cover

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title : Imaging in Oncology

author : Curati, Walter L.
publisher : Greenwich Medical Media Limited
isbn10 | asin : 1900151030
print isbn13 : 9781900151030
ebook isbn13 : 9780511043314
language : English
subject Neoplasms--diagnosis, Diagnostic Imaging--methods,
Cancer--Imaging, Neoplasms--radionuclide imaging,
Neoplasms--ultrasonography.
publication date : 1998
lcc : RA645.C3.I43 1998eb
ddc : 362.1
subject : Neoplasms--diagnosis, Diagnostic Imaging--methods,
Cancer--Imaging, Neoplasms--radionuclide imaging,
Neoplasms--ultrasonography.
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1
Imaging in Oncology

Introduction

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`Education is at the foundation of many initiatives to improve the health.' 1

One of many quotations linking health and education, this was selected for its publication date on the centenary of
the discovery of X-rays by W.C. Roentgen in 1895 and with this work we now celebrate 100 years of
clinical-radiological correlation as Antoine Béclère (1856 - 1939) was the first physician to use fluoroscopy to
diagnose pulmonary tuberculosis in 1897, only 2 years after Roentgen's discovery.2

Introduction

Imaging Strategies

`A well designed imaging strategy is an implicit component of the approach to a patient with cancer'.3

This quotation summarises the origin of the motivation to write and edit this book which is aimed at medical students
and colleagues in clinical practice. It seeks to improve the management of patients with cancer by providing the
essentials of modern imaging techniques as applied to organ-based investigations.

The book adopts an integrative approach to the use of the most recent imaging modalities in both the initial assessment
of a patient presenting with the symptoms and/or signs of cancer, and in further diagnostic and staging procedures.

In modern imaging we possess both the requisite technology and the clinical expertise to do a great deal for our patients.
There is, however, a third factor to be considered, the so-called `cost-benefit' equation for patient and society. The cost
element of this concept is not based only on the financial impact of imaging techniques, but also on the risks of ionizing
radiation for both the patient and the population as a whole. This problem was first addressed in detail in `Critical
Diagnostic Pathways in Radiology',4 a publication which has had a strong influence on the way we conduct and teach
modern imaging investigations. These issues are, if anything, even more important now than when they were first raised.

Medical decision analysis, discussed in more detail below, also depends on evidence-based medicine for sources of
information and can, with appropriate techniques, individualise the treatment of data, follow up the consequences of
decisions over long periods of time and generate cost effectiveness ratios.5

Algorithms

Algorithms or critical diagnostic pathways became a necessity for the day to day running of an Imaging Department in
the late `70s when CT scanning installations in the industrialised world provided a novel means of investigating the
human body. While CT of the brain provided an entirely new technique for the imaging of the skull contents and
replaced previous invasive techniques (often requiring general an aesthesia), the study of the rest of the body by CT
Body CT had to compete in a more serious fashion with traditional techniques. The use of the word traditional has a
negative connotation in a domain in which progress is generally taken to be synonymous with the alleviation of
suffering. The essence, the `raison d'être' of research in medicine, is the broadening of knowledge from molecular
biology to surgical technique or medical therapy including a spectrum of imaging procedures ranging from the simple
X-ray beam to complex Positron-Emission Tomography (PET scanning) and Magnetic Resonance Spectroscopy (MRS
imaging).

The French phrase `arsenal diagnostique' embraces the dual concept of both a range of techniques and a choice of
techniques. What may in an ideal set of circumstances be the best investigation may not, in the real world, be available
owing to scarcity of resources, different political priorities, etc., and the appropriate selection of tests from those which
are available will be determined by considerations of cost/efficacy, where efficacy is generally measured in terms of life
duration, and cost/utility, where the duration of life is weighted according to its quality.5 In addition to these
considerations the cost-benefit ratio of imaging in financial terms is a constant reminder that we do not live in Utopia
and in the non-industrialised world major epidemiological factors usually tend to direct resource allocation away from
high technology medicine.

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The defence of established techniques for the imaging of the chest and abdomen is undermined by two factors: time and,
paradoxically (because existent `conventional' studies are usually less expensive to implement), cost. The time factor is
the essence of algorithm philosophy: a more sophisticated one-step modality which can image a tumour and furnish the
means of obtaining a tissue diagnosis is preferable to a chain of simple techniques which would ultimately still require a
further (perhaps endoscopic) step to achieve access to a specimen of tissue. The other factor, cost, plays a part in all
diagnostic investigations whether undertaken during the course of a hospital admission or in a series of out-patient
attendances. In comparing the `fast lane' with the `slow lane' the benefit of the time-factor is superficially obvious but
we must not lose sight of its true implications: earlier treatment and a genuine reduction

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in pain, emotional distress and morbidity. The prolonged occupation of a hospital bed is financially and socially
`expensive'. The social implications (quality of life for the patient and for his/her family, and for subsequent patients on
the waiting list) merge with political implications with their own widespread consequences ranging from popularity
issues with the electorate to the potentially difficult reallocation of budget resources.

The last argument in favour of algorithms, but definitely not the least in our priority list, is the maxim `primum nil
nocere'. This applies to diagnostic techniques using ionizing or high energy radiations and to all interventional
procedures. A non-stochastic effect (not related to chance, but measurable with thresholds of reversible and irreversible
damage) is bad enough and requires discipline in radiation protection, but the stochastic effect (related to chance, the
`lottery of life'), implies the avoidance of any potentially harmful technique and alone imposes the concept of the proper
justification of any radiological procedure.

Going back 100 years to Roentgen and Béclère, the use of X-rays for the diagnosis and follow-up of pulmonary TB is
universally accepted, but we do not use fluoroscopy for this indication any more and should we now need to do so, we
would choose equipment with a modern image intensifier.

Logic in Medicine and Algorithms

What is `logic in medicine'? Logic, according to Paul Tomassi 6 is, in the most general sense of the term, simply the
study of the nature of reasoning, of argument. But the term is more often used in a much narrower sense as the study of
deductive reasoning and deductive argument. We must also recognise another kind of logic which is not deductive in
character but inductive and probabilistic which proceeds from a finite list of particular observations to a concluding
generalisation.

Algorithms consist of a series of questions linked by lines labelled with the answers, which lead to the next question or
to the diagnosis. (7) The terminology varies according to language; the French term `analyse decisionelle', for instance,
is linked to the `arbre de capture' which is equivalent to the English `flow chart' or `computer sequencing'.

Inverting a algorithm step-by-step leads to a process known today as audit. Audit has become an unavoidable process
implemented in order to counteract the questionable argument: `this is what good radiologists do, therefore it has to be
right'. The concept of Continuing Medical Education (CME) as applied by current (self)-regulatory bodies replaces the
more traditional self-disciplined approach of reading the current literature and a few recent books, and attending staff
rounds and a few national and international meetings.

Algorithms can be either:

1) A step beyond simple interpretation of images acquired by radiologists `consultants' in managerial terminology in the
process of helping clinicians (A recent article by Robinson8 addresses this issue: `Radiology's Achilles' Heel: error and
variation in the interpretation of the Roentgen image')

and/or

2) the integration of imaging modalities (and their `consultant') into the concept of organ-based medicine. Not so long
ago the Oncologist was the close relative of the radiologist as both shared a common basic knowledge in physics and
imaging interpretation. In the algorithms for many oncological situations multiple other investigative `windows' should
be opened: e.g. the diagnosis of a lung tumour includes not only the initial abnormal chest X-ray but also CT and
bronchoscopy, or bronchoscopy and CT. The symptoms and signs of gastric carcinoma justify endoscopy and/or
contrast studies, and further imaging for staging, etc.

We the editors of this book have been very fortunate in gathering together a formidable group of imaging experts, each,
within his or her special area, as comfortable in their knowledge of radiology as in clinical medicine. We extend to all of
them our most sincere thanks for their outstanding contribution, and to our partners and families our thanks for their
support and understanding.

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After so many months of gestation, the book is ready. Allow me in a final quote to paraphrase and (for once) disagree
with my favourite author, Antoine de Saint-Exupéry in the `Petit Prince': it is not the time we have lost but the time we
have given this book which makes it so important.

References

1. Craft, N. Lifespan: Conception to Adolescence. BMJ 1997; 315: 12027-12030 (8 November 1997).

2. Curati-Alasonatti, W. Modern Imaging techniques: 100 years of clinical radiological correlations. Postgrad Doctor
1997; 13: 237-240.

3. Bragg, DJ. Imaging Strategies for Oncologic Diagnosis and Staging in: Oncologic Imaging. Bragg DJ, Rubin P,
Youker JE. Editors Pergamon Press (New York) 1985.

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4. Eisenberg RL & Amberg JR. Critical Diagnostic Pathways in Radiology. JB Lippincott Co. (Philadelphia) 1981.

5. Junod AF. Decision analysis and/or evidence based medicine. Med et Hyg 1997; 55: 2027-9.

6. Tomassi P. Logic in Medicine, in logic in medicine (second edition) Phillips CI Editor. BMJ Publishing Group
(London) 1995.

7. Williams BT. Computer aids to clinical decisions. Vol I and II. Florida: CRC Press, 1982.

8. Robinson PJA. Radiology's Achilles' Heel: error and variation in the interpretation of the Roentgen image. BJR 1997,
70: 1085-98

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2
The Central Nervous System

Lloyd Savy and Ivan Moseley

Intra-axial brain tumours

Extra-axial brain tumours

The pituitary region and visual pathway

The pineal region

The skull base

The spine

Postoperative imaging and radiation effects

New imaging techniques

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Cross-sectional imaging has revolutionized the investigation and diagnosis of tumours affecting the central nervous
system. Computed tomography (CT) and subsequently magnetic resonance imaging (MRI) have entirely supplanted
conventional methods of visualizing intracranial neoplasia and dramatic improvements in resolution and scanning speed
have increased diagnostic sensitivity and lowered the clinical threshold for investigation. Radiographs still play a small
part in the diagnosis of spinal tumours, especially vertebral metastases, but MRI has almost completely replaced
myelography and CT as the definitive initial investigation for suspected neoplastic disease of the spine. MR
spectroscopy and functional MRI can now provide important information about the composition of tumours and effects
on adjacent brain respectively and imageguided interactive systems have greatly facilitated the surgical treatment of
brain tumours.

Intra-Axial Brain Tumours

The first and most important diagnostic step in the analysis of intracranial tumours on CT or MRI is the differentiation
between intra- and extra-axial location, i.e. whether the tumour lies within or outside brain parenchyma. This distinction
has important prognostic implications as many of the former are malignant with poor long-term prospects, whereas the
latter tend to be benign for which a surgical cure is frequently realistic. MRI is somewhat more sensitive than CT in the
detection and characterization of intra-axial tumours. 1 It allows multiplanar imaging and does not subject the patient to
ionizing radiation. However, cost and availability may favour CT, which can also demonstrate some diagnostic features
such as tumour calcification better than MRI. It may also be the investigation of choice in critically ill or confused
patients and is usually more practical for guiding biopsy.

Astrocytoma

An important criterion in the analysis of intra-axial tumours radiologically is the differentiation between diffuse,
infiltrative astrocytic tumours and localized, non-infiltrative tumours. The former have a worse prognosis; they include
fibrillary astrocytoma, anaplastic astrocytoma, glioblastoma multiforme and gliomatosis cerebri, in order of severity.2

Fibrillary astrocytomas have poorly defined margins. On CT they are usually of lower density than brain; about 20%
calcify and up to 50% may show irregular enhancement. On MRI they show non-specific high signal on T2-weighted
(T2W) and proton density (PD) sequences and mild low signal on T1W sequences. They may contain areas of subtle
high signal on T1W images, due possibly to calcification or microhaemorrhage. Apparent tumour cysts cannot be
differentiated from microcystic change by signal characteristics, but the presence of internal septa, partition levels
between fluids or fluid and debris, and fluid motion effects, may signify a drainable cyst.3 Peritumoural vasogenic
oedema is rare, but tumour cells may exist outside the region of abnormal density or signal.4 A minority dedifferentiate
to become more malignant tumours after an indolent period of many years.

Anaplastic astrocytoma is more likely to show enhancement and vasogenic oedema (Fig. 2.1).

Glioblastoma multiforme usually occurs in patients over 50 years old. It almost always enhances on CT and MRI,
usually with a thick ring of enhancement, which can be irregular or partly nodular, around a central area of
non-enhancing necrosis. This central area shows low density on CT and T2/PD high, T1 low intensity on MRI.5 These
aggressive tumours usually have extensive surrounding vasogenic oedema, which tracks through white matter and may
cross the midline at the corpus callosum. Intratumoural haemorrhage may occur and spread via the subarachnoid space
as well as direct invasion of bone may be seen. There is frequently midline shift and contralateral hydrocephalus due to
compression of the foramen of Monro. Other pathology which can mimic glioblastoma includes solitary metastasis,
anaplastic oligodendroglioma, lymphoma, radiation necrosis, abscess and cavernoma with recent haemorrhage.

Gliomatosis cerebri is a very diffuse gliomatous process involving both white and grey matter, causing little or no
reduction in attenuation on CT, but much more conspicuous confluent or multifocal T2/PD high signal change on
MRI.6 Little or no mass effect may be evident and only rarely enhancement. Neurological deficits may initially be
relatively mild, but there is remorseless progression and invariably a poor prognosis. The differential diagnosis
radiologically may include encephalitis and demyelination.

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Localized, non-infiltrative astrocytic tumours have a more favourable prognosis.7 Histologically they are frequently
pilocytic. Radiologically they are sharply demarcated and lobular, often with a cystic component, and almost always
some enhancement; they rarely exhibit oedema, calcification or haemorrhage. Other tumours in this

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Figure 2.1
Anaplastic astrocytoma in a 55-year-old woman, who presented with a single seizure. Initial MRI axial T2W
(a), enhanced axial T1W (b) revealed a small enhancing intrinsic lesion within the left anterior temporal lobe
white matter. Four months later there had been dramatic progression: axial T2W (c), unenhanced coronal T1W
(d), enhanced coronal (e) and axial (f) T1W images. A large tumour now involves left frontal and temporal
lobes and insula. There is irregular rim enhancement, central non-enhancing T1 low signal due to necrosis and
extensive vasogenic oedema, although only mild mass effect. The genu of corpus callosum is thickened despite
normal signal on both T1W and T2W images and there is a further area of tumour enhancement to the
right of the midline.

category include pleomorphic xanthoastrocytoma (a relatively benign, superficially-located glioma of young adults, often presenting
with seizures), and subependymal giant cell astrocytoma, seen characteristically adjacent to the foramen of Monro in up to 10% of
patients with tuberous sclerosis.

Oligodendroglioma

Calcification is the hallmark of oligodendroglioma, seen best on CT (50-90%) and optimally on MRI as low signal on T2W gradient
echo images. This tumour is usually located in frontal or temporal lobes, often superficially. 8 It is often slow-growing and has a better
prognosis than infiltrative astrocytoma, with an overall 5-year survival rate of approximately 50%, although the degree of malignancy is
variable. On CT, oligodendroglioma is usually a mixed hypo/isodense mass containing calcification, which may show enhancement,
focal cysts or haemorrhage. There are no specific signal characteristics on MRI, although the observation of calcification is useful.
Differential diagnosis includes astrocytoma, glioblastoma and dysembryoplastic neuroepithelial tumour.

Neuronal Tumours

Ganglion cell tumours such as ganglioglioma and gangliocytoma or mixed neural/glial cell tumours may be indistinguishable from
gliomas radiologically, with similar density and signal characteristics to astrocytomas. They typically present in children and young
adults as supratentorial intrinsic masses, frequently in the temporal lobes.9 About half contain cysts and 30% calcification. The solid
component usually enhances but surrounding oedema is not typical. Occasionally

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they are of grey matter density and signal and may mimic grey matter heterotopia.

A relatively rare tumour of neural origin with characteristic imaging appearances is central neurocytoma. This benign
tumour usually presents in young adults. CT and MR demonstrate a well-circumscribed, inhomogeneous, partly
calcified mass, typically within the third or lateral ventricles, close to the foramen of Monro or septum pellucidum (Fig.
2.2). 10 There is characteristically a broad-based attachment to the superolateral ventricular wall.11 The tumour may
return high signal or signal close to that of grey matter on T2W MRI. Hydrocephalus is almost always present.
Differential diagnosis includes other intraventricular tumours, such as ependymoma; oligodendroglioma and
astrocytoma may also lie predominantly or completely within the ventricles.

Dysembryoplastic neuroepithelial tumour (DNT) is another relatively recently characterized tumour of glioneuronal
origin.12, 13 This totally benign tumour which occurs most frequently in temporal lobe grey matter can be the cause of
complex partial seizures, which may be cured by its excision. Usually small at presentation, it may be overlooked on
CT, although

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Figure 2.2
Central neurocytoma in a 29-year-old man. Axial
T2W MRI (a) shows a large inhomogeneous mass
within the third and lateral ventricles, much of which
is of the same intensity as cortex. It causes obstructive
hydrocephalus. The majority of the tumour enhances
on post-gadolinium T1W image (b). Areas of T1 low,
T2 high signal suggest cystic or microcystic
components. Dense calcification is seen within parts
of the tumour on CT (c).

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larger lesions may be evident as a low density area with little if any mass effect; 50% calcify. On MRI the cortical location is
characteristic; high signal on T2W and PD and equal to or slightly lower than grey matter on T1W images is seen. A DNT often cannot
be distinguished from low grade glioma.

Ependymoma

Ependymomas are usually slow-growing, lobulated tumours, which arise from the ependymal lining of the ventricles or central canal of
the spinal cord. They are more common in children than adults, and in children most frequently lie within the fourth ventricle. The
tumour characteristically has a `plastic' appearance on imaging: it may extend through the outlet foramina of the ventricle and surround
the brainstem and upper cord with only minor distortion of the neuraxis (Fig. 2.3). In adults the majority of ependymomas are
supratentorial and these are usually extraventricular, although they may be partly or completely intraventricular. On CT ependymomas
are usually isodense; 50% calcify; most show moderate inhomogeneous enhancement; haemorrhage is uncommon. On MRI they yield
T1 low, T2 high signal, and the location and shape provide more specific clues to the diagnosis than signal and enhancement
characteristics. 14 There is a spectrum of anaplasia; the observation of central necrosis on CT or MRI suggests a more aggressive
tumour. Cerebral spinal fluid (CSF) seeding is not uncommon and is detected most accurately by MRI with gadolinium enhancement.

Haemangioblastoma

This uncommon tumour may occur in isolation, but 10-20% occur as part of von Hippel Lindau syndrome. The characteristic appearance
on CT or MRI is of an intrinsic cerebellar mass consisting of a relatively small, intensely enhancing nodule, often with a larger cyst
adjacent to it:15 a solid enhancing mass may be seen. Location in the brainstem or supratentorial compartment is rare. The tumour
nodules are multiple in a minority of cases and MRI is more sensitive than CT in demonstrating these small lesions in the posterior
fossa, as well as vascular signal voids which may be closely related to them. Only symptomatic lesions are treated surgically.

Lymphoma

The incidence of primary CNS lymphoma is increasing, both in patients who are immunodeficient, such

Figure 2.3
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Figure 2.3
Posterior fossa ependymoma in a 16-year-old boy.
Axial T2W MRI (a) shows a mixed signal intensity
mass within the inferior part of the fourth ventricle,
which extended through the outlet foramina. Coronal
T1W image (b) shows tumour of mixed signal, slightly
lower than that of grey matter, extending below the
foramen magnum. The post-gadolinium sagittal
image (c) shows intense, inhomogeneous
enhancement of the tumour, the shape of which
conforms to the subarachnoid space around the
neuraxis. Serpiginous areas of signal void are due to
distended posterior fossa veins.

as those with AIDS, organ transplant or congenital immunodeficiency, and in immunocompetent patients. In the latter
the peak incidence is in the sixth decade. The tumour is nearly always non-Hodgkin's lymphoma and has a dismal
prognosis, although radiotherapy can prolong life, particularly in patients with AIDS.

Lymphoma is typically located close to the ventricles, either in deep white matter or basal ganglia. Calcification is
absent and haemorrhage very uncommon. 16 On CT the mass is usually isodense or slightly denser than grey matter,
often spherical, and shows dense homogeneous or thick ring enhancement. Oedema occurs, but is usually less in degree
than with metastases or aggressive gliomas. In 20-40% of cases multiple sites are affected. On MRI tumour signal
characteristics are similar to grey matter, although either high or low signal on T2W sequences may be seen (the latter
due to dense cellularity).

In AIDS lymphoma, central necrosis and peritumoural oedema are more common,17 and the main differential diagnosis
is toxoplasmosis. Subependymal spread and enhancement along perivascular (Virchow-Robin) spaces are features
which favour lymphoma,18 whereas haemorrhage favours toxoplasmosis, despite occurring more frequently in AIDS
than non-AIDS lymphoma.

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Primary CNS lymphoma can also show a more diffuse, infiltrative pattern, which may be indistinguishable from
gliomatosis cerebri.

Metastases

Intra-axial metastases comprise 20% of clinically detected brain tumours and occur most frequently in the fourth to
seventh decades; 80% are supratentorial. The lung, breast, skin (melanoma), gastrointestinal tract and genitourinary
tract are the commonest primary sites. The optimal imaging method for detection of small metastases is
gadolinium-enhanced MRI,19 which can also differentiate small metastases from ischaemic areas. CT still has an
important role in investigating the acutely ill patient. The grey/white matter interface is a site of predilection, as there is
significant narrowing of cerebral arterioles at this level.20 Metastases exhibit florid vasogenic oedema, although this
tends not to cross the corpus callosum or involve cortex, in contradistinction to that associated with primary tumours.
Cortical metastases may show little or no surrounding oedema. Most metastases are of low density, T2/PD high and T1
low signal, but haemorrhage is present in 20% (particularly melanoma, choriocarcinoma and renal cancer). Melanin
itself has a characteristic MRI signal (T1 high, T2 low intermediate signal), although primary brain tumours as well as
metastases may be melanotic (Fig. 2.4); mucinous adenocarcinoma often yields T2 low signal. Metastases may calcify
or even ossify (especially osteosarcoma). Enhancement occurs on both CT and MRI: it may be nodular or consist of a
thick irregular ring, with a central non-enhancing area due to necrosis. This contrasts with the characteristically thin
enhancing rim of cerebral abscess, although the radiological appearance may be similar.

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Recently, the advent of stereotactic radiosurgery for solitary metastases and the use of adjuvant radiotherapy after surgery have
increased the importance of detecting small metastases.

Posterior Fossa Neoplasms of Childhood

In children infratentorial neoplasms are more prevalent than supratentorial neoplasms and present with symptoms of hydrocephalus,
cranial nerve palsies or cerebellar syndromes. The commonest tumours are juvenile pilocytic astrocytoma, primitive neuroectodermal
tumour (PNET) previously termed medulloblastoma, ependymoma and brainstem glioma. MR is the most useful imaging modality,
due to its clear depiction of posterior fossa anatomy 21 and facility to perform enhanced scans of the brain and whole spine at the time
of initial diagnosis, to demonstrate small leptomeningeal metastases which have spread via CSF.

Pilocytic astrocytoma frequently arises in the cerebellar vermis or hemisphere in children and young adults and is typically partly
cystic, partly solid. About 10% are calcified; enhancement is variable. PNET (medulloblastoma) occurs in a similar location, also
mainly in children, and may be indistinguishable, although it tends to be more homogeneous; it is usually relatively dense on CT and
may be of low signal on T2W MRI, due to dense cellularity. Enhancement is usually intense; haemorrhage and calcification are rare.
PNET shows early CSF dissemination, and preoperative gadolinium enhanced scans of the whole neuraxis are useful as postoperatively
small foci of leptomeningeal haemorrhage may be present. Like metastases these can also appear as tiny high signal areas on enhanced
images, but unlike metastases they are usually also of high signal on unenhanced T1W images.

Brainstem gliomas may be pilocytic or fibrillary astrocytomas. They are usually solid, low grade tumours, which expand the brainstem,
and are much more easily detected on MRI than CT.

Extra-Axial Brain Tumours

Neoplasms arising from structures around the brain are usually benign, but may cause neurological deficit

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Figure 2.4
caption overleaf

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Figure 2.4
Intraventricular tumour with unusual signal
characteristics which was shown histologically
to be a melanotic ependymoma. Unenhanced CT
(a) demonstrates a very large multilobular
hyperdense mass containing a little calcification,
which enhances homogeneously (b).
There is severe vasogenic oedema in the right
cerebral hemisphere (note the sparing of caudate
and lentiform nuclei), subfalcine herniation to the
left, compression of the ipsilateral lateral ventricle
and contralateral hydrocephalus. MRI strongly
suggests the intraventricular location of the mass.
Its low signal on the T2W image (c) and high
signal on the T1W image (d) are highly unusual
for ependymoma, and are due to the presence of
melanin in this case. Gadolinium enhancement of
the mass (e) is masked by its high signal, except for
a small tumour component which is isointense to
brain on the unenhanced scan.

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or even death by compressing the neuraxis. The mode of therapy and the prognosis depend on the location of the
tumour. It is therefore important for imaging studies to distinguish between extra- and intra-axial tumours, although this
can be difficult. MRI is superior to CT in this respect as it can demonstrate displaced cortex lying deep to extra-axial
tumours, compression of adjacent gyri, and also small intervening structures such as pial blood vessels, dura and
pockets of CSF, lying between tumour and brain (Fig. 2.5). It is particularly useful for suspected posterior fossa tumours
as its multiplanar capability helps to demonstrate the relationship of an extra-axial mass to the brainstem and
cerebellum. Furthermore, the beam hardening artefacts which degrade CT in the posterior fossa are avoided. MRI is
also better than CT at defining the margins of extension of extra-axial tumours, arterial encasement and dural sinus
compression or invasion. Gadolinium aids tissue characterization (meningioma and metastasis enhance whereas
dermoid and epidermoid do not), and also increases sensitivity for detection of small extrinsic tumours such as
metastases and lymphoma.

Meningioma

Meningioma is by far the commonest primary extra-axial intracranial tumour. It is twice as prevalent in women as men,
and presents most frequently in the fourth to seventh decades. It is very rare in children, in whom it is more likely to be
a manifestation of neurofibromatosis. Areas where arachnoid granulations are abundant are sites of predilection for
meningioma, including the parasagittal region and the meninges close to the pterion. The tumour can also arise from
pial meningeal cells and therefore can occur within the ventricles or Sylvian fissures.

CT shows an isodense or dense mass with a broad base to the overlying dura mater. Internal calcification is present in
20% and may be punctate or dense. There is almost always dense homogeneous enhancement. Oedema in adjacent brain
is common and variable in extent. An important sign on CT is thickening of adjacent bone (hyperostosis), which if
present is a strong pointer to the diagnosis. This may involve paranasal sinuses, particularly the posterior ethmoid air
cells adjacent to a meningioma of the planum sphenoidale, known as pneumosinus dilatans. The hyperostosis is usually
a reactive rather than neoplastic phenomenon, although infiltration and expansion of the skull vault or base by tumour
itself may also be seen; indeed meningioma can be solely intradiploic, arising from arachnoid cell rests in the diploic
space.

On MRI meningiomas usually yield signal close to that of grey matter on all sequences and if small may be
inconspicuous and easily overlooked. As on CT there is intense homogeneous enhancement of the mass and an
enhancing `dural tail' extending away from its base is characteristic, but not specific. The dural tail frequently does not
contain tumour cells. 22 Peripheral cysts may be seen on MRI and CT and can be intratumoural or subarachnoid.

To some extent meningioma subtypes can be identified by MRI signal.23 Angioblastic or syncytial tumours tend to
exhibit higher signal than cortex on T2W images; transitional tumours are isointense; fibroblastic tumours may show
lower T2W signal than cortex, due to calcification within psammoma bodies. The rare lipomatous form of meningioma
yields high signal on T1W images and is of low density on CT due to its fat content. Malignant meningioma is difficult
to predict radiologically. Invasion of the brain suggests it, but transcalvarial spread does not.24 Haemangiopericytoma
is usually indistinguishable from meningioma radiologically, but may be suggested by the absence of hyperostosis or
tumoural calcification.25

Angiography still occasionally plays a part in the preoperative assessment of meningiomas, both to indicate the degree
of tumour vascularity and to determine the patency or otherwise of adjacent dural sinuses, although MRI and MR
angiography (MRA) can also provide similar information. Angiography is also necessary in planning preoperative
embolization using particulates, to reduce the vascularity of the tumour and facilitate haemostasis at surgery.

Differential diagnosis depends on location: 8th nerve Schwannoma in the cerebellopontine angle; pituitary adenoma in
the suprasellar region; choroid plexus papilloma within the ventricles; metastasis, lymphoma or granuloma at any
extra-axial site are examples.

Nerve Sheath Tumours

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The commonest intracranial nerve sheath tumour is 8th nerve Schwannoma. It usually arises from the superior
vestibular nerve rather than the acoustic nerve and presents with sensorineural deafness and/or tinnitus. It is typically
bilateral in neurofibromatosis II. MRI has replaced CT in screening for this tumour as it is more sensitive and does not
subject a potentially large screened population to ionizing radiation. On 1.5 Tesla MRI, fast T2 sequences with high
spatial resolution may be sufficient to exclude small 8th nerve tumours, if the whole length of the nerve can be
visualized.26 If not, or on lower field strength systems, gadolinium-enhanced T1W sequences may be required. Small
lesions are of similar

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Figure 2.5
MRI of large frontotemporal meningioma arising in the region of the pterion in a 31-year-old man. Axial proton
density (a) and T2W (b) images. Coronal T1W images (c) before and (d) after gadolinium. Both the signal of the
tumour on PD and T2W images and the enhancement pattern are less homogeneous than usual. The
extra-axial location is signified by the displacement and compression of adjacent gyri and the presence of pial
vessels between tumour and brain, seen as small signal voids. Hyperostosis of the adjacent skull vault is evident,
in comparison with the opposite side. Vasogenic oedema within the underlying white matter is clearly seen on
the T2W image.

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intensity to brain on all sequences and therefore stand out against the high intensity of surrounding CSF on T2W
images. CSF motion effects may simulate a mass in the cerebellopontine angle, but lack of contrast enhancement will
exclude tumour. 8th nerve Schwannoma (Fig. 2.6) is characteristically cone-shaped, lying partly within the expanded
internal auditory meatus and partly within the cerebellopontine angle cistern. Larger tumours can compress the brain
stem and cause hydrocephalus. They may undergo central necrosis and form cysts and therefore show T2 high, T1 low
signal and central nonenhancement. Calcification is extremely rare, in contrast with meningioma, but haemorrhage is
more common. The shape of the tumour and absence of hyperostosis are also useful discriminators. Other tumours
which occur in the cerebellopontine angle include metastasis, epidermoid, exophytic glioma and ependymoma.

5th nerve (trigeminal) Schwannoma is the second commonest intracranial nerve sheath tumour and may be recognized
on MRI by its orientation along the line of the nerve.

Maldevelopmental Tumours and Cysts

Arachnoid cyst, lipoma, epidermoid and dermoid are all extra-axial masses which may compress the brain. However,
arachnoid cysts are common incidental findings on imaging, usually without clinical significance. Midline lipomas
occur in conjunction with developmental abnormalities, typically dysgenesis of the corpus callo-

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Figure 2.6
Bilateral 8th nerve Schwannomata in a patient with
neurofibromatosis type II. Coronal T1W MRI
(a) and axial T1W image after gadolinium injection
(b). Note the characteristic `ice-cream cone' shape of the
tumours, which occupy the expanded internal auditory
meatus and cerebellopontine angles and compress the
brain stem. Smaller Schwannomas are shown in the right
jugular foramen and (c) involving the left trigeminal nerve.

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sum. Epidermoids may grow and cause symptoms and require surgery or radiotherapy. They are characterized on
imaging by density and signal close to CSF, lack of calcification or enhancement, and unlike arachnoid cysts lobulated
margins. 27 Dermoids are inhomogeneous masses which tend to occur in the midline and may be identified on MRI or
CT by the presence of fat, or differentiated structures such as teeth within the mass.

Choroid Plexus Papilloma

This highly vascular benign intraventricular tumour accounts for 0.5% of intracranial neoplasms, but is one of the
commonest brain tumours in infants. It occurs most frequently in the lateral ventricle in children and the 4th ventricle in
adults, but also occurs in the 3rd ventricle. It may extend through the 4th ventricular outlet foramina and can also be
located solely within the cerebellopontine angle. Apart from intense homogeneous enhancement, the most characteristic
feature on imaging is a lobular, fronded appearance to its surface, more readily appreciated on MRI than CT.
Calcification is common and cyst formation and haemorrhage also occur. Hydrocephalus is also usually present and
may be secondary to repeated intraventricular haemorrhage or CSF oversecretion.28 Carcinoma of the choroid plexus is
much less common. It has similar appearances on imaging and features such as invasion of the brain and dissemination
via CSF do not distinguish it from papilloma.

Metastases

Intracranial metastases may be solely extra-axial, particularly breast and prostate carcinoma and neuroblastoma, and
cannot be reliably demonstrated without intravenous contrast enhancement.29 Enhanced MRI is much more sensitive
than CT. Lymphomatous involvement of the leptomeninges or dura mater (Fig. 2.7) may be primary or secondary,
solitary or multiple and occurs in a third of patients with systemic lymphoma.

Extra-axial metastases can have many deleterious effects on the CNS, including brain compression, cranial nerve
involvement, venous thrombosis, haemorrhagic meningitis and hydrocephalus, and all of these can be demonstrated by
MRI.

