histologic subtyping of lymphoma is crucial for chemother

apy and can be obtained by percutaneous core liver biopsy.
Focal splenic involvement and bowel involvement are observed in
32% and 26%, respectively, of ARLs, as compared to 9% and 12% in
other patient groups with similar histology. The incidence of renal le
sions is also increased. Imaging findings of splenic and renal ARLs in
clude solitary or multiple nodules, which are usually heterogeneous, hy-
poechoic on US and hypodense on CT scans (Fig. 10). Alimentary tract
lymphoma in AIDS patients has a wide variety of radiographic appear
ances. In patients with gastric or small bowel lymphoma, thickened folds,
multiple irregular masses and deep ulcerations can be noted on barium
studies. Colonic involvement may present as polypoid lesions, circum
ferential, diffuse wall thickening and bowel intersusception, and can also
present with perforation or obstruction. Compared to Kaposi's sarcoma,
lymphomatous masses tend to be bulky and are more commonly associ
ated with submucosal infiltration. Other sites of lymphomatous involve
ment are numerous and include the peritoneum, the pancreas and the
adrenals.
The appearance of lymphadenopathy in ARLs is nonspecific. Bulky
abdominal lymphadenopathy is common in ARLs, although it is seldom
the presenting feature. Moreover, central nodal groups are frequently in
volved without evidence of peripheral adenopathy. CT is the imaging
modality of choice in determining the extent of involvement and for guid
ing percutaneous needle biopsy.
Kaposi's sarcoma (KS)

KS is the most common malignancy in AIDS patients. For unknown rea
sons, its incidence is higher among homosexual men (44%) than in other
1324
RADIOLOGY IN AIDS
Figure 11.
Kaposi's sarcoma o f the
duodenum and proximal
ileum.
Note the presence o f multi
ple, irregular filling defects
associated with wall thick
ening.
patients with AIDS. The sites of involvement include the skin (93%),
lymph nodes (72%), the gastro-intestinal tract (48%) and both the liver
and spleen (34%).
Nodal involvement is characterized by bulky mesenteric and retroperi
toneal adenopathies with nodes more than 1.5 cm in diameter. On CT
scans, they are typically homogeneous with no low-density areas (as in
mycobacterial infection). However, KS cannot be distinguished from
other neoplastic or infectious causes and pathologic confirmation is
mandatory. It can be reliably obtained by fine needle aspiration biopsy.
Involvement of the stomach and small bowel is common, while the colon
is rarely affected. The lesions present as intraluminal filling defects on
barium studies, of variable size and number (Fig. 11). Central umbilica-
tion is characteristic of KS, with a ’’target" appearance on air-contrast
studies. Graded compression can help visualize a lesion hidden between
folds; coalescent lesions may produce thickened folds visible on CT
imges. Focal hepatic lesions of KS are rarely encountered on US or CT;
they include hepatic nodules and periportal infiltration with subsequent
dilatation of the intrahepatic bile ducts. As KS can involve almost any
abdominal organ, it can produce a variety of nonspecific lesions which
can be biopsied under CT guidance.
1325
Opportunistic infections
Oesophagus
Candida is the most frequent cause of oesophagitis in AIDS and oe
sophageal candidiasis is diagnostic of AIDS in a patient with known HIV
seropositivity. The main symptom is dysphagia. Double-contrast oe-
sophagography has a higher sensitivity (85-90%) in detecting esphageal
candiadiasis than single-contrast studies. Candiadiasis can produce a dif
fusely ulcerated shaggy mucosa or more limited lesions such as focal
plaques, subtle, longitudinally orientated filling defects and cobbleston
ing.
Cytomegalovirus (CMV) oesophagitis typically produces discretely
marginated diamond-shaped ulcers with a peripheral lucency that repre
sents a zone of edema against a background of normal mucosa.
Furthermore, CMV often involves the distal half of the oesophagus with
extension of the process in the stomach. Another unique feature of CMV
is its propensity for causing giant oesophageal ulcers resulting from both
infectious destruction of the mucosa and ischemic necrosis induced by
CMV vasculitis. Herpex simplex virus is the third major aetiology of oe
sophageal infection in AIDS patients. It produces radiographic findings
similar to those observed in CMV oesophagitis at both the early and ad
vanced stages of disease.
Stomach
Most infectious gastric lesions are detected on barium studies, performed
to evaluate the oesophagus or the small bowel in patients with dyspha
gia or diarrhoea. They rarely produce symptoms which suggest a diag
nosis or focus investigations on the stomach. CMV is the main aetio-
logical organism. It typically produces wall thickening of the OG junc
tion and antrum, associated with gastroesophageal ulcerations which can
lead to stricture formation and stenosis. Submucosal involvement can
appear as "thumbprint" lesions, usually more regular and less discrete
than the masses seen in KS. Gastric invasion by Mycobacterium tuber
culosis with lesser omental abscess has also been described.
Small bowel
On upper gastrointestinal barium studies, abnormalities are often multi
focal and affect the duodenum in 82% of the cases, the jejunum in 64%
1326
RADIOLOGY IN AIDS
and the ileum in 46%. The main clinical manifestations of small bowel
disease is diarrhoea. Mild diarrhoea is a frequent symptom in AIDS pa
tients which can be related to infection, tumours or drug therapy. Some
patients present with severe diarrhoea, accompanied by weight loss, de
hydration, electrolyte imbalance and m a l a b s o r p t i o n . The most common
cause of this serious syndrome is protozoan infection by Cryptosporidia
of Isospora belli. Radiographic findings include thickened folds in the
proximal small bowel, fragmentation, spasm, and mild dilatation. More
severe involvement produces mucosal atrophy with a subsequent "tooth
paste" appearance. Differential diagnoses include giardiasis, strongyloi-
dosis, acquired hypogammaglobulinemia, cystic fibrosis and mycobac
terial infections. Several antimicrobial treatments have been attempted
with limited success. Both Mycobacterium tuberculosis (MT) and
Mycobacterium avium intracellulare (MAI) may be encountered in the
small bowel. On barium studies, MAI infection is characterized by a
pseudo-Whipple appearance and marked hypertrophy of the valvulae
conniventes in the distal ileal loops. Associated mesenteric and retroperi
toneal lymphadenopathy, splenomegaly and ascites are usually shown
by CT.
CMV infection predominantly involves the distal ileum which has a
narrowed appearance with discrete submucosal nodules and thickened
folds. Ulceration, intestinal perforation or fistula are potential compli
cations of the necrotizing vasculitis induced by CMV.
Colon
Colitis may be due to opportunistic infections, as well as to the common
pathogens which are frequently encountered in homosexual men. The
"gay bowel syndrome" includes traumatic and infectious lesions of the
rectum and colon by pathogens such as amoebae, gonococci, salmonel-
lae, shigellae and Campylobacter. In 90% of homosexual men, CT shows
an infiltration of the perirectal fat and thickening of the rectal wall.
Although several colitides are unique to immunocompromised patients,
only CMV colitis produces distinctive radiographic findings. They in
clude diffuse mucosal granularity, aphthous ulcers and caecal spasm with
terminal ileal fold effacement. The presence on CT of a "target sign" due
to submucosal oedema as well as right-sided and ileal involvement, are
suggestive of CMV colitis. In advanced stages, CMV colitis may pre
sent with toxic megacolon, perforation, deep ulceration and submucosal
1327
Figure 12.
Hepatic abscess.
a) Contrast-enhanced CT
scan shows small hepatic
abscesses (arrows) with a
hypodense and nodular
appearance. Liver biopsy
was positive fo r MAI.
b) In another patient, con-
trast-enhanced CT scan
shows ill-defined area o f
low-density in the right
hepatic lobe (arrow).
Liver biopsy revealed
Candida albicans.
hemorrhage. Plain films occasionally show pneumatosis coli.
Liver. AIDS-related cholangitis

The most frequent pathogens involved in hepatic abscess formation are
MAI, CMV, Cryptococcus, Candida and Histoplasma capsulatum.
Imaging findings include multiple focal lesions on US with a hypodense
appearance on CT (Fig. 12 a). However, granuloma formation is fre
quently impaired in AIDS and disseminated hepatic infections can pre
sent as ill-defined lesions (Fig. 12 b) which can be difficult to detect with
US and CT and to differentiate from diffuse or focal steatosis. In these
patients, liver biopsy with culture almost always establishes the correct
diagnosis.
Abnormalities of the biliary tract in AIDS patients include acalculous
cholecystitis, papillary stenosis and cholangitis. The proposed patho
genic mechanisms are infection of the biliary tree by CMV or Cryp
tosporidia, and less probably, direct infiltration of the bile duct mucosa
by HIV or biliary inflammation due to the immune deficiency. Patients
1328
RADIOLOGY IN AIDS
Figure 13.
Adenopathy from
Mycobacterium tuberculosis
infection.
CT scan demonstrates bulky
retroperitoneal, coeliac and
periportal nodes with central
low density areas.
present with right upper quadrant pain, jaundice, fever or abnormal liver
function tests. US or CT can demonstrate segmental or diffuse dilata
tion, irregularity, and narrowing of the intra- or extra-hepatic bile ducts.
Wall thickening of the bile ducts and gallbladder is frequently associ
ated with enhancement of the wall of the bile ducts on CT. Periportal hy
perechogenicity due to fatty infiltration of the liver has been observed in
addition to cholangitis. Noninvasive imaging with US and CT may sug
gest AIDS-related cholangitis. However, direct cholangiography or
ERCP may be useful to document the presence of subtle cholangitis. The
only effective treatment is endoscopic sphincterotomy which can be per
formed in patients with isolated ampullary stenosis in order to obtain re
lief of the right upper quadrant pain.
Lymph nodes
Abdominal opportunistic infections produce clinical and radiographic
patterns that can be indistinguishable from AIDS-related Kaposi's sar
coma, lymphoma or even lymphadenopathy syndrome. MAI produces a
systemic infection and is more common than MT. Culture is necessary
to differentiate them. They typically involve the mesenteric and retroperi
toneal lymph nodes and produce bulky nodal masses. On CT images, the
presence of focal parenchymal lesions and low-attenuation lymph nodes
suggest MT (Fig. 13), whereas marked hepatic and splenic enlargement,
diffuse jejunal wall thickening and solid lymphadenopathy suggest MAI.
Low-attenuation lymph nodes in MT probably represent areas of necro
sis or caseation. Definitive diagnosis requires culture of the nodal tissue
which can be obtained by percutaneous biopsy.
1329
Genito-urinary tract
The incidence of urinary tract infection has been reported to be as high
as 50% in AIDS patients. Pyelonephritis is frequently complicated by
intrarenal or perinephric abscesses. CT in these patients shows swollen
kidneys with perirenal fascia thickening and focal areas of low density,
with a peripheral enhancement representing renal abscesses. MT and as-
pergilloma can present as multiple masses, with a hyperechoic appear
ance on ultrasonography. Hydronephrosis can be caused by an obstruc
tion due to fungus balls. Intrarenal areas of increased echogenicity have
been reported in patients with Pneumocystis carinii disease, MAI and
histoplasmosis. These changes can be associated with extrarenal infec
tions and with AIDS-related nephropathy which is characterized by in
creased echogenicity. Multiple pathologic processes have been proposed
to explain this increased echogenicity, including glomerulopathy, acute
tubular necrosis, interstitial nephritis, nephrocalcinosis, tubular dilata
tion and atrophy.
Diagnosis and role of imaging

Radiologists have a key role in evaluating abdominal disorders in AIDS
patients. In patients with dysphagia, diarrhoea, or colitis, barium studies
can identify the site of involvement of the GI tract, suggest a diagnosis
and guide the site of endoscopic search and site of biopsies.
Ultrasonography is the initial screening method in patients with abdom
inal pain and jaundice. It can reveal cholangitis, focal parenchymal le
sions and enlarged lymph nodes. However, CT remains the imaging
modality of choice for the diagnosis, staging and follow-up of abdomi
nal neoplasms including lymphoma and Kaposi' sarcoma.
1330
Index
(3-blocker 1173 acinar atelectasis 540

P-hemolytic streptococcal - disease 547
pneumonia 543 - nodule 541
(32-microglobulin amyloid acoustic impedance 27,65
deposition 336,343 acquired cholesteatoma 235
1 ,25-dihydroxyvitamin D 3 1128 - cystic disease 1142
1311 cholesterol adrenal imaging 1124 - heart disease 570
i3ij or 123j m i b g adrenal imaging 1124 - immune deficiency syndrome
1311-19-iodocholesterol 1211 (AID
131I-Hippuran 1122 - small-bowel obstruction (SBO) 583
3D reconstruction 810 - spinal stenosis 330
5-fluorouracil 154 - valvular disease 793
57Cr-EDTA 1122 acrania 1226
99m-Tc-HIDA 1046,1053 acro-osteolysis 441,504
99mTc Glucoheptonate 1122 acromelic 493
99mTc DMSA 1122 acromioclavicular joint
99mTc sestamibi 785 instability 403
99mTc DTP A 1122 ACTH 1209
99mTc MAG 1122 actinomycosis 736,966
A/D converters104 acute aortic insufficiency 797
A-mode 6 7 ,6 8 - arterial occlusion 825
abdominal aorta 820 - bowel ischaemia 1105
- circumference (AC) 1220 -cholecystitis 1051
- trauma 1107 - disseminated encephalo-
abortingtwin 1223 myelitis (ADEM) 21 6 ,2 1 7 , 623
abscess 6 2 2 ,6 5 2 ,1 0 7 2 ,1 1 9 5 - ischaemia o f the bowel 983
abscess drainage 159 - ischaemic colitis 1003
absent thumb 508 - osteomyelitis 442
absorbed dose 31 -o titis media 233
AC (abdominal circumference) 1220 -pyelonephritis 1150
acalculous cholecystitis 1052,1328 - rheumatic fever 570
accordeon pattern 502 - sinusitis 240
acetabular protrusion 440 - tubular necrosis 1156
achalasia 902 - viral pericarditis 802
achondrogenesis 492,496 acyanotic CHD 558
achondroplasia 330, 492, 493,495, 1227 Addison's disease 1209
XV
ADEM (acute disseminated alpha particle 28,61