The Pituitary Region and Visual Pathway

MRI has almost completely replaced CT for the assessment of chiasmal compression by tumours in the pituitary region.
Pituitary macroadenoma is by far the commonest cause, but meningioma, craniopharyngioma, teratodermoid and
metastasis may also involve the chiasmatic cistern, as well as intrinsic tumours of the optic pathway such as glioma
(usually pilocytic astrocytoma). The pituitary infundibulum may be the site of lymphoma or germinoma, as well as
adenoma and very rarely other primary tumours such as glioma and choristoma (granular cell tumour).30 The latter is
usually evident as an enhancing infundibular mass of similar density and signal to brain.

The multiplanar capability of MRI allows excellent demonstration of the relationship of a large pituitary tumour to the
cavernous sinuses and internal carotid arteries, and has obviated the need for angiography. On postoperative scans
artefact from surgical clips may obscure the region of interest less than on CT.

In the orbit CT still plays an important part in the diagnosis of tumours affecting the optic nerve/sheath complex. The
demonstration of calcification of the nerve sheath is virtually pathognomonic of meningioma; erosion or hyperostosis of
the optic canals or bony walls at the orbital apex are more readily identified than on MRI; fat within the rectus muscle
cone provides good inherent contrast with the nerves; narrow sections of 1-2 mm provide good spatial resolution for
small tumours. However, MRI usually separately identifies the nerve and its dural sheath, will show pathology within
the nerve more sensitively than CT, and avoids radiation to the lens. Gadolinium-enhanced, fat-suppression techniques
are sensitive to tumours of the nerve sheath such as meningioma. The patient's age at presentation is a good
discriminator of glioma and meningioma of the optic nerve/sheath complex: the former usually present in the first two
decades and the latter after this time. Orbital lymphoma is most prevalent in elderly women and typically has the
appearance of a diffuse, usually extraconal mass in the anterior part of the orbit, which is difficult to distinguish from
orbital granuloma.

Pituitary Adenoma

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Microadenomas are defined as tumours less than 10 mm in diameter and typically present with endocrine symptoms,
although many are asymptomatic, and they are a common incidental finding at autopsy. About 50% are prolactinomas
and for these, in the absence of visual signs, both the initial diagnosis and monitoring following medical therapy can be
achieved biochemically, without any need for imaging. Patients with acromegaly or Cushing's syndrome, or rarely
syndromes related to

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thyrotrophic or gonadotrophic hormone hypersecretion, may require imaging to locate the tumour within the pituitary
gland prior to surgery. This requires MRI using thin slices, small field of view and a fine matrix. Microadenomas are
usually of high signal compared with the pituitary on T2 fast spin echo images and of low signal on T1W images. They
enhance less than the remainder of the gland in the early phase following gadolinium injection and more than the gland
in the late phase. 31 Alteration in shape of the pituitary, signified by a bulge in its superior surface, depression of part of
the floor of the fossa, or displacement of the infundibulum, may help to locate a microadenoma but are less sensitive
signs than signal change and can be misleading. Rarely petrous vein sampling by catheterization via the femoral vein
may be required to distinguish Cushing's syndrome from syndromes of extraneous corticosteroid overproduction and to
assist in lateralization of tumour.

Pituitary macroadenoma may present with symptoms of optic pathway compression, but alternatively with

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Figure 2.7
A man of 70 years with systemic non-Hodgkin's
lymphoma, who presented with right 6th and 7th
nerve palsies. Axial T2W MR (a) shows no definite
abnormality in the cerebellopontine angle. The basilar
artery can cause slightly reduced signal in adjacent
CSF due to the effects of pulsation (arrow). However,
a gadolinium-enhanced T1W image (b) clearly
demonstrates enhancing tumour involving
the meninges at this site (arrow), and in contact with
the basilar artery. Enhanced coronal scan (c) also
shows the extent of tumour within the cistern.

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symptoms or signs of 3rd or 5th nerve compression, hypopituitarism, diabetes insipidus or pituitary apoplexy; in the
latter case, haemorrhage or infarct within the tumour may be seen on MRI (Fig. 2.8). These tumours enhance with
gadolinium, but unenhanced T1W images suffice for monitoring tumour size. On CT macroadenomas are isodense and
show intense enhancement, but rarely calcify.

Craniopharyngioma

Craniopharyngioma arises from squamous epithelial rests along Rathke's cleft and is usually predominantly suprasellar,
with an intrasellar component. It is more common in children than adults. On CT 90% show calcification, cyst
formation and nodular or rim enhancement. MRI may show multiple cysts of different signal intensity. 32, 33 The
presence of calcification and a solid component helps to differentiate this entity from Rathke's cleft cyst.

The Pineal Region

Pineal tumours constitute less than 1% of intracranial tumours. They may present with symptoms of hydro-

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Figure 2.8
Unenhanced T1W MR images showing a
haemorrhagic pituitary adenoma. Sagittal scan (a)
demonstrates an enlarged pituitary gland of abnormally
high signal causing expansion of the pituitary fossa.
The haemorrhagic tumour is of similar signal to
adjacent fatty marrow within the basisphenoid.
Coronal scans (b) before and (c) after gadolinium
show an area of normal signal within the right side of
the gland (arrow); however, this enhances to a
lesser degree than the cavernous sinus, suggesting
that it represents non-haemorrhagic tumour rather than
normal pituitary tissue.

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cephalus due to compression of the aqueduct, Parinaud's syndrome due to tectal plate compression, or endocrine
symptoms such as precocious puberty. They include pineal cell tumours (pinealoblastoma and pinealocytoma) and germ
cell tumours (germinoma and teratoma). These may be difficult to distinguish radiologically, but some features aid in
differential diagnosis. 34, 35

Teratoma typically presents in the first decade, predominantly in boys. It may be calcified, cystic or haemorrhagic, and
the presence of fat or differentiated structures such as teeth signifies the diagnosis. Germinoma usually has a more
homogeneous appearance on CT and MRI, is dense on CT and can be of the same intensity as grey matter on T2W
images. Its diagnosis is important as it responds to low-dose radiotherapy. It occurs most frequently in the first three
decades and 90% of patients are male. The primary tumour may arise in the suprasellar region or within the third
ventricle as well as from the pineal gland. Seeding through the CSF space is common, but such metastases may also
respond well to radiotherapy.

Pineal cell tumours are less common: pinealocytoma is a benign tumour of adults. Pinealoblastoma is a less well
differentiated malignant neoplasm found in young children. It is a subtype of primitive neuroepithelial tumour (PNET)
and has a strong tendency to metastasize within the subarachnoid space. It may appear less well encapsulated than other
pineal tumours, enhances less homogeneously and may invade adjacent brain, but there are no pathognomonic
radiological features.

Pineal cysts are a common incidental finding, seen in at least 5% of the population on MRI, and found much more
frequently at autopsy. They should have a signal close to or slightly higher than CSF with all MR sequences and have a
thin, well-defined, round capsule. They may show peripheral contrast enhancement. Any cyst greater than 1.5 cm in
diameter, however, should be regarded with suspicion.

The Skull Base

Neoplastic skull base lesions cause a wide variety of CNS symptoms depending on their location. They may compress
the base of the brain and brainstem and may involve cranial nerves, cavernous, lateral and sigmoid sinuses, or carotid
arteries. Meningioma and metastases can occur anywhere at the base of the skull. Nasal and sinus malignancy such as
carcinoma, rhabdomyosarcoma36 and olfactory neuroblastoma (esthesioneuroblastoma)37 can invade the anterior
cranial fossa. Each of these tumours exhibits bone destruction, but there are no specific density or signal characteristics
on CT or MRI, with non-specific T2 high, T1 low signal and enhancement following contrast medium; biopsy is almost
always required. MRI is more reliable for demonstrating the extent of the lesion.

Central skull base tumours involve the sphenoid and basioccipital regions. Pituitary tumours have been described above.
Chordoma is a relatively benign but locally invasive neoplasm, often with a poor outcome. It arises from the remnants
of the notochord and tends to involve the clivus in the midline. Apart from the location it does have other characteristic
imaging features: on CT a high percentage are calcified and severe bone destruction is usually evident; on T2W MRI38
it returns a very high signal, which may be higher than that of CSF and often has a strikingly inhomogeneous
appearance (Fig. 2.9); it enhances avidly. Chondrosarcoma is a very similar tumour histologically as well as
radiologically and orthographically, but typically arises lateral to the clivus. Either of these tumours can invade the
middle or posterior cranial fossae, as can nasopharyngeal carcinoma. The upper cervical spine may also be involved.
Other tumours which can involve the central skull base include trigeminal Schwannoma and juvenile angiofibroma.

Posterolateral skull base tumours involve the temporal bone. Glomus jugulare tumours may compress the neuraxis and
cause cranial nerve palsies. The irregular erosion of the jugular foramen and extent of petrous bone destruction are best
assessed by high resolution CT using narrow sections, but the relationship of the tumour to brain is seen more clearly on
MR. Angiography is used to define which branches of the external carotid artery supply the tumour and preoperative
embolization can reduce the size of the mass and aid haemostasis at surgery. Glomus tympanicum, like glomus jugulare,
is a highly vascular paraganglioma, but arises in the middle ear cleft. Either of these can reach the cerebellopontine
angle. Other tumours arising in the temporal bone region include squamous carcinoma of the external auditory meatus
and nerve sheath tumours arising from the 7th to 12th cranial nerves. Meningioma may occur at the surface of the clivus
or at the foramen magnum and can compress the brain stem or upper cord, often with relatively mild neurological signs
due to its slow growth.

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The Spine

MRI is now the primary imaging modality in the diagnosis of spinal tumours. It is more sensitive and specific than
scintigraphy in the detection of vertebral

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Figure 2.9
Skull base chordoma. (a, b)
Unenhanced CT shows a large
mass containing punctate calcification,
causing destruction of the basisphenoid
and compression of the brainstem. Axial
T2W MRI (c) shows the typical mottled
signal of chordoma, higher than that of
CSF, and displacement of carotid and
basilar arteries. Sagittal T1W image
following gadolinium (d) shows
inhomogeneous tumour enhancement
and clearly displays the extent of skull base
destruction and compression of the pons.

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metastases 39 and superior to CT myelography in the assessment of intraspinal tumours. CT still has a role in the
assessment of bone architecture prior to surgery for metastases and in the differential diagnosis of primary tumours of
the vertebrae.

Intramedullary Tumours

MRI is by far the best method of demonstrating features of intramedullary tumours such as subtle cord enlargement,
parenchymal oedema, haemorrhage and haemosiderin. Gadolinium enhancement may help to discriminate tumour from
surrounding oedema, particularly for metastases and haemangioblastoma.

The commonest intramedullary tumours are gliomas, of which astrocytoma and ependymoma are difficult to
differentiate on MRI. Each usually demonstrates focal expansion of the cord and non-specific T2W high signal, and
normal or low T1W signal, with variable, illdefined enhancement.40 Signs favouring ependymoma over astrocytoma
are; location in the lower cord or conus, central rather than eccentric position within the cord, a well-defined plane of
cleavage between tumour and normal cord and intratumoural haemorrhage: astrocytomas tend to be longer but less
bulky. Despite these differences, distinction between the two is frequently impossible.

Intramedullary cysts above or below the tumour may be lined by neoplastic cells, in which case the cyst wall may be
enhanced, or they may be due to a syringomyelic cavity filled with CSF.

Astrocytoma of the cord varies considerably in its degree of anaplasia. Most adult tumours are benign, but for malignant
tumours survival is usually less than 2 years. The overall survival rate following surgery and radiotherapy is
approximately 60% at 5 years and 23% at 10 years. The outcome for ependymoma is better and only 15% recur
following complete excision.

Haemangioblastoma constitutes 3% of intramedullary tumours and 30% of these patients have von Hippel Lindau
syndrome. The MRI appearance is more characteristic,41 with a small intensely enhancing nodule within or on the
surface of the cord (more often posteriorly), the majority with a large adjacent non-enhancing cyst, which is usually
non-neoplastic. Haemangioblastomas may be multiple. Meningeal varicosities on the dorsal surface of the cord are a
further pointer to the diagnosis. Treatment is usually surgical.

Intramedullary metastases (Fig. 2.10) are rare; the lung is the commonest source. Patients present with rapid clinical
progression of a cord syndrome. MRI typically demonstrates a small T2 high signal, enhancing lesion with adjacent
oedema which may be invisible on CT myelography. Unfortunately, despite radiotherapy, the majority of these patients
die within 6 months.

Intradural, Extramedullary Tumours

As with extra-axial brain tumours, the recognition of an extramedullary location for spinal tumours is important, as the
majority are benign, and surgical cure and alleviation of symptoms of cord compression are often realistic. The
commonest tumours located within the subarachnoid space are meningiomas and neurofibromas.42

Spinal meningioma is most prevalent in the 5th and 6th decades; 60-80% occur in women, in whom the thoracic spine is
usually affected. Symptoms are usually myelopathic rather than radiculopathic. The tumour is occasionally solely
extradural, in which case malignant histology is more likely. Plain radiography or CT may demonstrate erosion of
pedicles or enlargement of neural foramina. Like intracranial meningiomas, on CT the mass is usually iso- or
hyperdense, with homogeneous enhancement and sometimes dense calcification, although it may be impossible to
detect without intrathecal contrast medium (CT myelography). On MRI it is usually of similar signal to the cord or may
yield slightly higher signal on T2W and lower signal on T1W sequences. Gadolinium enhancement is usually intense
and can help to define the tumour margins. Signal may be very low if there is dense tumour calcification.

Characteristic features that differentiate meningioma from neurofibroma are a broad base on the dura mater, a single
tumour and location posterolateral to the cord. Neurofibromas are characteristically dumb-bell shaped as they transgress
the neural foramen along the line of the nerve; they therefore may be both intradural and extradural. They may be
multiple and tend to lie slightly anterior to the cord. There is considerable overlap in these characteristics however.

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Neurofibroma is the commonest intraspinal tumour and usually occurs as part of neurofibromatosis, whereas spinal
Schwannoma (neurinoma) is usually solitary and in patients without neurofibromatosis. Neurofibroma usually presents
in the fourth decade, most commonly in the cervical region, with pain and radiculopathy. On imaging it can sometimes
be differentiated from meningioma by the characteristic shape, a higher signal on T2W images, and absence of
calcification (Fig. 2.11).

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Figure 2.10
Intramedullary and extradural
metastases from breast carcinoma.
Sagittal T1W images (a) before and
(b) after gadolinium injection. The
lumbar expansion of the cord is
larger than normal and two
enhancing intramedullary masses are
shown. In addition small low signal
deposits are present in the D12 and
L5 vertebral bodies; these enhance
with gadolinium and therefore become
less conspicuous relative to the
surrounding marrow. On sagittal T2W
image (c) the intramedullary lesions
are of similar signal to cord, but the
larger one is identified because of the
high signal oedema above and below
it. The vertebral body deposits are
very inconspicuous, which is often
the case on T2W images. Axial
post-gadolinium T1W image (d) shows
the larger enhancing intramedullary
mass. The D12 vertebral body deposit,
despite some enhancement, is still
of lower signal than marrow.

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Spinal intradural extramedullary metastases occur with many CNS tumours by seeding through the subarachnoid space
(Fig. 2.12). These are frequently tiny lesions which require gadolinium-enhanced MR for their detection, and this
demonstrates tumour nodules in only about a fifth of cases with tumour cells within the CSF. The commonest primary
tumour is medulloblastoma in children, but glioblastoma, ependymoma, oligodendroglioma, astrocytoma and retinal,
pineal and choroid plexus tumours can all spread in this way. Malignant tumours from outside the CNS can metastasize
to the spinal meninges by direct invasion, lymphatic or haematogenous routes.

Extradural Tumours

Metastases are the commonest extradural tumours to cause cord compression and thecal impingement by such
metastases occurs in 5% of all systemic cancer. Frequent sites of primary tumour are prostate, lung and breast, and
vertebral lymphoma and myeloma also cause cord compression.

Plain radiography may demonstrate a lytic or sclerotic metastasis, sometimes with collapse of the vertebral body, and in
the thoracic spine paravertebral soft tissue swelling may be evident. CT shows paravertebral masses in more detail and
provides accurate information on the bone architecture of collapsed vertebrae, and in particular the integrity or
otherwise of posterior elements, as well as those of adjacent vertebrae, which may be infiltrated to a lesser degree. This
information may be important if surgical decompression and stabilization is contemplated. However, CT without
intrathecal contrast does not show the intraspinal extent of tumour or site and degree of cord compression, for which CT
myelography or MRI is required.

MRI is the optimal investigation in suspected metastatic cord compression. It is more sensitive than scintigraphy in
detection of vertebral metastases. It is much easier to perform than CT myelography in patients who are often immobile
and in severe pain, and will demonstrate intramedullary as well as extramedullary pathology. Most metastases yield low
signal on T1W images, and high, normal or low signal on T2W images, depending partly on whether they are lytic or
sclerotic. 43 Some fast T2W sequences are poor at differentiating metastases from marrow. Most metastases enhance
following gadolinium, but this can mask the lesion as it may then return the same signal as surrounding marrow,
therefore fat saturation techniques should be used for enhanced images. Gadolinium is also useful for characterizing the
exact site of epidural tumour spread within the spinal canal, differentiating epidural tumour from other pathology such
as prolapsed disc, and differentiating other causes of T1 low signal in vertebral bodies.

Spinal lymphoma is usually extradural, characteristically with vertebral body involvement, a paraspinal mass and
diffuse infiltration of the extradural space via neural foramina.

Vertebral haemangiomas are common incidental findings on spinal MR and usually return high signal on both T1W and
T2W images. They rarely affect the spinal cord, but if so surgery, radiotherapy or embolization may be necessary.

Other primary bone tumours very rarely cause cord compression. Most occur more frequently in the posterior elements
than in vertebral bodies, including osteoid osteoma, osteochondroma, osteoblastoma, aneurysmal bone cyst and giant
cell tumour. Malignant tumours such as chondrosarcoma, osteosarcoma and Ewing's tumour may be seen, but the latter
two are usually metastatic in the spine. In children, paravertebral tumours of neural origin such as neuroblastoma,
ganglioneuroblastoma and ganglioneuroma, may extend through neural foramina into the epidural space and cause cord
compression. Vertebral body chordoma is usually more malignant than clival or sacral chordoma, but shows similar
radiological characteristics.

Postoperative Imaging and Radiation Effects

Expected postoperative changes following resection or biopsy of intracranial tumours include haemorrhage at the
tumour bed and oedema and swelling around it. Signal change on MRI and enhancement in the line of resection may
persist for several weeks. Thus early postoperative imaging for assessment of residual tumour can be misleading,
although it has been suggested that imaging earlier than 48 hours postoperatively may avoid this.

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Radiotherapy to the central nervous system can cause transient white matter oedema or permanent diffuse leucomalacia,
as well as focal brain necrosis; the latter can be particularly difficult to distinguish from residual or recurrent tumour.
Calcifying microangiopathy and eventually focal or diffuse brain atrophy may occur. Necrosis is usually apparent at the
tumour bed on imaging between 6 months and 2 years after radiation treatment, depending on the dosage and rate of
delivery. It is

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Figure 2.11
A 50-year-old man previously treated
for Hodgkin's lymphoma presented with
a 6-week history of progressive leg
weakness and back pain. MR showed a
very well-defined extramedullary,
intradural mass causing severe cord
displacement and compression. The
tumour returns low/intermediate signal
on T1W (a) and high signal on T2W (b)
images. Axial post-gadolinium T1W image
(c) shows rim enhancement of the mass.
The intradural location and shape are
untypical of lymphoma, but characteristic
of neurofibroma; this was confirmed
histologically following surgery. (d) A
different patient with neurofibromatosis II.
Axial post-gadolinium T1W image shows a
small extramedullary Schwannoma to the
left of the cord. A larger tumour is seen
passing through the right neural foramen
and into the carotid sheath and a further
small tumour is present in the oropharynx.

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Figure 2.12
Intradural, extramedullary spinal metastases from pineal
germinoma. a, b) Sagittal and c) axial T1W post-gadolinium
images. Numerous enhancing nodules are seen on the
surface of the cord, and involving the cauda equina.

common after radiation seed placement. It may coexist with recurrent tumour and both may cause mass effect and ring
enhancement on CT and MR. More specific signs to signify recurrent tumour are progressive enlargement of a focal
mass lesion on serial scans, an anatomic pattern such as a butterfly distribution, and new enhancement at the tumour
site. In general MRI is poor at differentiating tumour from radiation effects, but techniques such as MR spectroscopy,
positron emission tomography (PET), single photon emission computed tomography (SPECT) 44 and functional MRI
all offer the potential to discriminate between them in some cases. Newer techniques which measure local cerebral
blood volume may be useful, such as echoplanar MRI with bolus gadolinium injection,45 and these seem to correlate
with indices of local cerebral metabolism provided by fluorodeoxyglucose-PET. However, these functional methods
may still be confounded by coexistent radiation necrosis and recurrent tumour.

Abnormal meningeal enhancement may be non-neoplastic, as a result of either surgery, shunt insertion or a previous
extracerebral collection. This is usually linear and diffuse and tends to persist unchanged, often for many years, whereas
nodular or increasing meningeal enhancement is more suggestive of residual or recurrent meningeal tumour.

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Radiation to the brain can also induce neoplasia and it is important to be aware of the potential development of both
meningiomas and gliomas many years after intracranial radiotherapy for other tumours.

New Imaging Techniques

MR angiography (MRA) can contribute to the preoperative assessment of intracranial tumours by demonstrating
displacement, compression, encasement or occlusion of major arteries, veins and dural sinuses, especially if used in
conjunction with MRI. Specific examples of its use are in the parasellar region, to show the relationship of the internal
carotid arteries to pituitary tumours; in the posterior fossa, the relation between a large 8th nerve Schwannoma and
surrounding veins and sinuses; and in the superior sagittal sinus, to show whether adjacent tumours such as meningioma
partially or completely occlude the sinus. MRA has largely replaced conventional cerebral angiography in these
instances.

Stereotactic CT is used to guide biopsy of brain tumours by calculating the precise three-dimensional position of an
intracranial probe tip using a frame fixed to the skull vault. Frameless MR stereotaxy utilizes skin markers on the scalp
and face to calculate the position of the probe tip during surgery. This allows real-time multiplanar display of the extent
of tumour resection to be depicted on preoperative gadolinium-enhanced scans.

Much research is being performed into the imaging and analysis of biochemical and physiological characteristics of
brain tumours, with the goal of tissue characterization to detect and grade malignant neoplasms, differentiate recurrence
from iatrogenic change, and differentiate neoplasm from other pathology, such as lymphoma and inflammatory disease
in AIDS. 46 Fluorodeoxyglucose-PET is sensitive but relatively non-specific in the diagnosis of high grade neoplasms,
as the radiopharmaceutical is also taken up by inflammatory processes and areas of cellular necrosis. Thallium is
concentrated in tumour but not in necrosis, and thallium-SPECT has been shown to be more accurate than CT but less
accurate than gadolinium-enhanced MR in detection and follow-up of gliomas.47

MR spectroscopy measures metabolite levels within a unit volume of brain tissue and can be targetted at specific areas
of abnormality on MRI. Gliomas are characterized by a reduction in N-acetyl aspartate, which is a neuronal marker, and
by raised choline levels, due to increased membrane turnover. However, these and other single metabolite resonances do
not classify tumours in terms of grade, whereas multiparametric statistical analysis may do so in future.48, 49

Functional MRI (fMRI) has potential clinical application in several aspects of the management of brain neoplasms.
Maps of regional cerebral blood flow are provided by functional MR perfusion studies, and tumour grade seems to
correlate with blood flow;45 this technique can therefore signify a higher tumour grade than suggested by MRI and
prompt biopsy or surgery. It can also direct biopsy to the more malignant part of a neoplasm and avoid the common
problem of under-grading. Another fMRI technique is diffusion imaging, which can help to distinguish the cystic and
solid components of a tumour. Surgical debulking of gliomas may be aided by task activation studies, which can
demonstrate the precise location of eloquent areas of motor or sensory cortex. These may be displaced or may have
relocated secondary to tumour.50 Functional MRI can be performed at the same time as conventional MRI and may
thus become a cost-effective alternative to PET and SPECT.

Acknowledgement

The authors gratefully acknowledge the assistance of radiographers at the Queens Square Imaging Centre and the
Addenbrooke's Hospital MRI Unit, Cambridge.

References

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2. World Health Organization. Classification of Brain Tumours. Zurich: WHO, 1990.

3. Kjos BO, Brant-Zawadzki M, Kucharczyk W, Kelly WM, Norman D, Newton TH. Cystic intracranial lesions:
magnetic resonance imaging. Radiology 1985; 155: 363-369.

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4. Earnest FIV, Kelly PJ, Scheithauer BW et al. Cerebral astrocytomas: histopathological correlation of MRI and CT
contrast enhancement with stereotactic biopsy. Radiology 1988; 166: 823-827.

5. Kieffer SA, Salibi NA, Kim RC et al. Multifocal glioblastoma: diagnostic implications. Radiology 1982; 143:
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6. Spagnoli MV, Grossman RI, Packer RJ et al. Magnetic resonance imaging determination of gliomatosis cerebri.
Neuroradiology 1987: 29: 15-18.

7. Forsyth P, Shaw E, Scheithauer B, O'Fallon J, Layton D, Katzmann J. 51 cases of supratentorial pilocytic

astrocytoma: a clinicopathologic, prognostic and flow cytometric study. Cancer 1993; 72: 1335-1342.

8. Lee Y, Tassel PV. Intracranial oligodendrogliomas: imaging findings in 35 untreated cases. AJNR 1989; 10: 119-127.

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9. Castillo M, Davis PC, Takei Y, Hoffman JC Jr. Intracranial ganglioglioma: MRI, CT and clinical findings in 18
patients. AJNR 1990; 11: 109-114.

10. Goergen SK, Gonzales MF, McLean CA. Intraventricular neurocytoma: radiologic features and review of the
literature. Radiology 1992; 182: 787-792.

11. Wichmann W, Schubiger O, von Demling A et al. Neuroradiology of central neurocytoma. Neuroradiology 1991;
33: 143-148.

12. Koeller KK, Dillon WP. Dysembryoplastic neuroepithelial tumors: MR appearance. AJNR 1992; 13: 1319-1325.

13. Ostertun B, Wolf HK, Campos MG et al. Dysembryoplastic neuroepithelial tumors: MR and CT evaluation. AJNR
1996; 17: 419-430.

14. Spoto GP, Press GA, Hesselink JR, Solomon M. Intracranial ependymoma and subependymoma: MR
manifestations. AJNR 1990; 11: 83-91.

15. Neumann HPH, Eggert HR, Schumacker M et al. Central nervous system lesions in von Hippel Lindau syndrome. J
Neurol Neurosurg Psychiatry 1992; 55: 898-901.

16. Jack CR Jr, O'Neill BP, Banks PM, Reese DF. Central nervous system lymphoma: histologic types and CT
appearance. Radiology 1988; 167: 211-215.

17. Johnson BA, Fram EK, Johnson PC, Jacobowitz R. The variable MR appearance of primary lymphoma of the
central nervous system: comparison with histopathologic features. AJNR 1997; 18: 563-572.

18. Dina T. Primary central nervous system lymphoma versus toxoplasmosis in AIDS. Radiology 1991; 179: 823-828.

19. Healy ME, Hesselink JR, Press GA, Middleton MS. Increased detection of intracranial metastases with intravenous
Gd-DTPA. Radiology 1987; 165: 619-624.

20. Russel DS, Rubinstein LJ. Pathology of Tumors of the Nervous System, 5th edn. Baltimore: Williams and Wilkins;
1989.

21. Lee BCP, Kneeland JB, Deck MDF, Cahill PT. Posterior fossa lesions: magnetic resonance imaging. Radiology
1984; 153: 137-143.

22. Tien RD, Yang PJ, Chu PK. `Dural tail sign': a specific MR sign for meningioma? J Comput Assist Tomogr 1991;
15: 64-66.

23. Elster AD, Challa VR, Gilbert TH, Richardson DN, Contento JC. Meningiomas: MR and histopathological features.
Radiology 1989; 170: 857-862.

24. Burger PC, Scheithauer BW. Tumours of meningothelial cells. In: Tumors of the Central Nervous System.
Washington DC: Armed Forces Institute of Pathology; 1994, pp. 259-286.

25. Chiechi MV, Smirniotopoulos JG, Mena H. Intracranial haemangiopericytomas: MR and CT features. AJNR 1996;
17: 1365-1371.

26. Press GA, Hesselink JR. MR imaging of cerebellopontine angle and internal auditory canal lesions at 1.5T. AJNR
1988; 9: 241-251.

27. Tampieri D, Melanson D, Ethier R. MR imaging of epidermoid cysts. AJNR 1989; 10: 351-356.

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28. Jelenik J, Smirniotopoulos JG, Parisi JE, Kanzer M. Lateral ventricular neoplasms of the brain: differential
diagnosis based on clinical, CT and MR findings. AJNR 1990; 11: 567-574.

29. Sze G, Soletsky S, Bronen R, Krol G. MR imaging of the cranial meninges with emphasis on contrast enhancement
and meningeal carcinomatosis. AJNR 1989; 10: 965-975.

30. Cone L, Srinivasan M, Romanul FCA. Granular cell tumor (choristoma) of the neurohypophysis: two cases and a
review of the literature. AJNR 1990; 11: 403-406.

31. Yuh WTC, Tali ET, Nguyen H et al. Sequential MR enhancement pattern in normal pituitary gland and pituitary
adenoma. SMRM Annual Meeting 1993, New York.

32. Pusey E, Kortman KE, Flannigan BD et al. MR of craniopharyngiomas: tumor delineation and characterisation.
AJNR 1987; 8: 439-444.

33. Eldevik OP, Blaivas M, Gabrielsen TO, Hald JK, Chandler WF. Craniopharyngioma: radiologic and histologic
findings and recurrence. AJNR 1996; 17: 1427-1439.

34. Chang T, Teng MMH, Guo W-Y, Sheng W-C. CT of pineal tumors and intracranial germ-cell tumors. AJNR 1989;
10: 1039-1044.

35. Tien RD, Barkovich AJ, Edwards MSB. MR imaging of pineal tumous. AJNR 1990; 11: 557-565.

36. Latack JT, Hutchinson RJ, Heyn RM. Imaging of rhabdomyosarcomas of the head and neck. AJNR 1987; 8:
353-359.

37. Regenbogen VS, Zinreich J, Kim KS et al. Hyperostotic esthesioneuroblastoma: CT and MR findings. J Comput
Assist Tomogr 1988; 12: 52-56.

38. Meyers SP, Hirsch WL Jr, Curtin HD et al. Chordomas of the skull base: MR features. AJNR 1992; 13: 1627-1636.

39. Avrahami E, Tadmor R, Dally O et al. Early MR demonstration of spinal metastases in patients with normal
radiographs and CT and radionuclide bone scans. J Comput Assist Tomogr 1989; 13: 598-602.

40. Sze G, Stimac GK, Bartlett C et al. Multicenter study of gadopentetate dimeglumine as an MR contrast agent:
evaluation in patients with spinal cord tumors. AJNR 1990; 11: 967-974.

41. Kaffenberger DA, Sah CP, Mortagh FR, Wilson C, Silbiger ML. MR imaging of spinal cord haemangioblastoma
associated with syringomyelia. J Comput Assist Tomogr 1988; 12: 495-498.

42. Matsumoto S, Hasu K, Uchino A et al. MRI of intradural extramedullary spinal neurinomas and meningiomas. Clin
Imag 1993; 17: 46-52.

43. Kamholtz R, Sze G. Current imaging in spinal metastatic disease. Sem Oncol 1991; 18: 158-169.

44. Carvalho P, Schwartz R, Alexander E et al. Detection of recurrent gliomas with quantitative thalium-201/technetiom
99m HMPAO single photon emission computerized tomography. J. Neurosurg 1992; 77: 565-570.

45. Aronen H, Gazit IE, Louis DN et al. Cerebral blood volume maps of gliomas: comparison with tumour grade and
histologic findings. Radiology 1994; 191: 41-51.

46. Slosman DO, Lazeyras F. Metabolic imaging in the diagnosis of brain tumors. Curr Opin Neurol 1996; 9: 429-435.

47. Rollins NK, Lowry PA, Shapiro KN. Comparison of gadolinium-enhanced MR and thallium-201 single photon
emission computed tomography in pediatric brain tumors. Pediatr Neurosurg 1995; 22: 8-14.

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48. Preul MC, Caramanos Z, Collins DL et al. Accurate non-invasive diagnosis of human brain tumors by using proton
magnetic resonance spectroscopy. Nature Med 1996; 2: 323-325.

49. Shimizu H, Kumabe T, Tominaga T et al. Noninvasive evaluation of malignancy of brain tumors with proton MR
spectroscopy. AJNR 1996; 17: 737-747.

50. Atlas SW, Howard RS, Maldjian J et al. Functional MRI of regional brain activity in patients with intracerebral
gliomas: findings and implications for clinical management. Neurosurgery 1996; 38: 329-338.

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3
The Head and Neck

Antonio Chiesa, Roberto Maroldi, Giuseppe Battaglia, Patrizia Maculotti and Davide Farina

Neoplasms arising from the upper aerodigestive mucosa

Neoplasms arising from nasosinusal mucosa

Non-mucosal and salivary gland lesions

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Some common features allow most head and neck neoplasms to be grouped into one of three homogeneous classes:
lesions arising from upper airway mucosa; lesions arising from the mucosa of paranasal sinuses; and extra-mucosal and
salivary gland lesions.

A number of significant clinical advantages have resulted from the application of CT, MR and ultra-sound in the
management of these neoplasms. As most head and neck malignancies arise from the mucosal epithelium, mainly the
upper aerodigestive tract, diagnosis can usually be made from direct or endoscopically-guided biopsy. Clinical
examination is essential for evaluating either superficial spread of neoplasms or functional data, e.g. impaired motility
of vocal cords. The goals of imaging are the precise assessment of deep tissues invasion and the detection of nodal
metastases.