encephalomyelitis) 2 1 6 ,2 1 7 ,6 2 3 - radiation 17
adenovirus 734 alpha-heavy chain disease 974
adenocarcinoma 244, 720, 974 aluminium filter 37
adenoid hyperplasia 247 alveolar cell tumor 720
adenoma 1006, 1032 -echinococcosis 1270
adenomatoid odontogenic tumor283, 284 - hydatid disease 1269,1270
adenomyomatosis 1053 -opacity 737
adenomyosis 1202 ameloblastic odontoma 283
adenopathy 553 ameloblastoma 283
adenovirus 549 amelogenesis imperfecta 272
aditus 230 American trypanosomiasis 1272
adrenal adenoma 1213 amniotic fluid 1230
-atrop h y 1210 - fluid index (AFI) 1220, 1231
- cortical adenoma 1208 -flu id volume 1220
- cortical carcinoma 1208,1213 amoebiasis 1239
-cy st 1215 amoebiasis o f the bowel 1239
-g la n d 1207 -c h e st 1245
- haemorrhage 607 -liv e r 1242
- hyperplasia 1208 amoebic hepatic abscess 1242
adrenogenital syndrome 1209 -hepatitis 1242
adult polycystic kidney disease - liver absces 1245
(APCKD) 595, 1140, 1155 - lung abscess 1245
adult respiratory distress syndrome amoeboma 1241
(ARDS) 743, 738, 758, 770, amplitude mode 68
adynamic ileus 1105 amyloid 345
AFI (amniotic fluid index) 1220, 1231 amyloid deposits 336, 346
aganglionic segment 585 amyloidosis 747, 1156, 1210
aganglionic colon 585 anaerobic infection 730
agaragar 131 analogue/digital transformation 103
AIDS (acquired immune deficiency analogue detectors 47
syndrome) 214, 754, 920, 1156 -im age 101
AIDS-related cholangitis 1328, 1329 - techniques 47
- complex (ARC) 1322, 1323 anaphylactoid (anaphylactic) shock 130
- infections 966 anaphylactoid reaction 127,129
- Kaposi's sarcoma 1329 anaphylatoxins 128
- lymphoma (ARL) 1321,1323 anaplastic astrocytoma 199
AIIMM 583 Ancylostoma duodenale 1281
ainhum 1296, 1297 ancylostomiasis 1281
air bronchogram 541, 542, 726, 726, 747 Anderson lesion 348
- embolism 813 anemia 503,607
- trapping 713 aneurysm 6 2 1 ,6 9 3 ,8 0 0 ,8 3 6
airways infection 547 aneurysm o f the aortic arch 707
akinesis 799 - ascending aorta 707
alamagna 176 aneurysmal bone cyst 288, 450
- parva 176 angina pectoris 799
ALARA (As Low As Reasonably angiocardiography 557,563,781
Achievable) 33 angiodysplasia 861, 1021, 1022
alcohol abuse 445 angiography 171
alcoholism 728 angiomyolipoma 1145
alevolar consolidation 724 angiotensin II 1132
allergoid (allergic) reaction 127, 129 angiotensin-converting enzyme 1131
XVI
INDEX
angular displacement 388 Apert syndrome 489

ankle injury 412 aphthoid ulcer 959, 963
ankylosing spondylitis apical segment 685
336, 338, 346, 430, 433,437, 751 apico-posterior segment 685
ankylosis 341 apophyseal joints 299, 347
Ann Arbor staging system 882,883 appendicitis 586,1093
annihilation 64 appendicolith 587
annulus fibrosus 300 aqueductal stenosis 619
anodontia 272 arachnoid cyst 226
anorectal evacuation disorder 1014 artificial ventilation 541
- malformation 583 ARC (AIDS-related complex) 1322, 1323
antegrade pyelography 161 architectural distortion 654, 655
antenatal screening 1220 ARDS (adult respiratory distress
anterior communicating artery 184 syndrome) 738, 743, 758, 770
- diaphragmatic hernia 707 argon-laser 856
- dislocation 402 ARL (AIDS-related
- fat pads 399 lymphoma) 1321,1323
- hernia 697 Armillifer armillatus 1301
-junction line 688 arterial embolization 825,1073
- longitudinal - occlusive disease 824
ligament 300 ,3 0 1 ,3 0 4 ,3 1 1 - switch procedure 567
- mediastinal masses 705 - thrombosis 825
- mediastinum 552 arteriovenous malformation
- sacral meningocele 361a (AVM ) 152, 171, 369, 624, 843, 1021
- segment 685 - fistula 864
- tibial artery 820 arteriosclerosis 657,1130
- tibial vein 822 arteritis 829, 831
anteroposterior radiograph 671 arthritis 432, 446
antiparallel protons 74 arthrography 376
antler sign 739 aryepiglottic folds 538
antrum 230 arytenoid cartilage 257
aortic aneurysm 837, 1106, 1173 asbestosis 744
- arch 819 ascariasis 1276,1278
- arteritis 1291 Ascaris lumbricoides 1276
- syndrome 832 ascaris infestation 968
- balloon pump 768 ascending phlebography 813
- dissection 677 - thoracic aorta 819
- diverticulum 571 ascites 1086
- insufficiency 797 ASD (atrial septal
- rupture 759, 760 defect) 558, 559, 564, 566
- stenosis 563, 792, 796 aseptic necrosis 516, 531
- valve 787 - spondyliltis 336
- valvular disease 796 Asian Oceanian Society o f
- valvular insufficiency 791 Radiology (AOSR) 15
- valvular stenosis 563, 837 Askin tumor 552
aortitis 829 Aspergillus 3 4 2 ,7 3 6 ,1 3 1 9
aortocoronary by-pass 765 aspergillus spondylitis 342
aortopulmonary window 688, 721 asphyxiating thoracic dysplasia 499
AOSR (Asian Oceanian Society aspiration 728
of Radiology) 15 aspiration pneumonia 769
APCKD (adult polycystic kidney - technique 634
disease) 595,1140,1155 - thromboembolectomy 145
XVII
asthma 710 Barkla, Charles C. 5

astrocytoma 197, 206, 351 Barlow maneuver 482
astroglial tumours 197 Barrett's oesophagus 907,916
asymmetrical density 654 - mucosa 904
atelectasis 716, 719, 725, 699, 768 Barton fracture 392
atherectomy catheter 145, 857 Basic Radiological System (BRS) 14
atheromatous plaque 826, 829 basilic vein 824
atherosclerosis 801,826, 1130 bat-wing 740
atherosclerotic aneurysm 841 Batson's venous plexus 339
atlas 299 BD (biparietal diameter) 1220
atom 19 Becquerel (Bq) 29
atresia o f the external ear canal 232 Behget's disease 964
atrial myxoma 793 benign calcification 657
- septal defect (ASD) 558 - cementoblastoma 283
atrioventriculare communis 561 - cystic leiomyoma 1202
atrioventricular canal defect (AVC) 561 - lymphoid hyperplasia
atrophy 6 1 7 ,6 1 8 (BLH) 946, 976
attenuation 24, 66 benign prostate hyperplasia (BPH) 1192
attenuation number 58 Bennett fracture 392
audio display 70 beta radiation 17
auricle 787 - particles 61
autoantibodies 433 beta-minus particle 28
AV-fistula 813 beta-plus particle 28
AVC (atrioventricular canal defect) 561 bifid rib 682
AVF (congenital arteriovenous bilateral multicystic kidney 1226
fistula) 843 Bilbao-Dotter tube 956
AVM (arterio-venous malformation) bilharzia 1177, 1246
152, 171,369, 624, 843, 1021 bilharziomas 1256
avulsion fracture 386, 402, 477 biliary atresia 588
axial imaging 18 - duct disease 1055
axillary artery 820 - imaging 1031
- vein 824 - obstruction 155
azygos lobe 684 biligraphy 1044
- node 688 Billroth II stomach resection 1097
-v e in 823 Binswanger’s disease 177, 180,219
В cell 502 Biparietal diameter (BD) 1220
В symptom 882 biphasic barium meal 927
B-mode 67 biplane technique 379
Bacillus fusiformis 1293 Bisacodyl 987
backwash ileitis 963, 997 bladder calcification 1252
bacterial endocarditis 794 - calculi 1178
- infection in HIV 1319 - hernia 1179
- pneumonia 549, 754 - tumors 1182
balloon angioplasty 143 blastomycosis 343, 736, 1210
- catheter 853 BLH (benign lymphoid
- dilatation 853 hyperplasia) 946, 976
- expandable stents 146 block vertebra 365, 368
bamboo spine 347 blood flow 173
Bankart lesion 402 - flukes 1246
barium platinocyanide screen 5 - volume 173
- sulphate 131,956 blood-brain barrier 123
- contrast media 131 bloody discharge 654
XVIII
INDEX
blow-out fracture 245 bronchial anomaly 674

blue sclerae 503 - arteriography 772
-lig h t 49 -c a n c e r 700
blunt abdominal - embolization 772
trauma 590,950,1107,1158 - erythematous plaque 1321
Bochdalek hernia 544,697 - wall thickening 548
Boerhaave's syndrome 923,924 bronchiectasis 6 7 4 ,7 1 4
bolus formation 894 bronchiole 686,711
bone bruise 385 bronchiolotis 549
-destruction 447,449 bronchitis 549
- dysplasia 492 bronchogenic cyst 553 ,7 0 7
-erosion 437,521 bronchography 6 7 4 ,7 1 1 ,7 1 6
- infarct 432 bronchopneumonia 549,725
-marrow 338 bronchopulmonary dysplasia
- marrow disease 880 (BPD) 4 6 5 ,5 4 3
-reaction 449 - foregut malformation 553
-sc a n 6 3,424,475 bronchoscopy 674
- scintigraphy 373 brown tumor 288, 527
bony ankylosis 437 BRS (Basic Radiological System) 14, 96
-exostosis 552 Brugia malayi 1299,1301
- sclerosis 338,503 Brunner's gland hyperplasia 946,9 5 0
- spurs 333 bubbly bulb 970
boot-shaped heart 564 buckle fracture 476
botryoid cyst 279 bucrylate 150, 369, 863
bowel bladder 1185 Budd-Chiari syndrome 867,1031
-ischaem ia 1108 Buerger's disease 829,831
-obstruction 1095 bulbar palsy 896
bowel-wall thickening 582 bulging disc 323,330
bowing fracture 475 bull's eye 941
bowler hat sign 993 bum injury 479
BPD (bronchopulmonary burst fracture 306, 313
dysplasia) 465,543 buscopan 900
BPH (benign prostate hyperplasia) 1192 butterfly vertebrae 363, 365, 368
Bq (Becquerel) 29 Caffey disease 528
brachial artery 820 calcaneonavicular coalition 491
brachiocephalic vein 824 calcification 452, 656, 731, 732, 747, 804
brachiocephalic vessel 687 calcified ligament 334
bradykinin 128 -ly m p h nodes 873
brain abscess 211 -p in e a l body 188
-dam age 623 - pleural plaque 702
- stem 205 calcifying epithelial odontogenic
-tum our 209 tumour 283
-tum our 611 calcium ipodate 1042
branchial cleft cyst 259 Caldwell projection 238, 263
branchial cyst 259 CAM (cystic adenomatoid
breast cancer 644,648 malformation) 545
- cancer mortality 665 campomelic syndrome 486
-D oppler US 631 Campylobacter 968
-irradiation 661campylobacter infection 1001
-self-exam ination 663 Candida albicans 1319
breech presentation 484 Candida oesophagitis 913,920
Brodie's abscess 442 - spondylitis 342
XIX
Capillaria philippiniensis 1283 cercaria 1246

capillary hemangioma 220, 843 cerebellar astrocytoma 206
- malformaton 843 - diameter (TCD) 1220
captopril 1132,1133 - infarction 180
captopril-enalpril renogram 1131 - medulloblastoma 206
captopril renography 1124 cerebellum 205
carboxy-methyl-cellulose 131 cerebral candidiasis 1313
carcinoid 971, 1012 - HIV infection 1309
carcinoma 65, 648 - infarction 177
cardiac catheterization 557, 563 - infection 621
- failure 698 - malformation 616
- injury 757 - masses 1311
cardiac tamponade 800 - non-Hodgkin's lymphoma 1312
cardiogenic congestion 739 - palsy 484, 620
cardiogenic edema 739 cerebritis 211
cardiomegaly 568, 569, 1290 cerebro-hepato-renal syndrome
cardiomyopathy 801 (Zellweger) 498, 1228
cardiophrenic fat pad 697 cerebro-spinal fluid circulation 618
cardiovascular malformation 557 cerebrovascular lesions 177
caries 274 cervical cancer 1200
Caroli's disease 1056 - plaque 218
carotid siphons 174 -r ib 364, 682
carpal coalition 489 - spine trauma 306
- fracture 395 CFI (colour flow imaging) 71, 1218
- instability 395 Chaga's disease 904, 1272
carpal-tarsal osteolysis 521 chagoma 1272
carpometacarpal joints 395 Chance fracture 316
cartilaginous growth plate 467 characteristic curve 49
cathecolamines 1132 characteristic X-radiation 20
cathode ray tube (CRT) 62 CHD (congenital heart diseasee) 558
cauda equina 350 chemo-embolisation 153
caustic oesophagitis 921 chemonucleolysis 343, 370
caval filter 846 chemotherapy 154, 450, 462, 732
cavemosometry 1198 chemotoxicity 120
cavernous haemangioma chest radiograph 669
209, 220, 843, 1032 chest wall 681,693
cavography 817 - injury 755
CD (Crohn's disease) -m a ss 551
478, 525, 933, 946, 958, 964, 966, 994, Chiari II malformation 366, 1228
996, 999, 1001, 1241 chiasm 174
CDH (congenital chiasmatic cistema 174
dislocation o f the hip) 482 Chiba needle 1045
CDI (colour doppler imaging) 1218 child abuse 479, 480
CDR (computed digital radiography) 1218 childhood stroke 624
celiac plexus block 165 chlamydia 1001
celiac trunk 820 Chlamydia trachomatis 1286
cellular fibroadenomas 631 choanal atresia 240, 536
cemental dysplasia 285, 287 - polyps 243
cementum 265 cholangiography 1044
central incisors 266 cholangitis 1328
cephalic vein 824 cholecystitis 1051, 1091
cephalometric projection 263 cholecystographic contrast media 133
XX
INDEX
choledochal cyst cleft palate 500