In addition, it should be noted that the prognosis of head and neck malignancies depends on several factors. None of the
biological properties of the neoplasm (grading, mitotic index) can be studied with imaging techniques, although positron
emission tomography (PET) and MR spectroscopy are promising modalities. The other significant prognostic factors are
related to the local extent of the neoplasm (T), and to nodal (N) or distant (M) metastases 1 and the assessment of TNM
staging represents the central goal of imaging in most head and neck malignancies.

Neoplasms Arising from the Upper Aerodigestive Mucosa

Neoplasms arising from the upper aerodigestive mucosa share four common features:

squamous cell carcinoma is the most common histotype;

the superficial spread of a neoplasm can be adequately assessed by direct examination or endoscopy;

a typical pattern of deep, extramucosal extent of neoplasms can be observed;

nodal metastases are frequent.

As a general rule, the deep spread of squamous cell carcinoma follows two different patterns:

progressive invasion through the submucosa, the muscular layer (e.g. the constrictor muscle at the level of the pharynx)
and, further, into fat tissue, vessels, nerves and bones of adjacent structures;

spread along pre-existing pathways, such as nerves and vessels.

As a consequence, an imaging technique is very dependent on the contrast it can achieve between tumour and fat tissue
layers, muscles, bones, vessels and nerves.

Detection of the Degree of Wall Invasion in Upper Aerodigestive Tract Neoplasms

This problem applies to malignant neoplasms arising from the nasopharynx, orohypopharynx, larynx and oesophagus.
Its solution requires discrimination between the abnormal signal of neoplasm and the normal wall. The thickness of the
wall (which determines its main signal) depends on its muscular content, e.g. the complex of constrictor muscles in the
pharynx.

Generally, the contrast resolution of CT is inadequate for distinguishing the muscle from the abnormal density of the
adjacent tumour.1 MR can, however, demonstrate the different signal intensities between the muscular layer
(hypointense) and the neoplasm (moderately hyperintense) (Fig. 3.1), particularly when spin echo (SE) turbo
T2-weighted sequences are used2 and MRI should be chosen for the precise evaluation of muscular wall invasion.3

Detection of Neoplastic Spread Beyond the Walls (Equivalent to Class T4 of TNM Staging)

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Demonstration of the replacement of fat tissue surrounding the wall by the tumour is the key indicator of neoplastic
spread beyond the upper aerodigestive tract walls. Usually, this information is adequately provided either by CT or MR.

Detection of Neoplastic Invasion of Muscles and Other `Key Areas`

This problem applies, for example, to the floor of the mouth muscles in cases of tongue neoplasms and to the vocal
cords and paraglottic spaces in cases of laryngeal neoplasms. Again, the replacement of muscle or fat tissue signal by
the tumour indicates neoplastic invasion. It should be noted that fat tissue actually behaves as a natural contrast agent
both for CT and MR.

This finding is critical if intrinsic muscles invasion by tongue neoplasms is to be accurately quantified. Since the fat
content of these muscles is noticeable, solid neo-

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Figure 3.1
Glosso-tonsillar squamous cell carcinoma. On MR the
tumour spreads circumferentially along the walls of the
glosso-tonsillar sulcus extending deep into the adjacent
structures. After Gd-DTPA injection the tumour enhances.
Base of the tongue has been invaded (short arrow). The
neoplasm spreads into the parapharyngeal space and
invades the medial pterygoid muscle. The external carotid
artery appears to be surrounded by neoplastic tissue
(arrowhead). The abnormal signal intensity of the
posterior oropharyngeal wall on the right side indicates
inflammation and oedema (long arrow). Level II partly
necrotic lymphatic metastasis (n). Abnormal hypointensity
of the medullary space of right mandibular ramus was
associated with neoplastic invasion (*).

plastic tissue replacing fat can be detected. Spin echo T1-weighted sequences show the hypointense neoplasms
obliterating the regular texture of the muscular fibres, normally separated by thin fat layers. 2, 4

In addition, an accurate assessment of tumour margins can be achieved by enhancement of neoplastic tissue with
intravenous administration of contrast agents (iodine for CT studies and gadolinium (Gd)-based for MR).1 Both CT and
MR clearly show the precise relationship between the tumour and lingual septum, because of the latter's fat content.
Finally, MR is definitely superior to CT in defining the degree of neoplastic invasion of the muscles of the floor of the
mouth muscles (Fig. 3.2).5

The vocal cord should be considered a crucial structure in the management of laryngeal neoplasms, since its extensive
invasion often requires aggressive surgical management (vertical hemilaryngectomies, supracricoid laryngectomies,
total laryngectomy) (Fig. 3.3).6 Furthermore,

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Figure 3.2
Base-of-tongue squamous cell carcinoma. a) On
enhanced axial T1 MR sequence, the neoplasm
extends from the left tongue base into the floor of
the mouth muscles. The tumour surrounds the left
lingual artery (arrow) and invades the styloglossus
muscle (a boundary between base of the tongue and
floor of the mouth) and a landmark for the XII nerve.
Two non-homogeneous adenopathies are at level II. b)
Displacement of both the genioglossus muscle (arrows)
and mylohyoid muscle (arrowheads) by the neoplasm
is better demonstrated on the coronal plane. On
both axial and coronal images the lingual septum (*)
appears not to have been invaded by the tumour.

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Figure 3.3
Right glottic squamous cell carcinoma. On enhanced
CT the hyperdense neoplasm (T) extends along the
entire surface of the right vocal cord. The vocal muscle
is partly invaded. The enhancing neoplastic tissue
spreads into the anterior commissur, which is
abnormally thickened (arrow). The asymmetrical
thinning of the right paralaryngeal space results from
oedema of the thyroarytenoid muscle. The tumour
approaches the vocal process of the right arytenoid
cartilage (sclerotic). No abnormality of the thyroid
cartilage is detectable.

surgical treatment is influenced by the demonstration of neoplastic spread into submucosal fat spaces of the larynx deep
to the lateral walls (paralaryngeal spaces). Conversely, deep invasion through the epiglottis into the pre-epiglottic space
does not change the surgical management, since the entire space is usually removed by conservative surgical
techniques. In contrast, this information is useful for planning radiation therapy. CT is reliable in calculating the volume
of a tumour invading the pre-epiglottic space, which is a valuable predictor of successful control of the disease (Fig.
3.4).

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Figure 3.4
Supraglottic squamous cell carcinoma. The neoplasm
arises from the infrahyoid epiglottis and spreads
circumferentially into both aryepiglottic folds. Partial
invasion of the pre-epiglottic space is shown (arrows).

Detection of Perineural or Perivascular Spread

This information is crucial in the management of nasopharyngeal neoplasms (because of the possible invasion of
trigeminal nerve, internal carotid artery and cavernous sinus), oral cavity and base-of-tongue neoplasms (hypoglossus
and laryngeal nerves, carotid artery). Direct signs of spread include changes in diameter or density/signal of nerves and
vessel walls. 7 Indirect signs are changes in bone structures (diameter or shape of skull base foramina and fissures),
obliteration of fat tissue within foramina or fissures and muscular atrophy indicating denervation.

CT usually only shows indirect signs, such as remodelling/erosion of skull base foramina or pterygo-palatine fissure
walls. MRI can demonstrate some cranial nerves (particularly the trigeminal nerve and its branches), both within or
outside the cranial cavity, and abnormalities of the walls of the internal carotid artery and jugular vein or cavernous
sinus.8 These advantages of MR allow earlier detection of perineural and perivascular spread (Fig. 3.5). Intravenous
contrast injection highlights the abnormal signal/density of the nerves or vessel walls involved. However, both CT and
MR are sometimes unable to distinguish neuritis from perineural neoplastic spread.

Detection of Bone or Cartilage Invasion

This information is critical for the management of neoplasms arising from the nasopharynx (because of the possible
involvement of the skull base and Eustachian tube), oral cavity (mandible, infrastructure, pterygoid plates) and larynx
(cartilage and hyoid bone). Detection requires the demonstration of the destruction of bones, ossified (provided by
cortical rims lining a medullary space) and non-ossified cartilage.

It should be noted that neoplastic invasion by squamous cell carcinoma seldom results in sclerosis of bone or cartilage.
Sclerosis usually indicates inflammatory changes caused by tumour, rather than invasion. This finding can be observed
either in the skull base and facial bones or in the ossified laryngeal cartilages.

CT is particularly useful in assessing bone destruction. Neoplasms seldom spread into the medullary space of bone and
cartilage (especially thyroid cartilage) without extensive destruction of the cortical rim. In these cases CT shows a
thinning of the cortical bone/ossified cartilage and an abnormal tissue density replacing the fat with-

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Figure 3.5
Undifferentiated carcinoma of the nasopharynx. a) On axial T1-weighted MRI sequence, the homogeneous
tumour fills the sphenoid sinus and extends into the fat tissue of both inferior orbital fissures (arrows).
Bilateral intracranial spread through the foramen lacerum and perivascular invasion of the carotid arteries
are demonstrated on axial (arrowheads) and b) coronal MR views (arrowheads). Level V adenopathy on the
left side (n) and bilateral retropharyngeal metastatic lymph nodes (n) are shown.

in the medullary space (Fig. 3.6). The reliability of MR in detecting intramedullary (and intracartilaginous) tumour spread is definitely
superior to CT (Fig. 3.7). 9,10,11,12

MRI is more sensitive but less specific than CT in detecting neoplastic cartilage invasion in laryngeal neoplasms. MR tends to
overestimate neoplastic cartilage invasion and may result in overtreatment, whereas CT tends to underestimate invasion and may lead
to inadequate therapy. Proton density SE MR sequences are particularly useful in the evaluation of the more resistant non-ossified
cartilage of the larynx.9, 6, 13

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Figure 3.6
T4 glottic squamous cell carcinoma. Diffuse invasion
of thyroid cartilage by tumour is shown by the
destruction of the ossified rims and replacement
of the medullary space by soft tissue. The barrier
provided by the outer pericondrium has prevented
neoplastic spread into the soft tissues of the neck
(pathologic observation). Destruction of the right side
of cricoid cartilage is demonstrated (*).

Figure 3.7
Retromolar trigon squamous cell carcinoma. Tumour
erases the `black' signal of the cortical rim of the
mandible (short arrows) and extends into the medullary
space, replacing its fat content. Infiltration of the medial
pterygoid, the masseter and the buccinator (curved
arrows) muscle is also present.

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Detection of Occult Adenopathies in Clinically Negative (NO) Necks

Patients treated for cancer arising from the upper aerodigestive tract often die of a disease related to the presence of cervical nodal
metastases, despite successful control of the primary tumour. The overall prognosis for these patients is directly related to the presence
or absence of metastatic adenopathies. 14, 15 Moreover, the most relevant prognostic factor for predicting recurrent cervical lymph node
metastases is the presence of nodal disease at the initial diagnosis.

In about 20% of clinically negative necks, histological examination reported positive lymph nodes, multiple metastatic nodes were
detected in 13% and a single positive node in 16%. These data are in keeping with the clinical observation that about 15% of NO necks
will eventually develop nodal recurrence (all primary sites of the neck considered).16 Different strategies have been developed by
clinicians to manage NO neck patients who have this 15% risk of occult metastases. Surgery or radiotherapy would constitute
unnecessary therapy for 85% of these patients but delaying treatment until nodal disease is detected would entail a slightly worse
prognosis for 15% of them. However, regardless of the particular treatment strategy adopted for clinical NO necks, the accurate
detection and staging of cervical metastases is crucial to patient survival.

Diagnosis relies on the detection of even microscopic neoplastic deposits within normal sized lymph nodes. However, as approximately
25% of electively operated on sides of the neck contain exclusively metastases smaller than 3 mm, the sensitivity of all imaging
modalities in these necks is limited to 75%. Currently, the reliable imaging criteria used in assessing abnormal lymph nodes are a
minimal axial diameter of the node not exceeding 11 mm in the jugulo-digastric group and 10 mm elsewhere (Table 3.1). It has been
proposed that retropharyngeal nodes should not exceed 8 mm in diameter. However, MRI can easily detect nodes of 4-5 mm and if they
show the same signal intensity as the primary nasopharyngeal tumour on T1- and T2-weighted images they are probably invaded.17 It
has also been suggested that the ratio of the maximal longitudinal length to nodal width should be > 2 for normal hyperplastic nodes and
< 2 for metastases (which are more often spherical in shape). Moreover, groups of three or more lymph nodes with maximal diameters
of 8-15 mm or minimal axial diameter of 9-10 mm in the jugulo-digastric area and of 8-9 mm elsewhere are suggestive of lymph node
metastases. Regardless of the lymph node size, the most reliable imaging feature of metastatic disease is `nodal necrosis', detected on
both enhanced CT and T1-weighted MR images as a low density (CT) or low intensity (MR) area > 3 mm (Fig. 3.8).18 The overall error
rate of these size criteria for both false-positive and false-negative CT and MR diagnoses is in the range is 10-20%.

Ultrasound has an accuracy of no more than 80%; however, when used to guide cytological sampling, its diagnostic accuracy rises to
95%. In the follow-up of treated patients, ultrasound is useful in the assessment of those patients in whom post-treatment fibrotic
changes do not allow correct clinical assessment. Retropharyngeal nodes cannot be evaluated by ultrasound.

New imaging modalities, such as immunoimaging with SPECT, thallium SPECT, PET and fused images, are developing rapidly.
Although these techniques are likely to become very accurate for the staging of the neck, it is doubtful whether they will be used
routinely because

Table 3.1 Modified American Joint Committee on Cancer radiological nodal staging guidelines.
Stage Definition
N0 All nodes < 15 mm in diameter with no central low density (on CT) or central low intensity (on MR)
N1 Single ipsilateral node 15-29 mm in diameter;
or single ipsilateral node < 15 mm with central low density (on CT) or central inhomogeneous intensity (on MR)
N2 Single ipsilateral node 3-6 cm in diameter or multiple ipsilateral nodes all <6 cm;
Single ipsilateral node 3-6 cm in diameter
N2a
Multiple ipsilateral nodes all < 6 cm
N2b
Bilateral or contralateral nodes, none of which is > 6 cm in diameter
N2c
N3 Node or nodes > 6 cm in diameter

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Figure 3.8
Right piriform sinus squamous cell carcinoma. On
enhanced CT the neoplasm extends into the apex of the
piriform sinus and spreads along the inferior constrictor
muscle, which inserts on the outer surface of the thyroid
cartilage ala. Therefore the neoplasm destroys the
cartilage from the outside (arrows). An abnormal node
presenting a central hypodense area with rim
enhancement is detectable on the ipsilateral side at level
III. The adenopathy has a normal diameter.

of cost and availability. Their role will probably be more important in the detection of unknown primaries, distant
metastases and follow-up after radiotherapy in case where there is clinical doubt. (Table 3.1).

Extranodal spread is present in more than 50% of nodes that are 20-30 mm in their greatest dimension and in more than
70% of lymph nodes that are >30 mm. Extranodal spread is more reliably detected on contrast-enhanced CT than on
MR: they consist of irregular nodal rim-enhancement with infiltration of adjacent fat planes. Once the neoplasm has
spread beyond the lymph node capsule, the most reliable criterion of vascular invasion is the degree of arterial/vein
circumferential involvement by neoplastic tissue: if the vessel is completely surrounded by tumour it is probably
invaded. When the fat planes are also totally effaced by the signal intensity of neoplastic tissue, the vessel is almost
certainly invaded.

Neoplasms Arising from Nasosinusal Mucosa

Nasosinusal neoplasms account for only 3% of all cancers of the head and neck area. They arise from the mucosal
surface of the nasal cavity and paranasal sinuses. The tumour may extend beyond the bony `boxes' of the facial
framework, either by destroying the walls or spreading along nerves and vessels that run through fissures and foramina
within the craniofacial bones.

Key to treatment planning is the determination of the following features:

nature (benign vs. malignant);

histotype: squamous cell carcinoma is the most frequent malignant lesion and it usually arises from the maxillary sinus,
whereas adenocarcinoma arises from the ethmoid sinus;

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superficial and deep (extramucosal) extent of the lesion.

In most cases, endoscopy allows tissue diagnosis through percutaneous biopsy and accurate staging of the superficial
spread. Therefore, differentiation between different neoplasms is not a main goal of CT or MR. Both techniques are
useful in the investigation of anatomical structures that cannot be reached by endoscopy, either because they are
submucosal (bones, vessels, orbital and intracranial contents) or because they are located deep in the paranasal sinuses.

The en bloc removal of neoplasm within normal adjacent tissues successfully controls the lesion. The development of
combined surgical approaches through the nasal cavity and the anterior cranial fossa was made possible by the precise
radiological mapping of submucosal spread towards the anterior cranial fossa, the orbit, the pterygo-palatine and the
superior orbital fissures. The degree of spatial/anatomical detail required in treatment planning, however, differs
significantly between surgery and radiotherapy. 19 A number of elementary questions can be used as a guide.

How Important is the Determination of the Most Probable Site of Origin of a Nasosinusal Neoplasm?

Patterns of spread of nasosinusal neoplasms depend on their site of origin. For this reason, it is useful to discriminate
between low (maxillonasal) and high (nasoethmoidal) lesions. A key point is to assess the

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most probable centre of growth of lesions. While this is easy for small neoplasms, it can be very difficult in advanced
neoplasms.

Critical sites in `low' lesions include the posterior wall of the maxillary sinus, a pathway to the infratemporal fossa and
pterygo-palatine fissure and the orbital floor. In `high' neoplasms, these include the posterior aspect of the lamina
papyracea, the orbital roof, the anterior skull base floor and the sphenoid sinus, particularly its roof.

Generally, the probable site of origin of the lesion can be inferred from CT and MR findings, combined with history and
clinical data. MR is better than CT at discriminating between the tumour and intrasinusal retained secretions or
mucoperiosteal inflammatory changes.

Is it Crucial to Differentiate Lesions Limited to the Sinusal Walls from Those Extending Beyond These Boundaries?

It should be noted that the periosteum is the most effective barrier to the spread of aggressive lesions, neoplastic or
inflammatory, beyond sinusal walls. It is particularly resistant in two of the most critical sinonasal areas: the skull base
(where it links to the dura) and the orbit (where the periosteum of seven bones becomes a continuous layer, the
periorbita). Therefore, an assessment of neoplastic spread beyond the periosteum of sinusal walls is critical for
therapeutic planning because it is related to dural or orbital infiltration.

Although MR cannot directly show the mineral content of bones, in some areas it can detect the connectival/periosteal
layer which limits the sinusal walls. 20 The sinusal walls in contact with the neoplasm may present various signal
changes. On MR, a thick hypointense sinusal wall (on T1 and T2 SE sequences), with focal areas of erosion, usually
indicates chronic inflammation. Again, periosteal thickening appears as an hypointense line parallel to the outer surface
of the sinusal wall. Inflammatory changes of the sinusal mucosa are always associated: they usually appear as a diffuse
mucoperiosteal thickening which is homogeneously hyperintense on T2-weighted sequences, and as a double layer of
signal intensities, enhanced mucosa, non-enhancing submucosa on CT or SE T1-weighted sequences after Gd-DTPA.

Bowing and displacement of a normal and continuous hypointense sinusal wall by the tumour excludes neoplastic
spread beyond the bony periosteal barrier. When the displacement is not caused by the tumour, a mucocele represents
the most likely explanation. Mucoceles generally arise from neoplastic obstruction of the sinusal ostium. Signal
intensity of mucoceles may vary widely vary on T2- and T1-weighted images, depending on the protein content of the
fluid, which is usually higher in older lesions.

Replacement of the hypointense signal of the sinusal walls by neoplastic tissue is a reliable sign of invasion.

Can Imaging Reliably Predict Orbital Exenteration?

A key point is that the orbit is usually preserved at surgery, provided the periorbita is not (or only minimally) invaded,
even though the bone has been completely eroded. In fact, a more aggressive approach does not improve survival. The
assessment of the thin bony lamina papyracea should not be underestimated; however, it is not crucial, since the lamina
itself is in most cases partly or completely resected at surgery for pathologic examination.

MR is of particular value in demonstrating the thin hypointensity of the non-invaded periorbita, which can still be
detected after erosion of the mineral content of the orbital walls (Fig. 3.9). An accurate MRI evaluation of the orbit
requires comparison between different sequences and planes since the walls have an oblique orientation.

Despite attempts to assess the integrity of orbital walls, the information provided by CT or MR has only limited

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Figure 3.9
Ethmoid sinus adenocarcinoma. The huge tumour
displaces both medial orbital walls causing bilateral
exophthalmos. On the left side, the hypointense line
separating the tumour from the intraorbital fat is still
detectable (arrows). On the right side, the same finding
can be identified only at the posterior third of the lamina
papyracea (arrowheads).

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impact on the surgeon's decision to resect the orbit or to save it, as this decision depends not only on imaging data but
also on other factors (e.g. intraoperative staging, vision of the contralateral eye, presence of metastases). Nevertheless, if
imaging suggests orbital infiltration, the patient should be informed that an exenteratio orbitae may be required. Indeed,
the final decision depends on the intraoperative staging. If the probability of exenteration were based only on
ophthalmic symptoms, the lesion would be overestimated in over 50% of cases. Conversely, the negative predictive
value of MRI residual hypointense line between tumour and orbital fat is effective. Focal areas of abnormal signal
intensity of the hypointense periorbita can be overestimated.

Are there Any Indications for Anterior Craniofacial Resection?

This problem applies to neoplasms in contact with the structures that separate the paranasal sinuses from the anterior
and middle cranial fossae. Generally, craniofacial resection (CFR) is recommended if the tumour extends to the mucosal
surface of these sinusal walls. If intracranial spread occurs, the precise grading of the lesion tumour confined to the dura
mater or invading the brain tissue affects not only surgical planning but also the patient's prognosis. In fact, while CFR
is more likely to control neoplasms, it carries the substantial risks of an aggressive surgical procedure. Whether the
precise extent of brain infiltration amount of brain resection, contralateral spread to the olfactory/frontal lobes, middle
cranial fossa invasion should contraindicate surgery remains controversial.

CT and MRI findings are good indicators of the feasibility of CFR. 19 MR is of remarkable value in grading the
neoplastic spread to the anterior cranial fossa, particularly when focal areas of skull base invasion are detected.21 A key
diagnostic observation concerns the signal intensity of the three tissue layers at the interface between the ethmoid roof
and the brain at the anterior cranial fossa: cribriform plate and its periosteum, dura mater, and subarachnoid space. On
enhanced sagittal and coronal spin echo T1-weighted MR sequences, the three layers give rise to a `sandwich' of
different signals (bone periosteum complex, dura and cerebrospinal fluid), where dural hyperintensity is due to a
hypervascular inflammatory reaction.22

Generally, three different patterns of neoplastic involvement of the skull base are observed: the neoplasm is in close
contact with an uninterrupted, hypointense cribriform plate; the neoplasm erases the hypointensity of the cribriform
plate, extending into the anterior cranial fossa (ACF) and displacing an uninterrupted, hyperintense and thickened dura;
the neoplasm encroaches on the dural hyperintensity, the hypointense CSF invades brain tissue. The latter finding is
easier to detect if the signal intensity of the neoplasm is lower than the enhanced dura surrounding the invaded segment.

Oedema surrounding the involved area and replacement of cerebral parenchyma by the signal intensity of neoplastic
tissue indicate brain invasion on MRI and CT (Fig. 3.10).22

Finally, it is essential to assess perineural or perivascular spread toward the middle cranial fossa, usually through
pterygo-palatine and orbital fissures (Fig. 3.11).

Discrimination of an Inflammatory Reaction and Retained Secretions from Neoplastic Tissue

MR can discriminate a neoplastic mass from surrounding retained secretions better than CT. On SE T2-weighted
sequences there is usually a significant difference in signal intensity between the neoplasm (exhibiting intermediate
signal because it is highly cel-

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Figure 3.10
Ethmoid sinus adenocarcinoma. On a sagittal
enhanced T1 MR sequence the neoplasm destroys the
floor of anterior skull base. A residual `sandwich' of
bone and hyperintense dura is still detectable at the
planum sphenoidalis (arrow). The enhancing tumour
extends into a blocked (hypointense fluid content with
mucosal rim enhancement) frontal sinus. Retained
secretions fill the blocked sphenoid sinus.

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Figure 3.11
Left maxillary sinus squamous cell carcinoma.
Follow-up CT after chemotherapy. Patient complains
of pain in the area of the second branch of the
trigeminal nerve. Perineural spread into the inferior
orbital and pterygopalatine fissures appears as soft
tissue surrounding the signal void of the
pterygopalatine artery (arrow). Retained secretions
and inflammatory changes of the maxillary sinus
mucosa are present. The hypointensity of the
posterior maxillary wall is not detectable
(arrowheads).

lular), adjacent structures (bone, muscles and fat tissue) and retained secretions (generally markedly hyperintense).
However, retained secretions may vary widely in signal intensity depending on their protein content. 21 Moreover,
variable enhancement of neoplastic tissue is obtained by Gd-DTPA infusion, usually resulting in a better discrimination
of tumour from adjacent tissues on SE T1-weighted images (Fig. 3.10).

Non-Mucosal and Salivary Gland Lesions

This heterogeneous group includes neoplasms that generally present as soft-tissue masses in the neck. They must be
differentiated from a number of benign lesions that arise from the different anatomical structures of the neck.

Understanding the anatomical organization of the neck is helped by thinking of it first as an axle, along which vessels,
nerves, airways and the upper digestive tract run from the cranium to the trunk, anchored to a robust musculoskeletal
support. Secondly, focus on the deep cervical fascia, which splits into three different layers that define several spaces.
These layers behave as barriers, preventing lesions from crossing their boundaries. Although the individual layers
cannot be detected on normal CT or MR scans, they are of great importance, since knowledge of the precise boundaries
and of the contents of the spaces allows a differential diagnosis unique to each particular space. Within these spaces
there are two important groups of glands: the exocrine glands, distributed around the oral cavity (parotid,
submandibular, sublingual) and the endocrine glands, located at the thoracic inlet (thyroid and parathyroids).
Furthermore, it should be noted that the neck is the body region with the greatest number and complexity of lymph
nodes: of the 800 in the entire body, 300 are located in this region.

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A simple physical examination permits the diagnosis of several soft-tissue masses of the neck because of the superficial
site of the lesion. Ultrasound is useful in assessing the content of lesion solid vs. liquid and it accurately evaluates
lymph nodes and guides cytological sampling. CT and MR are usually indicated to stage nodal spread of squamous cell
carcinoma of the upper aerodigestive tract. They are seldom required for the differential diagnosis of the soft-tissue
masses of the neck.

Neck Masses in Children

In most cases, the correct diagnosis can be obtained by simple clinical examination. Moreover, when clinical data
suggest acute lymphadenitis, imaging is not usually indicated and the case generally resolves after antibiotic treatment.
Non-mucosal and salivary gland neoplasms are rare among children, rhabdomyosarcoma and lymphoma being the two
most frequent head and neck malignancies. The differential diagnosis includes not only inflammatory diseases but also
congenital lesions (thyroglossal duct cysts, lymphangiomas, branchial cleft cysts).23

Thyroid Masses

Discovery of a single nodule or nodules in the thyroid on palpation in a non-hyperthyroid patient requires, as a first step,
a simple needle aspiration which, besides distiguishing solid or liquid content, permits cytological sampling, essential
for diagnosis. Ultrasound-guided sampling is indicated when fine needle aspiration cytology yields non-diagnostic
material.24

Neither radioactive scanning nor ultrasound can distinguish a malignant neoplasm, even if a `cold' lesion is suspected
(in 16% of cases the nodule is malignant). Radionuclide scanning is the procedure of choice for the work-up of a
diffusely enlarged thyroid and for hyperthyroid patients presenting single or multiple nodules.

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Malignant thyroid neoplasms are rare: their prognosis mainly depends on the histotype, sex, age and local extent of
disease. The assessment of local spread is usually accomplished by ultrasound (lesion limited to the capsule, detection
of nodal metastases). Aggressive neoplasms extending beyond the capsule may require CT or MRI to assess invasion of
the trachea, vessels and adjacent muscles, before surgical treatment (Fig. 3.12). 25

Extent of Salivary Gland Masses

Again, clinical examination and fine needle aspiration cytology can achieve all the information required for this
work-up. Ultrasound can accurately evaluate the gland parenchyma. If a deep lobe neoplasm is suspected or a large
malignant lesion is detected, CT or MR are appropriate.4 In fact, the tumour extent into the parapharyngeal space or the
invasion of the adjacent skull base are not detectable by clinical examination or ultrasound: they require scanning
techniques. Nevertheless, malignant salivary gland neoplasms are rare. Adenoidcystic carcinoma tends to spread slowly
along neural pathways and an MRI survey is therefore indicated.

Approach to Rarer Soft-Tissue Masses

Most are nerve sheath neoplasms: schwannomas or neurofibromas. Common sites include the vagus nerve, the cervical
roots and the sympathetic chain. A schwannoma usually presents as a painless, slow-growing mass in the anterolateral
neck. On MR, a schwannoma

Figure 3.12
Undifferentiated carcinoma of the left lobe of the
thyroid gland. On an axial T1 MR sequence the
neoplasm enhances and extends beyond the capsule
invading the common carotid artery (encased) (short
arrows). The left tracheal wall is infiltrated
(arrowheads). Thrombosis of the left internal
jugular vein is detected (curved arrow).

demonstrates a fusiform shape, absence of flow void within its tissue (differential diagnosis with paragangliomas),
well-circumscribed margins, uniform enhancement on T1-weighted sequences and variable hyperintensity on T2 (Fig.
3.13). The features of neurofibroma are indistinguishable from those of schwannoma, except for the diffuse plexiform
type that demonstrates an infiltrative pattern of growth.

Few lesions exhibit a specific density/signal. Among these, lipoma is the most frequent. Typical findings include a
well-circumbscribed lesion showing the same density/signal as adjacent fat. In most soft-tissue masses, however, biopsy
confirmation is necessary to obtain a definitive diagnosis.

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Figure 3.13
Cervical root neuroma. The lesion appears
hyperintense after Gd-DTPA injection on a T1 MRI
sequence. The typical fusiform shape of the lesion
along the course of a cervical root is detectable
(arrows). The vertebral artery is displaced anteriorly.

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3. Madison MT, Remley KB, Latchaw RE, Mitchell SL. Radiologic diagnosis and staging of the head and neck
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8. Laccourreye O, BÄly N, Halimi P, Guimaraes R, Brasnu D. Cavernous sinus involvement from recurrent adenoid
cystic carcinoma. Ann Otol Rhinol Laryngol 1994; 103: 822-825.

9. Becker M, Zbaren P, Laeng H, Stoupis C, Porcellini B, Vock P. Neoplastic invasion of the laryngeal cartilage:
comparison of MR imaging and CT with histopathologic correlation. Radiology 1995; 194: 661-669.

10. Castelijns JA, Brekel MW. Magnetic resonance imaging evaluation of extracranial head and neck tumors. Magn
Reson Q 1993; 9: 113-128.

11. Hermans R, Lenz M. Imaging of the oropharynx and oral cavity. Part I: Normal anatomy. Eur Radiol 1996; 6:
362-368.

12. Lenz M, Hermans R. Imaging of the oropharynx and oral cavity. Part II: Pathology. Eur Radiol 1996; 6: 536-549.

13. Zbaren P, Becker M, Laeng H. Pretherapeutic staging of laryngeal carcinoma. Clinical findings, computed
tomography and magnetic resonance imaging compared with histopathology. Cancer 1996; 77: 1263-1273.

14. Foote RL, Olsen KD, Davis DL et al. Base of tongue carcinoma: patterns of failure and predictors of recurrence
after surgery alone. Head Neck 1993; 15: 300-307.

15. McLaughlin MP, Mendenhall WM, Mancuso AA et al. Retropharyngeal adenopathy as a predictor of outcome in
squamous cell carcinoma of the head and neck. Head Neck 1995; 17: 190-198.

16. Jaulerry C, Rodriguez J, Brunin F et al. Results of radiation therapy in carcinoma of the base of the tongue. The
Curie Institute experience with about 166 cases. Cancer 1991; 67: 1532-1538.

17. Ross MR, Schomer DF, Chappell P, Enzmann DR. MR imaging of head and neck tumors: comparison of
T1-weighted contrast-enhanced fat-suppressed images with conventional T2-weighted and fast spin-echo T2-weighted
images. AJR 1994; 163: 173-178.

18. Som PM. Detection of metastasis in cervical lymph nodes: CT and MR criteria and differential diagnosis. AJR 1992;
158: 961-966.

19. Reisner K, Uhlig U. The influence of computer tomography on treatment strategies and follow-up in tumors of the
nasopharynx and the paranasal sinuses. A retrospective study on 104 patients. Strahlentherapie Onkologie 1996; 172:
1-8

20. Chong LY, Fan YF. Skull base erosion in nasopharyngeal carcinoma: Detection by CT and MRI. Clin Radiol 1996;
51: 625-631.

21. Allbery SM, Chaljub G, Cho NL, Rassekh CH, John SD, Guinto FC. MR imaging of nasal masses. Radiographics
1995; 15: 1311-1327.

22. Ahmadi J, Hinton DR, Segall HD, Couldwell WT. Surgical implications of magnetic resonance-enhanced dura.
Neurosurgery 1994; 35: 370-377.

23. Vazquez E, Enriquez G, Castellote A et al. US, CT, and MR imaging of neck lesions in children. Radiographics
1995; 15: 105-122.

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24. Vassilopoulou Sellin R. Management of papillary thyroid cancer. Oncology Huntingt 1995; 9: 145-151.

25. Takashima S, Nomura N, Noguchi Y, Matsuzuka F, Inoue T. Primary thyroid lymphoma: evaluation with US, CT,
and MRI. J Comput Assist Tomogr 1995; 19: 282-288.