587, 588, 1056, 1226, 1228 cleidocranial dysplasia 272, 274
cholelithiasis 573, 589 clemastin 130
cholesteatoma 234 clinodactyly 489
cholesterol embolism 825 clonorchiasis 1283
cholesterolosis 1053 Clonorchis sinensis 1283
chondral fracture 408 closed fracture 384
chondrification 297, 298, 363 clostridium difficile 1093
chondroblastoma 452 club foot 485, 498, 500
chondrocalcinosis 440 cluster o f malignant calcifications 660
chondrodysplasia punctata 498 CMV colitis 1327
chondroectodermal dysplasia 493, 498 CMV (cytomegalovirus)
chondrolysis 517 4 6 5 ,9 2 0 , 967, 1315
chondromatous tumors 452 CMV oesophagitis 920
chondrosarcoma 290, 452 congenital hepatic fibrosis 594
chordal rupture 794 C 0 2 insufflation 1098
chordoma 204, 359 coagulative systems 128
choriocarcinoma 1224 coalition 491
choroid plexus papilloma 201 coarctation of the aorta 5 6 1 ,5 6 3 ,6 9 4
- plexus cyst 1230 cobblestoning 959
chronic aortic insufficiency 798 Coccidioides immitis 1319
- arterial occlusive disease 825 coccidioidomycosis 343
- bronchitis 711,713 cochlea 230
- cholecystitis 1053, 1100 cochlear aqueduct 230
- cystitis 1177 coeliac angiography 1020
- glomerulonephritis 1155 - disease 950, 969
- ischaemia o f the bowel 984 coherence scattering 23
- lung diseases 728 cold injury 479
- nephrosclerosis 1155 colitis 1093
- osteomyelitis 443 collagen disorder 522
- otitis media 233 - vascular disease 750, 751,801
-pancreatitis 1069,1092 collar-stud ulcer 996
- pyelonephritis 1151 Colles fracture 389
- renal failure 933 collimator 62
- rickets 526 colloid intravascular contrast media 135
- sclerosing osteomyelitis 277 colloid cysts 201
- suppurative osteomyelitis 277 colonic adenoma 1008
chylothorax 698 - cleansing enema 987
chylous exudate 698 - diverticula 989
Ci (Curie) 29 - epithelial polyp 1006
cine CT 60, 775 - haemorrhage 1022
- angiography 773 - volvulus 1101
- fluorography 53 colonoscopy 1006
circle of Willis 174 colorectal carcinoma
circular constrictions 489 (CRC) 888, 1005, 1008
circumflex artery 787 colour-Doppler 818
circumvallate papillae 249 colour-flow Doppler 589
cirrhosis 1034 colour flow imaging (CFI) 71, 1218
cisplatin 154 colour Doppler imaging (CDI) 1218
cisternography 174 colpocystourethrography 1179
clavicle 403 column o f Bertin 1144
cleft lip 1226 columnar-lined oesophagus 916
XXI
comedo-type 654, 658 coronary angiography 781, 798, 799

comminuted fracture 187, 385 coronary artery abnormalities 569
common iliac artery 820 - fistula 569
- carotid artery 819 corrected transposition o f the
communicating vein 821, 822 great vessels 567
communication network 112 corrosive gastritis 933
compensatory emphysema 713, 764 cortical necrosis 1156
complement systems 128 costocervical tmnk 820
complete fracture 385 costochondral osteochondritis 695
complex odontoma 283 costophrenic angle 684, 698, 700, 72
compound odontoma 283, 285 coxa valga 440, 484, 488, 505
compression fracture 386, 388, 402 coxa vara 488, 490
Compton scattering 23, 24, 40 CPPD crystal deposition disease 441
computed digital radiography craniocervical junction abnormalities 364
(CDR) 1218 craniofacial dysostosis 274
computed tomography (CT) 18, 54 craniopharyngioma 224, 225
computerized axial imaging 18 CRC
congenital anomalies 488 (colorectal cancer) 888, 1005, 1008
- arteriovenous fistula (AVF) 843 CREST syndrome 901,094
- AV-malformation 861 cribriform 658
- cyst 250 cricoid lamina 257
- dislocation o f the hip (CDH) 482 - cartilage 257
- fibromatosis 530 cricopharyngeal bar 893
- heart disease (CHD) 489, 558 - prominence 897
- lobar emphysema 5 4 4 ,713 -w e b s 898
- pseudoarthrosis 486 crista supraventricularis 786
- short femur 488 CRL (crown mmp length) 1220
- spinal malformations 360 Crohn's disease (CD)
- ureteropelvic junction 596 478, 525, 933, 946, 964, 966,
congestive heart failure 802 994, 996, 999, 1001, 1241
Conn's syndrome 1209 Crookes William 6
Conradi-Hunerman 498 Crookes tube 5
consolidative pneumonia 547 croup 537
constipation 1017 crown 265
containment o f the hip 515 crown rump length (CRL) 1220
continuous wave mode (CW) 70 CRT (cathode ray tube) 62
contracture 489 cryptococcal disease 1313
contracture syndromes 484 cryptococcal meningitis 1315
contrast 43 cryptococcosis 343, 736
contrast media kinetics 122 Cryptococcus neoformans 1319
- media for roentgen rays 116 Cryptosporidium 967
- resolution 55, 106 CSF fistula 192
contusion injuries 188 - oligoclonal bands 219
- o f lung tissue 757 - spaces 618
conus medullaris 350 CT (computed tomography) 18
conventional tomography 18 CT angiography 59, 1029
Cooper's ligament 653 - arthrography 376
copper 37 - myelography 318
copper deficiency 527 - number 58
cord 298 -portography 1029, 1037
corkscrew oesohagus 904 cubital fossa 824
comer fracture 479 Curie (Ci) 29
XXII
INDEX
Cushsing's syndrome 224,1208 demyelinating diseases 214

cutaneous naevi 368 demyelination 215
-am oebiasis 1245 dens 299
-leishm aniasis 1293 dens invaginatus 271
CW (Continuous Wave Mode) 70 dense breast 630,645
cyanosis 563,568 density 49
cyanotic CHD with decreased dentigerous cyst 279, 280
pulmonary blood flow 563 dentin 265
- CHD with increased dentino-enamel junction 265
pulmonary blood flow 566 dentinogenesis imperfecta 272
cylindrical bronchiectasis 715 depression fracture 186,386
cyst 1072 dermatomyositis 751
cystic adenomatoid malformation dermoid 203, 220, 222, 250, 705, 802
(CAM) 545 descending aorta 819
-bronchiectasis 715 desmoplastic reaction 1173
- degeneration o f the adventitia 835 destructive spondylarthropathy 336, 343
-fibrosis 583 -b r a in damage 616
-hygrom a 259,552 detection rate of breast cancer 664
- lung disease 544 - bias 663
-teratoma 1232 developmental dysplasia
cysticercosis 213,1304,1305 o f the hips (DDH) 482
cystitis 1177,1252 diabetes mellitus 728,1156
cystograpahy 1116,1178 diagnostic ultrasound 64
cystoides coli 1005 - peritoneal lavage (DPL) 951
cysts o f the jaw 279 diaphragm 691
cytomegalovirus diaphragm injury 761
(CMV) 4 6 5 ,9 2 0 ,9 6 7 ,1 3 1 5 diaphragmatic hernia 544
-oesophagitis 1326 diaphyseal fracture 468,475
D/A converters 104 diastematomyelia3 6 1 ,3 6 5 ,3 6 7 ,3 8 6
D. medinensis 1302 diastolic closure rate (DCR) 796
DALY (Disability-adjusted diastrophic dysplasia 498
life years) 8 7 ,8 8 dicheiria 489
darkness level 108 Die Presse 10
DCBE (double contrast diethylene-triamine-penta-acetic-acid
barium enema) 986 (DTPA) 136,138
DCBM (double-contrast diffuse generalized pulmonary
barium meal) 9 2 5,926,933 disease 736
DCIS (ductal carcinoma in situ) 658 - oesohageal spasm 904
DCR (diastolic closure rate) 796 - pulmonary fibrosis 743
DDH (developmental dysplasia digital fluorography 54
of the hips) 4 8 2 ,4 8 3 ,4 8 4 - fluoroscopy 54
decay constant 30 -im a g e 101
decompensated aortic stenosis 791 digital image plates 104
deep femoral artery 820 - mammography 632
- femoral vein 822 - matrix 53
- palmar arch 821 - subtraction device 39
-plantar vein 821 - projection radiograph 56
- vein thrombosis (DVT) 845,1233 -radiography 53,371
degenerative disease 317 - radiological unit 111
-jo in t disease 421 - subtraction angiography
-d is c disease 338 (DSA) 5 4 ,1 0 8 ,1 7 1 ,8 1 7
deglutition 896 dilated cardiomyopathy 791
XXIII
dimer 118 - outlet right ventricle 567

dimple 361 Down's syndrome 584, 1226
diphenhydramine 129 doxorubicin 154
dipyridamole 853 DPL (diagnostic peritoneal lavage) 951
direct fluoroscopy 51 dracunculiasis 1302
- pyelography 1115 drill catheter 857
- radiography 48 dromedary hump 1144
- splenoportography 1075, 1078 drooping lily sign 1159
dirofilariasis 1302 drowning 741
disability-adjusted life years (DALY) 87 drug abuse 445
disc 300 drug-induced oesophagitis 921
disc height 340 DSA (Digital Subtraction
- herniation 323, 325, 327, 332, 333 Angiography)5 4 ,1 0 8 ,1 7 1 ,8 1 7
- pseudoarthrosis 348 DTPA (diethylene-triamine-
- space 338 penta-acetic-acid) 136, 138
- space narrowing 341 dual energy x-ray absorptiometry
discography 3 2 1 ,3 7 0 (DXA) 524
dislocation o f the elbow 399 duct ectasia 653
- o f the hip 407 - o f Santorini 1067
- o f the patella 408 -ofW irsu n g 1067
displacement 3 8 8 ,4 1 5 ductal carcinoma 654
disruption o f the anterior ductal carcinoma in situ (DCIS) 658
cruciate ligament 409 ductectasia 657
dissecting aneurysm 829, 836, 838, 839 ductography 628
dissection o f the intima 813 ductus arteriosus 560
disseminated intravascular Dukes classification 1009
coagulation 770 dumb-bell neurinoma 356
distal interphalangeal (DIP) joint 436 duodenal atresia 577
diuresis renography 1124, 1173 - carcinoid tumour 953
diverticula 898, 993, 1175 - disease 944
diverticular disease 989 - diverticula 952
diverticulitis 990, 991.993 - haematoma 951
diverticulosis 990 - laceration 950
Doppler 589 - lymphoma 953
Doppler angle 70 - neoplasm 953
- echocardiography 782, 797 - nodular filling defect 946
- effect 69 - perforation 950, 951
- frequency shift 70 - stenosis 577
- pressure measurement 809 - ulceration 577, 948
- sonography 69 duodenography 1061
- transducer 69 duodenojenunal junction 580
- ultrasound 64 duplex ultrasound scanning 818
dorsal dermal sinus 3 6 1 ,3 6 6 - scanning 71,817
dorsalis pedis artery 820 duplication o f the renal
dose rate 32 collecting system 1159
dose equivalent 31 DVT (deep vein thrombosis) 845, 1233
double aortic arch 536, 571 dwarfism 498
- bubble 579 DXA (dual energy x-ray
- contrast barium enema (DCBE) 986 absorptiometry) 524
- meal (DCBM) 925, 926, 933 dynamic contrast study 1068
double halo 958 dysentery 1285
- limb 489 dysfunction o f swallowing 896
XXIV
INDEX
dyskinesis 799 emission computed tomography 63

dysmyelination 214 emphysema 711
dysostosis mandibulo-facialis 233 emphysematous bullae 680, 703
dyspepsia 928 - cyst 703
dysphagia 892, 893, 898, 930 empty sella 224, 225
dysraphism 352 empyema 2 1 2 ,7 0 1 ,7 0 2 ,7 2 8
dysthyroid myopathy 222 enalpril 1132,1133
E. coli 442, 728 encapsulated fluid 700
E. coli infection 1001 encephalitis 623
E. granulosus 1260 enchondroma 4 5 1 ,4 5 2 ,5 5 2
E. histolytica 1239 end plate 340
E. multilocularis 1260 endo-anal sonography 1018
E. oligarthrus 1260 endocardial cushion defect 561
E. vogeli 1260 - fibroelastosis 569
EAR (European Association endocrine tumour 1066,1072
of Radiology) 15 endoderm 297
early gastric cancer (EGC) 938 endoluminal ultrasound 988
Ebstein anomaly 564 endometrial carcinoma 1202
ebumation 341 - chocolate cyst 1232
ECG gated spin echo imaging 775 endometriosis 1012, 1205
ECG gating 680 endomyocardial fibrosis 801
echinococcosis 1260 endoscopic gastrostomy 158
echo time (ТЕ) 80, 1085 - retrograde cholangiography
echo-encephalography 188 (ERC) 155,1045
echocardiography - cholangiopancreatography
557,564, 680, 781,793,838 (ERCP) 1061, 1064, 1065
eclampsia 1233 - ultrasound (EUS)906, 909, 910, 928
ectoderm 297 endoscopy 892
ectopic islet-cell tumour 953 endosonography 1018
-pregnancy 1222, 1223 energy 20
- ureter 598 Entamoeba histolytica 736, 1239
- ureterocele 599 enteric cyst 553,579
EGC (early gastric cancer) 938 - duplication 553
Ehlers-Danlos syndrome 836 - neo-bladder 1185
Eisenmenger physiology 558 - stricture dilatation 1024
ejection fraction 791 - tube 1025
Eklund views 642 enteritis 1093
electrical injury 479 enterocele 1018
electrocardiogram 557 enteroclysis 9 5 5 ,9 5 6 , 961
electrocardiographic (ECG) gating 680 enthesitis 437
electromagnetic (em-) radiation 20 entrapment syndrome 835
electron shells 20 enzyme kinetics 173
electron 19, 28 eosinophilia 1281,1304
Ellis van Creveld syndrome 498 eosinophilic enteritis 964
embolism 681 - gastritis 933
embolization 150, 1041, 1109 - granuloma 529
embolization o f plaque 813 ependymoma 197, 207, 351,356
- procedures 861 epidermoid 203
- therapy 150 epidermoid cyst 250
embolotherapy 1021 epididymitis 1195
embryonal tumors 352 epidural hematoma 621
EMI-scanner 54 epidural space 323
XXV
epiglottis 5 3 7 ,5 3 8 extracorporeal shock wave lithotripsy