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4
The Lung and Mediastinum

Geraldine Walsh and Christopher Flower

Bronchial carcinoma

The solitary pulmonary nodule

Superior sulcus tumour

Pulmonary metastases

Lymphoma and haematological malignancies

Mediastinal tumours

Pleural malignancy

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A wide range of neoplasms arise in or secondarily involve the thorax. These include primary lung cancer, mediastinal
tumours, pleural malignancy and thoracic spread of extrathoracic malignancies. Frontal and lateral chest radiographs
remain the initial imaging investigation in suspected intrathoracic neoplasia and are frequently supplemented with
computed tomography (CT), which gives excellent anatomical definition and allows for accurate localization and
staging of the tumour. Histological diagnosis is frequently possible from percutaneous CT-guided biopsy, particularly in
cases of peripheral pulmonary and pleural neoplasia. Magnetic resonance imaging (MRI) has a complementary role to
CT in selected instances such as in the assessment of superior sulcus tumours and occasionally in the evaluation of the
mediastinum.

Bronchial Carcinoma

Bronchial carcinoma is one of the commonest primary cancers with an overall 5-year survival rate of just 10%. 1 It is
classified on the basis of histology into small cell carcinoma (approximately 20% of cases) and non-small cell
carcinoma (80%). Non-small cell carcinoma may be further divided according to cell type into squamous cell, large cell,
adeno- and bronchiolo-alveolar carcinoma. The relative incidence of squamous cell carcinoma appears to be decreasing
while that of adenocarcinoma, which is more common in females, is on the increase. Bronchioloalveolar carcinoma is
usually considered separately from adenocarcinoma and may account for up to 15% of primary lung cancer.2, 3

The poor prognosis for most patients with lung cancer compared with the greatly improved survival for those with
isolated small peripheral cancers has led to the use of screening programmes using chest radiography for high risk
populations. Despite the relative insensitivity of this technique, it detects a significant number of early stage cancers.
However, in none of the screening programmes to date has there been any significant reduction in mortality in the
screened population as compared to controls.4, 5

The diagnosis of primary lung cancer is usually suspected from a combination of specific signs and symptoms. These
include cough, particularly in association with haemoptysis, dyspnoea, chest pain and persistent pneumonia. The chest
radiograph may show direct or indirect signs of carcinoma; the primary tumour may be visible as a pulmonary mass or
features such as volume loss and hilar displacement may indicate the presence of an underlying bronchial occlusion.

Appropriate staging of the patient with bronchial carcinoma is important as stage of disease determines the surgical
resectability and ultimately the prognosis. Some information can be obtained from the chest radiograph such as tumour
size, the presence of gross hilar and mediastinal lymphadenopathy, evidence of pleural effusion and features of
haematogenous spread such as rib metastases, but in most cases CT is essential. Staging is based on the TNM
classification (Table 4.1) and includes:

1. Assessment of the primary tumour: CT is used to assess size and local spread of tumour. The presence of mediastinal
and chest wall invasion is important as it determines if the tumour constitutes a T2 (resectable) or T3 (unresectable)
lesion. Both CT and MRI detect gross invasion accurately (Fig. 4.1), but are relatively insensitive for lesions which abut
but have not obviously extended into the mediastinum or chest wall.

2. Assessment of nodal spread: There is some variation in the size of normal nodes depending on their location within
the mediastinum; however, they measure less than 1 cm in short axis diameter on CT. Whilst CT depicts nodes
accurately it is relatively insensitive for N staging as normal sized nodes may be involved by tumour and a significant
proportion of enlarged nodes represent an inflammatory reaction and are not involved by tumour. In this regard, CT and
MR have similar sensitivities of 60-70%. Despite these difficulties, CT is invaluable in providing a `roadmap' for nodal
sampling at mediastinoscopy and thereby preventing unnecessary thoracotomies (Fig. 4.2).6, 7

3. Assessment of extranodal spread: A significant proportion of patients will have extrathoracic metastases at initial
presentation, the prevalence being greater for adenocarcinoma, and in many cases these metastases are occult.8
Systemic features such as weight loss are ominous and suggest a poor prognosis.9 In these cases, evaluation for
extrathoracic spread to liver, brain and bone is warranted. Patients with organ-specific clinical findings should also
undergo appropriate evaluation for metastatic spread. A high incidence of CNS metastases has been noted in patients
with adenocarcinoma and mediastinal node involvement and preoperative evaluation of this group should probably
include MRI of the brain.10

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At our institution, all patients with suspected lung cancer proceed to CT evaluation of the thorax and upper abdomen.
This establishes the presence of tumour and evaluates the best approach to biopsy (whether by fibre-

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Table 4.1 TNM definitions for the International Staging System for Lung Cancer
Primary tumour (T)
TX: Tumour proved by the presence of malignant cells in bronchopulmonary secretions but not visualized
roentgenographically or bronchoscopically, or any tumour that cannot be assessed as in a retreatment staging.
T0: No evidence of primary tumour.
T1S: Carcinoma in situ.
T1*: A tumour that is 3 cm or less in greatest dimension, surrounded by lung or visceral pleura, and without evidence of
invasion proximal to a lobar bronchus at bronchoscopy.
T2: A tumour more than 3 cm in greatest dimension, or a tumour of any size that either invades the visceral pleura or has
associated atelectasis or obstructive pneumonitis extending to the hilar region. At bronchoscopy the proximal extent of
demonstrable tumour must be within a lobar bronchus or at least 2 cm distal to the carina. Any associated atelectasis or
obstructive pneumonitis must involve less than an entire lung.
T3: A tumour of any size with direct extension into the chest wall (including superior sulcus tumors), diaphragm, or the
mediastinal pleura or pericardium without involving the heart, great vessels, trachea, oesophagus, or vertebral body; or a
tumour in the main bronchus within 2 cm of the carina without involving the carina.
T4: A tumour of any size with invasion of the mediastinum or involving the heart, great vessels, trachea, oesophagus,
vertebral body, or carina, or presence of malignant pleural effusion.
Nodal involvement (N)
N0: No demonstrable metastasis to regional lymph nodes.
N1: Metastasis to lymph nodes in the peribronchial or ipsilateral hilar region, or both, including direct extension.
N2: Metastasis to ipsilateral mediastinal lymph nodes and subcarinal lymph nodes.
N3: Metastasis to contralateral mediastinal lymph nodes, contralateral hilar lymph nodes, ipsilateral or contralateral
scalene, or supraclavicular lymph nodes.
Distant metastasis (M)
M0: No (known) distant metastasis.
M1: Distant metastasis present - specify sites.

optic bronchoscopy or fine needle biopsy) and assesses both intra- and extra-thoracic spread. (Fig 4.3) Depending on the CT findings,
further preoperative evaluation may include biopsy of nodes at mediastinoscopy or mediastinotomy and CT-guided biopsy of likely
abdominal metastases.

The following standard CT imaging protocol can be used. Initial 10 mm collimation sections at 10 mm intervals through the thorax
are followed by spiral volumetric image acquisition through the mediastinum and central airways (3 mm collimation, table feed of 4.5
mm/s) during intravenous injection of iodinated contrast medium (50 ml of low osmolar, non-ionic contrast medium at a rate of 3-4
ml/s with a delay of 10-12 s).

Further spiral image acquisition through the upper abdomen (8 mm collimation, table feed of 12 mm/s) immediately post contrast
medium administration completes the study.

These images allow documentation of tumour size, the size and extent of hilar and mediastinal lymphadenopathy and likely
mediastinal and pleural invasion by tumour. Metastases to the liver and adrenals are also visualized (Fig. 4.4). Occasionally, there is
uncertainty whether a hepatic or adrenal lesion represents metastatic involvement or an incidental benign lesion; CT-guided
percutaneous biopsy of these masses is then required to establish the diagnosis. MRI may also be used to distinguish between an
adrenal metastasis and an adenoma. Korobkin et al 11 showed that adrenal masses can be characterized as adenomas using chemical
shift with a high specificity and acceptable sensitivity by visually comparing the opposed-phase and in-phase gradient echo (GRE)
images; only adenomas showed an increase in relative signal intensity ratio on opposed-phase chemical shift images. Krestin et al12
reported that adenomas and non-adenomas have different patterns of gadolinium enhancement on fast GRE images.

Haemoptysis

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Haemoptysis is an important clinical symptom and a common mode of presentation of bronchial carcinoma. It merits full evaluation
even though the aetiology is established in only about 50% of cases.13 Patients with

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Figure 4.1
CT scan shows squamous cell carcinoma in apical segment of right upper lobe eroding the
adjacent rib and vertebral body (arrows).

this symptom tend to fall into two categories: those with a normal chest radiogaph and those with radiographic findings
suggestive of underlying disease.

Patients with clinical or radiographic findings suggestive of carcinoma require fibre-optic bronchoscopy. CT plays an
important role in assessing these patients prior to bronchoscopy as it provides a `roadmap' for biopsy and also stages the
tumour. In patients with a normal chest radiograph, CT has a potentially valuable role in determining which patients
should be bronchoscoped. Several studies have emphasized the value of high-resolution CT 14,15,16 which detects as
many as or more tumours than bronchoscopy. In addition, it will demonstrate non-neoplastic processes which may be
responsible for haemoptysis (e.g. bronchiectasis which accounts for approximately 15% of cases). A case can be made
for using CT as the initial screen for patients with a normal chest radiograph and haemoptysis, reserving bronchoscopy
for those with CT evidence of bronchial carcinoma or those with persisting haemoptysis in the face of a negative CT.

Pleural Effusion

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Approximately 15% of patients with bronchial carcinoma will have an associated pleural effusion at initial presentation
and over 50% of patients with disseminated disease will develop an effusion. The fluid may indicate malignant pleural
involvement or be secondary to lymphatic obstruction. Effusions are also found in association with pulmonary
atelectasis or pneumonia distal to endobronchial obstruction. The diagnosis of malignant pleural involvement may be
established by ultrasound-guided pleural aspiration and biopsy.

The Solitary Pulmonary Nodule

Determination of the nature of a solitary pulmonary nodule (SPN) is an important and relatively common problem in
radiological practice. A SPN is defined as a circumscribed spherical pulmonary opacity < 5 cm in

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Figure 4.2
CT scan shows collapse of the right upper lobe (due to a bronchoscopically proven
carcinoma occluding the right upper lobe bronchus) and enlarged paratracheal nodes
which were involved by tumour at mediastinoscopy (arrows).

diameter which is not associated with significant abnormality elsewhere in the thorax. Having established that the lesion
is definitely intrapulmonary and not an artefact or innocent chest wall lesion, it is important to determine if it is benign
or malignant and in particular whether it represents a primary bronchial carcinoma; 40-60% of bronchial carcinomas
present as SPNs but only a number of SPNs are malignant. In the United States, where the prevalence of granulomatous
disease is high, only 30% of SPNs are due to primary lung cancer whereas in Europe the likelihood of a SPN being
malignant is significantly higher.

The following features are helpful in differentiating benign from malignant lesions:

1. Past radiographs: A lesion which has not changed in size over a period of 2 years is likely to be benign.

2. Computed tomography: CT is used to assess the size and shape of a nodule and to characterize its architecture.

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Size: Clearly visible lesions of less than 1 cm in diameter are more likely to be benign than malignant. Small bronchial
carcinomas tend to have ill-defined borders and are difficult to detect on chest radiographs when less than 1 cm in
diameter. Benign lesions such as hamartomas and granulomas are denser and more sharply defined and are therefore
visible at smaller sizes.

Shape: Malignant lesions tend to be ill-defined and irregular in shape with lobulated or spiculated margins. Benign
lesions are more commonly well-defined and circular or oval in shape.

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Figure 4.3
Percutaneous needle biopsy under CT control of a mass in the right lung which is
beyond the range of bronchoscopic vision.

While these generalizations hold true for the majority of SPNs, there are sufficient exceptions to make these
assessments of limited value in the individual case. More precise predictive features are:

Calcifications: The determination of the presence or absence of calcification is of great importance. While 5-10% of
malignant lesions exhibit evidence of calcification on CT, this is usually granular or sandlike in nature. Laminated
calcification or a central nidus of calcification within a lesion is invariably evidence of a benign granulomatous process.
`Popcorn' calcification is a characteristic but uncommon manifestation of a hamartoma. Eccentric calcification may
represent a benign granulomatous lesion which has been engulfed by tumour.

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CT densitometry: Since its advent, CT has been used to categorize the morphology of SPNs in an attempt better to
distinguish between benign and malignant lesions. CT is clearly of value in defining the presence of calcification and
fat; the latter being a good predictor of a hamartoma. Absolute assessment of CT attenuation has also been used.
Recently, Swensen et al 17 demonstrated the usefulness of CT densitometry following intravenous injection of
iodinated contrast medium. Enhancement of greater than 20 Hounsfield Units (HU) was found in all malignant lesions,
although a proportion of benign lesions also showed significant enhancement. CT densitometry post contrast medium
administration therefore appears to be a sensitive but relatively non-specific test for the differentiation of benign from
malignant lesions.

Superior Sulcus Tumour

Superior sulcus or Pancoast's tumours are apical tumours of any cell type,18 which invade the chest wall

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Figure 4.4
CT reveals several low attenuation lesions in the liver due to metastases from an adenocarcinoma.

and the lower cords of the brachial plexus and the sympathetic chain to produce the classic complex of pain in the upper limb and
Horner's syndrome.

The chest radiograph shows an apical mass in 50-75% of cases and an apical cap resembling pleural thickening in the remainder. 2
The latter tumours may be particularly difficult to diagnose on standard radiographs and CT is valuable in these cases. Bone
destruction, involving the adjacent ribs and the spine, is present in approximately one-third of cases.

MRI is currently the imaging modality of choice for further evaluation of superior sulcus tumours. Imaging in both the coronal and
sagittal planes allows evaluation of the extrathoracic extent of the tumour and involvement of the brachial plexus and subclavian
vessels is optimally visualized. T1-weighted and short T1 inversion recovery (STIR) images in sagittal and coronal planes with 5 mm
collimation are recommended.19,20,21

Pulmonary Metastases

The primary tumours which most commonly metastasize to lung arise in the breast, colon, kidney, prostate and head and neck.
Metastases may be visible on the chest radiograph as multiple pulmonary nodules which frequently, although not invariably, have
well defined margins. CT allows detection of a significantly increased number of nodules partly because of its superior resolution and
also because the cross-sectional images of CT are free from overlying structures (Fig. 4.5). Haematogenous metastases are
characteristically found in the outer one-third of the lung and CT is superior to the chest radiograph for evaluation of this region.
Spiral scanning is the optimal CT technique as continuous volume acquisition during a single breathhold is advantageous in the
detection of small lesions which may be missed or duplicated by incremental CT because of respiratory inconsistencies.22

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Figure 4.5
Lung metastases demonstrated by CT. These were barely visible on the chest radiograph.

Lymphangitis Carcinomatosa

This particular form of metastatic disease is particularly well demonstrated by high resolution CT, which is significantly
more sensitive than the chest radiograph and is used when there is a clinical suspicion of lymphangitis in the presence of a
normal or equivocal chest radiograph. The CT features of lymphangitis include interlobular septal thickening with
bronchial wall thickening and centrilobular micronodules (Fig. 4.6).

Lymphoma and Haematological Malignancies

Thoracic involvement is a well recognized feature of the lymphomas. Intrathoracic disease is found in 67-84% of patients
with Hodgkin's disease (HD) 23, 24 and in 40-50% of those with non-Hodgkin's lymphoma (NHL) at initial presentation
and tends to worsen the prognosis. In North et al's series,25, 26 the 5-year survival for patients with stage I and II disease
and mediastinal involvement was 88% versus 98% for those with similar stage disease without mediastinal adenopathy.

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The mediastinum is the most frequently involved site. In HD, all nodal groups may be affected but the anterior mediastinal,
tracheobronchial and paratracheal nodes are particularly favoured. NHL may have similar appearances but the contiguity
of nodes characteristic of HD is frequently absent (Fig. 4.7). Pulmonary involvement by lymphomas is much less common.
In HD, it is usually associated with hilar and/or mediastinal disease,24, 27 whereas in NHL, pleural or pulmonary
involvement may be found in the absence of mediastinal or hilar adenopathy.

While the chest radiograph is the initial imaging investigation, CT is particularly well suited for displaying both
mediastinal and pleuropulmonary involvement and is used routinely in the staging and follow-up of

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Figure 4.6
Lymphangitis carcinomatosa demonstrated on high resolution CT. The patient complained of dyspnoea
and had a normal chest radiograph. The thickening of the interlobular septa (arrows) is characteristic.

lymphoma. The nodal masses usually have a characteristic appearance but there may be difficulties in differentiating focal
disease from primary mediastinal tumours such as thymomas and in differentiating multiple symmetrical nodes from
sarcoidosis.

When the lungs are involved, CT shows soft tissue opacities surrounding patent bronchi, often mimicking the consolidation
of pneumonia. Discrete pulmonary lesions are also seen; they usually take the form of nodules with poorly defined borders.
The least common manifestation of pulmonary parenchymal involvement is an interstitial pattern representing disease spread
along lymphatic routes. 26

AIDS-Related Lymphoma

Pulmonary lymphoma is the second most common intrathoracic malignancy linked to human immunodeficiency virus (HIV)
positivity and while NHL constitutes an AIDS-defining illness, HD does not.28, 29 B cell NHL is the commonest
AIDS-related lymphoma and tends to be an aggressive neoplasm with a predilection for extranodal sites including the
pulmonary parenchyma.30, 31 Blunt & Padley32 found the chest to be the major site of involvement in AIDS-related
lymphoma in 15 of 116 patients (12%); the pattern of disease tends to be different from lymphoma in the immunocompetent
patient with pleural and pulmonary masses, frequently peripheral and cavitating, being the commonest CT finding.

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Treated Lymphoma

CT is used to monitor response to chemo- and radiotherapy, for regular follow-up of patients in remission and to detect
evidence of relapse. Patients may develop direct complications of their therapy; these are assessed with chest radiography
and CT when appropriate.

Direct complications include radiation-induced pneumonitis which may progress to pulmonary fibrosis. It classically
develops 8-12 weeks after completion of

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Figure 4.7
CT scan reveals multiple enlarged nodes mainly in the anterior mediastinum (arrows) in a patient with
non-Hodgkin's lymphoma.

therapy and patients present with cough, dyspnoea and pleuritic chest pain. The chest radiograph may show pulmonary infiltrates
which typically lie within the radiation portal. Occasionally, CT will demonstrate changes not visible on the chest radiograph. 33

The chemotherapeutic agents most frequently associated with pulmonary toxicity in lymphoma patients are bleomycin, methotrexate,
chlorambucil and procarbazine. Toxicity is related either to cumulative dosage or to a hypersensitivity reaction and in most cases
results in diffuse alveolar damage with interstitial fibrosis. High resolution CT is a much more sensitive technique than the chest
radiograph for detection of lung damage and whilst the appearances are seldom diagnostic, they are often characteristic of the disease
(Fig. 4.8).

Indirect complications of therapy usually result from bone marrow suppression and steroid therapy. Thrombocytopenia may give rise
to diffuse pulmonary haemorrhage and increased susceptibility to infection results from neutropenia, lymphopenia and steroid therapy.

Infections encountered in the normal immunocompetent host may occur but these immunocompromized individuals are also
susceptible to opportunistic infections of which the most frequently encountered are cytomegalovirus (CMV), Pneumocystis carinii
pneumonia (PCP), invasive pulmonary aspergillosis and Candida albicans pneumonia.

CT has an important role in imaging patients with suspected infection. The CT appearances may be sufficiently characteristic to
enable treatment without a tissue diagnosis and this is particularly important in patients who are at risk from bronchoscopic biopsy
such as those with a low platelet count. PCP produces patchy ground glass change,34 whilst invasive aspergillosis typically causes
ill-defined nodules with a surrounding halo of haemorrhage; these develop air crescents as the neutrophil count improves.35
However, it may be difficult on the basis of the imaging findings alone to differentiate drug-induced change and pulmonary
parenchymal involvement by lymphoma from infection

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Figure 4.8
CT scan reveals bilateral reticular shadowing at the periphery of both lower lobes which is
characteristic of bleomycin toxicity.

and tissue acquired at transbronchial or open lung biopsy is often required for definitive diagnosis

Mediastinal Tumours

Many mediastinal tumors are asymptomatic and symptoms when present are relatively non-specific. Approximately
one-third of tumours are malignant. Division of the mediastinum into anterior, middle and posterior compartments is
helpful in the differential diagnosis of the lesion. Imaging of mediastinal tumours is with standard chest radiographs, CT
and/or MRI.

The chest radiograph determines the position of the lesion within the mediastinum, thus limiting the differential diagnosis,
and in a proportion of cases the appearances may suggest a specific diagnosis, as in cases of aortic aneurysm and
neurogenic tumours.

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Most patients are then evaluated further with CT. MRI may be performed either after or instead of CT. Advantages of MRI
include its multiplanar capabilities, its superiority to CT in tissue characterization and its ability to demonstrate spinal
canal involvement in neurogenic tumours.

Anterior Mediastinum

Thymoma is one of the commonest primary mediastinal tumours and is found in approximately 10% of patients with
myasthenia gravis (Fig. 4.9). More frequently, it occurs as an isolated finding in patients with non-specific symptoms. The
CT appearances are usually characteristic and the size and extent of the tumour can be assessed as well as the likelihood of
local invasion.

Germ cell tumours are most commonly found in young adults. There is a variety of histological types, including seminoma
and the non-seminomatous germ cell tumours which include teratoma and embryonic cell carcinoma. Whilst the chest
radiographic appearances are very similar to thymoma, CT may show diagnostic features such as fat or fat/fluid levels or
suggestive fea-

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Figure 4.9
CT scan of a patient with myasthenia gravis reveals a lobulated
thymoma lying anterior to the ascending aorta and main pulmonary
artery (arrows).

tures such as cystic components in benign teratoma.

Thyroid masses are superior mediastinal lesions with characteristic features, including their paratracheal location, areas
of high attenuation on CT representing normal thyroid tissue interspersed with rounded foci of low attenuation and
calcification. CT is used to assess the size of the tumour and its secondary effects on the trachea. Lymphoma may arise
in anterior mediastinal nodes or within the thymus. When this is an isolated finding, the lesion may mimic a thymoma
or germ cell tumour.

Posterior Mediastinum

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Neurogenic tumours account for the large majority of posterior mediastinal lesions and 30% are malignant. They arise
from peripheral nerves, sympathetic and parasympathetic ganglia and are usually found in the paravertebral gutter. The
chest radiograph may show rib erosion and an increase in the size of the intervertebral foramena but either CT or MRI
are required to define the extent of the tumour. MRI has the advantages of accurate definition of the intraspinal
component and of differentiation between neurogenic tumours and lateral meningoceles.

Pleural Malignancy

Pleural malignancy may be due to primary pleural tumour (mesothelioma), metastases from extrapleural sites or direct
spread within the thorax.

First described in the North Western Cape Province of South Africa, mesothelioma is the commonest primary pleural
malignancy. There is a strong association with occupational asbestos exposure and it is estimated that approximately 6%
of asbestos workers will die of diffuse malignant mesothelioma. The incidence of mesothelioma in the United Kingdom
continues to

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increase, reflecting the lack of protection for asbestos workers until relatively recently coupled with the long latent
period (usually 20-40 years].

Pleural metastases are the commonest cause of pleural malignancy accounting for 95% of cases and the majority relate
to a primary tumour in the breast, bronchus or gastrointestinal tract. Bronchial carcinomas frequently involve the pleura
and chest wall by direct extension. Uncommon pleural malignancies include thymoma (which may seed directly within
the pleura) and lymphoma.

Pleural malignancy commonly results in a pleural effusion. In most instances, this is well demonstrated on the chest
radiograph which may provide further clues to the diagnosis such as the underlying bronchial carcinoma. More
frequently, the diagnosis is established by cytological analysis of the pleural aspirate and closed pleural biopsy. When
the effusion is small or loculated, ultrasound is invaluable for localization of fluid prior to aspiration and biopsy. CT
may also be helpful in patients presenting with effusions by demonstrating the underlying pulmonary disease (bronchial
carcinoma, lymphangitis carcinomatosa or pulmonary metastases), pleural tumour masses or chest wall invasion. It is
usually reserved for those patients in whom a diagnosis cannot be reached from the chest radiograph and pleural
aspiration.

A significant number of patients with pleural malignancy do not develop an effusion. They usually present with chest
pain and the chest radiograph may show lobulated pleural masses or diffuse pleural thickening. Rarely, there is evidence
of associated rib destruction. CT plays an important role in the further investigation of these patients. Not only does
cross-sectional imaging better delineate the disease, it also allows differentiation between benign and malignant pleural
thickening with a high degree of sensitivity. 36 Nodular pleural thickening of greater than 1 cm, involving the
mediastinal pleura and forming a circumferential sheath with lung encasement, is a feature of malignant pleural disease
(Fig 4.10). Finally, CT-guided biopsy is an extremely useful technique in patients with either focal or diffuse pleural
thickening when a tissue diagnosis is required.37 It is carried out under local anaesthesia as an outpatient procedure.

More recently, MRI has been used to differentiate benign from malignant pleural disease. Falaschi et al38 found
malignant lesions to be hyperintense relative to muscle on proton-density and T2-weighted sequences with a sensitivity
of 100%, a specificity of 87% and a negative predictive value of 100%. MRI may therefore have a complementary role
to CT in the evaluation of pleural thickening.

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Figure 4.10
Mesothelioma encasing the right lung. The tumour has a
lobulated outline which is a characteristic feature.

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References

1. Rosado de Christenson M. Staging of Lung Cancer. Proceedings of the Armed Forces Institute of Pathology.
Washington, DC, Armed Forces Institute of Pathology, April 1994.

2. Armstrong P. Neoplasms of the lungs, airways and pleura. In: Armstrong P, Wilson AG, Dee P, Hansell DM (eds)
Imaging of Diseases of the Chest, 2nd edn. St. Louis: Mosby, 1995, pp. 272-368.

3. Auerbach O, Garfinkel L. The changing pattern of lung carcinoma. Cancer 1991; 68: 1973-1977.

4. Heelan RT, Flehinger BJ, Melamed MR et al. Non-small cell lung cancer. Results of the New York Screening
Program. Radiology 1984; 151: 289-293.

5. Melamed MR, Flehinger BJ, Zaman MB et al. Screening for early lung cancer. Results of the Memorial
Sloan-Kettering study in New York. Chest 1984; 86: 44-53.

6. Grover FL. The role of CT and MR in the staging of the mediastinum. Chest 1994; 106 (Suppl): 3915-3965.

7. Webb WR, Jenson BG, Gollitto R et al. Bronchogenic carcinoma: Staging with MR compared with CT and surgery.
Radiology 1985; 156: 117-124.

8. Hillers TK, Sauve MD, Guyatt GH. Analysis of published studies on the detection of extrathoracic metastases in
patients presumed to have operable non small cell lung cancer. Thorax 1994; 49: 14-19.

9. Bragg DG. The diagnosis and staging of primary lung cancer. Radiol Clin North Am 1994; 32: 1-14.

10. Gamsu G. Extrathoracic evaluation of suspected pulmonary malignancy. Proceedings of the Fleischner Society.
26th Annual Conference on Chest Disease, Vancouver, 1996, pp. 187-191.

11. Korobkin M, Lombardi TJ, Aisen AM et al. Characterization of adrenal masses with chemical shift and
gadolinium-enhanced MR imaging. Radiology 1995; 197: 411-418.

12. Krestin GP, Steinbrich W, Friedmann G. Adrenal masses: evaluation with fast gradient-echo MR imaging and
Gd-DPTA-enhanced dynamic studies. Radiology 1989; 171: 675-680.

13. Müller NL. Hemoptysis: High-resolution CT vs bronchoscopy. Chest 1994; 105: 982-983.

14. Set PAK, Flower CDR, Smith IE et al. Hemoptysis: Comparative study of the role of CT and fiberoptic
bronchoscopy. Radiology 1993; 189: 677-680.

15. McGuinness G, Beacher JR, Harkin TJ et al. Hemoptysis: Prospective high-resolution CT/bronchoscopic
correlation. Radiology 1993; 189: 677-680.

16. Naidich DP, Funt S, Ettenger NA et al. Haemoptysis: CT-bronchoscopic correlations in 58 cases. Radiology 1990;
177: 357-362.

17. Swensen SJ, Brown LR, Colby TV et al. Pulmonary nodules: CT evaluation of enhancement with iodinated contrast
material. Radiology 1995; 194: 393-405.

18. Attar S, Miller SE, Sallerfield J et al. Pancoast's tumor: irradiation or surgery? Ann Thorac Surg 1979; 28: 578-586.

19. Hamlin DJ, Burgener FA. CT including sagittal and coronal reconstruction in the evaluation of Pancoast tumors. J
Comput Assist Tomogr 1982; 6: 35-40.

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20. Heelan RT, Demas BE, Caravelli JF et al. Superior sulcus tumors: CT and MR imaging. Radiology 1989; 170:
637-641.

21. McLoud TC, Filion RB, Edelman RR et al. MR imaging of superior sulcus carcinoma. J Comput Assist Tomogr
1989; 13: 233-239.

22. Touliopoulos P, Costello P. Helical (spiral]) CT of the thorax. Radiol Clin North Am 1995; 33: 843-861.

23. Castellino RA, Blank N, Hoppe RT et al. Hodgkin disease: Contributions of chest CT in the initial staging
evaluation. Radiology 1986; 160: 603-605.

24. Filly R, Blank N, Castellino RA. Radiographic distribution of intrathoracic disease in previously untreated patients
with Hodgkin's disease and non-Hodgkin's lymphoma. Radiology 1976; 120: 277-281.

25. North LB, Fuller LM, Hagemeister FB et al. Importance of initial mediastinal adenopathy in Hodgkin disease. AJR
1982; 138: 229-235.

26. North LB, Libshitz HI, Lorrigan JG. Thoracic lymphoma. Radiol Clin North Am 1990; 28: 745-762.

27. Kaplan HS. Contiguity and progression in Hodgkin's disease. Cancer 1971; 31: 1811-1813.

28. Dee P. AIDS and other forms of immunocompromise. In: Armstrong P, Wilson AG, Dee P, Hansell DM (eds).
Imaging of Diseases of the Chest, 2nd edn. St Louis: Mosby, 1995, pp. 229-271.

29. Boring CC, Brynes RK, Chan WC et al. Increase in high grade lymphoma in young men. Lancet 1985; 1: 857-859.

30. Kuhlman JE. Diseases of the Chest in AIDS. Proceedings of the Fleischner Society 26th Annual Conference on
Chest Disease, Vancouver, 1996, pp. 57-71.

31. Sider L, Weiss AJ, Smith MD et al. Varied appearance of AIDS-related lymphoma in the chest. Radiology 1989;
171: 629-632.

32. Blunt DM, Padley SPG. Radiographic manifestations of AIDS related lymphoma in the thorax. Clin Radiol 1995;
50: 607-612.

33. Ikezoe J, Takashima S, Morimoto S et al. CT appearances of acute radiation-induced injury in the lung. AJR 1988;
150: 765-770.

34. Bergin CJ, Wirth RL, Berry GJ et al. Pneumocystis carinii pneumonia: CT and HRCT observations. J Comput
Assist Tomogr 1990; 14: 756-759.

35. Kuhlman JE, Fishman EK, Burch PA. Invasive pulmonary aspergillosis in acute leukemia: the contribution of CT to
early diagnosis and aggressive management Chest 1987; 92: 95-99.

36. Leung AN, Müller NL, Miller RR. CT in differential diagnosis of diffuse pleural disease. AJR 1990; 154: 487-492.

37. Scott EM, Marshall TJ. Flower CDR et al. Diffuse pleural thickening: Percutaneous CT-guided cutting needle
biopsy. Radiology 1995; 194: 867-870.

38. Falaschi F, Battolla L, Mascalchi M et al. Usefulness of MR signal intensity in distinguishing benign from
malignant pleural disease. AJR 1996; 166: 963-968.

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5
The Breast

William E Svensson

Cancer diagnosis

Cancers

Imaging following breast cancer diagnosis

Imaging follow-up of the breast cancer patient

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Breast cancer is the commonest malignancy affecting women in North America and much of Europe. In the UK 1 in 10
women will develop breast cancer and it is the commonest cause of death in women in the 35-55 year age group. In the
US just over half of women in whom breast cancer is detected will die of breast cancer and it is the second commonest
cause of cancer mortality in women (17%).

Significant risk factors are age, previous breast cancer, a family history of breast cancer involving a first-degree relative
(sisters, mother, aunts or grandmothers). High risk is associated with carriage of the BRCA1 and BRCA2 genes,
previous biopsies demonstrating atypia or a typical ductal or lobular hyperplasia. Even higher risk is associated with
lobular carcinoma in situ and well-differentiated ductal carcinoma in situ.

Other factors which are associated with increased risk of breast cancer include a history of fibroadenomas (though
fibroadenomas themselves are not premalignant), early menarche, late menopause, no previous pregnancy or late first
pregnancy, no breast feeding, post-menopausal obesity, a history of exposure to significant radiation and, possibly,
cystic breast disease. The contraceptive pill and hormone replacement therapy have both been implicated in very slight
increases of breast cancer but mainly in association with prolonged and/or early usage.

Cancer Diagnosis

Breast Screening

Many studies have shown the benefit of breast screening, particularly in those over 50 years. There is strong evidence
for screening between the ages of 40 and 50 but the screening cost per life saved is very high compared with other
medical interventions. The age of starting screening and screening interval depend on the relative risk factors of the
population being screened and the relative benefits as well as costs. In the general population under the age of 35 the
risks to the population as a whole of screening are greater than the risks of not screening (the number of cancers caused
by screening is almost certainly greater than the number of lives that would be saved). Between 35 and 40 years the
risks are about even. From 40 to 50 the risks of not screening begin to increase over the risks of screening and from 50
onwards the risks of not screening are significently greater than the risks of screening.