epilepsy 615,621 (ESWL) 163
epinephrine 129, 130 extradural haematoma 191
epiphrenic diverticula 922 - tumors 359
epiphyseal injury 468 extrarenal haematoma 1159
epiphysis 461, 468, 469 extrauterine pregnancy (EUP) 1107
epithelial proliferation 656 extremity-preserving surgery 450
epitympanon 230 extruded disk 325
equinous deformity 485 facet joints 299
ERC (endoscopic retrograde facetectomy 334
cholangiography 155, 1045 facial cleft 274
ERCP (endoscopic retrograde facial hemiatropathy 274
cholangiopancreatography - nerve schwannoma 236
1061, 1064, 1065 - skeleton fractures 244
Erlenmeyer flask 508 Fallopian tube recanalization 163
erosion 4 3 4 ,4 4 0 false aneurysm 836
erosive degenerative disc disease 343 - diverticula 922
- gastritis 932 familial adenomatous
- osteochondritis 336 polyposis (FAP) 942, 953, 1008
erythema nodosum 748 fast screens 50
erythrocytcylinduria 1174 fat necrosis 649, 657
erythrocytes 128 - pad sign 399
Escherichia coli 442, 728 fatigue fracture 418
ESWL (extracorporeal shock fatty marrow 342
wave lithotripsy) 163 - infiltration 1039
ethanol 151 FDG-glucose 881
ethibloc 863 female genital organs 1198
ethmoid air cells 239 femoral vein 821
EUP (extrauterine pregnancy) 1107 - head coverage 516
European Association femorotibial rotation 408
o f Radiology (EAR) 15 femur length 1220
EUS fetal abnormality 1221, 1225
(endoscopic ultrasound)909, 910, 928 - adrenal haemorrhage 1227
eustachian tube 247 - urine 1230
evacuation proctography 1015 fibre optics 856
Ewing sarcoma 529, 552, 555 fibreoptic-endoscopy 1108
excited electrons 104 fibrinolysis 805, 846, 858
exit dose 33 fibrinolytic systems 128
Exner 10 fibroadenolipoma 649
exostoses 287 fibroadenoma 649, 657
expiratory frontal view 671 fibrocystic changes 645
exstrophy o f the bladder 602 - disease 645, 653, 657
extension 301 fibrodysplasia ossificans
extension injury 311 progressiva 522, 523
- tear-drop fracture 313 fibroglandular tissue 643
- iliac artery 820 fibrolipoma 361
extension iliac vein 822 - o f the filum terminale 366
- herniation 1095 fibromuscular hyperplasia 1131
extra nipple 647 - dysplasia 833
- digits 489 fibrosing alveolitis 743
extraadrenal pheochromocytoma 1211 fibrosis 732, 804, 960
extraaxial infratentorial tumours 201 fibrotic reaction 653
XXVI
INDEX
- stricture 960 fracture-dislocation 392,395

fibrous dysplasia 285, 552 fracture-dislocation o f the elbow 399
fibula 409 - hip 407
field size 34 - Lisfranc joint 416
filariasis 698, 1299 - tarsometatarsal joint 416
film contrast 629 fragmentation of the femoral head 514
filtration 37 frequency 20
filum terminale 350 frequency spectrum 83
-syndrom e 361 frontal sinus 238
fine needle aspiration biopsy (FNAB) Frostberg's sign 1061
456,631,633,651,1025,1037,1073 frostbite 479, 528
fistula 455, 702, 962 FTG-glucose PET Scanning 886
flattening o f the femoral head 514 full spectral display 70
flexion 301 functional luteal cyst 1232
flexion injury 310 fungal disease in HIV 1319
- tear-drop fracture 310 - pneumonia 736
fluid overload 570 - spondylitis 342
fluorogram 52 funnel-shaped sternum 693
fluorography 52 fusion anomaly 1136
fluoroscopy 18, 671, 672 GA (gestational age) 1221
FNAB (fine-needle aspiration biopsy) gadolinium compounds 137
456, 631, 633, 651, 1025, 1037, 1073 galactocele 650
focal disc bulge 325 galactography 628, 636
-hyperplasia 1032 Galeazzi fracture 399
- neurological signs 194 gallbladder carcinoma 1054
- nodular hyperplasia 1032 - disease 589
focus 36 Gallium 67 scanning 6 3 ,8 8 1 ,8 8 4
folds o f Kerkring 1097 gallstone 589,1044
follow-through examination 954 gallstone disease 1048
Fontaine classification 824 - ileus 1100
foot deformity 485 gamekeeper's thumb 397
foramen magnum 366 gamma 49
- ovale 821 gamma camera 28,61
- of Luschka 207 - photons 61
- o f Magendie 207 - quantum 22, 29
forearm 389 - radiation 17, 20, 29
fossa o f Rosenmuller 247, 248 -r a y s 61
fracture 384 gammascintigraphy 1046
fracture o f the acetabulum 406 gangliocytoma 201
- femoral neck 404 ganglioglioma 201
- femoral shaft 407 ganglion cells 584, 605
- fibula 409 ganglioneuroblastoma 605
- intertrochanteric region 404 ganglioneuroma 605
-olecranon 399,401 gangrenous cholecystitis 1091
- patella 408 Gardner's syndrome 2 7 2 ,9 5 3 ,1 0 0 8
- pubic rami 406 Garre osteomyelitis 443
- radial head and neck 399 gasless abdomen 997
-r ib 755 gastric atrophy 933
- sternum 756 gastric carcinoma 938
- tibia 409 - diverticula 936
fracture in transverse processes 315 - lymphoma 943
fracture o f the vertebral body 315 - retention 1097
XXVII
- rotation 929 glucoerebroside hydrolase 508

-u lc e r 5 7 7 ,9 3 3 ,9 3 7 ,9 3 8 glucosylceramide 508
gastritis 932 gluteal artery 820
gastro-oesophageal reflux glycogen storage disease 569
(GOR) disease 575, 893, 898, 911 goitre 707
gastrocnemius vein 8 2 1 ,8 2 2 Goodpastures syndrome 1156
gastrografin 9 2 5,1104 Goodspeed A.W. 8
gastrointestinal bleeding 1108, 1109 GOR (gastro-oesophageal reflux)
- haemorrhage 1019 575, 893, 8 9 8 ,9 1 1 ,9 1 6
- reflux 573 Gorlin's syndrome 281
gastro-oesohageal reflux 901 Graf 482
Gaucher disease 508,516, 522 graft-versus-host disease (GVHD) 964
gauss 73 gram negative pneumonia 728
gay bowel syndrome 1327 - infections 728
Gd-BOPTA 139 granulation tissue 339
Gd-DOTA 139 granulation 336
Gd-DTPA 136, 138 granuloma 209
Gd-DTPA-BMA 139 granulomatous colitis 999
Gd-EOB-DTPA 139 GRE sequences 338
G d-HP-D03A 139 great saphenous vein 821
GE-sequences 338 green light 49
gelatin sponge 1021 greenstick fracture 385, 476
gelfoam 150, 151,863, 1021 Greulich and Pyle 467
general anesthesia 534 grey matter 170
generations o f CT scanners 55 grid 40
genetic counseling 493 gross needle biopsy 1190
geniculate ganglion 230 growth disturbance 465, 468
genioglossus muscle 249 - lines 462
geniohyoid muscle 249 - plate 461,468
genital hernia 1180 - injury 474
geographic lesions 338 -rate 617
germ-cell tumor 552 Gruntzig, Andreas 804
germinal tumor 707 guided fine-needle biopsy 1040
germinoma 356 guinea worm infection 1302
gestational age (GA) 1221 GVHD (graft-versus-host disease) 964
giant cell granuloma 288 haemangioblastoma 202, 207, 354
- tumour 288, 452 haemangioma 361, 452, 552, 1032
Giardia lamblia 1280 haemangiopericytoma 220
giardiasis 966, 1280 haematological effects 123
gibbus formation 336,337, 341 haematoma 649
glenohumeral dislocation 402 haematotympanon 235
glioblastoma 199 haematopoietic marrow 342
glioblastoma multiforme 197 haematuria 1174
glioma 197 haemobilia 1073
glomerular filtrate 1127 haemochromatosis 1210
- filtration rate 1122 haemodialysis 831,864
glomerulonephritis 1156 haemoglobin 182
glomus jugulare tumors 236 haemoperitoneum 951
- tumours 236 haemophilia 440, 1156
- tympanicum 236 Haemophilus influenzae
- vagale 237, 260 442, 538, 549, 728
glucagon 900 haemopneumothorax 757
XXVIII
INDEX
haemoptysis 675,772 higher energy shell 19

haemorrhage 624 hilar enlargement 709
haemorrhagic effusion 698 Hilgenreiner line 482
- lesion 623 Hill-Sach's defect 402
- necrotic pancreatitis 1068 hilum 688
-pancreatitis 1067 hindbrain 366
- pleural fluid 703 hindgut 583
haemosiderin 182 hip effusion 511
haemothorax 755,757 Hippel-Lindau syndroem 1211
hairy tuft 361 Hirschsprung disease 584
half-life 30 HIS ("Hospital Information System") 110
halo 650 histamine 128
hamartoma 226, 649, 942, 1145, 1214 histiocytosis X 452, 529, 552
Hamman-Rich disease 743 Histoplasma capsulatum 736, 1319
Hand-Schuller-Christian disease 529 histoplasmosis 7 4 7 ,9 6 6 ,1 2 1 0
hang-man fracture 311 Hittorf J.W. 6
hard palate 249 Hittorf vacuum tube 5
head circumference (HC) 617, 1220 HIV infection 920
head and neck tumors 888 - leukoencephalopathy 1314
headache 621 -m yelopathy 1316
healing o f diaphyseal fracture 476 - polyneuropathy 1316
heart failure 568 HLA-B27 346
- surgery 765 Hodgkin's disease
heart volume 789 874, 882, 8 8 4 ,1 2 1 5 ,1 3 2 3
Heliobacter pylori 929, 968 Holt Oram syndrome 508
helminthoma 1282, 1283 honeycomb lung 743
hemiazygous vein 823 hookworm infestation 968,1281
hemimelia 488 hormone replacement therapy 643
hemimyelocele 365 horseshoe kidney 594
hemiplegia 623 Hospital Information System (HIS) 110
hemivertebra 365,368 hot balloon 856
Hensen's mode 297 hot tip 856
heparin treatment 845 Hounsfield unit (HU) 58
Heparin 865 HPS (hypertrophic pyloric stenosis) 577
hepatic venography 1031 humeral shaft fracture 401
-b leed ing 1041 Hurler form (MPS IH) 511
hepatitis В 1034 hyaline membrane disease 465
hepatobiliary scinitgraphy 588 hydatid cyst 1262
hepatocellular carcinoma 1034 hydatid disease 1260,1262,1266
hepatoma 1034 hydatidiform mole 1224
hepatosplenomegaly 594 hydranencephaly 1226
herpes simplex encephalitis 213 hydrocele 1195,1196
- oesophagitis 920 hydrocephalus 192, 611, 617, 618
herpes virus 734 hydrocortisone 130
herpes zoster 734 hydrogen nuclei 73
Herz (HZ) 20 hydromyelia 352,368
heterotopic gastric mucosa 946 hydronephrosis 5 7 3 ,5 9 6 ,1 1 5 0
hiatus hernia (HH) hydrosalpinx 1206
573, 575, 696, 893, 916, 918, 929 hyoscine butylbromide 900, 925
HIDA 928 hyperaeration 549
high resolution CT 675, 714 hypercementosis 287
high-energy photons 25 hyperemia 434, 440, 462, 519
XXIX
hyperextension 311 -manipulation 106

hyperextension fracture 311 - quality 42
-in ju ry 311 -subtraction 108
hyperinflation 542,713 imaging geometry 41
hyperodontia 272 -plates 53
hyperoxaluria 1155 immobilization device 459
hyperparathyroidism 2 6 2 ,5 2 6 ,5 2 7 ,8 3 1 immunoblastic sarcoma 1323
hyperplasia o f the coronoid impaction fracture 386
processes 272 imperforate anus 489,583
hyperplasia o f the face 274 impotence 1197
- maxillary tuberosities 272 incisive foramen 266
hyperplastic cholecystosis 1053 incomplete abortion 1223
hypertension 791,1131 -fracture 385
hyperthyroidism 222 incontinence 1018
hypertrophic cardiomyopathy 792 increased intracranial pressure 619
- gastritis 933 - intracapsular pressure 432,444
hypertrophic pyloric stenosis (HPS) 577 incus 230
-sy n o v itis 445 indirect splenoportography 1075,1078
hypoalbuminemia 661 indium-labeled leukocyte
hypodontia 272 scintigraphy 337
hypoglossus muscle 249 infantile polycystic kidney disease
hypokinesis 799 (PCKD) 594
hypopharyngeal carcinoma 257 infarct 799
-diverticulum 898 infarction 621,1210
hypopharynx 2 4 9 ,2 5 7 infection 528
hypophosphatasia 5 0 0 ,5 2 7 infectious adenopathy 553
hypophosphatemic rickets 525 - gastric lesion 1326
hypoplasia o f the face 274 - oesohagitis 920
-fib u la 490 infective discitis 348
- ilia c bones 440 inferial orbital fissure 176
hypoplastic left heart 1226 inferior mesenteric artery 820
hypothalamus dysfunction 224 - ophthalmic vein 176
hypothyroidism 4 6 7 ,5 1 7 ,1 0 1 7 -v e n a cava 823,824
hypotonic drug 900 infertility 1206
hypotympanon 230 infiltrating epitheliosis 655
hysterosalpingography 1117,1206 inflammation 447,647
Hz (Herz) 20 inflammatory aneurysm 839
1-123 SAP (serum amyloid P - bowel disease (IBD) 994
component) 1031 -carcinoma 661
IBD (inflammatory bowel disease) 994 - disc degeneration 343
ICRP (International Commission on - spine process 337
Radiological Protection) 97 influenza 549
idiopathic arteritis 1291 influenza А, В, С 734
- bone cavity 274 infraction 531
- endomyocardial fibrosis 1290 infrared radiation 20
- respiratory distress syndrome 540 - imaging 17
ileocolic intussusception 1109 - photon 25
ileus 582 infratentorial tumours 192
iliolumbar artery 820 infundibulum 174
image compression 111 inguinal ligament 822
-com m unication 112 inhalation o f gases 742
-intensifier 3 9 ,5 2 initial hematuria 1174
XXX
INDEX
inner ear malformation 232 -v o lu m e 617