The frequency of screening (screening interval) is determined by cost and the number of cancers which develop or are
detected (interval cancers), between screening rounds. Another factor which needs to be considered is one or two views
at initial screening and at subsequent screening rounds.

In the UK current practice is two-view screening (oblique lateral and cranial caudal views) mammography at initial
screen followed by single views (oblique lateral views) (Fig. 5.1) at follow-up mammography. The female population
between the ages of 50 and 65 years is invited for screening at 3-year intervals. Women over the age of 65 are screened
at their request. Screening detects approximately one-third of all breast cancers in the breast screening population and
the remaining two-thirds are interval cancers which present between screening rounds. (The woman notices a lump
within the breast or a lump is detected during a routine examination for some other medical problem.) The arguments
for and against more frequent screening are influenced not only by cost but also whether interval cancers are more
aggressive cancers and therefore less likely to benefit from more frequent screening. In patients with symptomatic
breast problems, recent screening should not be taken to indicate that breast cancer is not present and if a woman
presents with a breast problem after recent screening she should still be evaluated in the normal way.

The Symptomatic Breast

All breasts are lumpy and the degree of nodularity varies from `millet seed' to `dried apricots and figs'. The degree of
nodularity for most women is in the `dried fruit and nuts' range. Large nodules or masses need further evaluation at first
presentation. Large nodules or masses which have been previously evaluated and have not changed at all since
evaluation may not necessarily need further investigation provided no concerns have been raised previously.

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Breast pain is a common presentation and in the under 35s with no risk factors does not require imaging investigation
provided there is no asymmetry or variation of nodularity within the breast at the site of pain or elsewhere. If pain is
associated with mass or significant thickening, imaging evaluation may well be necessary. As a general rule masses
which have been present for less than 1 month should be observed for a complete menstrual cycle to determine whether
they are transitory masses associated with the menstrual cycle.

Persisting palpable masses should always be evaluated to obtain a diagnosis which can definitively exclude cancer.
Masses that are discovered at well women clin-

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Figure 5.1
Oblique lateral views of right and left breasts. In the mid-part of the right breast there is an
area of increased density which is somewhat ill defined and merges with the surrounding
breast parenchyma. This appearance may be associated with a cyst or, as in this case, a
carcinoma. This screening mammography appearance would result in the woman being
recalled for further evaluation. Further investigation might include ultrasound and, if there
was a palpable mass, also fine needle aspiration cytology (FNAC) or core biopsy if
ultrasound showed the mass to be solid rather than a simple cyst.

ics or during a screening examination for another medical problem, are often of no significance if the patient is unable
to demonstrate them herself on a subsequent occasion, though there are rare occasions when such lesions are significant.
If the patient is aware of a lump or nodule and can regularly demonstrate it, however small and however benign the
examining clinician may think it is, it should always be evaluated further as on occasions women detect small cancers
before they are obvious to examining clinicians, even experienced breast surgeons. As well as examination by an
experienced breast surgeon, evaluation should include imaging and fine needle aspiration cytology (FNAC) or needle
for biopsy for histology (triple assessment).

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Increasing the number of tests performed improves sensitivity at the cost of worsening specificity. Focused groups of
tests can however reduce surgical biopsy rates. FNAC with ultrasonography and mammography is a particularly good
combination and is very useful in `one stop' breast clinics and often allows management decisions to be made the same
day. This has a particular advantage for women who are shown to have a benign breast problem as they can be
reassured the day of their investigation that they either do not have cancer or almost certainly have a benign problem.

Breast Imaging

Mammography

The main imaging modality for the breast is mammography using a dedicated mammography unit. Conventional
radiographic equipment does not provide sufficient sensitivity to demonstrate soft tissue differences and does not have
the resolution necessary to

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show the fine soft tissue connective strands and micro-calcifications within the breast. A dedicated mammography
X-ray tube contains a molybdenum target which produces lower energy radiation suited to demonstrating the small
differences in density of different soft tissues. It has a very fine focal spot to provide high definition. Mammographic
films (high detail, singlesided emulsion) and cassettes (carbon fibre) are also designed to give high resolution, good
contrast and the Buckey (film cassette holder on the mammography unit) has a high detail moving grid to improve
contrast.

For each view the breast is compressed as much as possible to improve tissue differentiation and resolution whilst
ensuring as much of the breast as possible is demonstrated on a single view. The compression also reduces the amount
of superimposition of tissues making interpretation easier than when a greater thickness of breast is X-rayed.

Two views of each breast are conventionally taken to ensure that the whole of the breast is imaged. Though much of the
breast is seen on both views, regions at the edge of the breast may only be seen on one. In particular, the axillary region
is seen only on the oblique lateral view and the medial edge only on the craniocaudal view.

Modern equipment helps to reduce the radiation dose to the breast whilst maintaining image quality. The US
Mammography Quality Standards Act 1992 requires all mammography facilities to be certified by the FDA. Radiation
doses of > 300 mrad per exposure require corrective action. The Breast Screening Service of the UK aims to maintain
single image radiation doses to at or below 200 mrad.

Mammography should be performed in a specialist mammography unit by a radiographer who has had mammography
training under the supervision of a recognized breast screening training centre. Interpretation should be performed by an
experienced radiologist with suitable breast imaging training. Best results are obtained in units with a sufficiently high
throughput to ensure that expertise is maintained. (The ACR recommends a minimum 40 examinations per month for
any unit performing mammography; others suggest double that number. Ideally specialist units should be performing at
least these numbers in a week).

Mammography is not recommended in the under 35 year old except in rare individual cases which have been discussed
with the radiologist, such as when FNAC or core biopsy and ultrasound have been inconclusive in the evaluation of a
suspicious area for which open biopsy is refused or has relative contraindications.

Over the age of 35 mammography is part of the work up in the symptomatic breast (Table 5.1). This may be the
evaluation of unexplained recent pain, recently noticed asymmetry, or a mass causing clinical concern. Its main use in
the evaluation of palpable lumps is the demonstration of microcalcifications and to evaluate margins and extent of
lesions. Mammography is helpful in the staging and evaluation of a known carcinoma at any age and for screening the
contralateral breast for an occult second primary. Impalpable mammographic abnormalities can be localized
mammographically using stereotaxic mammographic attachments which can be used for FNAC), biopsy or wire
localization for surgical excision biopsy. Most current equipment requires the patient to be wedged, sitting erect with
the breast compressed in the mammography machine for upwards of 10 min whilst the procedure is performed. Quite
frequently the procedure has to be abandoned if the patient experiences a vasovagal attack.

In the absence of a palpable mass, mammography is a screening procedure and the same indications apply as for breast
screening. The risks of mammography causing breast cancer are greater in young or large breasts than old or small
breasts. Law 1 has estimated, for the UK, that beginning screening at 30-34 years would cause 1 cancer for every 3
detected if two views are

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Table 5.1 Indication for mammography

Breast screening
Over 50 Indicated: national screening programmes, e.g. U.K.
Over 40 Debatable, but there is increasing evidence to suggest that it is
indicated.
Under 40 Not indicated, but if a first-degree relative developed breast cancer
before the menopause, screening may be indicated from the same
age at which the relative's cancer was diagnosed.
The symptomatic breast
Over 35 No recent previous mammogram
and
Palpable mass
or
Evaluation of breast pain, deformity or
asymmetry
and/or
Clinical suspicion of carcinoma.
Under 35 ONLY if there is a strong clinical suspicion of malignancy in the
presence of a normal breast ultrasound AND negative needle core biopsy.

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taken for each breast. At age 40-44 it is 1 for every 30 detected while at 50-54 it decreases to 1 for every 90 detected.
Mammographic screening, because of the cumulative effect of radiation, is currently not indicated below the age of 40
and between the ages of 40 and 50 the benefits are hotly debated. Over the age of 50 there is a clear benefit from breast
screening.

Digital mammographic imaging systems are becoming more accurate with improved image quality and have the
additional advantage of quantitative analysis. In due course they will improve on conventional mammography,
particularly with the development of more effective computer-aided diagnosis and image interpretation. The major
problem is related to image display and resolution. A single 18 cm X 24 cm mammogram with a resolution of 10 line
pairs/mm (the minimum required for acceptable detection of microcalcifications and parechymal strands) requires a
monitor of 3600 X 4800 pixels for display. The technical problems of image production and display are being overcome
but currently remain prohibitively expensive.

Ultrasound

Breast ultrasound has a significant role in the diagnosis of benign and malignant breast masses. Used in conjunction
with FNAC it provides high diagnostic accuracy for cancers and reduces the need for diagnostic excision biopsies of
benign lesions. It is the examination of choice in patients under the age of 35 and during pregnancy (Table 5.2). Over
the age of 35 there is debate as to whether ultrasound or mammography is the first imaging method of choice in aiding
the diagnosis of a clinically suspicious mass. In expert hands ultrasound is probably the most suitable. Mammography is
still necessary if it has not been performed recently to exclude impalpable abnormality in the remainder of both breasts.

Ultrasound should be performed by an experienced breast radiologist or ultrasonographer using a high-resolution linear
array probe (7-10 MHz) on an ultrasound machine, designed for high-resolution, small parts soft tissue imaging, with
colour Doppler, if it is to be used to its full potential. Many benign lesions can now be diagnosed ultrasonographically
with a high degree of certainty, reducing the need for open biopsy. If FNAC is not performed serial ultrasound
measurement, with high definition images, can confirm absence of change in ultrasonically benign lesions. For example,
fibroadenomata are now managed conservatively, with FNAC and/or follow-up ultrasound examinations, in many
centres.

Table 5.2 Indication for breast ultrasound

Characterisation of:
palpable breast masses
impalpable breast masses of uncertain aetiology seen
on mammography.
Primary evaluation of palpable masses:
In women under 35,
In pregnant or lactating women.
Evaluation of:
Asymmetry or distortion on mammography
Lesions seen in only one mammographic projection.
Guidance for interventional techniques:
Cyst aspiration
Abscess aspiration
Fine needle aspiration for cytology
Needle core biopsy
Localization for surgery either with skin marker or
internal localization wire.

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Imaging of:
The augmented breast.
The male breast with a suspicious mass or unilateral
gynaecomastia
Inflammation
The tender breast
The postoperative breast:
To identify haematoma and seromas
To evaluate new lumps in the scar of patients
who have had previous surgery for cancer.

The two imaging methods are now recognized as being complementary rather than competitive. Fine
microcalcifications, detected by mammography, are often not associated with any palpable mass in ductal carcinoma in
situ and are not easily seen with ultrasound. Conversely mammography is often unhelpful in the dense breast and in the
evaluation of densities which have moderately well defined margins. As well as evaluating palpable masses, ultrasound
may on rare occasions detect impalpable small cancers which are not demonstrated on mammography.

Ultrasound-guided interventions include ultrasound-guided FNAC, needle core biopsy and localization for open
excision biopsy, are all simple procedures. Localization for open excision biopsy may just involve marking the
overlying skin with the patient positioned as she would be in the operating theatre or using a localization wire. As well
as managing ultrasound abnormalities, breast ultrasound is frequently very useful for identifying and localizing the
impalpable mammographic mass for FNAC, biopsy or localization. As

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interventions are performed with the patient lying in a comfortable supine position, vasovagal attacks are very rare and
if they occur are unlikely to result in abandonment of the procedure. The ultrasound-guided techniques are more
acceptable to the patient and preferred by experienced operators who have experience with both ultrasound- and
mammographic-guided interventions. Ultrasound is real-time imaging and always allows optimum placement of needle
tips under direct vision.

Using ultrasound to screen for occult breast cancer is less sensitive than mammography because it does not detect much
of the microcalcification associated with ductal carcinoma in situ (DCIS). The other major disadvantage of ultrasound
breast screening is the expense, which is much greater than that of mammographic breast screening, because it requires
a lot of time from experienced breast ultrasonographers. Breast ultrasound is safe, because it does not use ionizing
radiation; unfortunately its lower sensitivity and cost make it unsuitable for screening at present.

Other Imaging Modalities

Other imaging modalities are second-line diagnostic methods which are used in complex cases or potential first-line
imaging methods which are currently too expensive and/or are under evaluation.

Nuclear Medicine

Nuclear medicine methods for imaging breast cancer include 99mTc-methyoxy-iso-butyl-isonitrile (MIBI), which is
selectively taken up by both the primary carcinomas and lymph node metastases (Fig. 5.2). 201Thallium also is taken up
by breast cancers, presumably due to the increased metabolism within them. Radiolabelled monoclonal antibodies are
also under evaluation. Positron emission tomography (PET) using 18fluorine-labelled FDG is showing promise in the
diagnosis of of primary breast cancer and breast cancer recurrences, detecting tumour foci as small as 0.4 cm in
diameter. Lymphoscintigraphy, which used only to be of help in the evaluation of lymphoedema (an important
complication of breast cancer treatment), is now important as a staging investigation using technetium-labelled
microaggregated albumin or sulphur colloid.

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) alone has not lived up to early expectations as a method of breast imaging (Fig.
5.3). MRI, with intravenous gadolinium contrast agents to show vascularity, is a rapidly

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Figure 5.2
A MIBI scintigram of a patient with a right breast
carcinoma. P is the primary tumour in the breast, N an
axillary lymph node containing tumour, H the heart which
takes up MIBI (which is also used for cardiac
scintigraphy), L the liver, S the left submandibular
gland and T the left lobe of the thyroid. In this case
the MIBI demonstrated a large lymph node deposit high
in the lateral side of the right axilla as well as the
known primary.

expanding area of research (Fig. 5.4). Gadolinium-DTPA dynamic enhancement profiles are helping to differentiate
malignant tumours from benign lesions with the aid of digital subtraction techniques. Interpretation, however, often
requires a large number of images to be examined. Gadolinium-containing melanin polymers coupled to monoclonal
antibodies specific for breast carcinoma are being synthesized for targeted MRI.

Despite a wide variety of imaging sequences and techniques, even with dedicated coils and IV contrast agents, the
current indications for MRI are still mainly restricted to:

imaging breasts with silicone implants to demonstrate adjacent malignancy or implant defects (leakage);

differentiation of scarring from malignancy;

detection of malignancy in dense breast tissue (including the diagnosis of multifocal disease in the presence of a known
malignancy);

monitoring the response to chemotherapy.

Cost and availability of equipment in many countries are important additional considerations.

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Figure 5.3
Magnetic resonance sectional image of a carcinoma
in the upper part of the right breast. Note the irregular
margin and radiating strands particularly in the area
beneath the tumour.

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Figure 5.4
Magnetic resonance sectional image following
intravenous enhancement with gadolinium DTPA.
Note how the signal is stronger from within the
tumour (the tumour is brighter than on the
unenhanced image in Fig. 5.3).

Ductography

Ductography, classically, is the demonstration of a duct by injection of X-ray contrast after cannulation of the duct.
Indications are continuing discharge after previous surgery and suspicion of ductal abnormality despite a normal
ultrasound examination. However, intraductal lesions of sufficient size, such as intraductal papillomata, are
demonstrated on ultrasound. Smaller lesions can be demonstrated with ultrasound ductography (saline is injected into
the duct and duct wall irregularity can be easily demonstrated).

Research Modalities

Thermography, like transillumination, does not have sufficient specificity or sensitivity to be recommended as a routine
examination. Research into the use of light for breast cancer diagnosis is concentrating on infrared and near infrared
light, i.e. that part of the electromagnetic spectrum that humans feel as heat. Modern infrared cameras can detect
temperature variations of <0.1° C at 1 m. Of greater interest is the use of near infrared light spectroscopy in which the
breast is transilluminated with laser light; fibreoptic detectors detect small changes of frequency when the light is
reflected by moving red cells. Spectral mapping of the changes may allow the increased and altered vascularity
associated with breast tumours to be detected.

Cancers

Invasive Ductal Carcinoma

Invasive ductal carcinoma is the most common type of breast cancer (approximately 75% of all breast cancers).
Clinically the woman usually presents with a palpable mass which may be associated with distortion or skin retraction,
particularly with larger tumours. The mammographic appearance most commonly is that of a spiculated mass (Fig. 5.5),
often associated with local architectural distortion and skin thickening if the tumour is close enough to the skin surface.
It may on occasions present as a more rounded, well-defined or partially-defined mass with a more benign appearance
(Fig. 5.6). Though this appearance is also commonly associated with the rarer breast cancers, because invasive ductal
carcinoma is so common, it is the commonest cause for this mammographic presentation. There may be associated
malignant microcalcifications if there is a combination of invasive ductal carcinoma and ductal carcinoma in situ (see
below).

The ultrasound appearance is also most commonly that of a spiculated mass with distortion of the surrounding
parenchyma. It usually shows loss of echogenicity centrally with quite marked posterior shadowing (Fig. 5.7). Invasive
ductal carcinoma can also present as a more defined lesion of low, fairly

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Figure 5.5
A small mass in the left breast with a stellate shape. Note the strands radiating
from it and the way in which it distorts the adjacent fairly homogeneous
breast parenchyma. This is a typical appearance of a small invasive
ductal carcinoma.

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Figure 5.6
A more rounded tumour which has a more defined shape. Its edges
are slightly irregular with a `brush border' appearance. There are also stellate
radiating strands into the adjacent breast similar to the small carcinoma in Fig.
5.5. This is also an invasive ductal carcinoma but the more rounded definition
might also occur in one of the rare breast cancers such as a medullary or
mucinous carcinoma.

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Figure 5.7
A typical ultrasound appearance of an irregular
stellate carcinoma with absorption of the sound
centrally resulting in a central anechoic area with
posterior shadowing. Like the stellate carcinoma on a
mammogram it has strands extending into the
surrounding normal tissues.

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Figure 5.8
A carcinoma with a lobulated shape and slightly
reduced heterogenous internal echogenicity (arrows).
There is some `bright up' with higher echogenicity in
the tissues deep to it (arrow heads).

homogeneous internal echogenicity with good through transmission of sound and a posterior increased echogenicity,
`bright up' (Fig. 5.8).

Invasive Lobular Carcinoma

Invasive lobular carcinoma is the cause of approximately 10% of all breast cancers. It is often bilateral with a reported
incidence in some series as high as 28%. It can be difficult to diagnose as a discrete mass, may not be palpable and
mammographically may be associated with very subtle diffuse changes. Only half present as a focal mass (usually
spiculated) and in the other half parenchymal asymmetry and architectural distortion are the only signs. This is also the
finding on ultrasound, although when there is distortion there is often quite marked posterior shadowing which if focal
can be helpful in diagnosis.

Ductal Carcinoma in Situ

A quarter to almost a half of all breast cancers diagnosed mammographically are ductal carcinoma in situ (DCIS). Many
patients are asymptomatic as the majority of these cancers are impalpable and the apparent rise in incidence of DCIS is
attributed to high-quality mammographic screening. Just under one-third of biopsyproven DCIS progress to invasive
disease. The treatment of DCIS is controversial and is being evaluated in a number of trials.

Mammographically, DCIS has microcalcifications orientated in the line of the ducts, often with branching
microcalcifications (Fig. 5.9). These may be seen on ultrasound as very bright echoes, occasionally with shadowing.
Less commonly, DCIS is associated with welldefined mammographic or ultrasound masses which may not have the
associated malignant type calcifications.

Rare Breast Cancers

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The remaining rarer types of carcinoma, which have a better prognosis, are mainly detected on screening and in the
most part rarely present clinically.

Lobular Carcinoma in Situ

This is most commonly an incidental finding in breast biopsies performed in premenopausal women carried out for
other reasons. Approximately 30% of these women go on to develop invasive carcinoma, which may be either ductal or
lobular, over the following 20 years. It is often bilateral and multifocal and there is

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Figure 5.9
Fine microcalcifications in the breast associated
with extensive ductal carcinoma in situ (DCIS). On
examination this patient's breasts felt quite normal
and there was no mass. She had a routine screening
mammogram because of a family history of breast
carcinoma. In this magnified image, multiple irregular
small flecks of microcalcification can be seen. Some
are linear in shape and are arranged in rows, some of
which are branching. The calcifications are associated
with carcinoma extending along the duct lumen.
The branching of the microcalcifications occurs when
the ducts branch. At operation, this patient was found
to have DCIS and invasive ductal carcinoma.

great debate as to whether it represents a true carcinoma. This debate extends to the management of these women,
ranging from observation to prophylactic bilateral mastectomy. There is no mammographic or ultrasound abnormality in
these patients until the development of the invasive carcinoma, which is more easily detected if it is ductal than lobular
(see above).

Tubular Carcinoma

In its pure form, tubular carcinoma occurs in <2% of breast cancers. It is multicentric in over a quarter of patients and
may be bilateral in a similar number. It presents as a small spiculated lesion on mammography and may be difficult to
differentiate from radial scars.

Medullary Carcinoma

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Approximately 5% of breast cancers are medullary carcinoma. It is commoner in young women. Both on
mammography and ultrasound it presents as a rounded mass with not particularly well defined borders (Fig. 5.6). On the
ultrasound it shows reduced echogenicity. It is often locally quite aggressive but the prognosis is often better than with
infiltrating ductal carcinomas.

Mucinous Carcinoma

Approximately 2% of breast cancers are mucinous carcinomas. They are more common in older women and have a
good short-term prognosis, although systemic recurrences more than 10 years after initial treatment have been reported.
Again mammographically they tend to be lobulated or rounded, moderately welldefined masses (Fig. 5.1). On
ultrasound they are quite well defined with reduced echogenicity which has a heterogeneous echo pattern and increased
echogenicity posteriorly (Fig. 5.8). On colour Doppler they show a marked increased blood flow within them.

Papillary Carcinoma

Papillary carcinomas account for approximately 1-2% of all breast cancers. They usually occur in older patients
presenting with a clinical history of nipple discharge or nipple retraction. They are often large, lobulated, palpable
masses in the subareolar region. They appear as quite well-defined masses on mammography. On ultrasound they may
be complex cystic masses with internal echogenicity or may be mainly solid.

Paget's Disease

Between 1 and 5% of all breast carcinomas present as Paget's disease and approximately half show a palpable mass. On
mammography, if there is no significant mass, the only signs may be nipple and areolar thickening or nipple
calcifications and in many patients mammography may be normal.

Male Breast Cancer

Approximately 1 in 200 breast cancers occur in males. The mean age of 64 is older than that for female breast cancers.
It usually presents as a painless hard mass. It should always be excluded in patients who are otherwise thought to have
gynaecomastia. The majority (85%) are infiltrating ductal carcinomas with the remainder divided between intraductal or
papillary carcinomas. Lobular carcinoma is extremely rare. On mammography, male breast cancers can range from well
circumscribed (Fig. 5.10) to spiculated masses and microcalcifications occur in up to one third of patients. Similarly,
ultrasound appearances are those of welldefined circumscribed (Fig. 5.11) to spiculated masses

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Figure 5.10
Craniocaudal views of the right and left breast of a
63-year-old male with unilateral enlargement of the
left breast area. This was thought to be gynaecomastia
by the referring physician. The mammogram shows a
non-specific increase in density which is asymetric
behind the left nipple. Careful examination (see inset
of magnified view of mass) shows there are abnormal
small calcifications within the mass which means it
cannot be benign gynaecomastia. This was an
invasive ductal carcinoma in a male.

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Figure 5.11
Ultrasound of the male breast carcinoma shown in
Fig. 5.10. The mass is moderately well defined with
fairly heterogenous internal echoes. It has increased
abnormal vascularity (colour Doppler positive), the
vessels are both around the edge and within the
tumour (arrows) and there is quite prominent posterior
`bright up' deep to the tumour (arrow heads).

which have a different appearance from the breast tissue development associated with gynaecomastia.

Imaging Following Breast Cancer Diagnosis

Staging of Breast Tumours

Final staging of breast tumours is done postsurgically for accurate assessment of tumour size and determination of nodal
status, because micrometastases in nodes cannot be imaged before surgery. Because of the low pick up rate of
metastatic disease in node negative T0 and T1, some centres do not routinely search for metastatic disease at
presentation. Staging for metastatic disease is often left until operative staging is completed, particularly if the initial
tumour is T0 (impalpable) or T1 (<2 cm). Larger tumours, however, benefit from preoperative staging as the stage often
determines the extent of the initial surgery and many centres also stage before surgery for smaller tumours. Imaging
plays an important part in both these situations.

Mammography and Ultrasound

If the diagnosis is made prior to mammography, mammography is still indicated to exclude multifocal or bilateral
carcinoma. It is often helpful in assessing the size of the tumour. Breast ultrasound is also useful for assessing tumour
size and the two imaging techniques are often complementary in this situation as the tumour may be better evaluated
with one rather than the other.

Ultrasound evaluation of axillary lymph nodes is useful in staging of breast cancer. High-resolution ultrasound, with
careful examination, is sensitive for detecting macroscopic involvement of lymph nodes. Irregular and/or enlarged
nodes if supported by an increase in vascularity are very suspicious of malignant infiltration. Micrometastases may not
cause any significant architectural change in lymph nodes or any increase in blood flow.

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Abdominal ultrasound, particularly of the liver, is a sensitive means of detecting metastatic disease within the liver.
Well-defined target lesions are pathognomonic of liver metastases (Fig. 5.12). More diffuse metastatic disease
associated with diffuse heterogenecity of the liver can be difficult initially to differentiate from focal fatty change which
is associated with factors such as previous hepatitis, significant alcohol intake, obesity and some drug therapies as well
as adjuvant chemotherapy treatment. These changes are not only seen with the more toxic chemotherapeutic agents but
also with hormonal therapeutic agents such as tamoxifen.

Nuclear Medicine

Bone Scintigraphy

Tc99m MDP bone scintigraphy is the most sensitive method for detecting bony metastatic disease (Fig. 5.13). It detects
bony metastatic disease up to 6 months before there is sufficient bony destruction for demonstration on plain film
radiography. It may require plain film radiography of increased activity to exclude other causes of `hot spots' such as
degenerative change or osteoporotic collapse. It can be helpful in assessing response to treatment, although the flare
response of increased activity which occurs in the first 3 months of response to chemotherapy can be confusing to those
unfamiliar with the use of bone scintigraphy in the treatment of metastatic disease.

Figure 5.12
Ultrasound of the liver in sagittal section. There is
a metastasis (arrow heads) just deep to the gallbladder
(arrows). Note the low echo rim of the metastasis with
the brighter central echoes, the so-called `target lesion'
appearance.

Breast Lymphoscintigraphy

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Ultrasound of axillary nodes can be helpful in confirming nodal involvement, but as already mentioned is less helpful
for excluding it. Breast lymphoscintigraphy following the injection of radiolabelled colloid into the breast primary
allows identification of lymph node drainage from the tumour and can be used to demonstrate the site of the sentinel
node, biopsy of which is a good predictor of nodal involvement. Accurate sampling of the drainage lymph nodes also
allows greater accuracy in determining routes of lymph node drainage, thus reducing the need for more extensive lymph
node sampling with its increased risk of postoperative arm swelling (lymphoedema). Dye injections just prior to surgery
provide similar information but do not show as easily the site of the sentinel node, which can be used for histology to
determine the likelihood of microscopic disease.

Imaging in Primary Treatment

Ultrasound is particularly useful for patients with large tumours who are treated with primary chemotherapy and
radiotherapy to reduce the bulk of the primary and allow less radical surgery with a better cosmetic result. Follow-up
with ultrasound can be used to confirm response. Colour Doppler flow changes in response to therapy (an increase in
vascularity is associated with increasing tumour size while decreasing vascularity is associated with decrease in size)
can occur up to 4 weeks before clinical or ultrasound measured changes in many patients.

Imaging Follow-Up of the Breast Cancer Patient

Mammography should be performed annually for the first 5 years following breast cancer treatment. Thereafter patients
should be screened every 2 years because of the increased risk of a second cancer developing in the contralateral breast.
Recurrence at the sight of previous surgery may often be masked by changes due to the surgery and radiotherapy so that
the first postoperative mammograms are often less helpful in the diagnosis of local recurrence than subsequent
mammograms.

Ultrasound is helpful in detecting breast cancer recurrence at the site of previous surgery by demonstrating regions of
reduced echogenicity. While ultrasound does not detect the microcalcifications associated with recurrence, it often
detects local recurrences which may not

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be demonstrated on mammography. Thus the two techniques are complementary in this important problem. Ultrasound
is less helpful in early recurrence where the only change is distortion of tissue with no obvious mass deposits. The
usefulness of colour Doppler in diagnosing early recurrence in areas which have an appearance of disruption due to scar
formation is uncertain but is under investigation in conjunction with ultrasound contrast media.

Bone scintigraphy is the most sensitive method for determining early bone metastases. Plain film radiography is useful
to exclude other causes of increased activity but is not indicated, however, in the routine follow-up of patients with
breast cancer. Abdominal ultrasound is the first examination for the detection of liver metastases. In equivocal cases
computed tomography (CT) may be indicated to demonstrate the occasional metastases which are not shown by
ultrasound. Very occasionally, 18fluorine FDG PET scanning is useful in diagnosing tumour or tumour recurrence
which is not diagnosed by any other method (Fig. 5.14) and the expense of this very sensitive test for tumour can be
justified.

Figure 5.13
Anterior and posterior views of an MDP 99m
Tc bone scintigram of a patient with multiple
bone metastases from a breast carcinoma
primary. Note the multiple areas of increased
activity in thoracic and lumbar vertebrae, ribs,
both shoulders, pelvis and upper femora. The
patient has had a previous right mastectomy.
The anterior ends of the left ribs are not as
clearly seen as on the right because the
thickness of the left breast tissue attenuates
the photons which arise in the ribs on the left.

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Figure 5.14
A 18fluorine FDG PET whole body scan of a patient
who has had a bilateral mastectomy for previous
bilateral carcinoma. The sites of the bilateral mastectomy
were scarred and nodular. Previous fine needle
aspiration cytology (FNAC) of some of the
nodules had not revealed any evidence of recurrence of
carcinoma. The PET scan was performed to see if there
was any evidence of local or distant recurrence. The
three sectional images (coronal anterior, transaxial
mid-thorax and right sagittal) show that there is a
small area of increased activity at the medial end of
the right mastectomy scar. Subsequent biopsy
confirmed that this was an area of local recurrence.

References

1. Law J. Variations in individual radiation dose in a breast screening programme and consquences for the balance
between associated risk and the benefit. Br J Radiol 1993; 66: 394-397.

2. Adler DD, Wahl RL. New methods for imaging the breast: techniques, findings, and potential. AJR 1995; 164: 19-30.

3. Buscombe JR, Cwikla JB, Thakrar DS, Hilson AJW. Scintigraphic imaging of breast cancer: A review. Nuclear Med
Commun 1997; 18: 698-709

4. Gardenosa G (ed). Breast Imaging Companion. Philadelphia: Lippincott-Raven, 1997.

5. Jack D. Hot spots inside the body. Lancet 1997; 350: 790.

6. Khalkali I, Mena I, Diggles L. Review of imaging techniques for the diagnosis of breast cancer: a new role of prone
scintimammography using technetium-99m sestamibi. Eur J Nuclear Med 1994; 81: 357-362.

7. Sabel M, Aichinger H. Recent developements in breast imaging. Phys Med Biol 1996; 41: 315-368.

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8. Scheidhauer K, Scharl A, Pietrzyk U et al. Qualitative (18F)FDG positron emission tomography in primary breast
cancer: clinical relevance and practibility. Eur J Nuclear Med 1996; 23: 618-623.

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9. Svensson WE. A review of the current status of breast ultrasound. Eur J Ultrasound 1997; 6: 77-101.

10. Tuck AK (ed) Textbook of Mammography. Edinburgh: Churchill Livingstone, 1993.

11. Tohno E, Cosgrove DO, Sloane JP (eds). Ultrasound Diagnosis of Breast Diseases. Edinburgh: Churchill
Livingstone, 1994.

12. Veronesi U, Paganelli G, Galimberti V et al. Sentinel-node biopsy to avoid axillary dissection in breast cancer with
clinically negative lymph-nodes. Lancet 1997; 349: 1864-1867.

Acknowledgements

The author thanks Helen Young for the PET images, Nandita De Souza for the MR images, Muhammad Mubashar for
the MIBI image and Damien Sell and Graham Reed for preparation of all the figures.

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6
The Oesophagus, Stomach, Duodenum and Small Intestine

Daniel J Nolan

Oesophagus

Stomach

Duodenum

Small Intestine

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Oesophagus

Oesophageal carcinoma is fairly common and accounts for about 2.5% of all malignancies and for almost all primary
oesophageal malignant neoplasms. 1 Rare primary oesophageal malignancies include adenosquamous carcinoma,
carcinosarcoma, pseudosarcomas, oat cell carcinomas and melanomas.

Carcinoma

Clinical Aspects

Oesophageal carcinoma has a poor prognosis with a 5-year survival of less than 10%.2 Numerous factors can
predispose to oesophageal carcinoma but in Western Europe and North America smoking and alcohol, particularly a
combination of the two, are by far the most important. Previously squamous carcinoma accounted for about 90% of
carcinomas while most of the rest were adenocarcinomas; currently there is an increase in the incidence of
adenocarcinoma. Squamous carcinomas are distributed throughout the oesophagus, although involvement of the
oesophagogastric junction is unusual. Adenocarcinomas arise in the lower third of the oesophagus on a background of
columnar metaplasia, probably induced by gastroesophageal reflux.3

Most patients present with dysphagia. Unfortunately this usually indicates that the neoplasm has reached an advanced
stage at the time of presentation. Some patients locate the dysphagia accurately to the site of the lesion, while in others
the perceived site of food sticking does not correspond to the location of the carcinoma. Anorexia, weight loss, chest
pain and anaemia are other, less frequently encountered, symptoms.