innominate artery compression 536 intraductal carcinoma 636, 656, 658
instability 301 intradural extramedullary tumors 354
insufficiency fracture 418, 446 - lipomas 366
intensifying screens 49 intramedullary metastases 351
interactions o f electrons 22, 24 -tum ours 351
- photons 22 intramural bleeding 1097
- radiation 19 - gas 582
- ultrasound 26 - haematoma 951
interactions o f X-rays 21 intranuclear cleft 341
Interamerican C ollege o f Radiology 15 intraoral radiography 263
intercostal artery 820 intraorbital expanding lesions 219
interfacetal dislocation 310 intraosseous phlebography 816
interlobar pleural fluid 680 intraparenchymal haematoma 1037
intermediate growth 450 intraperitoneal seeding 974
internal auditory canal 230 intrarenal haematoma 1159
- herniation 1095 - haemorrhage 1158
- iliac artery 820 intrathoracic stomach 930
-jugular vein 824 intravenous cholangiography 1044, 1055
- mammary artery 820 - urography (IVU) 1111
- pudendal artery 820 intraventricular bleeding 189
International Commission on - haemorrhage 625
Radiological Protection (ICRP) 97 -m eningiom as 197
International Lung Cancer intravesical ureterocele 599
TNM Staging System 886 intussusception 573, 585, 1098, 1099
International Society o f Radiology invagination 1095
(ISR) 15 invasive lobular carcinoma 655
interosseous artery 820 inverted 3-sign 1061
interpedicular distance 495 ion-imbalance 120
intersegmental arteries 298 ionic contrast media 119
interstitial edema 540, 543 ionization chamber 31
- fibrosis 543 ischaemia of the small intestine 983
- opacity 737 ischaemic brain damage 625
intervertebral disc spaces 347 -cardiomyopathy 791
-joints 323 - heart disease 799
intestinal duplication 579 - lesion 623
intimal hyperplasia 866 - necrosis of bone 432
intra-abdominal injury 1108 ischiopubic synchondrosis 461
intra-peritoneal gas 1087 islet-cell hyperplasia 949
intra-uterine infection 620 isometric phlebography 816
intraarterial stents 861 isotope cystography 592
intraaxial infratentorial tumours 205 isotope imaging 17
intrabulbar tumours 220 - scanning 784
intracapsular bleeding 1078 ISR (International Society
intracerebral calcifications 168 o f Radiology ) 15
- haemorrhage 625 ivalon 150, 151,863
- haematoma 181 IVP (intravenous urography) 1111
intracortical striations 525 IVU (intravenous urography) 1111
intracranial air 187 J-guidewire 811
- haemorrhage 619 Jaccoud's arthropathy 441
- medulloblastoma 356 Jansen form 501
- pressure 186 jaundice 607
XXXI
JCA (juvenile chonic arthritis) 438 - papyracea 245

JDMS (juvenile dermatomyositis) 522 laminectomy 334
Jefferson fracture 3 0 6 ,3 1 4 Langerhans cell histiocytosis 529
jejunal diverticulosis 969, 977 lanthanide screens 49
Jeune syndrome 499 laparoscopic cholecystectomy 157, 1045
joint capsule 433 large bowel ileus 1097
- disease 519 - volvulus 1101
- effusion 387 large cell carcinoma 720
- instability 422 Larmor equation 74
- laxity 408 Larmor frequency 74
- space reduction 440 Larsen syndrome 507
JRA (juvenile rheumatoid arthritis) 519 laryngeal movement 894
jugular bulb 230 laryngocele 257
juvenile angiofibroma 247 laryngotracheobronchitis 537
- arthritis 438 larynx 255,257
- chronic arthritis (JCA) 438 laser angioplasty 145, 853, 856
- dermatomyositis (JDMS) 522 lateral decubitus view 671
- polycystic disease o f kidney - disc herniation 327
and liver 594 - hemivertebra 363
-p o ly p 1008 - periodontal cyst 279
- rheumatoid arthritis (JRA) 478, 519 - pharyngeal protrusion 899
Kaposi's sarcoma - pouches o f Retzius 1085
(KS) 976, 1300, 1316, 1320, 1324 - recess 323, 330
karyotyping 1225 - segment 685
Katayama syndrome 1248, 1255 - semicircular canal 230
Kawasaki disease 570 - spinal stenosis facet
Keats 461 hypertrophy 330
keratocyst 279, 281, 295 Lauge Hansen classification 412
Kerley A lines 739 LCIS (lobular carcinoma in situ) 659
Kerley В lines 568, 686, 739 LCP (Legg-Calve-Perthes
kerma 31 disease) 513,51 4 ,5 1 6
kidney-ureter-bladder survey Le Fort fracture 246
(KUB) 1111 lead grid 34, 40
Killian's dehiscence 898 - lines 464
kinin systems 128 - time bias 663
klebsiella 339, 442, 754 leather bottle stomach 939
Klebsiella pneumoniae 728 Lecher 10
Klippel-Feil syndrome 364 left anterior descending artery (LAD) 787
Klippel-Treaunay syndrome815, 844, 852 - atrial enlargement 792
Kohler 461 - atrium 785, 787
KS (Kaposi's sarcoma) - auricle 795
976, 1300, 1316, 1320, 1324 - common carotid artery 820
KUB (kidney-ureter-bladder survey) 1111 - iliac artery 820
Kundt, August 3 - coronary artery 787
kyhposcoliosis 364.693 - subclavian artery 820
lacrimal gland 177 - ventricle 785, 787
lacrimal gland tumour 220 Left ventricular enlargement 791
lacunar infarction 177,180 - failure 768
LAD (left anterior descending artery) 787 left-to-right shunt 709
Ladd bands 581 Legg-Calve-Perthes disease
Ladd operation 581 (LCP) 5 1 3 ,5 1 4 ,5 1 6
lamina dura 266 leiomyosarcoma 974, 1202
XXXII
INDEX
Leishmaniasis 1303 low-energy photons 25

Lenard P. 5 ,6 lower airway foreign body 555
length bias 663 - gastrointestinal haemorrhage 1021
Lennep 1 - oesophageal reflux 901
leprosy granulomas 1297 lucent band 503
leprosy 1297 - metaphyseal bands 465, 521
Leriche syndrome 827 lumbar artery 820
lethal dwarfism 1226 - lordosis 315
Letterer-Siwe disease 529 - nerve-rootblock 323
leukaemia - vein 823
2 2 1 ,5 5 5 ,5 2 1 ,5 2 8 ,5 5 2 ,6 1 1 ,8 8 0 - vertebra 691
leukemic lines 465 lung 685
leukocytes 128 lung abscess 728
leukopenia 503 - biopsy 771
ligamentous injury 397, 468 - cancer 720
-tear 304 - infection 723
ligamentum flavum 301,323 - injury 757
light scanning 628 - transplantation 714
light photon 25 - tumour 554
limey bile 1053 lymphocytic interstitial pneumonitis
line pair 44 (LIP) 1321
linear fractures 187 lymph node 645, 649
- opacity 745 - flow 875
- ulcer 914 lymphadenopathy 260
- striations 465 lymphadenopathy syndrome 1329
lingual thyroid 251 lymphangiography 874
lingular segment 685 lymphangioma 220, 552
LIP (lymphocytic interstitial lymphangitic carcinoma 722
pneumonitis) 1321 lymphatic malformation 843
lipiodol ultrafluid 132 lymphatic obstruction 687
lipohemarthrosis 405 lymphocytes 128
lipoma 204, 366, 452, 552, 1011 lymphogranuloma venereum 1286
lipomyelomeningocele 366 lymphography 132
Lisfranc dislocation 416 lymphoma
liver cirrhosis 1040 201, 220, 221, 222, 244, 248, 289,
- failure 661 555, 647, 677, 707, 880, 972, 1329
- fluke 1283 lymphosarcoma 585
Loa loa 1299 M. leprae 1297
lobar pneumonia 725 M. avium-intracellulare 1319
lobectomy 764 M. kansasii 1319
lobular carcinoma in situ (LCIS) 659 M-mode 68
- calcification 658 M-mode 67
local aggressiveness 450 Mach band 650
- tumor extension 452 MacLeod's syndrome 713
localised dissecting aneurysm 839 macrocystic renal disease 594
loculi 700 macronodular hyperplasia 1208
long saphenous vein 821 Maffucci syndrome 506
longitudinal defects 489 magnetic field 73
- epiphyses 498 - examination 25
loop of Henle 1128 - field gradient 80
lordotic view 671 - imaging 17
low energy shell 19 - resonance 76
XXXIII
Magnetic Resonance medial retinaculum 408

Angiography (MRA) 8 2 ,1 7 1 ,8 1 8 - segment 685
Magnetic Resonance Imaging (MRI) 72 mediastinal biopsy 771
Magnetic Resonance - bleeding 755
Spectroscopy (MRS) 83 - fibrosis 708
magnification technique 636 - injury 759
major interlobar fissure 684 - lesion 705
malabsorption 969 -m a ss 552, 680, 693
malaria 1303, 1304 mediastinitis 708
male genital organs 1191 mediastinum 687
malformations o f the jaws 271 Mediterranean lymphoma 974
malformations o f the teeth 271 medullary sponge kidney 1142
malignancy 446 medulloblastoma 207, 357
malignant calcification 658 megacolon 1094
- disease 445 megalodactyly 489
- external otitis 237 megaureter 597
-lym ph om a 8 8 2,1 21 5 meliodosis 1289
- melanoma 220 membrane formation 297
- mesothelioma 746 MEN (multiple endocrine
malleus 230 neoplasia) syndrome 1211
Mallory-Weiss laceration 924 Menetrier's disease 933
malrotation 5 7 3 ,5 8 0 meningeal cysts 213
mammography 628, 630, 638 meningioma 1 9 3 ,2 0 3 ,3 5 4 ,3 5 7
mandible 249 meningitis 2 1 1 ,3 3 6 ,6 1 9 , 621,623, 1315
mandibular canal 268 meningocele 360
- condyle 293 meningoencephalitis 336
mandibulofacial dysostosis 272 mental nerve 268
march fracture 419 mesenteric angina 984
Marfan syndrome 836 - venous thrombosis 984
massa lateralis 311 mesoblastic nephroma 1226
mast cells 128 mesoderm 298
mastitis 6 52,661 mesodermal abnormalities 507
maxilla 266 - defect 507
maxillary antra 240 mesomelic 493
- cuspid 270 mesothelioma 703,802
-s in u s 238 mesotympanon 230
maxillary zygomatic process 268 metabolic bone disease 524
MCDK (multicystic dysplastic - disease 447
kidney) 595 metabolism 173
McKusick form 502 metacarpal bones 396
meandering artery 843 metameric arteries 298
measurements 376 metaphyseal chondrodysplasia 501, 527
mechanical bowel obstruction 1095 - lines 464
-recanalisation 145 metaphysis 461, 468, 469
Meckel diverticulum 583, 585, 978, 979 metastasis 201, 206, 209, 220, 222, 289,
meconium 583 359, 647, 707, 722, 1012
meconium aspiration 540, 541, 542 metastatic nodal disease 885
- ileus equivalent 583 - disease 555, 650
- peritonitis 583 metatarsophalangeal joint 436
meconium-plug syndrome 583 metoclopramide 956,958
MED (multiple epiphyseal Mexican-hat sign 993
dysplasia) 440, 516 МНЕ (multiple hereditary exostoses) 504
XXXIV
INDEX
microcephaly 1226 mucosal necrosis 543

microcoils 151 -p o ly p 942
microcystic disease 657 mucous retention cysts 242
microcystic renal disease 499, 594 multicentric tumors 452
microfracture 422 multicystic kidney 1227
micrognathia 272 - dysplastic kidney (MCDK) 595
microinvasion 658 multilocular cystic nephroma 596
middle cerebral artery 179, 184 - renal cyst 596
middle lobe 686 multiplanar imaging 338
middle mediastinum mass 707 multiple enchondromatosis 506
midgut volvulus 580,581 - endocrine neoplasia (MEN)
migrating polyarthritis 441 syndrome 1211
miliary tuberculosis 13 02 - epiphyseal dysplasia
minor interlobar fissure 684 (MED) 440,516
missed abortion 1223 - exostoses 552
mitomycin С 154 - hereditary exostoses (МНЕ) 504
mitral orifice 787 - myeloma 1156
- stenosis 793, 795 - sclerosis 215
-v a lv e 787 Murphy’s sign 1091
- disease 792, 793, 795 muscle thickening 222
-prolapse 794 musculus levator palpebrae 176
Mn-DPDP 139 Mycobacterium
molar pregnancy 1222 tuberculosis 442, 730, 1316, 1318
molars 267 Mycobacterium avium intracellularae 967
molybdenum 29 Mycoplasma pneumoniae 733,735
molybdenum tube 628 mycotic aneurysm 838
Mondini malformation 232 myelination 297
monochromatic gamma quantum 28 myelitis 218
monochromatic quantum 20 myelocele 360, 365
radiation 22 myelocystocele 360, 367
monoclonal antibody imaging 888 myelodysplasia 469,484
monomer 118 myelographic block 349, 356
Monteggia lesion 398, 399 myelography 318, 349
Morgagni hernia 697, 707 myelolipoma 1214
Morquio syndrome (MPS IV) 511 myeloma 289,880
moulage sign 969 myelomeningocele 360, 365
MPS IV 511 mylohyoid muscle 249
MPS III (San Filippo form) 511 myocardial infarction 799,802
MPS IH (Hurler form) 511 myofibromatosis 530
MPS (mucopolysaccharidoses) 493, 509 myopia 500
MR signal 75, 76 myxoma 801
MRA (magnetic resonance Monkeberg's medial sclerosis 831
angiography) 82, 171,818 nasal fossa 267
MRI contrast media 136 - fracture 244
MRI (Magnetic Resonance Imaging) 72 - polyps 243
MRS (Magnetic Resonance - regurgitation 894
Spectroscopy) 83 nasopharynx 246
mucinous adenocarcinoma 1160 near-drowning 556
mucoceles 242 NEC (necrotizing enterocolitis) 582
mucoepidermoid carcinoma 289 Necator americanus 1281
mucoid degenerations 300 neck 258
mucopolysaccharidoses (MPS) 493, 509 necrotic pancreatitis 1067
XXXV
necrotizing enterocolitis (NEC) 582 non-ionic contrast media 119

- external otitis 237 non-obstructive jaundice 155
negative contrast media 116, 135 non-odontogenic
NEMD (non-specific oesophageal developmental cyst 279, 281
motility disorder) 901, 904 non-renal retroperitoneal abscess 1190
neodynium yag-laser 856 non-specific oesophageal motility
neonatal adrenal hemorrhage 607 disorder (NEM D) 901,904
- hepatitis 588 - duodenitis 948
- meningitis 62 non-steroidal anti-inflammatory
- pneumonia 540, 541, 542 drugs (NSAIDs) 964
neoplastic adenopathy 553 non-tropical sprue 969
nephroblastoma 602 nonunion 477
nephrocalcinosis 1155 notochord 204, 297, 298
nephrographic phase 1111 NSAIDs (non-steroidal
nephronopthisis 499 anti-inflammatory drugs) 964
nephrostomy 1188 nuchal thickening 1230
nerve compression 331 nuclear medicine imaging 17
nerve-root compression 333 - cystogram 600
nerve-roots 327 - magnetic resonance (NMR) 17
net magnetic moment 74 nucleus 19
neural foramen 327 nucleus pulposus 300
- arch 299, 306 nutcracker oesophagus 904
- groove 297 nylon 854
neurinoma 203, 354, 357, 359 oblique eye muscles 176
neuroaxis 298 - talus 485
neuroblastoma 359,522,552,555,605,607 -v ie w 671
neuroblasts 605 obstetric ultrasound 1217
neuroembolization 154 obstructive hydronephrosis 1160
neurofibroma 2 2 0 ,5 0 7 -jaundice 155
neurofibromatosis (NF) obturator artery 820
354, 506, 486, 552, 694, 1131, 1211 occipito-frontal diameter (OFD) 1220
neurogenic bladder 6 0 0 ,1 1 7 8 occlusal caries 274
neurolation 297 occult spinal dysraphism 366
neurosonograhpic examination 613 odontogenic infection 276
neurosonography 625 - myxoma 283, 285
nevoid-basal cell carcinoma 281 - tumours 283
NF (neurofibromatosis) - fracture 315
354, 486, 506, 552, 694, 1131, 1211 odontoid process 306
NHL (non-Hodgkin's lymphoma) -process 2 8 4 ,2 9 9 ,3 0 6
882, 884,972, 1215, 1323 odynophagia 921
nipple retraction 653 oedema 660, 1003
Nitinol 146 oedematous pancreatitis 1068
NMR (nuclear magnetic resonance) 17 oesophageal atresia 489, 573
nocardial brain infection 1313 - bolus obstruction 910
nocardiosis 736 - carcinoma 907
nodular opacity 738 - diverticula 922
non-bacterial pneumonia 733 - duplication 576
non-cardiogenic congestion 741 - dysmotility 911
- edema 741 - foreign body 575
non-ectopic ureterocele 1160 - injury 913
non-Hodgkin lymphoma (NHL) -intramural pseudodiverticulosis 918
882, 884, 1215,972, 1323 - manometry 900
XXXVI
INDEX
- motility disorders 901 osseous ankylosis 347

- perforation 923 - spina bifida 367
- rupture 759 - spinal abnormalities 363
- stricture 906 ossiculum terminale 364
- transit studies 900 ossification 297, 298
- varices 925 ossification anomalies 455
- web 916 - center 298, 461
oesophagitis in AIDS 1326 ossification of posterior longitudinal
oesophagitis 913,918 ligament (OPLL) 334
oesophago-gastro-duodenoscopy osteitis 441
(OGD) 891 osteoarthritis 421, 445,456
oesophago-tracheal fistula 925 osteoarthrosis 421, 423,430
oesphageal stenting 158 osteoarthrosis o f the ankle 428
OFD (occipito-frontal diameter) 1220 - distal interphalangeal joint 429
OGD (oesophago-gastro- - elbow 429
duodenoscopy 891 - first metacarpal joint 429
Ogden 469 - hip 427
01 (osteogenesis imperfecta) - knee 427,428
478, 482, 488, 492, 502 - patellofemoral compartment 427
oligodendroglial tumours 197 - proximal interphalangeal joint 429
oligodendroglioma 199 osteoblast activity 373
oligohydramnios 1230, 1231 osteocartilaginous fragment 419
Oilier syndrome 506 osteochondral fracture 408
omovertebral bone 364 osteochondritis
onchocerca volvulus 1299 dissecans 4 1 5 ,4 1 9 , 420, 518
oncocytoma 1146 osteogenesis imperfecta
onion-peel appearance 449, 450, 451 (OI) 478, 482, 488, 492, 502
opaficied sinus 244 osteogenic sarcoma 289
open fracture 384 osteoid osteoma 443
open-mouth projection 306 osteolysis 447
ophthalmic artery 176 osteolytic destruction 450
OPLL (ossification o f posterior - lesions 168
longitudinal ligament) 334 - metastases 373
opposed phase GRE sequences 338 osteoma 287, 452
optic chiasm 224 osteomalacia 525
-g lio m a 2 2 0 ,2 2 1 ,2 2 6 ,5 0 7 osteomyelitis 276, 277, 441, 442, 449,
- meningioma 220, 221 454, 469, 522, 531
- neuritis 216, 221 osteonecrosis 432, 445, 446
- nerves 174 osteonecrosis of the femoral head 407
- nerve canal 176 osteopenia 337, 478
optical cables 112 osteopetrosis 286, 503
orchitis 1195 osteophytes 317, 333, 423
organ ablation 152 osteoporosis 524
organ dose 33 osteoradionecrosis 276
orofaciodigital syndrome 272, 274 osteosarcoma 443, 452
oropharyngeal swallowing 893 osteosclerosis 449
- dysphagia 896 ostium primum defect 561
oropharynx 246, 249 ostium secundum ASD 559
Ortolani maneuver 482 oval window 230
os odontoideum 364 ovarian cyst 1227
osmolality 120 ovarian malignancy 1232
osmotoxicity 120 ovarian tumor 1203,1204,1232
XXXVII
ovarian vein 823 paravertebral lesions 338

overgrowth 477 parietal pleura 683
overpenetrated film 671 Park lines 462
overriding o f the aorta 563 Parkes-Weber syndrome 844
oxygen 130 parotid salivary gland 253
P. westermani 1287 particle radiation 20
packing deformity 486 PAT (percutaneous aspiration
PACS (Picture Archiving and thromb-embolectomy) 858
Communications Systems) 104,110 patella alta 408
Paget's disease 286 patent ductus arteriosus (PDA)560, 566
pair production 23 - foramen ovale 564, 566
palatal dysfunction 894 Paterson-Kelly syndrome 898
palatine tonsils 249 pathological fracture 478
palatoglossal arch 249 patient dose 30
palatoparhyngeal arch 249 PCKD (polycystic kidney disease) 594
Palmaz stent 861 PCNL (percutaneous
pampiniform plexus 823 nephrolithotomy) 1116
Pancoast tumor 721 PCP (pneumocystis carinii
pancreas annulare 1067 pneumonia) 736, 1316, 1317
- divisum 1067 PD (Pulsed Doppler Mode) 70, 71
pancreatic angiography 1065 PDA (patent ductus arteriosus)560, 566
- island 1067 pear-shaped bladder 1177
- tumours 1070 pectin 131
pancreatitis 1051, 1064, 1091 pedicles 299
pancuronium bromide 1228 pelvic vein 823
panoramic radiography 263 pelvimetry 1234
panorex view 238 penetrating trauma 1108
papillary muscle rupture 794 peptic ulcer disease 576
- necrosis 1153 percutaneous abscess drainage 1024, 1190
- stenosis 1328 - aspiration thromb-embolectomy
papilloma 649 (PAT) 858
papillomatosis 636 - biopsy 1190
papillotomy 1059 - catheter drainage o f the kidney 161
Papova JC virus 1315 - cholecystostomy 157
para-oesophageal hernia 929 - discectomy 370
paracardiac mass 680 - gastroenterostomy 158
paraganglioma 236, 237, 260, 1211 - gastrostomy 1025
paragonimiasis 1287 - litholysis 163
parahilar opacities 548 - nephrolithotomy (PCNL) 1116
parainfluenza 549 -nephrostomy 162, 1188
parallel protons 74 - neurolysis 165
paralytic ileus 1105 - porto-systemic shunting
paramagnetic contrast media 137, 341 (TIPPS) 1041
paranasal sinus 238 - pyelolysis 163
parapharyngeal tumors 260 - stricture dilatation 1190
parasellar tumours 192 - sympathectomy 165
parasitic brain infections 214 - transcatheter embolization
paraspinal fluid abscess 338 o f the renal artery 1187
- fluid collection 338 - thrombolysis 1187
parathyroid gland 261 - transhepatic cholangiography
paratyphoid infection 1284 (PTC) 154, 1045
parauterine mass 1232 - portography (РТР) 1031, 1066
XXXVIII
INDEX
-transluminal angioplasty (PTA) 143 phakomatoses 616, 620

- balloon angioplasty 853 phalangeal fractures 396
- coronary angioplasty - bones 396
(PTCA) 804 pharyngeal bar 897
- renal angioplasty - constrictors 249
(PTRA) 1186,1187 - foreign body 899
perforated ulcer 1094 pharyngocele 899
perforating vein 821 pheochromocytoma 1212
peri-ampullary duodenal carcinoma 953 phlebolith 844
perianeurysmal fibrosis 1173 phlegmasia cerulea dolens 849
periapical cyst 279 phocomelia 489, 508
- osteitis 276 phosphoethanolamine 500
- granuloma 276 photoelectric absorption 23
periarteritis nodosa 1156 photographic emulsion 48
peribronchial cuffing 548, 549 photomultiplier tubes 62
pericardial cyst 697, 707, 802 photon 19, 20
- disease 802 phrenic paresis 695
- drainage 806 Phrygian cap 1048
- fat pad 707 physeal fracture 468
-flu id 802 - injury 468
-tum or 802 physis 461, 462,467
pericarditis 803,804 picket-fence pattern 983
pericardium 788 picture element 101
pericolic inflammation 992 picture archiving and communi
periductal fibrosis 653 cations systems (PACS) 104, 110
perimesencephalic cistern 203 PIE (pulmonary interstitial
perinephric space 1207 emphysema) 541,545
periodontal disease 278 piezoelectrical crystals 65
- ligament 266 Pigtail 812
periosteal pin hole imaging 514
elevation 475, 521, 526, 528, 530 pineal germ cell 201
- reaction 449, 451 pipe-stem colon 996
- membrane 450 pituitary microadenoma 1208
periostitis 449 - adenoma 224
peripheral embolisation 154, 813 - tumour 192
peripheral neuron 350 pixel 5 3 ,8 1 ,1 0 1 ,5 7
peritoneal bands 581 placenta praevia 1231
peritonitis 1093 placode 365
perivascular fibrosis 829 plain film radiography 371
periventricular leukomalacia 624 plaques 216
peroneal artery 820 plasma cell myelomas 373
-v e in 822 platelet activating factor 128
peroperative cholangiography 1045, 1055 platelets 128
peroral cholceystography 1042, 1047, pleueral metastases 555
1051 pleura 683
perpendicular periosteal reaction 449 pleural adhesion 732
perpendicular striations 451 - cavity 683
persistent corpus luteum cyst 1226 - effusion 539, 680
PET (Positron Emission -flu id 700,746,771
Tomography) 63, 64, 173, 881 - lesion 698
PET-camera 28 - plaque 745
Peutz-Jegher syndrome 942,976, 1008 - transudate 698
XXXIX
- thickening 699, 702, 732 - fossa 205

plicae collicularis 601 -hemivertebra 363
Plummer-Vinson syndrome 898 - hernia 697
PML (progressive multifocal - longitudinal ligament 300, 301, 325
leukoencephalopathy) 1315 - mediastinal mass 707
PNET 555 - rib fracture 480
pneumatosis coli 1005, 1088 - segment 685
pneumococcal pneumonia 726 - semicircular canal 230
pneumocolon 1098 - tibial artery 820
pneumoconiosis 744 - vein 822
pneumocystis carinii - urethral valve 601, 1226
pneumonia (PCP) 736, 1316, 1317 posteroanterior radiograph 671
pneumocystogram 651 postinfectious encephalitis 623
pneumomediastinum postirradiation oedema 661
541,547, 556, 759, 761 - reaction 661
pneumonectomy 763 postoperative
pneumonia 723, 770 cholangiography 1046, 1055
pneumopericardium 547, 759 - scarring 654
pneumoperitoneum 585,1 0 8 7 postthrombotic syndrome 850
pneumothorax 541, 547, 556, 582, 694, PRC reaction 889
703,704, 732, 757, 7 6 1 ,7 7 2 , pre-diverticular disease 990
polyarteritis nodosa 751 precession 73
polychromatic radiation 22 precocious puberty 467
polycystic kidney disease 594 prednisolone 130
- disease 1033 preeclampsia 1233
polydactyly 489, 496 premature closure o f the physes 440
polyethylene 854 presby-oesophagus 904
polyethylene-teraphthalate 854 prevertebral hematoma 304, 311
polyhydramnios 1230, 1231 primary adenocarcinoma 963
polyp 585, 993 -aldosteronism 1209
polyposis syndrome 1008 - CNS lymphoma 1309
Polytechnic o f Zurich 2 - lymphoma 1316
Polyurethane 854 - lung cancer 886
popliteal artery 820 - oesophageal peristalsis 901
- vein 821, 822 primitive neuroectodermal tumor 552
porcelain gallbladder 1053 progressive subacute HIV
porocephalosis 1301 encephalitis 1314
portal hypertension 589, 594 - multifocal
portal vein thrombosis 589 leukoencephalopathy (PML) 1315
positive contrast media 116 prolapse 325, 1018
positively charged electron 28 proliferative mastopathy 631
positron 28 prominent pulvinar 484
positron emission - colonic lymphoid follicle 1012
tomography (PET) 63, 64, 173, 881 - thymus 550
positron-emitting radionuclides 173 pronation-dorsiflexion 412
post-embolization syndrome 154 pronation-extemal rotation 412
post-myelography 361 prostaglandin 128,1132
post-traumatic epilepsy 616 prostaglandin therapy 528
postaxial polydactyly 489 prostate cancer 889,1193
posterior atlas 313 prostatic abscess 1192
- dislocation 402 prostatitis 1191,1192
- fat pads 399 proton density 75, 77
XL
INDEX
proton density (PD) weighted imagesi 79 - haemorrhage 542