In many cases the carcinoma has spread beyond the oesophagus so that it is inoperable at the time of diagnosis. Lack of
serosa around the oesophagus and the thin nature of the oesophageal wall encourage early spread of carcinoma. Spread
of oesophageal carcinoma is by direct extension, lymphatic permeation and blood-borne metastases. Direct extension is
mostly to adjacent mediastinal structures such as the trachea, bronchi, lung parenchyma, aorta and pericardium.
Bronchoesophageal fistulae and occasionally aortoesophageal fistulae may develop. Spread to the fundus of the stomach
is frequently seen in patients with adenocarcinoma of the lower end of the oesophagus. In such cases it may be
impossible to establish whether the adenocarcinoma originated in the oesophagus or fundus of the stomach. Lymphatic
spread is mostly to the peri-oesophageal lymph nodes and nodes in the mediastinum and neck.4, 5 Spread to lymph
nodes below the diaphragm with involvement of the paracardial, gastric lesser curve and coeliac lymph nodes can occur.
Blood-borne metastatic spread is mostly to liver, lung, adrenals, kidneys, pancreas and peritoneum and bones.2

Radiological Diagnosis

The barium swallow remains an extremely efficient initial investigation for suspected oesophageal malignancy. The
examination takes 10-15 minutes to perform, requires no sedation, the patient does not need to be accompanied and
normal activities, such as work, can be resumed afterwards. The only requirement is that the patient should be fasting
for 6 hours. A barium swallow should be performed as a matter of urgency on any patient who presents with dysphagia.
Views of the whole length of the oesophagus, fully distended by the barium suspension, should be obtained and these
should be supplemented by air-contrast views. When an oesophageal stricture is present the upper limit is normally well
shown but the lower limit may be difficult to define. It is important, however, to demonstrate the lower limit and thus
the full extent of the lesion, whenever possible. Double-contrast views are obtained by getting the patient to hold the
nostrils closed while swallowing barium suspension in the upright position. Double-contrast views are best for showing
early oesophageal carcinoma, mucosal abnormalities and small polypoid lesions.

Early oesophageal carcinoma is shown on double-contrast views as a small sessile intraluminal filling defect or a
plaque-like lesion of abnormal mucosa.6 Most patients, however, develop dysphagia when the lumen of the oesophagus
is considerably narrowed by the carcinoma and characteristic appearances are then seen on barium swallow.
Oesophageal carcinomas are frequently shown as an irregular stricture with shouldering of the margins (Figs. 6.1 and
6.2). Others are shown as a polypoid mass (Fig. 6.3) and occasionally an infiltrating neoplasm produces a tapering
stricture (Fig. 6.4). Adenocarcinoma may be indistinguishable from squamous carcinoma involvement of the gastric
fundus makes adenocarcinoma much more likely.

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Staging

Staging of oesophageal carcinoma is necessary to define the extent of spread as many carcinomas are inoperable at the
time of presentation. A chest radiograph is normally taken at the time of diagnosis to establish whether there is evidence
of advanced disease in the mediastinum or chest. Computed tomography (CT) is cur-

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Figure 6.1
Carcinoma of the oesophagus: barium swallow
shows an irregular stricture with mucosal destruction
and well-defined margins in the lower oesophagus.

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Figure 6.2
Carcinoma of the oesophagus: barium swallow
shows an irregular stricture, with some polypoid filling
defects near its lower end, occupying much of the
lower third of the oesophagus.

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rently the most widely used technique for staging oesophageal carcinoma (Fig. 6.5). CT has the ability to demonstrate
the extent of mediastinal involvement and thus help to decide whether or not an attempt at curative surgical resection
may be made. Spread outside the oesophagus is assessed on CT by showing whether there is evidence of spread to
adjacent mediastinal structures as shown by loss of the fat planes between the oesophagus and adjacent structures,
enlargement of lymph nodes (Fig. 6.5) and the presence of hepatic, pulmonary or abdominal metastases. 7 A paucity of
mediastinal fat can make interpretation of the CT examination difficult.8 Normally, there is no fat plane separating the
oesophagus from the trachea or left main bronchus, which can make airway invasion difficult to diagnose. Aortic
invasion may also be difficult to assess as many patients do not have a fat plane separating the oesophagus from the
aortic arch or descending thoracic aorta. There can be difficulty deciding whether there is evidence of spread to lymph
nodes as involved perioesophageal lymph nodes are frequently of normal size, even though they are engulfed by
tumour.8 Despite these limitations, CT remains the most useful technique for staging oesophageal carcinoma. Evidence
of mediastinal invasion, liver metastases and abdominal adenopathy, as demonstrated on CT, predict a shortened
survival time regardless of the type of treatment.9

Endoscopic ultrasound is a new technique using high frequency, high resolution, real-time ultrasound

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Figure 6.3
Carcinoma of the oesophagus: barium swallow
shows a large irregular polypoid mass on the right
side of the cervical oesophagus. (Reproduced from
Phillips and Nolan 1995 89 with permission).

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Figure 6.4
Carcinoma of the oesophagus: barium swallow
shows a tight infiltrating stricture with slightly
irregular margins in the mid oesophagus. The marked
obstruction caused by the stricture makes it difficult
to identify its lower margin.

images obtained from within the oesophagus by an ultrasound probe incorporated into the tip of a fibreoptic
endoscope.10 The depth of oesophageal invasion is shown by identifying the layers of the oesophageal wall that are
involved by tumour (Fig. 6.6). Metastatic involvement of peri-oesophageal lymph nodes can also be identified. Involved
lymph nodes are usually > 10 mm in diameter and are frequently spherical.11 Endoscopic ultrasound can also make it
possible to determine whether the neoplasm has infiltrated adjacent structures.

Other Primary Malignancies

Leiomyosarcomas are rare and may be polypoid or infiltrating or show a combination of these features. They may be
indistinguishable radiologically from carcinoma.

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Pseudosarcomas and carcinosarcomas may represent carcinomas that have undergone metaplasia, giving rise to
sarcomatous elements.12 These neoplasms consist predominantly of malignant-looking spindle cells with a small
localised component of carcinomatous material usually in the margin of the neoplasm or superficially invading the
mass.1 They have a more favourable prognosis than carcinoma when treated surgically. These rare oesophageal
neoplasms are characteristically seen on barium swallow as large polypoid masses.

Secondary Neoplasms

Oesophageal involvement is not unusual in patients in the late stages of other malignancies.13 Secondary neoplastic
involvement of the oesophagus frequently occurs by direct spread from a neoplasm in an adjacent organ such as the
pharynx, thyroid, bronchus or stom-

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Figure 6.5
Carcinoma of the oesophagus: (a) CT shows a
mass (arrow) involving the posterior and lateral
walls of the oesophagus. The anterior wall is
spared. (b) Involvement of a retrocrural lymph node
(arrow) is seen on another section. (Courtesy of
Dr Niall Moore).

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Figure 6.6
Carcinoma of the oesophagus: endosonography
showing the extent of carcinoma in the wall of the
oesophagus (arrow). (Courtesy of Dr James Virjee).

ach. Radiologically, most of these are seen as extrinsic compression or invasion of the oesophageal wall or lumen and
may simulate a primary oesophageal carcinoma. Usually, however, an associated extrinsic mass allows the correct
diagnosis to be identified. Lymph node metastases may develop and the resulting enlarged adjacent lymph nodes may
produce radiological evidence of extrinsic compression with a mass pressing and protruding into the oesophageal
lumen. Bloodborne metastases may be from lung or breast, although metastases from the kidneys, bladder, pancreas and
cervix have been described. 1

Stomach

Carcinoma is by far the most common primary malignant neoplasm of the stomach. Lymphoma, although much less
common, is occasionally seen and may be difficult to differentiate from carcinoma. Other primary malignant neoplasms
that are occasionally encountered include carcinoid tumours and leiomyosarcoma.

Carcinoma

The incidence of carcinoma of the stomach has declined in recent years, although there is an increasing incidence of
carcinoma of the cardia. Previously, carcinoma of the stomach was more common in males but the male: female ratio is
now about 1: 1.14 The incidence of carcinoma of the stomach varies in different geographical locations; this is due to
environmental factors rather than genetic predisposition. A number of conditions predispose to gastric carcinoma and
these include pernicious anaemia, gastric atrophy, adenomatous gastric polyps and partial gastrectomy.

Gastric carcinoma is nearly always adenocarcinoma, although squamous carcinoma and adenosquamous carcinoma are
occasionally encountered. In the great majority of cases gastric carcinoma is at a late stage when the diagnosis is made
and as a result the prognosis is poor with a 5-year survival rate of less than 20%.

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This is because symptoms are absent or are trivial in the early stages. In Japan, where the incidence of gastric carcinoma
is high, screening programmes using endoscopy or barium studies enable gastric carcinoma to be diagnosed at an early
stage. This has led to the concept of `early gastric cancer' with a more favourable prognosis and a 5-year survival rate of
over 90%. Early gastric cancer is defined as being localised to the mucosa or submucosa regardless of the presence or
absence of lymph node involvement and may be seen as a depressed, protuberant or flat lesion. 15 Because of the low
incidence of carcinoma of the stomach in Western countries screening programmes are not justified. Gastric cancer
detected at an early stage in the West similar to the Japanese early gastric cancer has a prognosis of nearly 70% 5-year
survival.16, 17

Presenting symptoms of gastric carcinoma include anorexia, weight loss, anaemia and epigastric pain. Symptoms are
frequently late developing and are often vague. As a result most carcinomas are diagnosed when they have reached an
advanced stage.

Gastric carcinoma spreads by direct extension, lymphatic permeation and blood-borne metastases. Direct spread from
the gastric wall occurs early and extends to involve adjacent structures. Transperitoneal dissemination is common once
the neoplasm has broken through the gastric serosa. Peritoneal metastases can spread to other organs such as the ovaries
giving rise to a Krukenburg tumour. Direct extension across the gastroesophageal junction is common with carcinoma
of the cardia and these neoplasms may present with dysphagia. In the past, extension across the pylorus to the
duodenum was considered unusual but in a recent study transpyloric spread occurred in 25% of adenocarcinomas of the
gastric antrum.18

Spread to lymph nodes is common. The most frequently involved are the perigastric lesser curve nodes followed by
greater curve nodes, and the coeliac and porta hepatis groups. Spread to supradiaphragmatic lymph nodes, including the
supraclavicular and mediastinal groups, is well recognised. Lymphangitis carcinomatosis may develop secondary to
mediastinal lymph node involvement. Metastatic spread to the liver is common but may also occur to the lungs, skin,
ovaries, adrenals and bone.

Radiological Diagnosis

Gastric carcinoma is well demonstrated on barium studies. Most carcinomas are seen as a nodular or polypoid
intraluminal mass (Fig. 6.7). The lesions have an irregular surface and the margins are usually well-defined.

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Figure 6.7
Carcinoma of the stomach: barium examination
shows a large irregular polypoid mass occupying the
upper half of the stomach.

An ulcer crater is the predominant feature of ulcerating carcinomas. Malignant ulcers tend to be greater in width than
depth, often with nodularity of the floor and the edge of the ulcer may show a nodular appearance. Radiating mucosal
folds may be tapered, clubbed, fused or terminate abruptly. Gastric ulcers should preferably be biopsied endoscopically
to firmly establish whether the lesion is benign or malignant. The linitis plastica appearance is seen in scirrhous
carcinoma when there is extensive submucosal infiltration by the neoplasm. On barium examination the gastric lumen is
markedly narrowed with nodularity and distortion of the mucosal fold pattern. The limited ability of the stomach to
distend is confirmed by using large quantities of an effervescent agent (Fig. 6.8). Endoscopic biopsies are frequently
negative in patients with linitis plastica. and as a result the diagnosis may be missed at endoscopy. If there is any
suspicion of linitis plastica at endoscopy further evaluation by barium examination or CT is indicated.

On CT polypoid carcinoma is seen as a mass protruding into the lumen of the stomach. Ulcerating carcinoma can be
difficult to detect on CT if there is not much thickening of the gastric wall. Linitis plastica shows marked gastric wall
thickening on CT (Fig. 6.9).

Staging

A number of imaging modalities may be used to stage gastric carcinoma and assess whether the neoplasm is resectable.
A chest radiograph is useful for detecting the presence of pulmonary or mediastinal lymph node spread or the presence
of lymphangitis carcinomatosis.

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Figure 6.8
Carcinoma of the stomach: the typical features of
linitis plastica are shown on a barium study in this
patient with an infiltrating carcinoma. There is only
slight mucosal irregularity. During the examination
the stomach failed to distend.

Ultrasound is widely used to detect hepatic metastases. Ultrasound may also show subdiaphragmatic lymph node
enlargement and demonstrate ascites. The characteristic ultrasound appearances of gastric carcinoma have been
described. 19, 20 Although ultrasound is not frequently used for staging gastric carcinoma it is

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Figure 6.9
Carcinoma of the stomach: CT, with oral contrast
medium, shows marked irregular thickening of the wall
of the stomach. Small volume lymph node metastases
and `mucky' peritoneal fat is seen between the
stomach and aorta. (Courtesy of Dr Fergus Gleeson).

important for those performing abdominal ultrasound to recognise gastric wall thickening or a mass lesion so that
further investigation can be directed towards the stomach in patients referred for ultrasound with nonspecific upper
abdominal symptoms due to underlying gastric carcinoma.

At the present time CT is the technique of choice for staging carcinoma of the stomach. CT is able to demonstrate
gastric wall thickening, extension into adjacent viscera, nodal involvement, hepatic and adrenal metastases and
ascites.21, 22 It has been shown that the CT findings correlate well with the surgical and pathological findings and the
high accuracy rate of CT can help to avoid unnecessary laparotomy in many patients.22

Other Primary Neoplasms

The stomach is the most frequent site of gastrointestinal lymphoma and accounts for 2-5% of all gastric malignancy.23,
24 The great majority of gastrointestinal tract lymphomas are non-Hodgkins in type. Symptoms are similar to those of
gastric carcinoma.

The antrum and body of the stomach are the most frequent sites of involvement. Lymphoma tends to occur in a
submucosal or intramucosal location and gives rise to diffuse thickening of the gastric wall with a lobulated surface and
thickening of the mucosal folds. The surfaces of these thickened mucosal folds are relatively smooth in contrast to the
irregularity seen in widespread carcinoma. The volume of the stomach is preserved, unlike in carcinoma and the
lymphomatous stomach retains its distensibility.25 Gastric lymphoma may manifest itself as ulceration and these ulcers
may be large and can be multiple and may be associated with a mass lesion. Single or multiple polypoid lesions are
occasionally seen, usually on a background of thickened mucosal folds. Lymphoma may infiltrate across the
gastro-oesophageal junction. Spread of lymphoma across the pylorus into the duodenum is fairly common in patients
with antral involvement and was seen in 50% of the patients reviewed by Cho and colleagues.18

Primary carcinoid tumours of the stomach are recognised but are rare. They are usually seen as a small intramural lesion
protruding into the lumen and are usually about 2cm in diameter with ulceration in about 40%.26 Rarely gastric
carcinoids may be seen as multiple small sessile polyps occurring throughout the stomach or in clusters.27
Radiologically they are similar to multiple polyposis and as biopsy is superficial polypectomy is necessary to achieve a
definitive diagnosis. Rarely carcinoid tumours are seen as large polypoid masses or large

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malignant ulcers radiologically indistinguishable from primary carcinoma. 26 The primary neoplasm and secondary
deposits grow slowly and long survival may be achieved by surgical resection of the primary lesion and the metastases.

Secondary Neoplasms

The stomach may be involved by direct spread from carcinomas in adjacent structures such as oesophagus, pancreas,
transverse colon, left kidney and left adrenal. Spread of adenocarcinoma from the lower oesophagus is not uncommon,
although it is unusual for squamous oesophageal carcinoma to spread to the stomach. Carcinoma of the transverse colon
can spread along the greater omentum to the stomach.

The most common blood-borne metastases to the stomach are from malignant melanoma and carcinoma of the breast.
Metastatic melanoma is characteristically seen in the submucosa and produces an intraluminal polypoid mass which
frequently shows central ulceration, giving it the characteristic `bull's eye' appearance.28 The most frequent
manifestation of metastatic breast carcinoma is diffuse infiltration producing a linitis plastica-type appearance (Fig.
6.10).29 The gastric mucosa usually remains intact, although it may develop a serrated or nodular configuration.
Metastases from other organs have been described.30

Duodenum

Primary malignant neoplasms of the duodenum are uncommon. Carcinoma is the most frequently encountered

Figure 6.10
Secondary carcinoma of the stomach: marked
narrowing and irregularity of the gastric antrum is
seen, resulting from infiltration by metastatic breast
carcinoma.

and accounts for 80-90% of primary duodenal malignancies.31 Leiomyosarcoma32 and lymphoma are seen much less
frequently. Other neoplasms that rarely involve the duodenum include carcinoid tumour, Kaposi's sarcoma, malignant
schwannoma, lymphangiosarcoma and plasmocytoma.33 Secondary neoplastic involvement of the duodenum occurs as
a result of direct spread from an adjacent organ or as metastases.

Primary Neoplasms

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About half of all small intestinal carcinomas arise in the duodenum while most of the remainder develop in the
jejunum.34 Carcinoma of the duodenum can be classified into carcinoma of the papilla of Vater and true carcinoma of
the duodenum.35 Patients with carcinoma of the ampulla of Vater usually present with obstructive jaundice. Carcinoma
of the ampulla is shown on barium studies as irregular enlargement of the papilla, sometimes with spiculation and
ulceration.36

Non-papillary duodenal carcinoma mostly presents clinically with symptoms of duodenal obstruction, mostly abdominal
pain, nausea and vomiting. Other presenting symptoms are varied and can mimic peptic ulceration, hiatus hernia and
pancreatic or biliary disease.37 Barium examination shows the carcinoma as an annular lesion with shouldered margins
(Fig. 6.11), as a polypoid mass or as an ulcerative lesion. The appearances are similar to carcinomas elsewhere in the
gastrointestinal tract. CT shows duodenal carcinoma as asymmetrical thickening of the duodenal wall or as a

Figure 6.11
Carcinoma of the duodenum: an irregular polypoid
stricture with mucosal destruction is shown on a
barium study obstructing the third part of the
duodenum.

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polypoid mass. 33 It may be difficult to differentiate duodenal carcinoma from pancreatic carcinoma invading the
duodenum.33

Leiomyosarcomas are very uncommon, but may develop in the duodenum. Clinical presenting symptoms include
gastrointestinal bleeding, abdominal pain, obstructive jaundice or a palpable mass.38 Leiomyosarcomas are usually
large and are mostly shown on barium studies as a large cavitating mass with much of the tumour extending
extraluminally. There is frequently compression of adjacent organs but leiomyosarcomas do not usually invade them.33
CT shows leiomyosarcoma as a large lobulated cavitating mass with inhomogeneous attenuation and varying contrast
enhancement, often with hypervascular liver metastases.39 Characteristically no evidence of lymphadenopathy is seen.

Primary duodenal lymphoma is rare. Most lymphomas involve the duodenum either from transpyloric spread of gastric
lymphoma or secondary encasement by paraduodenal lymph nodes.33 Primary duodenal lymphoma may be an
infiltrative lesion of the duodenal wall or as a cavitating mass indistinguishable from leiomyosarcoma.

Secondary Neoplasms

The duodenum may be invaded by malignant neoplasms from adjacent organs or it may be the site of blood-borne
metastatic deposits.

The most common neoplasms to invade the duodenum are gastric carcinoma and gastric lymphoma extending across the
pylorus. In a recent series transpyloric spread occurred in 40% of lymphomas and 25% of adenocarcinomas of the
gastric antrum, demonstrating contour deformities and nodular filling defects in the duodenum.18

Carcinoma of the head of the pancreas may cause a double contour, irregularity of the inner border (Fig. 6.12) and
sometimes stricturing of the second part of the duodenum. The reversed `3' sign of Frostberg is a well recognised but
infrequent finding.40 It is not unusual for carcinoma of the body of the pancreas to invade the fourth part of the
duodenum (Fig. 6.13) resulting in obstruction or bleeding.

Other carcinomas that may invade the duodenum include carcinoma of the colon, kidney, gallbladder or common bile
duct. Colon carcinoma, particularly lesions in the hepatic flexure may distort and invade the duodenal loop (Fig.
6.14).41 Occasionally carcinoma of

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Figure 6.12
Carcinoma of the pancreas involving the duodenum:
barium examination shows narrowing of the lumen and
distortion of the mucosal folds of the mid second part
of the duodenum. A double contour is seen on the
medial aspect at the junction of the second and third
part of the duodenum (arrow). A spiculated
appearance is seen on the inner border of the
duodenum and this most marked in the third part of
the duodenum.

the left kidney spreads through the lymphatics to the fourth part of the duodenum.33

Barium studies are excellent for showing the luminal changes in the duodenum caused by neoplasms invading from
adjacent organs. CT is ideal for demonstrating the full extent of the primary neoplasm.

Blood-borne metastases to the duodenum are uncommon. Metastatic melanoma is the one that most frequently
metastasises to the duodenum. Other primary carcinomas that metastasise to the duodenum include colon, kidney, lung,
uterus, breast and testis (Fig. 6.15). The radiological appearances of metastases to the duodenum are similar to those
seen in the jejunum and ileum and will be described in the following section.

Small Intestine

Malignant neoplasms are uncommon in the small intestine and account for less than 2% of all primary

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Figure 6.13
Carcinoma of the pancreas involving the duodenum:
a barium study shows complete obstruction to the
fourth part of the duodenum (arrow). Carcinoma of the
body of the pancreas was subsequently confirmed.

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Figure 6.14
Carcinoma of the colon involving the duodenum:
barium examination shows a fairly tight stricture of
the second part of the duodenum is seen (arrow)
resulting from invasion of the duodenum by
carcinoma of the colon.

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Figure 6.15
Duodenal metastasis: CT shows a large irregular
duodenal mass (arrow). This proved to be metastatic
teratoma of the testis. Note the metastatic deposits in
the liver. (Courtesy of Dr Fergus Gleeson).

malignancies of the gastrointestinal tract. 42,43,44,45 The diagnosis of small intestinal neoplasms is difficult. Most
patients present with insidious symptoms and vague, mild non-specific complaints that are often overlooked and easily
dismissed.45 In the series of 153 cases reviewed by Hancock46 more than half were initially considered to be neurotic.
Delay in diagnosis is due to a combination of factors; patients are reluctant to seek early medical attention because of
the mild symptoms, physicians frequently do not recognise the importance of the presenting symptoms, resulting in a
delay requesting the relevant imaging investigations. Further delay in diagnosis is often because of inadequate or
incorrect interpretation of radiological examinations.

Radiological Investigation

The small intestine is the longest and most inaccessible part of the gastrointestinal tract. As yet endoscopy is not a
practical procedure for routinely examinating the small intestine and the barium examination remains the method of
choice for demonstrating changes in the lumen of the jejunum and ileum.

Each barium examination is a challenge to the radiologist. This is because of the length of the intestine and difficulty
manipulating the barium suspension so that all segments are clearly visualised.47 A number of barium techniques are
available and are based on the small intestinal follow-through, using orally administered barium or enteroclysis (small
bowel enema). The barium follow-through is the most widely used technique,

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although enteroclysis is being introduced in an increasing number of centres

During enteroclysis the barium suspension is introduced directly into the small intestine through a tube. 48, 49
Enteroclysis is superior to the follow-through because the intestine is well distended by the barium suspension,
providing optimum visualisation of the jejunum and ileum. There is sometimes a reluctance to perform enteroclysis
because it is necessary to intubate the duodenum. Duodenal intubation can be performed easily, quickly and with only
minor patient discomfort, using one of the newer 10 French tubes.50 The enteroclysis technique is easy to learn and the
radiologist and quickly become more skilled using this examination than the time-consuming repeated fluoroscopy
required for the barium follow-through.51

The available evidence indicates that enteroclysis is superior to the barium follow-through for detecting and
demonstrating morphological abnormalities in the intestine.52 Keats and Sakai53 reported 84 cases of primary small
intestinal neoplasms and found that on the barium follow-through neoplasms were reported in 50%, another 9% were
described as abnormal and in the remaining 41% the report was negative. A retrospective study of 71 patients with
histologically proven primary malignant neoplasms were reported by Bessette and colleagues.54 Fourteen had been
examined by the follow-through, 16 by enteroclysis and 4 by both techniques. Eleven of the 18 follow-throughs were
abnormal and the actual neoplasm was shown in 6 of the 18. Nineteen of the 20 enteroclysis examinations were
abnormal and the neoplasm was shown in 18 out of 20. My own experience would indicate that enteroclysis provides
excellent visualisation of carcinomas,55 lymphoma,56 carcinoid tumours57 and secondary neoplasms.58

CT plays an important role in the evaluation of neoplastic disorders of the small intestine. Unsuspected disorders may
be seen at CT and localised to the small intestine in patients referred for unusual or nonspecific abdominal
complaints.59 Mural and extraluminal components of neoplasms can be evaluated by CT, including changes in the
lymph nodes, mesenteric surfaces and peritoneal reflections.59, 60

Ultrasound has a limited role in evaluating intestinal neoplasms. Like CT unsuspected abnormalities may be detected by
ultrasound and require further evaluation by other imaging modalities. Intestinal neoplasms may be diagnosed using a
dedicated ultrasound technique.61, 62

Angiography is frequently used in the investigation of obscure gastrointestinal bleeding and may occasionally detect a
malignant neoplasm as the cause of the bleeding. Otherwise angiography has a very limited role in the evaluation of
small intestinal malignancy. Different neoplasms show specific features at angiography.63

Nuclear medicine imaging does not have a significant role in small intestinal malignancy although the development of
tumour specific imaging agents may, in the future, lead to an increasing use of nuclear medicine studies in the
diagnosis, management and therapy of functioning small intestinal neoplasms.64

Primary Neoplasms

The most frequently encountered primary malignant small intestinal neoplasms are adenocarcinoma, lymphoma,
carcinoid tumours and leiomyosarcoma

Carcinoma

Adenocarcinoma of the small intestine is uncommon and represents approximately 0.6% of all primary gastrointestinal
malignancies.65 Despite its rarity and even when lesions in the duodenum are excluded, adenocarcinoma is probably
the most common primary neoplasm of the small intestine, with a peak incidence in the 6th and 7th decades.66
Adenocarcinomas are mostly located in the duodenum and proximal jejunum. Most patients present with abdominal
pain, which can be vague, intestinal obstruction or chronic blood loss. The prognosis for adenocarcinoma is poor with a
five-year survival of 15-28%.67, 68

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Barium studies are more reliable than CT or ultrasound for detecting primary adenocarcinoma69 and enteroclysis is
excellent for demonstrating the neoplasm.55 Adenocarcinomas are mostly located in the jejunum, particularly the
proximal jejunum. The appearances on enteroclysis are similar to those of adenocarcinoma elsewhere in the
gastrointestinal tract. Most are infiltrating and are shown as short, well-demarcated, symmetrical, constricting lesions
with mucosal destruction and shouldered margins (Fig. 6.16). There is frequently a degree of intestinal obstruction and
pre-stenotic dilatation may be present. Polypoid adenocarcinomas are less common and are shown as an irregular filling
defect or an irregular polypoid mass with mucosal destruction. Ulceration is seen in most adenocarcinomas, particularly
in infiltrating lesions. The ulcers are usually small, although occasionally adenocarcinoma presents as a large cavitating
mass.

Lymphoma

Lymphoma is one of the more common neoplasms encountered in the small intestine. The majority are

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Figure 6.16
Carcinoma of the jejunum: an irregular stricture with
mucosal destruction and shouldered margins is shown
at an enteroclysis examination.

non-Hodgkins lymphoma. Lymphoma arises in the small intestine either as a primary neoplasm, arising focally from
lymphoid tissue 70 or as part of a more widespread disease process.71 Intestinal lymphoma is considered to be primary
if the predominant lesion is in the intestine, the initial presenting symptoms are related to intestinal involvement and
there is no evidence of a generalised or intestinal predisposing factor.56 Disorders that predispose to lymphoma are
coeliac disease, chronic lymphatic leukaemia, previous extra-intestinal lymphoma, immunoproliferative small intestinal
(α chain) disease and immunological dysfunction, including acquired immunodeficiency syndrome (AIDS).66 Most
primary intestinal lymphomas are in the ileum, where lymphoid follicles are most numerous, with the jejunum the site
of involvement in a small percentage of cases.

Abdominal pain, diarrhoea, weight loss and blood loss are the most frequent presenting symptoms. Patients occasionally
present acutely with perforation. Intestinal lymphoma has a poor prognosis with an overall 5-year survival of 36%.56, 72

A broad spectrum of radiological signs is demonstrated by enteroclysis. Characteristic features include luminal
narrowing with stricturing, broad-based ulceration, cavitation, thickening of the valvulae conniventes, discrete
intraluminal filling defects and an extraluminal mass.56, 66 A large cavitating mass is highly characteristic (Fig. 6.17),
although similar lesions may be seen in leiomyosarcoma and metastases. Rarely, the characteristic `aneurysmal'
dilatation may be seen. The lesions are multifocal in up to 40% of patients.56 Occasionally, small lesions or polyps may
be distributed throughout the intestine.

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A variety of appearances are exhibited by CT in patients with intestinal lymphoma. These include bulky masses with
central cavitation, nodules, aneurysmal dilatation and irregular fold thickening.59 Lesions in the intestinal wall are
relatively homogeneous and there is less contrast enhancement in lymphoma than that seen in leiomyosarcoma or
epithelial neoplasms. Evidence of mesenteric lymph node enlargement may be seen and the characteristic `sandwich'
appearance may be seen when the enlarged lymph nodes surround the mesenteric vessels.73

Carcinoid

Carcinoid tumours are mostly located in the ileum, particularly in the terminal ileum and are multifocal in about
one-third of cases. Small intestinal carcinoids are

Figure 6.17
Lymphoma of the small intestine: a large cavitating
mass (arrow) is seen in the ileum in an elderly patient
who presented with an episode of acute
gastrointestinal bleeding.

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considered to be of low grade malignancy with a likelihood to metastasise. The primary lesion may be small and
frequently patients present with the carcinoid syndrome in which the characteristic cutaneous flushing and diarrhoea are
the dominant symptoms, occurring in the presence of extensive hepatic metastases. The primary tumour, although
usually small, may cause abdominal pain which may be non-specific or colicky, characteristic of intestinal obstruction
that may be due to recurrent intussusception. A large mass resulting from local invasion and fibrosis may be palpable at
the time of presentation. The prognosis is related to tumour size and resectability and prolonged survival is not
uncommon with a 5-year survival rate of up to 75% for localised or operable cases.

The radiological signs shown on enteroclysis may be those of the primary lesion itself, those of a secondary mesenteric
mass, or those developing from interference with the ileal blood supply. 57, 66 Primary ileal carcinoids are seen as
sharply defined intramural or intraluminal filling defects with regular margins in the ileum, particularly the distal ileum
(Fig. 6.18). Multiple lesions may be present.74 Narrowing of the lumen with stricture formation is sometimes seen.
Hypertrophy of muscle tissue occurs as a result of tumour infiltration with radiologically evident thickening of the
valvulae conniventes. In patients with extensive mesenteric fibrosis adjacent loops of ileum are separated, and
compressed, making it impossible to identify the primary tumour.

Figure 6.18
Small intestinal
carcinoid tumour:
enteroclysis shows
a well-defined
intraluminalfilling
defect (arrow) in the
ileum in a patient
who was shown to
have multiple ileal
carcinoids.

Sharp angulation or kinking of one or more intestinal loops may be seen.

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CT shows the intestine, mesentery, lymph nodes and liver in a single investigation and is ideal for staging carcinoid
tumours. In patients with extensive mesenteric fibrosis CT demonstrates displacement, kinking or angulation of adjacent
loops and the characteristic stellate radiation of mesenteric neurovascular bundles (Fig. 6.19).75

Leiomyosarcoma

Leiomyosarcoma is encountered less frequently than adenocarcinoma, lymphoma and carcinoid tumour. Most
leiomyosarcomas attain a large size and much of the mass grows extraluminally. Acute bleeding is a common clinical
presentation, although occasionally patients present with perforation. Leiomyosarcoma is seen radiologically as a
cavitating mass outlined with barium. On CT the rim of the neoplasm around the cavity enhances markedly following
intravenous contrast medium.76

Kaposi's Sarcoma

Kaposi's sarcoma may be seen in the small intestine in association with AIDS and in many cases is asymptomatic. The
radiological appearances cover a wide spectrum, including thickened valvulae conniventes, mural thickening,
submucosal nodularity, polypoid filling defects and plaque-like lesions.66

Other Primary Malignant Neoplasms

A variety of other extremely rare malignant neoplasms have been reported in the small intestine. They include

Figure 6.19
Carcinoid tumour of the small intestine: CT shows
a mass (arrow) with the characteristic stellate radiation
of mesenteric neourvascular bundles and thickening
of the walls of the adjacent ileum.

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angiosarcomas, fibrosarcomas, liposarcomas, malignant schwannomas, lymphangiosarcomas and malignant

mesotheliomas 66 The clinical features and radiological appearances do not differ significantly from those of other
small intestinal malignancies.