protons 73 - hydatid cyst 1266
protozoal pneumonia 736 - hypertension 558, 793, 794
protrusion 325 - infarction 722,723
provisional ossification 464 - infection 547
proximal caries 274 - insufficiency 794
- focal femoral deficiency 490 - interstitial emphysema
- interphalangeal (PIP) joint 436 (PIE) 541,545
pseudo-achalasia 904 - ligament 683
pseudo-allergic reaction 127 - orifice 786
pseudo-anaphylactic reaction 127 - perfusion studies 63
pseudoacetabulum 4 8 3 ,4 8 4 - pseudocyst 545
pseudoaneurysm 813 - sling 536,571
pseudobulbar palsy 896 - tuberculosis 693
pseudocyst 1072 - vein 785
pseudohypoparathyroidism 467 - venous hypertension 569, 794
pseudomembrane 914 pulmonic valve 786
Pseudomonas aeruginosa 237, 728, 754 pulp chamber 266
Pseudomonas pseudomallei 1289 pulpitis 274
pseudopolyposis 996 pulse-spray method 859
pseudotumor 220, 550, 1144 pulsed Doppler mode (PD) 70,71
pseudotumoural plaques 219 pulsion diverticula 922
psoriatic arthropathy 437 pulsless disease 832
- arthritis 430, 433 punched-out ulceration 959
psycho-motor development 619 punctate erosion 914
- delay 619 pyelitis 1162
psychological deprivation 462 pyknodysostosis 504
psychosocial dwarfs 462 pyogenic spondylitis
PTA (percutaneous transluminal 3 3 6 ,3 3 9 , 340, 341,342
angioplasty) 143 pyonephritis 1163
PTC (percutaneous transhepatic pyramidal eminence 230
cholangiography) 154, 1045 pyriform sinus 257
PTCA (percutaneous transluminal pyrophosphate synovitis 440
coronary angioplasty) 804 quality control 667
PTP (percutaneous transhepatic quantum 19, 25
portography) 1031, 1066 RA (rheumatoid arthritis)
PTRA (percutaneous transluminal 4 2 1 ,4 3 0 , 4 3 3 ,5 2 5 , 647
renal angioplasty) 1186, 1187 radial absence 489
pull-through method 868 - artery 820
pulmonary adaptation syndrome 539 - hypoplasia 489
- amoebiasis 1245 - scar 653,655
- angiography 674 radiation enteropathy 986
- arterial disease 677 - induced oesohagitis 922
- arterial pressure 124 - nephritis 1156
- arterial stenosis 709 - protection 30, 33, 534
- arteriovenous malformation 677 radicular cyst 279
- calcification 731 radio frequency (rf-) radiation 26
- congestion 738, 739, 765, 769 - frequency interference pattern 26
-ed em a 7 3 8 ,7 3 9 ,7 6 9 ,7 9 7 - waves 20
- embolism radiographic report 388
63, 680, 722, 723, 769, 846 radiography 18
- fibrosis 744, 750 radioisotope scanning 63
XLI
radioisotopes 28 -dysplasia 1137

radiological measurements 110 - ectopia 594
- information system (RIS) 110 - failure 742
Radiological Society of North - fusion 594
America (RSNA) 15 -lym hom a 1149
radionuclide imaging 60 - tubular ectasia 594
radionuclides 60 - osteodystrophy 517, 527
radiopharmaceuticals 28, 60, 172 - retroperitoneal abscess 1190
radiotherapy 450 - scintigraphy 593
raised intracranial pressure 194 - transplantation 1156
Rashkind ballon atrial septostomy 566 - tuberculosis 1152
ratio 120 - vein 824
Raynaud phenomenon 829, 835, 836 -sam pling 1188
Raynaud's disease 835 -throm bosis 1136
Raynaud's syndrome 835 Rendu-Osler-Weber disease 844
RCA (right coronary artery) 787, 788 renin
rCBF 172 renovascular hypertension 1131, 1132
RDS (respiratory distress repetition time (TR) 79
syndrome) 540, 542 residual cyst 280
reactive arthritis 430, 433, 437 - thyroid tissue 251
- bone formation 449 -urine 1178
- fibrosis 654, 655 resolution 43
- patterns o f bone 447 resonance frequency 73
real-time scanners 69 respiratory syncytial virus 549
receptor kinetics 173 - distress syndrome (RDS) 540, 542
rectocele 1018 reticular opacity 737
recurrent incontinence 1180 reticulo-endothalial system 880
recurrent pneumonia 720 reticulonodular opacity 738, 745
reflux 9 1 1 ,9 1 8 retinoblastoma 220
reflux nephropathy 1151 retrieval o f lost foreign bodies 149
- oesophagitis 902, 950 retrobulbar tumours 219
regional sclerosis 337 retrocalcaneal bursa 437
regurgitation 898 retrograde phlebography 815
Reiter's syndrome 433, 437 retrogressive differentiatioan 297
remodelling 477 retroperitoneal adenopathy 1149
Remscheid 1 -em physem a 1088
renal abscess 1150 - fat 697
- adenoma 1145 -fibrosis 851,1173
-a g e n e sis 1136,1226 - fluid 951
- anomaly 489 -tum or 1173
- arteriography 1118 retrosternal goitre 705
- arteriovenous fistula 1135 reverse Colles fracture 390
- artery 820 rhabdomyosarcoma 220, 222, 248, 552
- artery aneurysm 1134 rheumatic fever 441,794
- artery percutaneous - heart disease 793
angioplasty 1186 rheumatoid arthritis
- artery stenosis 1130 (RA) 4 2 1 ,4 3 0 ,4 3 3 ,5 2 5 ,6 4 7
- atrophy 1168 - disease 751
- biopsy 1135 rhino virus 734
- cell carcinoma 1146 rhinorrhoea 192
- contusion 1158 rhizomelic 493,498
- cystic disease 594 rib notching 563, 694
XLII
INDEX
- fracture 694 sapphire tip 856

rickets 4 6 5 ,5 1 7 ,5 2 5 sarcoidosis 221, 747, 748, 750
right aortic arch 536 SBE (small bowel enema) 955,956
- atrial enlargement 793 SBO (small-bowel obstruction) 583, 980
- atrium 785 scanogram 56
- coronary artery (RCA) 7 87,788 scaphoid fracture 395
- subclavian artery 819 scaphoid-trapezoid joint 429
- ventricle 7 85,786 scapholunate dissociation 437
- ventricular enlargement 793 scapula 403
- hypertrophy 563 scar tissue 328, 336
right-sided aortic arch 564, 688 scattered radiation 40
ring ulcer 964 SCFE (slipped capital
- apophysis 298 femoral epiphyses) 516,517
RIS (Radiological Schatzki ring 892, 893, 916
Information System) 110 schistosomal cirrhosis 1257
Roentgen, Wilhelm Conrad 1 schistosomiasis 1246
Rokitansky-Aschoff sinus 1053 Schwachman syndrome 527
Rolando fracture 395 schwannoma 260
root caries 274 scintillation crystal 61
root-canal 330,331 scleroderma 747,1156
root-sleeve 318, 331 sclerosing adenosis 657
Rotacs system 857 - agents 863
rotating device 857 - cholangitis 1056
rotator cuff 403 - osteogenic sarcoma 286
round window 230 - osteomyelitis 286
- pneumonia 549 sclerosis 341,423
roundworm infestation 968 sclerosis o f the femoral head 514
RSNA (Radiological Society sclerotic lines 462
of North America) 15 - r im 450
rt-PA 853,859 scoliosis 318
Ruhmkorff induction coil 5 scout view 56
Ruhmkorff H.D. 6 screen-film combination 39
rupture o f the diaphragm 755, 761 screening 51
S. haematobium 1246,1247, 1249, 1252 screening for breast cancer 662
S. intercalatum 1247 scrotal enlargement 1195
S. japonicum 1247, 1254 sebaceous cyst 649
S. mansoni 1247, 1254 secondary achalasia 904
S. mekongi 1247 - lobule 686
S. stercoralis 1279 - oesophageal peristalsis 901
saccular cyst 257 - peritonitis 1091
sacral agenesis 364 sedation 534,613
sactosalpinx 1206 seizures 194
sagittal measurement 309 Seldinger technique 811
salivary gland tumors 255 self selection bias 663
salivary glands 252 self-expandable stents 146
salmonella 339, 968 sella turcica 174
salmonella colitis 1001 seminoma 1195
- infection 1284 sensitivity 170,613
- osteitis 1286 sepsis 742
Salter and Harris classification 469 septic arthritis 430, 441, 444, 445
sampling error 634 septic spondylitis 336
San Filippo form (MPS III) 511 sequester 325
XLIII
sequestration 336 ,5 5 3 - maturation 466, 467

sequestrum 443 - trauma 467
serial changers 50 skin dose 33
serofibrinous exudate 698 skip lesion 961,94
seronegative chronic arthritis 438 skull radiography 168
- spondyloarthropathy 430, 433, 437 - fracture 168,480
seropositive arthritis 438 SLE (systemic lupus
serotonin 128 erythematosus) 441, 1156
serum alkaline phosphatase 500 slice o f thicknes 59
- amyloid P compound sliding hernia 929
(1-123 SAP) 1031 slipped capital femoral epiphyses
shearing injuries 189 (SCFE) 516, 527
shigella dysentery 1001 small bowel adhesion 981
shiny comer 348 - atresia 579
shivers oesophagus 912 - enema (SBE) 955, 956
short saphenous vein 821 - ileus 1097, 1100
- inversion time (STIR) 338 - lymphoma 972
- ribs 496 - meal 955
shortening 388 - neoplasm 970
shunt function 619 - obstruction (SBO) 583, 980
-p a ten cy 619 - stenosis 579
sialoectasis 254 - tuberculosis 962
sialography 254 - series 955
sialolithiasis 253 small cell carcinoma 720
sickle cell disease 516, 530, 531, 1156 smearing technique 634
sigmoidoscopy 1006 Smith type fracture 390, 392
signal to noise ratio 43 smooth muscle tumour 974
silent abdomen 1105 social history 482
silicate crystals 747 sodium ipodate 1042
silicone dioxide 747 soft palate 249
- prosthesis 642 somites 298, 363
- spheres 863 sorbitol 131,958
- implant 631 South American blastomycosis 966
silicosis 7 4 4 ,7 4 7 spatial resolution 55,58, 105
silver bromide 48 specificity 170,613
simple bone cyst 282 specific radiologic pattern 452
-c y st 6 4 9 ,1 1 3 9 specimen radiogram 635
- renal cyst 595 SPECT (single photon emission
- ureterocele 1160 computed tomo-
Simpson catheter 145 graphy) 6 3 ,6 4 , 172, 881
Simpson-atherectomy catheter 857 spermatocele 1195, 1196
single umbilical artery (SUA) 1230 sphenoid sinus 238
- contrast barium enema 986 sphincterotomy 1059
- photon emission computed spiculated border 653
tomography (SPECT)63, 64, 172, 881 - tumor 648
sinography 455 spina bifida 368, 1226, 1229
sinus 962 - aperta 365, 367, 370
sinus tympani 230 - occulta 365
- venosus 559 spinal arteriovenous malformations 369
- tract 455 - canal 297
Sjogren's syndrome 254, 751 - cord MS 218
skeletal hydatid disease 1267 - cord tumor 507
XLIV
INDEX
- dysraphism 360, 365, 600 stricture 916

- infections 338 stroke 623
- ligament calcification 346 strongyloidiasis 966, 1279
- ligament ossisfication 346 styloglossus muscle 249
- lipoma 361,366 SUA (single umbilical artery) 1230
-sten osis 318,319, 330, 333 subacute osteomyelitis 442
- trauma 301 subarachnoid spread 349
- tumours 348 - haemorrhage 171
spinnaker sail 602 subarcuate canal 230
spinous process 301 subcapsular haematoma 1037
spiral CT 59 subchondral cyst formation 423
splanchnic neurolysis 165 subclavian vein 824
splenic infarction 1076 - artery 820
- rupture 1078 - vessel 688
splenomegaly 1074, 1076, 1304 subcortical atherosclerotic
splinter fragments 223 encephalopathy 177,219
split notochord syndrome 367 - fracture of the femoral head 514
spondylitis 336, 240, 707 subcutaneous emphysema 761, 1088
spondyloepiphyseal dysplasia 493, 500 - lipoma 360
spondylolisthesis 330 subdural haematoma 190
spondylosclerosis hemispherica 343 - effusion 621
spongioblastoma 209 subependydomas 201
spontaneous transmural perforation 923 subependymal lesion 1315
spot filming 52 sublingual salivary gland 253
Sprengel's deformity 364 subluxation 310
squamous cell carcinoma 237, 244, 248, submandibular gland 253
252, 289, 720, 1160 submentovertex projection 263
stacked coin appearance 952 submucosal haemorrhage 1003
Stafne cyst 274 -tu m o r 941
standard views 384 subpial-juxtamedullary lesions 366
Stanford classification 838 subtrochanteric fracture 407
stapes 230 subvalvular aneurysms 1291
staphylococcal pneumonia 727 superficial femoral artery 820
Staphylococcus 442 - femoral vein 822
Staphylococcus aureus 339, 549, 727 - palmar arch 821
static brain scintigraphy 172 superior gluteal artery 820
status epilepticus 616 - mesenteric artery 820
steel coils 151 - mesenteric artery syndrome 952
stenosis 829 - ophtalmic vein 176
stents 146 - orbital fissure 176
stereotactic localization 633 - sagittal sinus 180
STIR (short inversion time) 338 - semicircular canal 230
strangulation 1095,1100 - sulcus tumor 677, 721
strawberry gallbladder 1053 - vena cava 684, 687,785
Strecker stent 861 - vena caval syndrome 677
Streeter bands 489 supernumerary teeth 272
Streptococcus 339, 342 superparamagnetic contrast media 137
Streptococcus pneumoniae 549, 726 supination-adduction 412
- pyogenes 549 supination-external rotation 412
streptokinase 805 supracondylar fracture 399, 401,408
stress fracture supraglottic airway 249
41 8 ,4 1 9 , 443,446, 455,4 7 8 suprarenal vein 824
XLV
suprasellar aneurysms 226 ТЕ (echo time) 80, 1085

- meningioma 224, 225 tear-drop bladder 1177
supratentorial extraaxial tumours 193 tears o f the menisci 409
- hydrocephalus 205 technetium 29
- intraaxial tumours 197 technetium 99m 785, 881
-tu m ou rs 192 technetium-99m-methylene
surgical biopsy 656 diphosphonate 373
- neck fracture 402 technetium-labelled red cells 1019
Swan-Ganz catheter 767 TEF (tracheoesophageal fistula) 573
swimmer's itch 1246 teflon catheters 143
sympathoblasts 605 teleradiology 113
symphalangism 489 temporomandibular joint
syncytial virus 734 (TMJ) 290, 293,436
syndactyly 489 tension pneumothorax 547, 755, 757
syndesmophytes 346 teratoma 552
synovial membrane 433 terminal hematuria 1174
synovial proliferation 434 tertiary oesophageal contraction 901
synovitis 425, 445, 521 Tesla (T) 73
syphilis 465 testicular cancer 1195
syringohydromyelia 349, 351, 352, 367 -rupture 1195
syringomyelia 352 -torsion 1197
systemic adenosis 751 -trauma 1197
- collateral arteries 566 -tum or 1195
- disease 432 -v e in 823
- lupus erythromatosus tethered cord 361,367
(SLE) 4 4 1 ,1 1 5 6 tetralogy o f Fallot 563, 564
- malignant lymphoma 1316 tetraplegia 311
- sclerosis 904, 978, 969 TGV (transposition o f great vessels) 566
-v a scu litis 751 thallium 201TI 785
T (Tesla) 73 thanatophoric dysplasia 492,495
T cell 502 thermography 17,628
T. saginata 1304 thoracentesis 700
T. solium 1304, 1305 thoracic aortic aneurysm 837
Tl relaxation 78 - disease 677
T l-w eighted images 79 - drain 763
Tl-weighting 77 - kyphosis 315
T2 relaxation 77 - venous disease 677
T2-weighted images 79 - outlet syndrome 833
T2-weighting 77 thoracic trauma 698
ТА (truncus arteriosus) 568 - tumours 549
taeniasis 1304 thoracoepigastric vein 824
Takayasu's arteritis 832,11 3 1 ,1 2 9 1 thoracoplasty 693,732
talipes equinovarus 485 thoracotomy 675
talocalcaneal coalition 491 threatened abortion 1222
Tantalum 146 three-dimensional biplane technique 379
tapeworm 968, 1304 thrombectomy 845
TAPVR (total anomalous pulmonary thromboangitis obliterans 831
venous return) 568 thrombolysis 146,858
tarsal coalition 489, 491 thromboxane A2 128
tarsus 415 thumbprinting pattern 983, 994, 1003
Tausig-Bing complex 567 thymic tumor 552
TCD (cerebellar diameter) 1220 thyreocervical trunk 820
XLVI
INDEX
thyroglossal duct cyst 251,259 transition zone 450

thyroid adenoma 262 transitional cell carcinoma 1160
- cartilage 257 transluminal angioplasty 1186
- gland 261 transmitted radiation 60
-tum or 552 transmitter sensor 17
thyrotoxicosis 221 transplanted kidney 1125
tibia 409 transposition of great vessels (TGV) 566
tibial plateau fracture 408 transrectal ultrasonograhy 1192, 1193
tibioperonteal trunk 820 transurethral resection
Tietze syndrome 695 o f the prostate (TURP) 163
TIPPS (percutaneous - biopsy 184
porto-systemic shunting) 1041 transurethral ultrasonography 1184
tissue plasminogen activator (TPA) 805 transvaginal ultrasound
- glues 151 (TVUS) 1205, 1218
- contrast 38 transvenous pacemaker electrode 768
TMJ (temporomandibular transverse shear injury 316
joint) 2 9 0 ,2 9 3 ,4 3 6 trauma 447,754
toddler 478 traumatic arterial perfusion disorder 836
tomography 51, 671, 673 - bleeding 151
tongue movement 894 - bowing 385
tooth anomalies 271 - subarachnoid haemorrhage 189
- follicle 270 Treacher Collins syndrome 233, 272
- formation 270 trematodes 1246
torsed ovary 1203 trephine needle 456
torsion 1195 trichorhinophalangeal syndrome 516
torus fracture 385,476 tricuspid atresia 564
total contrast 39 - insufficiency 793, 794
- linear attenuation coefficient 55 - stenosis 793
- anomalous pulmonary - valve 786
venous return (TAPVR) 568 tricuspid valvular defect 796
Towne projection 263 triphalangeal thumb 508
toxic colitis 1094 triplane fracture 474
- dilatation 1094 tripod fractures 245
toxicity 117 trisomy 18 1226, 1228
toxicology 119 tropical eosinophilic lung 1301
toxolasmosis 214, 1311 - splenomegaly 1303
toxoplasmic abscess 1311 - sprue 969
- granuloma 1311 - ulcer 1293
Toxoplasma gondii 736 true aneurysm 836
TPA (tissue plasminogen activator) 805 - diverticula 922
TR (repetition time) 79 - vocal cords 257
tracheo-bronchial angle 684,688 truncus arteriosus (ТА) 568
- rupture 759 Trypanosoma cruzi 904,1272
tracheoesophageal fistula (TEF) 573 tuberculoma 732
tracheomalacia 536 tuberculosis 549, 730, 732,
tracheomembranous cartilage 536 736, 965, 1313, 1318
traditional fluoroscopy 51 tuberculous abscess 342
- tomography 51 - cerebritis 1313
transabdominal ultrasound 988, 1103 - lymphadenopathy 732
transchondral fracture 385 - meningitis 1315
transient tachypnea o f the newborn 539 - oesophagitis 920
transillumination 628 - pleurisy 702
XLVII
- spondylitis 342 urodynamic evaluation 1178

tuberous sclerosis 620 urokinase 146, 805, 853, 858
tubular adenoma 1006 US (Ultrasonography) 64, 65
- ectasia 1142 uterine anomaly 1201
tubulovillous adenoma 1007 uterine fibromyoma 1232
tumour 624 UTI (urinary tract infection) 600
tumour embolization 152 vacuum phenomenon 511
- calcification 168 valgus deformity o f the foot 485
tungsten 19 Valsalva manoeuvre 815
tungsten tube 628 valvular aplasia 852
Turner syndrome 467 - pulmonary stenosis 563
TURP (transurethral resection valvuloplasty 806
o f the prostate) 163 vanishing tumor 701
TVUS (transvaginal ultrasound) 1218 varicella 734
typhoid 968 varicella virus 734
typhoid infection 1284 varicocele 1195,1196
UC (ulcerative colitis) 994 varicose venous disease 850
ulcerative colitis vascular anomaly 842
(UC) 994,995, 1001, 1241 - compression syndrome 833
ulcerative jejunoileitis 970 - congestion 539
ulnar artery 820 -le sio n 415
- dislocation o f the wrist 521 - malformation 842
ultra fast CT 775, 793 -rin gs 570
ultrafiltrate 1127 vasoactive substances 128
ultrasonography (US) 64, 65 vasomotor nephropathy 1156
ultrasound examination 17 vasopressin 150, 1021
ultrasound contrast media 139 vasovagal reactions 129
ultraviolet light 20 VATER association 508
uncinate process 299, 300 VCUG (voiding cystourethrography) 591
unco vertebral joints 334 vena cava filters 149
unilateral headache 621 venae comitantes 822, 824
unilateral emphysema 713 veno-lymphatic obstruction 661
University o f Wurzburg 4 venography 813
upper extremity venography 816 venous angioma 186
- gastrointestinal haemorrhage 1020 venous arch 821
- motor neuron 350 - dysplasia 852
urachus 1177 - insufficiency 850
uremia 802 - malformation 843
ureteral balloon dilatation 163 - valve 821
- ectopia 598 ventilation scintigraphy 681
- obstruction 1150, 1152 ventricular septum 785
- occlusion 1191 - outflow tract obstruction 563
- stenting 163 - septum rupture 800
ureteritis 1162 - septal defect (VSD) 558, 566
urethral catheterization 1181 ventriculography 799
- stricture 1181,1190 ventriculomegaly 618
- trauma 1181 vertebra plana 509, 529
- tumors 1181 vertebral anomalies 489
urethrography 1116 - artery 820
urinary ascites 602 - body 299
urinary calculi 1165,1166 vertical force 313
urinary tract infection (UTI) 600 - talus 485
XLVIII
INDEX
vesicoureteral reflux (VUR) 591, 601 wet-lung disease 539, 541, 542
vestibular aqueduct 230 Whipple's disease 968, 969
vestibule 230 WHIS (WHO Imaging System) 14, 96
video urodynamics 1178 WHIS-Manual 98
videophlebography 816 WHIS-RAD 96
vigorous achalasia 902, 904 white matter 170
villous adenoma 1006 WHO "Manual of Radiographic
viral pneumonia 549, 733 Technique" 94
Virchows triad 846 WHO Imaging Systems (WHIS) 14, 96
visceral pleura 684 WHO Basic Radiological System 96
visible light 20 WHO (World Health Organization) 85
visual display 70 WHO-BRS 96
vitamin A poisoning 528 WHO-designed x-ray unit 95
- В 12 deficiency 977 Wilms' tumor 596, 602, 605
- D dependent rickets 526 window width 108
- D hypovitaminosis 831 wolfian duct 598
- D resistant rickets 525 workstations 113
vocal cord 257 World Health Organization (WHO) 85
voiding reflex 1129 worm-shaped polyposis 999
voiding cystourethrograhy (VCUG) 591 wormian bones 503
volume scanning 810 Wuchereria bancrofti 1299
volvulus 573,1101 Wurzburg University 3
vomiting 573 Wtirzburg Physical Medical Society 9
von Hippel-Lindau disease 103 3 X radiation 17
voxel size 58 X-ray guided FNAB 633
voxel 57,81 X-ray examination 17
VSD (ventrcular septal defect) 558, 566 X-ray spectrum 24
VUR (vesicoureteral reflux) 591, 601 X-ray 20
Waldeyer's ring 884 X-ray generator 36
Wallstent 861 X-ray tube 36
wash-in defect 795 xanthogranulomatous pyelonephritis 1152
water solubility 119 xenon-133 681
water siphon test 913 Xenonchloride-excimer-laser 856
Waters view 238 Y cartilage 482
Waters projection 263 Yersinia enterocolitica 959, 966, 1001
watershed infarctions 178 Zellweger syndrome (cerebro-
wavelength 20 hepatorenal syndrome) 498, 1228
wedge fracture 310 Zenker's diverticulum 893, 898
Wegener's granulomatosis 751, 1156 Zollinger-Ellison syndrome933, 948, 949

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A Global TextBook of Radiology II

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T h e N IC E R C e n te n n ia l

The NICER Institute

Reprinted papers are available from The NICER Institute

This book is partly based on a Scandinavian Textbook of Radiology

Editors of the Scandinavian Textbook:

Chapter 1 W.C. Roentgen and the discovery of X-rays............. 1

Chapter 12 The spine.................................................................... 297

Chapter 18 The lungs and mediastinum...................................... 669

David J. Allison, BSc, MD, Marie-France Beilin, MD

Olle Ekberg, MD Derek Harwood-Nash, MB,

Hassen A. Gharbi, MD Stig Holtas, MD

Philippe Grenier, MD Kjell Jonsson, MD

Frode Laerum, MD Con Metreweli, MB, BChir,

Holger Pettersson, MD Giuseppe Scotti, MD

The lungs and mediastinum

Alf Kolbenstvedt, Arnulf Skjennald and

A chest radiograph is the most frequently performed radiological exam­

Chest radiographs with supplementary methods of

radiograph as a starting point, supplementary radiographs using special

Fluoroscopy is used to localize and adjust special projections in order

Tomography involves sectional imaging. In conventional tomography,

placed by computed tomography (CT).

chronic haemoptysis it may be necessary to examine the vessels sup­

Computed tomography (CT)

Magnetic resonance imaging (MRI)

1. Thoracic aortic disease including aortic dissection and aneurysm

Figure 8. ECG gated spin echo images

Figure 9. ECG gated spin echo image in the

6. Evaluation of brachial plexopathy

A variety of MRI techniques are applicable in the assessment of thoracic

lae, pneumonia, etc. In order to distinguish embolism from other condi­

NORMAL ANATOMY AND VARIATIONS

It is important to be familiar with the appearance of the ribs, and to be

Figure 16. Lobes and segments o f the lungs.

clip, lost during thoracotomy may appear on a frontal radiograph of the

to the position of the middle lobe on the right side.

gestion, lymphatic obstruction, or in some cases of pneumoconiosis.

The posterior part of the mediastinal shadow is made up of the tho­

of the ribs by radiography. If an accompanying pneumothorax is sus­

pain in the front of the chest wall, costochondral osteochondritis (Tietze

Table 1. Causes o f elevation o f both domes o f the diaphragm

Table 2. Causes o f elevation o f one dome o f the diaphragam

Volume loss of the lung produces elevation of the diaphragm, causing a

Sinus not free- Loteral decubitus view with patient lying

Figure 28. Standing and lateral decubitus views o f the thorax.

resorbed and the appearance returns to normal, this type of interlobar

Pleural fluid Adhesion

Figure 31. Development o f pleural adhesions

Extensive nodular pleural thickening is seen with mesothelioma, a ma­

or damage to the diaphragm combined with rupture of part of the in­

germinal tunors. Goitre usually causes deviation and compression of the

CT scans can precisely define the location o f mediastinal masses and

Respiratory diseases and emphysema

Table 3. Classification o f emphysema

Type Clinical association

Scanty peripheral vascular shadows,

The chest film diagnosis of emphysema (Fig. 42) is based on:

The overall diagnostic accuracy is 65-80% depending on the clinical

to misinterpretation of normal variation of vascularity, abnormalities of

Another cause o f unilateral emphysema is unilateral lung transplanta­

struction. There is often a combination of causes. Cylindrical bronchiec­

Bronchography has been a common supplementary examination when

Table 4. Causes o f bronchial obstruction

Atelactasis of right upper lobe Atelectasis of left lower lobe

A chest radiograph is the most frequently performed radiological exam

chronic haemoptysis it may be necessary to examine the vessels sup

lae, pneumonia, etc. In order to distinguish embolism from other condi

The posterior part of the mediastinal shadow is made up of the tho

of the ribs by radiography. If an accompanying pneumothorax is sus

Extensive nodular pleural thickening is seen with mesothelioma, a ma

or damage to the diaphragm combined with rupture of part of the in

Another cause o f unilateral emphysema is unilateral lung transplanta

struction. There is often a combination of causes. Cylindrical bronchiec

The histological classification is of significance because small cell car

of blood through the bronchial circulation is sufficient to prevent the oc

Healed infarct or bleeding may be seen as residual linear opacities, of

considerably in appearance and distribution. In some types of pneumo

Pulmonary congestion and edema develop in two stages. Initially, in

segments, and are symmetrical, may be used in the differential diagno

muscles), there may be pronounced congestive changes without simul

Disseminated lupus erythematosus is the most common of the col

velopment of a secondary transudate. Contusion injuries may cause hy

tral venous catheter is therefore carried out to diagnose possible com