Secondary Neoplasms

Malignant neoplasms can spread to the small intestine by direct invasion from adjacent structures, by lymphatic
extension, by intraperitoneal seeding and by embolic blood-borne metastases.28, 30, 77 In some patients more than one
mechanism of spread occurs; a combination of direct spread and intraperitoneal seeding is the combination most often
seen.78

Direct Extension

Direct invasion of the small intestine from carcinomas of the colon, ovary, uterus and kidney may occur and this
indicates that an aggressive malignant neoplasm has broken through fascial planes.28 Intestinal obstruction is the most
frequent indication that there is invasion of the small intestine by recurrent colon carcinoma (Fig. 6.20) or
gynaecological malignancy, particularly ovarian carcinoma.79 It is important to distinguish secondary involvement by
gynaecological malignancy from chronic radiation enteritis. Chronic radiation enteritis has characteristic appearances,
including thickening of the valvulae conniventes, stenosis, mural thickening, mucosal tacking, effacement of the
mucosal pattern and adhesions.80 On CT characteristic appearances of peritoneal metastases are seen and these include
omental caking, infiltration of mesenteric lesions and soft tissue attenuation along loops of intestine.59, 81, 82

Lymphatic Spread

Lymphatic extension plays a minor role in the spread of neoplasm to the small intestine. A characteristic example is
spread of caecal carcinoma to the terminal ileum with resulting stricture formation.83,84 The first manifestation of
caecal carcinoma may be when the patient presents with intestinal obstruction. from ileal stenosis (Fig. 6.21).
Narrowing of the lumen with effacement of the mucosal pattern is the characteristic appearances seen at enteroclysis
(Fig. 6.21).79

Intraperitoneal Seeding

Intraperitoneal seeding of abdominal neoplasms to the small intestine occurs as a result of spread via ascitic fluid.
Primary neoplasms and even intraperitoneal lymph nodes metastases can shed malignant cells into the ascitic fluid when
they break through the peritoneal

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Figure 6.20
Small intestinal invasion by colonic carcinoma:
enteroclysis shows a constricting lesion with mucosal
destruction, an irregular ulcerating lumen and a degree
of shouldering of the margins in the proximal jejunum.
At operation this proved to be direct invasion from
recurrent carcinoma of the colon. (Reproduced from
Nolan 199779 with permission).

cavity, although it is not necessary to have much ascites for the transport and deposit of maligant cells.77 In the
peritoneal cavity ascitic fluid flows preferentially along the small intestinal mesentery towards the right lower quadrant.
Forty per cent of intraperitoneal seeding is localised in the right lower quadrant and at the lower end of the small
intestinal mesentery.85

Radiological examination shows characteristic changes in the terminal ileum. These include separation of adjacent
loops, often with parallel configuration, multiple scalloped deflections, sometimes with gross mass deflections and
distorted, tethered mucosal folds on the mesenteric border. Angulation, fixation and separation of distal ileal loops can
occur, particularly in gastric, colonic, pancreatic and ovarian carcinoma.85

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Figure 6.21
Secondary involvement of ileum from carcinoma of
the caecum: on enteroclysis a stricture with mucosal
destruction and shouldered margins is seen at the
terminal ileum. At operation this proved to be a caecal
carcinoma that had spread via the lymphatics to the
terminal ileum.

Embolic Metastases

The small intestine is an uncommon site for embolic blood-borne metastases from primary neoplasms at other sites. 28,
30 Embolic metastases are frequently multiple and tend to be submucosal. Gastrointestinal bleeding is a common
presentation from the central ulceration that develops as the metastases outgrow their blood supply. Other clinical
presentations include obstruction, often due to intussusception, and occasionally perforation. Melanoma is one of the
most common neoplasms to metastasise to the small intestine.

On barium studies melanoma metastases are mostly seen as multiple filling defects with central ulcers or

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Figure 6.22
Metastatic melanoma of the small intestine: on
enteroclysis a cavitating mass is demonstrated in the
ileum (arrow). The patient, a middle-aged female who
had previously had a malignant melanoma resected,
presented with acute gastrointestinal bleeding.

cavities outlined with barium. They may be solitary and be seen as a large cavitating mass on barium examination86
(Fig. 6.22) or CT (Fig. 6.23).

Breast carcinoma occasionally spreads to the small intestine. Metastatic breast carcinoma is mostly seen as an
infiltrating lesion that results in stricture formation and obstruction.28, 87 There may be long segment of intestinal
narrowing (Fig. 6.24) similar to the infiltrating linitis plastica appearance of breast carcinoma metastatic to the
stomach.79

Figure 6.23
Metastatic melanoma of the small intestine: a large
cavitating mass is shown on the left side of the
abdomen on CT. (Coutesy of Dr Fergus Gleeson)

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Figure 6.24
Metastatic breast carcinoma: a long segment of
narrowing is seen in a segment of ileum with
effacement of the mucosa on the upper border of the
narrowed segment. (Reproduced from Nolan 199779
with permission).

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Carcinoma of the lung and kidney metastasise on rare occasions to the small intestine. Metastatic lung carcinoma may
present as perforation, bleeding or obstruction and is shown radiologically as a large mesenteric mass with infiltration of
the intestinal wall. 28 Metastatic renal carcinoma is usually seen as a solitary, bulky intramural mass.28, 88

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7
The Colon and Rectum

Clive I Bartram

Colorectal cancer

Carcinoid tumours

Lymphoma

Kaposi sarcoma

Leiomyosarcoma

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Malignant tumours of the colorectum may be considered as being of epithelial origin or from some other component of the
bowel wall, but those of epithelial origin are by far the most important. Colorectal cancer (CRC) is now the second commonest
cancer in England and Wales, with about 28 000 new cases and 19 000 related deaths annually. Some 20% present with
metastases and the 5-year survival rate of 40% has remained unchanged for some years.

In the non-colitic population, CRC arises from changes in adenomatous tissue described as the adenoma-cancer sequence. An
adenoma is a circumscribed elevation of intraepithelial neoplasia. Dysplasia within adenomas may be graded as mild, moderate
or severe. Severe dysplasia is more frequent in large or villous type adenomas. Penetration of dysplastic cells into the
submucosa defines cancer.

The level of lymphatic supply to the mucous membrane of the gastrointestinal tract varies. Dysplastic cells must be able to
enter the lymphatic circulation for the tumour to behave as a cancer. There is no lymphatic tissue in the mucosa of the colon
and rectum, only relatively few lymphatics in the muscularis mucosa, but a rich plexus in the submucosa. As a result lymphatic
spread occurs in colorectal tumours only when dysplastic cells have crossed the muscularis mucosa layer into the submucosa.
This is the basis for the definition of CRC and why `carcinoma in situ' is not recommended as a term to describe severe
dysplasia that does not penetrate beyond the muscularis mucosa.

The meticulous analysis of resected rectal cancer specimens by Dukes demonstrated a clear relationship between the extent of
tumour invasion of the rectal wall, lymph node involvement and survival. The Dukes classification (Table 7.1) has been widely
modified, but remains the basis for staging CRC. Tumour permeation into the submucosal veins seems to have little effect on
prognosis, but once the extramural thick-walled veins become affected, there is a significant reduction in survival due to
metastatic disease, which is independent of the Dukes stage. Metastases may involve the liver (75%), lungs (15%), bones (5%)
and brain (5%). Tumour penetration of the visceral peritoneum results in transcoelomic spread. Malignant cells may be
implanted at anastomotic, abdominal wall incision or colostomy sites, but locoregional recurrence implies continued growth of
residual malignant tissue from inadequate resection.

Imaging has several roles in CRC: diagnosis of the precursor of CRC, the adenomatous polyp, and of overt cancer and staging
of that cancer. Interventional imaging-based techniques may play an increasing role in the management of advanced cancer.
Treated patients require follow-up and first-degree relatives should be investigated to exclude polyps.

Colorectal Cancer

Diagnosis

Although the number of barium enemas is falling due to increasing primary referral to colonoscopy, the barium enema and in
particular the double contrast barium enema (DCBE) remains an important method for polyp and cancer detection. Compared
to colonoscopy, the DCBE is cheaper and considerably safer with a mortality of < 1 in 50 000 1 and should always demonstrate
the proximal colon. Total colonoscopy is difficult in about 25% where diverticular disease is present or in females with long
transverse colons.2 Colonoscopic localization of tumours is difficult. This rarely causes problems with standard surgical
resection, but if laparoscopic resection is planned, DCBE is useful to confirm the site of the tumour, as resection of a tumour in
the transverse colon is not feasible technically.

Size, shape, surface texture and number should be used to define polyps (Fig. 7.1). The risk of cancer is negligi-

Table 7.1 Dukes staging for colorectal cancer.

Stage Description 5-year survival (rectal: colonic)
A Muscularis propria not breached 80: 85%
B Muscularis propria breached but no nodal involvement 55: 67%
C Regional nodes involved 32: 37%
NB This staging is based on histological examination of the resected specimen. Stage C has been divided into C1
where the apical node is not involved and C2 where it is. Stage D may be used to indicate the presence of distant
metastases, but was not part of the original description by Dukes.

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Figure 7.1
Two sessile polyps on a DCBE. One shows a
meniscus around the base of the polyp only
(arrowhead), the other a meniscus around the base
and a coating over the surface to form the classical
''hat sign".

ble (< 1%) in polyps < 1 cm in diameter, increasing to > 20% for polyps of > 2 cm. Most series relating the incidence of
cancer to polyp size are based on endoscopic measurement. There is considerable magnification during DCBE, so that a
polyp measuring 1 cm may be only 7 mm endoscopically. A radiological size of < 1 cm is therefore conservative.
Polyps that are pedunculated are often considered benign, but this is a misconception. The incidence of cancer in the
head of the polyp is similar to that for a sessile lesion. However, even if the head of the polyp is malignant, the risk of
spread into the bowel wall is negligible providing the stalk is intact. Once this is invaded, the lesion reverts to a sessile
appearance.

The natural history of adenomas remains unclear, but recent work suggests that small polyps (< 1 cm) frequently
undergo spontaneous regression. 3 Larger polyps may have mutated oncogenes that make further growth with malignant
transformation more likely.

Cancers are typically either polypoid or annular, depending on invasive growth within the bowel wall. Flat, plaque-like
lesions represent an early stage of annular growth and are the most difficult to image on DCBE (Fig. 7.2). The detection
rate for CRC by DCBE is 85-9%.4 Perceptive error is the commonest reason for missing a lesion and highlights the
value of double reading examinations.5

Flexible sigmoidoscopy followed by DCBE detects all significant colorectal neoplasia6 and may be used in

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Figure 7.2
Carcinoma adjacent to the ileo-caecal valve,
presenting as a irregular mass (arrowheads).

cancer screening where flexible sigmoidoscopy is negative to exclude proximal disease (Fig. 7.3).

Cancers may be picked up on routine transabdominal US. Filling the colon with water has been used to improve
detection and staging.7 In elderly, infirm patients, where bowel preparation would be difficult, an unprepared CT is a
useful alternative to DCBE or colonoscopy.8 Helical CT and fast MR sequences enable large volumes of data to be
acquired in a single breath hold, and has increased the utility of these techniques for examining the bowel. However, the
data sets obtained are too large to review in a standard fashion. Advances in computer processing and 3D software
developments have allowed volume rendering and cine

Figure 7.3
Algorithm for CRC detection based on initial flexible
sigmoidoscopy6

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loop techniques to be applied. CT colography can resolve 70% of polyps of 5 mm in diameter. 9 IV contrast
enhancement highlights any neoplastic lesion as both adenomas and cancers are highly vascular, which helps define the
tumour. Although 3D reconstructions are currently time consuming, this technology holds great promise and may soon
find a place in routine investigation.

If a distal cancer has been diagnosed, total colonic examination is still indicated to exclude further neoplasia that may be
impalpable at operation. Synchronous lesions are present in 4-5%. Colonoscopy may be difficult as the tumour inhibits
manipulation of the endoscope. Bowel preparation is often poor, so that visualization of the proximal colon is not ideal.
The same restriction also applies to a DCBE, but a complete examination should usually be possible and sufficient to
exclude a further carcinoma or large polyp.11

Staging

Dukes classification is a pathological one. For cross-sectional imaging, the TNM system12 is more relevant (Table 7.2).

Figure 7.4
Normal rectal wall on endosonography. The
submucosa is a prominent central reflective layer
(small arrowhead). Outside this is the muscularis
propria, divided into two layers by a thin reflective
fascia. Inside the submucosa is the low reflective
layer of the deep mucosa and then the first interface
reflection with the surface of the mucosa. A small
benign lymph node (large arrowhead) is noted.

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Table 7.2 TNMM Classification of CRC.12

Description
T Stage
T1 Tumour invades submucosa
T2 Tumour invades muscularis propria
T3 Tumour invades through muscularis propria into subserosa or
non-peritonealized pericolonic or perirectal tissues
T4 Visceral peritoneum or adjacent structure invaded
N Stage
N0 No regional node metastasis
N1 1-3 pericolic or perirectal nodes involved
N2 > 3 pericolic or perirectal nodes involved
N3 Involved nodes along any named vascular trunk
M Stage
M0 No distant metastasis
M1 Distant metastases

The Primary Tumour (T Staging)

`T' staging describes how far the tumour has penetrated the bowel wall and related structures. CT and MRI are limited
to showing if a lesion is intramural (i.e. T1 or T2) or extramural (i.e. T3 or T4). The only modality capable of defining
the various wall layers is endosonography and this is the most accurate method for staging rectal cancers.

The normal rectal wall has a five-layer sonographic pattern (Fig. 7.4), which is made up of interface reflections as well
as reflections from actual tissue layers. Interface reflections occur at junctions between tissue layers of different acoustic
impedance. The thickness of the reflection depends on the axial resolution of the transducer. The five layers are as
follows:

1. The first inner layer is a narrow bright interface between the water-filled balloon and mucosal surface.

2. Deep to this is a narrow band of low reflectivity from the deep mucosa. The muscularis mucosae is not visualized as a
separate layer and is thought to be part of an interface reflection merging into the submucosa.

3. The submucosa is a prominent central reflective band. This appears wider sonographically than it is histologically, as
the interface reflection with the muscularis propria extends down into the muscle layer, making this appear narrower
and the submucosa wider.13

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4. The muscularis propria is of low reflectivity. A thin reflective fascial plane divides the inner circular layer from the
outer longitudinal layer. This may be detected using high resolution probes of 10 MHz or more.

5. At the outer border of the muscle layer is the fifth outer layer, which is another interface reflection with the fascia and
perirectal fat.

A disposable enema is required to cleanse the rectum. Rigid probes may be inserted blind into the distal rectum, but
higher insertion necessitates passing the probe through a short sigmoidoscope to negotiate the rectal folds. A
water-filled balloon system maintains acoustic contact with the rectal wall.

Rectal endosonography (RES) requires experience. It is important to view the entire lesion at right angles to the wall to
obtain proper staging. This is difficult with lesions on the posterior wall of the ampulla and is a significant cause of
incorrect staging. 14 Most systems for RES use axial imaging. This is one instance where a linear probe is helpful.
Artefacts during RES are common.15 A typical problem is air, either in the balloon or between the balloon and the
lesion, causing acoustic shadowing.

Cancers are of low reflectivity and easy to distinguish from normal bowel wall (Fig. 7.5). A peritumoural reaction
composed of inflammatory cells, oedema and fibrosis is usually present and is the most likely explanation as to why the
T2 tumours are most frequently overstaged. Maier et al16 suggest that this layer may be

Figure 7.5
T3 cancer showing tumour extending outside the
muscle layer (arrowhead) into the perirectal fat.

recognized as a rim of reduced reflectivity around the lesion. Excluding this layer from the staging process increased
accuracy from 70% to 95%.

Endoscopic sonography17 allows a tumour in any part of the colon to be staged. However, this facility is not widely
available. Colonic hydrosonography, where a water-filled colon is scanned by transabdominal US, may be used instead
with 70% accuracy and a claimed 100% sensitivity for infiltration of adjacent structures.18 Endoscopic staging could be
important in the resection of malignant polyps to exclude deep infiltration of the bowel wall or lymph node involvement.

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CT is more accurate than MRI in staging rectal cancer for > T3 (74 vs 58%),19 but has about the same accuracy for
colon cancers (62 vs 64%).

The majority of cancers are resected regardless of stage and preoperative knowledge of the tumour stage is required in
relatively few situations:

1. Large rectal tumours that seem fixed on clinical examination require imaging to confirm invasion of adjacent
structures. CT pre- and post-radiotherapy indicated.

2. Small rectal tumours that are mobile and suitable for local excision transanally should be examined sonographically.
The lesions should be T2, N0, of low grade malignancy and < 3.5 cm in diameter for a local excision.

3. Malignant change in large villous adenomas is difficult to detect clinically but contraindicates submucosal resection.
RES is indicated preoperatively.

4. Adjuvant chemotherapy (5 flurouracil ± levamisole or folinic acid) may be recommended for more advanced cancers
(< T2). Developments in adjuvant chemotherapy are potentially the most important indication for preoperative staging.

5. If laser therapy is planned, it is important to know the thickness of a tumour and proximity of structures such as the
bladder.

Lymph Node Involvement (N Staging)

Infiltration of the lymphatic system is a highly significant factor in survival, as indicated by the Dukes classification,
where lymphatic involvement places the tumour into grade C regardless of the depth of bowel wall infiltration.

In vitro sonography of perirectal and pericolic lymph nodes suggests that benign nodes are typically ovoid,
heterogeneous in reflectivity and < 5 mm in diameter,

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whereas malignant nodes are rounded, homogeneous in reflectivity and >5 mm in diameter. Nodal enlargement may be
due to tumour infiltration or non-specific inflammatory change. Tumour replacement of the internal nodal architecture
should produce a homogeneous echopattern of low reflectivity. The internal architecture is maintained with non-specific
changes and typically these nodes show increased reflectivity. However, there is considerable overlap and some 60% of
nodes cannot be differentiated on sonographic images. 20 Only about half the nodes present in an operative specimen
can be seen during in vitro scanning and during in vivo endosonography it is impossible to scan a field equivalent to that
of the surgical specimen with a rigid rectal probe. It is therefore not surprising that endosonography is relatively
inaccurate in determining N stage. From pooled data a kappa of only 0.58 is reported.21

CT and MRI have a lower sensitivity than endosonography, of about 45% for detecting malignant adenopathy. This is
based on visualizing a node of any size in a position where nodes are not normally seen, i.e. the perirectal fat, or
demonstrating nodes > 1 cm anywhere.

Overall the imaging of nodal involvement is very disappointing. The fundamental problem lies in the nature of
metastases to lymph nodes. Micrometastases within an otherwise normal node will not be detected, and nodes involved
by micrometastases may be very small. In one study metastases were present in 32% of nodes of 5 mm or less and in
8% of nodes of 2 mm or less along the superior rectal artery chain.22 Clearance of involved perirectal nodes is essential
to prevent local recurrence. Tumour rests may be found in the mesorectum for up to 3 cm distal to the primary tumour.
Lymph node clearance up to 5 cm is therefore recommended for tumours in the mid and lower rectum and is achieved
by total mesorectal (perirectal fascia) excision.23 Incomplete clearance is considered to be the cause of high local
recurrence rates (> 10%). Internal iliac nodes are involved in 30% and are always secondary to mesorectal node
involvement.

Advances in immunoscintography may improve imaging in this field, but the problem of micrometastases is still a
limiting factor.

Metastasis (M Staging)

About 20% of patients presenting with CRC have metastatic spread and > 50% will develop hepatic metastases during
the course of the disease. There are two main pathways for haematogenous spread depending on the site of the primary
tumour. Tumour cells from rectal cancers may enter the systemic circulation as the rectal venous plexi drain via the
middle and inferior rectal veins into the hypogastric veins and inferior vena cava. Only the portal circulation is involved
in colonic tumours, with drainage via the superior and inferior mesenteric veins. Pulmonary metastases may develop
without hepatic involvement in rectal cancers, whereas these are always secondary to hepatic spread in colonic lesions.

Documentation of hepatic metastases has become important as hepatic resection is now a practical therapeutic option.
Imaging has a vital role in patient selection. Criteria for resection are the presence of < 5 liver metastases and the
absence of systemic spread or hepatic nodal involvement. At least 30% of normal liver must remain following resection
to avoid liver failure. About 12% of CRC cases have metastases confined to the liver and some 25-50% of these may be
suitable for surgical resection. Successful resection significantly improves 5-year survival.

It is probable that many tumour cells enter the portal circulation. Metastases are more common in the right lobe, not
only because this is larger, but also a lamella flow may direct dependent tumour emboli into the right portal branch.
Most of these perish in the endothelial lining of the sinusoids without implantation. It is possible that some pass directly
through into the hepatic veins and pulmonary circulation, but most pulmonary metastases, with the exception of rectal
cancer, arise from cells shed by hepatic metastases. An alternative route for metastatic emboli to reach the pulmonary
bed is via the lymphatic system. Tumour cells may escape from the nodal chain into the thoracic duct and so into the
systemic venous system.

Pulmonary and bony metastases are seen in about 5% at the time of diagnosis. A chest radiograph is part of routine
preoperative screening and is adequate in most cases. Skeletal investigation with nuclear medicine scanning is
undertaken only for symptomatic disease.

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There are two particular situations where metastatic disease detection is poor: hepatic lymph node involvement and
small volume deposits on the peritoneal surface. There is early spread from liver metastases via lymphatics into the
hepatic nodes. These are located deep to the common duct surrounding the first part of the duodenum and are extremely
difficult to image. Peritoneal seeding of < 0.5 cm in size is also not detectable even with a meticulous CT technique.24

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Imaging Techniques for Liver Metastasis

Transabdominal US has the advantages of being a simple, rapid and readily available technique ideally suited for
screening, though it is less accurate, especially for smaller metastases, than other cross-sectional modalities. The
reflectivity of metastases may be equal, increased or decreased relative to normal parenchyma. There is often a
surrounding low reflective halo of compressed tissue that helps outline the lesion. Cystic change is not seen with CRC
metastases, though larger metastases may undergo necrosis. Punctate calcification is diagnostic of a metastasis from a
mucinous secreting adenocarcinoma (Fig. 7.6). Diffuse disorganization of the hepatic parenchyma is a subtle pattern to
recognize. A mass effect from the metastasis alters the contour of superficially placed lesions or compresses central
tubular structures.

In one series the overall detection of focal liver lesions was 68% for CT, 63% for MRI and 53% for US. 25 Only 20%
of lesions of < 1 cm in diameter were detected by US, compared to 49% by CT. Reports26,27,28 suggest that Doppler
measurement of the ratio of hepatic artery to the portal vein blood flow, termed the Doppler perfusion index (DPI), is a
highly sensitive index for metastatic disease. Of those 80 consecutive cases whose DPI was normal, 97% were
disease-free after 2 years, compared to recurrent disease in 78% of those with elevated DPI.27 It is suggested that an
abnormal DPI is a significant risk factor for metastatic disease, sufficient to warrant chemotherapy (28). Intraoperative
US is capable of detecting lesions of £ 5 mm in diameter and is

Figure 7.6
US of the liver showing a large diffuse metastasis
with some scattered bright foci. These were due to
microcalcifrication from a mucinous secreting
adenocarcinoma. A small area of necrosis is noted in
part of the metastasis.

considered more accurate than CT arteriography.27 However, follow-up of patients with negative intraoperative US29
has shown that 16% develop liver metastases, proving that a significant proportion of metastases escape all attempts to
be imaged.

Metastases receive their blood supply mainly from the hepatic artery, with only a little from the portal venous
circulation. Intravascular contrast may be used to enhance contrast between tumour and normal parenchyma to improve
tumour conspicuity.30 Intraarterial injection into the hepatic or superior mesenteric artery has been used to maximize
filling of tumour circulation when the parenchymal background will only be minimally enhanced as during the arterial
phase there will be no contrast in the portal circulation. This will be most beneficial with hypervascular tumours. CRC
metastases are generally hypovascular, nevertheless CT arteriography of the liver has been considered the most accurate
method for the preoperative detection of CRC metastases.

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CT arteriography will be impractical for most UK departments. Scanning in the portal venous phase after IV contrast is
essential to maximize tumour detection (Fig. 7.7). Injection of 100 ml of contrast agent at a rate of 3 ml/s using a pump,
with 5 mm slices is recommended after a 45 s delay. If the patient is given a bowel preparation, gas insufflation of the
colon with IV buscopan to prevent bowel motility, may be used to visualize the primary lesion. If the tumour is known
to be in the pelvis, this should be scanned at 5 mm slices, otherwise 10 mm for the abdomen (Fig. 7.8). An entire

Figure 7.7
Enhanced CT scan of the liver during the portal
phase revealing a number of metastases of varying
size. Some ascites is present.

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Figure 7.8
CT scan just below the liver revealing a
large peritoneal deposit (arrowhead).

assessment of the primary tumour and intra-abdominal or hepatic spread may therefore be made during one study. 10

Follow-Up

Within a year of surgery, a `clean' colon, i.e. one without any polyp, should be established. Colonoscopy is preferred for
this as a polyp of any size may be significant. After this baseline examination, DCBE or colonoscopy may be
recommended at 3-5 yearly intervals until the age of 70, although there is no evidence that this increases survival.
Repeat liver scanning is recommended for the first 2 years to detect any potentially resectable metastasis. With a high
grade rectal tumour and low anterior resection, repeat rectal endosonography is indicated31 to pick up recurrent disease
early and at a resectable stage. Locoregional recurrence is about 10%. A rising CEA titre is a useful marker for recurrent
disease and warrants repeat CT, chest X-ray and possibly bone scan.

There is a problem differentiating scar tissue from recurrence on CT. Where applicable, needle biopsy provides
histological confirmation. PET scanning and MRI may also be helpful.32

The family history is important in CRC and the patient's relatives must also be considered. The risk of CRC in
first-degree relatives is 2-4 times that of the general population. Two genetically determined conditions place relatives
at a much greater risk. Familial adenomatous polyposis accounts for 1% of CRC in the UK and should be picked up by
the presence of numerous adenomas throughout the colon and rectum. All members of the family will need screening
and a Polyposis Registry conducts this most effectively. Hereditary non-polyposis colorectal cancer (HNPCC) is more
common, accounting for about 5% of CRC. In the Lynch Type I variant (hereditary site-specific colon cancer) flat
adenomas may be present, there is a greater incidence of right-sided cancers and the risk of syn-

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Figure 7.9
Algorithm for CRC management

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chronous tumours is very high, estimated at 3% annually. In the Type II (or cancer family syndrome) cancers may be
found at other sites, notably uterus, breast, ovary, stomach and pancreas. HNPCC patients require more intensive
screening of the colon and in Type II cancers other sites must also be screened with mammography and pelvic US.

Carcinoid Tumours

Carcinoid tumours arise from the enterochromaffin cells belonging to the Amine Precursor Uptake and Decarboxylation
(APUD)-cell system. Overall, they account for about 6% of all malignant epithelial lesions in the colon and rectum. A
small (< 1 cm) submucosal nodule in the rectum is a common presentation. Large polypoid lesions may develop in the
colon. Ulceration suggests the lesion has metastasized. Size is a good indication of the risk of metastasis, with 15% of
those < 1 cm metastasizing, rising to > 75% for tumours of > 2 cm in size. As liver metastases are hypervascular they
are best seen in the hepatic arterial phase of biphasic helical CT, 30 and tend to be well defined and bright on US. The
carcinoid syndrome is relatively rare with colorectal tumours, but when present implies diffuse metastatic disease.

Lymphoma

Primary lymphoma of the colon represents < 1% of all malignant colorectal tumours. It is commonest in the caecum or
rectum at the sites where lymphoid tissue is most abundant. The tumour may be annular, polypoid or ulcerated, and is
frequently larger than CRC. Aneurysmal dilatation may occur. Another rare presentation is diffuse polyposis, with
multiple small submucosal nodules that are typically umbilicated. The differential diagnosis for this is malignant
melanoma or metastatic carcinoma. Lymphoid polyposis should not be confused with familial adenomatous polyposis
or lymphoid hyperplasia, where the lesions are not umbilicated in adults, < 2 mm in size and usually limited to part of
the colon.

The primary lesion may be diagnosed on DCBE, but CT will be required for staging nodal and extranodal involvement.

Kaposi Sarcoma

Kaposi sarcoma is a systemic multifocal tumour of the reticuloendothelial system that is common in AIDS patients. The
process starts with diffuse submucosal nodules, which coalesce to form a narrowed segment with irregular folds.
Typical changes are seen on DCBE. CT will demonstrate surrounding inflammatory change in the mesentery and local
lymph node enlargement.

Leiomyosarcoma

Now classified as being neurogenic in origin, these tumours are of low grade malignancy, with local recurrence and the
capability to metastasize. They are most commonly situated in the rectum and only the intraluminal part is visible on
DCBE. CT or TRUS reveal the mural and extramural components.

Conclusion

Micrometastases in lymph nodes and the liver limits the accuracy of current imaging techniques. Developments in
radiolabelled monoclonal antibody using a hand held detector during surgery might provide a way forward,33 but there
is still a major role for imaging during the oncological management of colorectal neoplasia.

References

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2. Saunders BP, Fukumoto M, Halligan S et al. Why is colonoscopy more difficult in women? Gastrointest Endosc
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621-626.

25. Wernecke K, Rummeny E, Bongartz G et al. Detection of hepatic masses in patients with carcinoma: comparative
sensitivities of sonography, CT and MR imaging. Am J Roentgenol 1991; 157: 731-739.

26. Leen E, Angerson WG, Cooke TG, McArdle CS. Prognostic power of Doppler perfusion index in colorectal cancer.
Correlation with survival. Ann Surg 1996; 223: 199-203.

27. Solomon MJ, Stephen MS, Gallinger S, White GH. Does intraoperative hepatic ultrasonography change surgical
decision making during liver resection? Am J Surg 1994; 168: 307-310.

28. Leen E, Goldberg JA, Robertson J et al. Early detection of occult colorectal hepatic metastases using duplex colour
Doppler sonography. Br J Surg 1993; 80: 1249-1251.

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29. Paul MA, Blomjous JG, Cuesta MA, Meijer S. Prognostic value of negative intraoperative ultrasonography in
primary colorectal cancer. Br J Surg 1996; 83: 1741-1743.

30. Oliver III JH, Baron JH. Helical biphasic contrast-enhanced CT of the liver: technique, indications, interpretation,
and pitfalls. Radiology 1996; 201: 1-14.

31. Ramirez JM, Mortensen NJ, Takeuchi N, Humphreys MM. Endoluminal ultrasonography in the follow-up of
patients with rectal cancer. Br J Surg 1994; 81: 692-694.

32. Ito K, Kato T, Tadokoro M et al. Recurrent rectal cancer and scar: differentiation with PET and MR imaging.
Radiology 1992; 182: 549-552.

33. Cote RJ, Houchens DP, Hitchcock CL et al. Intraoperative detection of occult colon cancer micrometastases using
125 I-radio-labled monoclonal antibody CC49. Cancer 1996; 77: 613-620.

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8
The Liver, Biliary System and Pancreas

Michel Lafortune and Luigi Lepanto

Hepatic tumours

Bile duct tumours

Pancreatic neoplasms

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This chapter describes the imaging methods used in the investigation of tumours of the liver, bile ducts and pancreas.
The algorithms used may vary from centre to centre, depending on available modalities and expertise. Knowledge of the
strengths and weaknesses of each examination allows the physician to select appropriate screening and to understand
the logical order of further tests.

Hepatic Tumours

Presenting symptoms in patients with liver tumours are often non-specific. Symptoms reflect the primary disease in
patients with metastases or cirrhosis, or may be due to increased liver size. Clinical signs include jaundice and a right
upper quadrant mass. Most liver tumours are incidental findings at sonography or CT performed for other reasons.
Table 8.1 shows the pathologic classification of liver tumours. 1, 2 The commonest tumours in clinical practice are
discussed.

Table 8.1 Pathologic classification of liver tumours.

Benign tumours
hepatocellular:
simple cyst
focal nodular hyperplasia
adenoma
nodular regenerative hyperplasia
mesenchymal:
haemangioma
lymphangiomatosis
angiomyolipoma
lipoma
epithelial and mesenchymal
teratoma
Malignant tumours
Primary
hepatocellular:
hepatoblastoma
hepatocellular carcinoma
fibrolamellar carcinoma
vascular:
angiosarcoma
haemangioendothelioma epithelioid
muscle tissue:
leiomyosarcoma
rhabdomyosarcoma
Secondary:
metastasis

Benign Tumours

Simple Cysts

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One of the most frequent masses of the liver (up to 20%), cysts are usually incidental findings at sonography performed
for other reasons. Single or multiple, they are lined by a single layer of cuboidal epithelium. The differential diagnosis
includes biliary cysts and echinococcal infections; the latter usually results in multilocular cysts. When multiple (as in
association with polycystic kidneys), they may cause liver enlargement. Rarely they cause pain and jaundice by
compression of bile ducts and surgical treatment is needed.3 The diagnosis of a simple cyst is straightforward at
sonography and complementary tests are rarely required. When first seen with CT, sonography may be used to confirm
the diagnosis.

Haemangioma

This is the most frequent benign mesenchymal tumour of the liver and occurs in 0.7-7% of the general population, with
a peak incidence at age of 30-50 years. Haemangiomas are thought to represent hamartomatous lesions, a consequence
of an acquired hepatic arteriolar malformation. Because haemangiomas occur more frequently in women than in men, a
possible relationship with oestrogen or progesterone has been suggested. Haemangiomas are usually found incidentally
at sonography or CT. Haemangiomas of >4 cm may manifest as right upper quadrant pain, hepatomegaly or as an
abdominal mass.4 This lesion is not pre-malignant. Bleeding after trauma or biopsy is a rare but potentially serious
complication. The tumours are well demarcated, ranging in size from a few millimetres to more than 20 cm. They are
composed of blood-filled spaces of varying size. The centre of the lesion, especially when large, is mucinous or fibrous.

On sonography the majority (+ 70%) of haemangiomas are hyperechogenic and show acoustic enhancement. They are
usually smaller than 3 cm. Some lesions are atypical (hypoechogenic, isoechogenic or heterogenous) especially when
greater than 3 cm in diameter or when the lesion occurs in a fatty liver. Very large haemangiomas (>5 cm) usually have
a hyperechogenic external rim and a hypoechogenic centre. When compressed, haemangiomas may `disappear', being
suddenly isoechogenic with the rest of the parenchyma. This phenomenon is easily observed in the operating room
where compression of the haemangioma by the transducer is easy. No blood flow is detected with Doppler sonography.5

On CT, lesions are classically hypodense before injection of contrast medium and the periphery of the lesion

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enhances rapidly after injection. The centre becomes progressively filled with contrast on delayed sequences (3-60 min
after the injection). 6 This description is true in 55-80% of haemangiomas. Small lesions, multiple lesions or lesions
with fibrosis tend to be more difficult to categorize with CT. Rarely, metastatic lesions may mimic haemangiomas on
CT studies.

MRI is sensitive and specific, both over 90%, in the diagnosis of haemangiomas (Fig. 8.1). The lesion is hypointense on
T1-weighted images and hyperintense on T2-weighted images. The latter persist even on images with longer TE.
Haemangiomas are homogenous, well circumscribed, often with polylobulated contours. Specificity and sensitivity of
MRI for the diagnosis of hemangiomas is over 90%. Cysts may look like haemangiomas at MRI, but are readily
characterized with sonography. The injection of paramagnetic agents serves as a diagnostic tool for giant hemangiomas.
The sequences of enhancement from the periphery to the centre of the lesion is similar to that seen with CT.

Haemangiomas, especially when large (>2 cm), can be readily diagnosed with red blood cell scintigraphy. The
combination of a photopenic lesion on HIDA or colloid scans, decreased perfusion on the flow study and increased
activity within the lesion on the blood pool study is characteristic of haemangiomas. The sensitivity and specificity of
radionuclide scintigraphy is between 80 and 90%.

Biopsy of haemangiomas is rarely performed because of the danger of haemorrhage, which may be fatal. However,
haemorrhage after biopsy is very rare, especially when the lesion is surrounded by normal liver parenchyma which
tends to contain any haemorrhage. Biopsy of peripheral lesions should be avoided.

What should be done in practice? If a lesion is thought to be a haemangioma at sonography. and if the patient is
asymptomatic, with normal liver tests, no other test is necessary. A follow-up study is performed 6 and 12 months later.
Haemangiomas usually have not grown on subsequent exams.7 If the patient is cirrhotic or if the patient has cancer,
MRI is performed. If the lesion is more than 3 cm in diameter, MRI is still the best tool, but CT and scintigraphy can be
used.

Focal Nodular Hyperplasia

Focal nodular hyperplasia (FNH) is a benign lesion of unknown origin; it may represent a hamartoma or a response to a
vascular malformation.8 It affects all ages and is more common in women. Anovulant therapy may stimulate growth of
FNH. FNH is usually asymptomatic (75%) and is usually an incidental finding on CT or ultrasound. FNH is a
well-demarcated, non-encapsulated nodule, often solitary, measuring less than 5 cm in diameter. Characteristically there
is a central scar with radiating vascular structures encased in fibrous septa. Between the septa are hyperplastic nodules
composed of normal hepatocytes. The lesion usually projects from the surface of the liver and is often pedunculated.

On sonography FNH is usually a homogenous lesion, isoechogenic with the surrounding liver. It lacks a capsule and
may therefore be difficult to detect. A bulge on the surface of the liver may be the initial manifestation. Sometimes a
central scar is seen. Doppler sonography (Fig. 8.2) may be quite characteristic: a feeding artery is seen in the centre of
the lesion which gives rise to arteries which radiate in a spoke-wheel fashion. Contrary to malignant tumours, venous
signals are rarely seen within FNH.9

On MRI FNH is typically an isointense lesion on all pulse sequences. A central scar is present in 70-85% of lesions: it is
hypointense on T1-weighted images and hyperintense on T2 weighted images. FNH is enhanced by contrast injection.
No capsule is seen. When all these features are present, the MRI diagnosis is specific.

With Technetium 99m colloid scintigraphy, FNH shows three patterns of uptake: iso-, hypo- or hyper-fixation. Iso- and
hyper-fixation are the most frequent and the most characteristic.

FNH is iso- or hypo-dense on pre-contrast CT examinations. Soon after bolus injection of contrast medium, there is
contrast enhancement of the lesion. During the portal phase, the lesion becomes isodense. The central scar is visible in
only 15-45% of patients.

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What should be done in practice? FNH is a benign lesion and there is no reason for excision, except for the rare
situation where the lesion causes symptoms (abdominal pain due to torsion or compression). If FNH is suspected at
Doppler sonography, and MRI confirms the diagnosis, the investigation can stop there. Annual follow-up of the lesion
with Doppler sonography may be undertaken.

Adenoma

This rare tumour bleeds readily and occurs mainly in women (male:female = 1:9), between the ages of 15 and 45 years.
It is related to the use of oral contraceptives: the incidence increases 20-100 fold after 5 years and 500-fold after 7 years
of anovulant therapy. Regression of adenomas has been reported after with-

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Figure 8.1
Haemangiomas. MRI of the liver: a) T1-weighted image shows a 2 cm hypointense mass in the right lobe.
b) The lesion becomes hyperintense on T2- weighted image. c) Sonographic examination (another example):
a uniformly hyperechogenic mass is outlined. d) No Doppler signals are identified with colour or e) power mode.

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Figure 8.2
Focal nodular hyperplasia: Colour Doppler sonography shows vessels radiating from the centre
of a mass towards the periphery. This is a classic appearance of a FNH at Doppler sonography.

drawal of oral contraceptives. Since 1990, the incidence of adenoma has declined, probably because the dose of oestrogen
in anovulants has been greatly reduced. Patients with glycogenosis (type I and III) and males treated with androgenic
steroids also have a higher incidence of adenomas, and their risk of malignant transformation is higher than in women
taking oral contraceptives. The patient with an adenoma may be asymptomatic or may present with an abdominal mass or
chronic abdominal pain. When bleeding occurs in the mass or the peritoneum, patients may have acute abdominal pain.
Serum α-fetoprotein levels are normal. Adenomas are well demarcated, occasionally encapsulated, solitary tumours, that
can be quite large (5-30 cm). At histology, adenomas are composed of hepatocytes slightly larger than normal, which
frequently have a pale cytoplasm because of glycogen or fat accumulation. Infarction and haemorrhage are frequently
present and are followed by fibrosis. Unlike normal liver parenchyma, adenomas do not have portal or central veins, nor
bile ducts. They are vascularized by large arteries entering from the periphery of the mass.

On sonography adenomas usually have the same echogenicity as the surrounding liver. However, they are often
heterogeneous with hypoechogenic (necrotic) areas. They can be well demarcated with a hypoechogenic rim. The
surrounding vessels are compressed, but not invaded. The hepatic artery feeding the lesion is usually dilated. Peripheral
vessels are well visualized with colour Doppler sonography and identified as arteries or veins with pulsed Doppler. The
centre of the mass usually contains vessels with venous flow. Sonographic surveillance of the lesion is indicated when
surgery is contraindicated.

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Adenomas usually present as photopenic lesions on sulphur colloid scintigraphy.

Adenomas differ from FNH in their heterogeneous architecture. On T1-weighted MR images, adenomas are usually hypo-
or iso-intense. In 30%, a hypointense rim is present. Haemorrhagic areas or fat within the mass are seen as hyperintense
signals. On T2-weighted images, hypointense bands of tissue are seen and represent necrosis or haemorrhage. 10

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Haemorrhagic areas are usually clearly seen with unenhanced CT. After contrast injection the lesion is seen as a
heterogeneous mass. No central scar is identified.

As the treatment is often surgical, adenomas are rarely biopsied. If doubt exists as to the exact mature of an adenoma,
excision is indicated, since the distinction between adenoma and hepatocarcinoma may be impossible to make with
imaging methods.

What should be done in practice? When MRI with or without CT indicates that the lesion is not FNH or if doubt
persists, the diagnosis of adenoma is likely but must be distinguished from hepatocarcinoma. Surgery may be necessary.
The role of biopsy (guided with sonography or CT) is still uncertain.

Malignant Tumours

Hepatocarcinoma

Hepatocarcinoma (HCC) usually occurs in association with chronic liver disease, especially cirrhosis. There is a higher
incidence of HCC where viral hepatitis is common, especially in Asia and sub-Saharan Africa, and where there is
exposure to various hepatocarcinogens (e.g. aflatoxine). HCC is rare in the western hemisphere. Non-alcoholic
postnecrotic cirrhosis is more frequently associated with HCC than alcoholic cirrhosis. HCC has an earlier age of onset
in countries with a high incidence of hepatitis (third decade rather than seventh to eighth decade). HCC occurs more
frequently in men than in women. In countries with a low incidence of HCC, the onset of symptoms is insidious and
includes malaise, anorexia, fever and abdominal pain. Jaundice is rare. In regions with a high incidence of HCC, the
clinical symptoms may be more dramatic and include abdominal distension and spontaneous tumour rupture, with
massive haemoperitoneum. The α-fetoprotein levels are often elevated in patients with HCC. Several classifications
exist, based on the gross appearance of HCC. Eggel's (1901) is still much in use and serves as the basis for newer
classifications. There are three types:

1) Massive: there is a single large mass (with or without satellite nodules);

2) Nodular: there are multiple small nodules;

3) Diffuse: multiple, indistinct nodules are seen throughout the liver.

Tumour masses tend to necrose and bleed. Capsules are frequent and tend to become thicker as tumour size increases.
They are composed of fibrous tissue and compressed vessels and bile ducts. 11 HCC tends to invade portal veins and,
more rarely, hepatic veins, the inferior vena cava and bile ducts.11 Metastatic seeding tends to occur via the portal veins
within the liver. Extrahepatic spread of tumour occurs late in the course of the disease.

The sonographic appearance of HCC is variable. In Asia, HCC may have a high fat content (fatty metamorphosis) and
the lesion may present as an echogenic mass. Elsewhere, HCCs are usually hypoechogenic, sometimes heterogeneous
(especially if >3 cm), with a surrounding hypoechogenic rim. The chaotic intratumoural vascularization can be outlined
with colour and pulsed Doppler sonography. A network of neovasculature with abnormal blood flow is often detected
with Doppler sonography: high systolic Doppler shifts are outlined, as well as evidence of arteriovenous shunting. This
is the result of angiogenesis stimulated by the tumour. Such Doppler shifts are detectable at the periphery of a number
of malignant tumours within the abdomen. Tumour thrombi within the portal veins may contain arterial blood flow,
detected with pulsed Doppler (Fig. 8.3); this is characteristic of tumour thrombus. The sensitivity of sonography in the
diagnosis of HCC is good (around 90%). It tends to be less sensitive in eastern countries, probably because HCC grows
in cirrhotic livers, where small tumours blend into the nodular liver architecture. Tumours are difficult to detect until
they reach 2-3 cm in diameter. The same is true of HCC complicating metabolic diseases in children (e.g. tyrosinaemia
and glycogenosis).

HCCs are photopenic at sulphur colloid scintigraphy. There is an accumulation of gallium in 90% of masses.

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The appearance on T1-weighted MR images is variable (low-, iso-, high- or mixed-intensity). They are hyper-intense on
T2-weighted images. Fat content and the surrounding pseudocapsule are hyperintense on T1-weighted images. Invasion
of vessels by HCC is clearly shown with MRI.

On unenhanced CT, HCCs are usually hypodense. On dynamic CT the mass enhances rapidly during the arterial phase
but becomes iso- or hypo-dense in the portal phase. The capsule usually enhances and necrosis within the tumour is
seen as an hypodense area. Haemoperitoneum and invasion of portal and hepatic veins and of the inferior vena cava can
be detected with CT. Because HCCs trap the contrast agent Lipiodol that is injected into the hepatic artery, the tumours
become highly visible on CT and remain so for several weeks. Small seeding tumours, which are otherwise difficult to
detect, become readily visible with this technique.

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Figure 8.3
Hepatocarcinma: vascularized tumour thrombus.
a) The sonographic examination of the left lobe of the
liver shows thrombus extending into the lumen of the
left portal vein. b) Colour Doppler shows signals
originating from the thrombus. c) At pulsed Doppler,
these are identified as high velocity signals,
characteristic of flow in tumour vessels.

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HCC is a vascular tumour that is seen on arteriography The hepatic arteries are usually enlarged, with
neovascularization, arteriovenous shunts and vascular invasion. Arteriography is rarely performed for diagnostic
purposes, but rather as a therapeutic gesture or for the study of the extension of HCC using Lipiodol.

Chronic liver disease carries an increased risk of HCC and any nodule within the already heterogeneous cirrhotic liver
may be an HCC. If α-fetoprotein levels are high, a nodule is most probably an HCC. If levels are low, a nodule could
still be an HCC, but could also represent a metastasis or a regenerative nodule. A nodule in a cirrhotic patient is more
likely to be an HCC than any other focal lesion. If excision or embolization is planned, guided biopsy is performed. If
liver transplantation is planned, biopsy is avoided because of the possible recurrence of HCC along the path of the
biopsy.

What should be done in practice? Routine screening for HCC is performed with sonography. 12 The majority of HCCs
are clearly seen on sonography, as long as the lesion diameter is at least 2 cm and technical factors are optimal. Where
clinical doubt exists and the α-fetoprotein level is elevated, other imaging methods are useful in detecting the HCC,
especially CT following intraarterial Lipiodol injection. Doppler sonography, CT and MRI are good tools to evaluate
the portal and hepatic veins and possible invasion by the tumour.

Metastasis

Common primary sites of liver metastasis include the lung, colon, breast and pancreas. As many as 50% of patients
dying of cancer have hepatic metastases. In western countries, metastases are the commonest liver tumour. HCC is
relatively more frequent in Asia. Symptoms from metastases relate to their number, the primary cancer site and the
hepatic reserve. At times a patient may present with liver metastases when no primary site is known. Patients may be
asymptomatic for a long time before hepatic insufficiency occurs. Jaundice and ascites are late events. When metastases
are found the patient is referred for the optimum specific treatment. Surgical removal of liver metastases from a colon
cancer in patients who have undergone resection of the

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primary tumour and regional lymphadenectomy and who have no evidence of extrahepatic metastatic disease gives a
5-year survival of 25%. 13

On sonography metastases are visualized as nodules of various echogenicity. Most are hypoechogenic and surrounded
by a poorly defined halo. Their size and architecture are unrelated to the primary tumour. Many studies have compared
the rate of detection of metastasis with sonography to other imaging techniques and have shown that the sensitivity of
sonography is at best equal to CT and MRI. The experience of the operator, the time taken to perform the study and the
quality of the ultrasound machine are important factors in determining the precision of the sonographic examination.
Intraoperative sonography is more sensitive and highly useful in guiding excision. Ultrasound contrast agents are used
in clinical practice in some centres in Europe and are used experimentally in North America. These agents improve
contrast between lesions and liver parenchyma and enhance the detection of tumour vascularity.

Single-photon-emission CT is more sensitive than conventional planar scintigraphy. Scintigraphy is less sensitive than
CT or ultrasound, and for this reason, is not used as the primary screening method for metastatic disease.

On CT the typical appearance of a liver metastasis is that of a focal, round lesion that is less dense than the normal
surrounding parenchyma. Other patterns may also be seen: heterogeneous architecture, hyper- or isodense or diffuse
invasion. The use of intravenous contrast agents increases contrast between the focal lesion and the normal liver. On
dynamic CT there may be mild enhancement of the periphery of the lesion; conversely, the entire lesion may be less
dense than the contrast-enhanced parenchyma. On delayed CT, metastatic adenocarcinoma may display a distinct
pattern: the centre is dense and the periphery has low uptake of contrast. CT arterial portography is the most sensitive
tool for detecting liver metastases.

Most metastatic lesions are homogeneous and less intense than normal liver on T1-weighted MR images and
inhomogeneous and hyperintense on T2-weighted images.

Biopsy of a possible metastasis is performed before specific treatment. It can be performed with CT or ultrasound
guidance to confirm that the lesion is linked to the known primary cancer.

What should be done in practice? In screening for hepatic metastasis the sensitivity and specificity of the imaging
method should be high and the examination cost effective. In experienced hands, sonography is quite sensitive and
specific, low in cost and widely available. CT and MRI are complementary tests. CT arterial portography is helpful in
certain circumstances such as before a segmental hepatectomy in a patient who has already undergone a
metastasectomy. There is an increasing number of tumours markers (CEA, CA 125, AFP, CA-50, etc.) but none is
specific for liver metastasis.

Bile Duct Tumours

In terms of clinical presentation, neoplasms of the biliary tree can be divided into three groups according to their site of
origin: intrahepatic biliary tree, extrahepatic biliary tree and gallbladder. Tumours originating from the intrahepatic
ducts present much like other liver lesions. Signs and symptoms are often non specific and jaundice is uncommon
unless disease is widespread. On the other hand, jaundice is the hallmark of tumours of the extrahepatic biliary tree.
Neoplasms of the gallbladder have a more insidious onset at presentation and are usually discovered incidentally or
when disease is advanced. A more comprehensive classification of biliary tree neoplasms is outlined in Table 8.2. Most
of these tumours are rare and only those encountered most frequently are discussed.

Biliary Cystadenoma Cystadenocarcinoma

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Tumours originating from the intrahepatic bile ducts behave clinically like other intrahepatic tumours. Although
classified as a benign tumour, cystadenoma has the potential for malignant transformation and surgical excision is
indicated. Furthermore, there is no way to distinguish between cystadenoma and cystadenocarcinoma on the basis of
imaging criteria alone.14 There is a strong female preponderance and 90% of these tumours arise from the intrahepatic
bile ducts. When small these tumours are usually discovered serendipitously during evaluation of the upper abdomen
with ultrasound or CT. When large enough to cause symptoms, these are usually non-specific and include right upper
quadrant discomfort and only rarely jaundice. On both ultrasound and CT examinations these appear as multiloculated
cysts with thickened septations and mural nodules.

Adenoma of the Gallbladder

Benign neoplasms of the biliary tree are rare, with the exception of adenomas of the gallbladder. These are most often
an incidental finding during abdominal ultrasound and present as solitary, small polyps originating from the wall. They
are not mobile and do not produce acoustic shadowing. Malignant potential is low and they

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Table 8.2 Pathologic classification of neoplasms of the bile duct and

gallbladder.
Bile duct
Benign neoplasms
papillary adenoma
cystadenoma
granular cell tumour
mesenchymal tumours
heterotopic gastric mucosa
Malignant neoplasms
cholangiocarcinoma
periampullary carcinoma
embryonal rhabdomyosarcoma
Gallbladder
Benign neoplasms
adenoma
granular cell tumour
mesenchymal tumours
Malignant neoplasms
primary adenocarcinoma
mesenchymal sarcoma
metastatic carcinoma

are usually followed sonographically. Criteria for surgical excision include a size greater than 1 cm, a solitary lesion,
associated gallstones, age greater than 50 years and progression on serial ultrasound examinations. 15

Adenocarcinoma of the Gallbladder

Adenocarcinoma of the gallbladder is more common in older female patients and is associated with gallstones in 90% of
cases. Porcelain gallbladder is associated with an increased incidence of carcinoma of the gallbladder.16 Jaundice is not
as commonly seen as in cholangiocarcinoma, unless the disease is widespread. Adenocarcinoma of the gallbladder has a
propensity to spread locally, invading the liver, the common hepatic and common bile ducts, and adjacent intestinal
structures.

In patients with right upper quadrant pain but no jaundice the initial imaging study is undoubtedly abdominal
ultrasound. The presence of a mass in the gallbladder fossa, a poorly discernible gallbladder and the presence of
gallstones are compatible with the diagnosis (Fig. 8.4). In fact, gallbladder carcinoma is more commonly associated
with a solitary stone, especially if it is displaced by a mass or focal wall thickening.17 The diagnosis is not always easy
to make and one must maintain a high degree of clinical suspicion in the proper clinical context.

CT plays a complementary role and helps confirm the diagnosis and determine the extent of tumour spread. Ultrasound
and CT are usually sufficient to diagnose carcinoma of the gallbladder and can guide percutaneous biopsy when
necessary. Usually, the malignant nature of the disease process is not in doubt and imaging serves to confirm the
diagnosis and determine surgical resectability.

Cholangiocarcinoma

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Cholangiocarcinoma is most commonly extrahepatic in location; however, 20% of cholangiocarcinomas occur

intrahepatically and their clinical presentation is indistinguishable from other intrahepatic focal lesions. Intrahepatic
cholangiocarcinomas can be further subdivided into peripheral and central lesions. The peripheral tumours are mass
lesions occurring deep in the liver parenchyma while central lesions, also known as Klatskin's tumour, involve the bile
duct bifurcation and are rarely identified as a mass lesion.17,18,19,20 Cholangiocarcinoma involving the extrahepatic
bile ducts invariably presents with jaundice. Clinically it is usually indistinguishable from other periampullary tumours
which include carcinoma of the ampulla, pancreatic cancer and duodenal carcinoma.

Ultrasound is the screening test of choice to eliminate hepatic causes of cholestatic jaundice.21 Cholangiocarcinomas
are often small and not seen on imaging studies which show biliary dilatation to the point of obstruction, usually the
distal common hepat-

Figure 8.4
Adenocarcinoma of the gallbladder. Sononographic
examination of the gallbladder: The poorly defined
mass (arrows) invading the liver in the gallbladder
fossa represents adenocarcinoma of the gallbladder.

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ic duct or the proximal common bile duct. This should suggest the diagnosis.

The site of obstruction can usually be reliably determined by a combination of ultrasound and CT. These modalities also allow
elimination of extrinsic compression (e.g. liver masses, hilar adenopathy) as a cause of obstruction.

Confirmation of the site of obstruction is usually obtained by direct opacification of the bile duct either endoscopically (i.e. endoscopic
retrograde cholangiography) or transhepatically (i.e. transhepatic cholangiography). Cholangiography reveals a severe segmental
stenosis, an abrupt cut-off, or, more uncommonly, a filling defect. The transhepatic approach is usually favoured because of the risk of
contamination with enteric organisms with a retrograde approach. 22

Magnetic resonance cholangiography is a new technique which may represent a non-invasive alternative to depict the biliary tree.23

What should be done in practice? The purpose of imaging is to establish the diagnosis, but also to determine the extent of disease and
the possibility of surgical cure. The combination of ultrasound and CT allows the assessment of hepatic metastases, local and regional
lymph nodes and contiguous spread to adjacent organs. Vascular invasion can be assessed with angiography; however, new techniques
with spiral CT and 3-dimensional vascular reconstructions may preclude the use of angiography (Fig. 8.5a and b). Although there are
reports of MRI in the evaluation of tumours of the biliary tree, this modality is not used routinely in the work-up of these patients.

Pancreatic Neoplasms

The pancreas functions both as an endocrine and an exocrine gland. Neoplasms can be classified according to the cell type of origin
(Table 8.3). In terms of clinical presentation, however, these tumours can be divided into three groups: tumours of the head of the
pancreas, tumours of the body of the pancreas and islet cell tumours. This is not a histologic classification but, from the perspective of
imaging work-up, it is useful to divide pancreatic neoplasms in this way. Tumours of the head of the pancreas often present with
jaundice and are indistinguishable, on purely clinical grounds, from cholangiocarcinomas and periampullary tumours. Neoplasms of the
body and tail of the pancreas usually present with epigastric pain radiating to the back, anorexia and weight loss. These tumours are
usually discovered later than those of the head of the pancreas and are subsequently larger at the time of diagnosis.

Ductal Adenocarcinoma

The commonest neoplasm of the pancreas is ductal adenocarcinoma.

Figure 8.5
Cholangiocarcinoma. a) CT of the liver: Small tumour (arrow) in the porta hepatis is a
cholangiocarcinoma. There is a an endoprosthesis in the bile duct (arrowhead). b) Three-dimensional
vascular reconstruction following spiral CT shows partial encasement of the hepatic artery (arrow).

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Table 8.3 Classification of pancreatic neoplasms

Duct cell origin
Solid:duct cell adenocarcinoma
solid and papillary epithelial neoplasm
variant carcinoma
Cystic:congenital cyst
microcystic adenoma
mucinous cystic adenoma
Acinar cell origin
acinar cell carcinoma
acinar cell cystadenocarcinoma
Islet cell origin
insulinoma
gastrinoma
glucagonoma
somatostatinoma
VIPoma

Ultrasound is a useful initial imaging test to rule out hepatic causes of jaundice, but CT is the examination of choice for
the diagnosis and staging of pancreatic cancer. 15 With proper technique, over 95% of tumours are detected. CT after
intravenous contrast administration typically demonstrates lesions as hypoattenuating masses within the pancreas (Fig.
8.6). Associated pancreatic duct and biliary duct dilatation is also seen. When the tumours are large, areas of necrosis
with cystic changes can be seen centrally. Less commonly, adenocarcinoma presents as diffuse involvement of the
gland. When the tumour is small, only the indirect sign of pancreatic duct dilatation is seen. Imaging is important in
staging disease to determine surgical resectability.

Findings that render lesions inoperable include regional lymph node metastases, distant metastases (e.g. liver), vascular
encasement, contiguous spread to adjacent organs (e.g. kidney, bowel) and ascites. CT and angiography have
traditionally been used to rule out vascular involvement, but spiral CT (i.e. CT-angiography) with or without
3-dimensional vascular reconstructions, as well as Doppler ultrasound, are now more widely used and may replace
angiography for this particular purpose.24, 25

At times very small tumours can only be demonstrated at endoscopic retrograde pancreatography (ERCP), which shows
abrupt cut-off or short segmental stenosis with proximal dilatation. Dilatation of the pancreatic duct and the common
bile duct (i.e. the double duct sign) is a classic finding.

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Figure 8.6
Ductal adenocarcinoma of the pancreas. CT of the
abdomen: Hypoattenuating mass in the head of the
pancreas (short arrow) with intrahepatic bile duct
dilatation (long arrow) and gallbladder distension
(arrowhead).

The role of MRI was recently evaluated in a multicentre study and was found to offer no significant advantage over
CT.26

Biopsy is not indicated if surgical cure is possible because of the risk of tumour seeding along the biopsy needle tract.
Biopsy is sometimes requested to obtain histologic confirmation of the disease when the tumour is deemed inoperable.

Cystic Tumours of the Pancreas

Cystic tumours of the pancreas are much less common and include microcystic adenomas (serous cystadenoma) and
macrocystic adenomas (mucinous cystadenoma). Both have a higher incidence in female patients. Microcystic
adenomas are found in older patients and have no malignant potential, whereas macrocystic adenomas occur in younger
patients and have malignant potential.

Distinguishing features can be demonstrated both by ultrasound and CT. Microcystic adenomas contain numerous small
cysts whose diameters do not exceed 1-2 cm. Septa are usually thin and there is sometimes a central scar that can
calcify. These tumours can occur anywhere in the pancreas, but are more frequent in the head. Macrocystic adenomas
are multiloculated with multiple cystic lesions each measuring more than 2 cm in diameter (Fig. 8.7). Septa are thick
and can contain calcifications. These tumours tend to be larger than microcystic adenomas with mean diameter of 10 cm
and tend

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to occur in the body and tail of the pancreas. Biopsy can aid in differentiating these two cystic tumours since
microcystic adenomas contain glycogen with little or no mucin, while macrocystic adenomas contain mucin. 27

Islet Cell Tumours

Islet cell tumours are dealt with separately because of their different histologic origin (i.e. the endocrine gland) and their
distinctive clinical presentation. These neoplasms include gastrinomas, insulinomas, glucagonomas, VIPomas and
somatostatinoma. Most are hormonally active and cause symptoms associated with hypersecretion of the hormone
produced. Although most of these lesions are adenomas, the biologic behaviour is better assessed by the presence of
regional spread or metastatic disease.

CT and nuclear medicine are the initial imaging modalities used. The detection rate with CT varies from 75% to 85%
and lesions usually appear as hyperattenuating nodules after intravenous administration of iodinated contrast. When
these modalities fail to identify the tumour, more invasive procedures such as angiography, portal vein venous sampling
and even intraoperative ultrasound are used.28, 29 Approximately 20% of islet cell tumours are non-functioning or
produce hormone levels that are subclinical. These neoplasms are the third most common of the islet cell tumours after
insulinomas and gastrinomas and present

Figure 8.7
CT of the abdomen: Mucinous cystadenoma of the
pancreas. The cystic mass (arrow) originates from the
body and tail of the pancreas.

quite late and are usually large and widespread at diagnosis. Clinically, they present much like other neoplasms of the
body and tail of the pancreas. An imaging feature that distinguishes these lesions from the more common
adenocarcinoma of ductal origin is the presence of calcification which is seen in up to 20% of tumours. Although once
thought to be uncommon, necrosis or cystic degeneration and vascular invasion can be seen with large tumours.30

References

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1. Okuda K, Korio M, Okuda H. Neoplasms of the liver. In: Schiff L, Schiff ER (eds) Diseases of the Liver.
Philadelphia: WB Saunders, 1993, pp. 1236-1296.

2. Ros PR, Li KC. Radiology of Malignant and Benign Liver Tumors: Part 11: Benign Liver Tumors. St Louis: Year
Book Medical Publishers, 1989 (Current Problems in Diagnostic Radiology, vol 18).

3. Vogl S, Koperna T, Satzinger U, Schulz F. Nonparasitic liver cysts. Overview of therapy with long-term results.
Langenbecks Arch Chir 1995; 380: 340-344.

4. Valls C, Rene M, Gil M, Sanchez A, Narvaez JA, Hidalgo F. Giant cavernous hemangioma of the liver: atypical CT
and MR findings. Eur Radiol 1996; 6: 448-450.

5. Lin ZY, Chang WY, Wang LY et al. Duplex pulsed Doppler sonography in the differential diagnosis of
hepatocellular carcinoma and other common hepatic tumours. Br J Radiol 1992; 65: 202-206.

6. Freeny PC, Marks WM. Patterns of contrast enhancement of benign and malignant hepatic neoplasms during bolus
dynamic and delayed CT. Radiology 1986; 160: 613-618.

7. Mungovan JA, Cronan JJ, Vacarro J. Hepatic cavernous hemangiomas: lack of enlargement over time. Radiology
1994; 191: 111-113.

8. Wanless IR, Mawdsley C, Adams R. On the pathogenesis of focal nodular hyperplasia of the liver. Hepatology 1985;
5: 1194-1200.

9. Mathieu D, Rahmouni A, Anglade MC et al. Focal nodular hyperplasia of the liver: assessment with
contrast-enhanced turboflash MR imaging. Radiology 1991; 180: 25-30.

10. Arrive L, Flejou JF, Vilgrain V et al. Hepatic adenoma: MR findings in 51 pathologically proved lesions. Radiology
1994; 193: 507-512.

11. Kadoya M, Matsui O, Takashima T, Nonmura A. Hepatocellular carcinoma: correlation of MR images and
histopathologic findings. Radiology 1992; 183: 819-825.

12. Khakoo SI, Grellier LF, Soni PN, Bhattacharya S, Dusheiko GM. Etiology, screening, and treatment of
hepatocellular carcinoma. Med Clin North Am 1996; 80: 1121-1145.

13. Adson MA. Mass lesions of the liver. Mayo Clin Proc 1986; 61: 362-368.

14. Pitt HA, Dooley WC, Yeo CJ, Cameron JL. Malignancies of the biliary tree. Curr Prob Surg 1995; 32: 1-90.

15. Freeny P, Traverso. L, Ryan J. Diagnosis and staging of pancreatic adenocarcinoma with dynamic computed
tomography. Am J Surg 1993; 165: 600-606.

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16. Fromm D. Carcinoma of the gallbladder In: David C, Sabiston Jr (eds) Textbook of Surgery: The Biological Basis of
Modern Surgical Practice, 15th edn. Philadelphia, WB Saunders, 1997. 16. pp. 1148-1151

17. Wibbenmeyer LA, Sharafuddin MJA, Wolverson MK, Heiberg EV, Wade TP Shields JB. Sonographic diagnosis of
unsuspected gallbladder cancer: Imaging findings in comparison with benign gallbladder conditions. AJR 1995; 165:
1169-1174.

18. Soyer P, Bluemke DA, Reichle R et al. Imaging of intrahepatic cholangiocarcinoma: 2. Hilar cholangiocarcinoma.
AJR 1995; 165: 1433-1436.

19. Soyer P, Bluemke DA, Reichle R et al. Imaging of intrahepatic cholangiocarcinoma: 1. Peripheral
cholangiocarcinoma. AJR 1995; 165: 1427-1431.

20. Neumaier CE, Bertolotto M, Perrone R, Martinoli C, Loria F, Silvestri E. Staging of hilar cholangiocarcinoma with
ultrasound. ??? 1995; 23: 173-178.

21. Robledo R, Muro A, Prieto ML. Extrahepatic bile duct carcinoma: US characteristics and accuracy in demonstration
of tumors. Radiology 1996; 198: 869-873.

22. Vauthey JN, Blumgart LH. Recent advances in the management of cholangiocarcinomas. Sem Liver Di 1994; 14:
109-114.

23. Reinhold C, Bret P. Current status of MR cholangiopancreatography. AJR 1996; 166: 1285-1285.

24. Angeli E, Venturini M, Vanzulli A et al. Color Doppler imaging in the assessment of vascular involvement of
pancreatic carcinoma. AJR 1997; 168: 193-197.

25. Cameron JL, Hruban RH, Pitt HA, Siegelman SS, Soyer P, Fishman EK. Potentially resectable pancreatic
adenocarcinoma: spiral CT assessment with surgical and pathologic correlation. Radiology 1995; 197: 381-385.

26. Megibow A, Zhou X, Rotterdam H et al. Pancreatic adenocarcinoma: CT versus MR imaging in the evaluation of
resectability report of the diagnostic oncology group. Radiology 1995; 195: 327-332.

27. Lewandrowski K, Lee J, Southern J, Centeno B, Warshaw A. Cyst fluid analysis in the differential diagnosis of
pancreatic cysts: a new approach to the preoperative assessment of pancreatic cystic lesions. AJR 1995; 164: 815-819.

28. Van Hoe L, Gryspeerdt S, Marcha l, Baert AL, Mertens L. CT for the preoperative localization of islet cell tumors
of the pancreas: value of arterial and parenchymal phase images. AJR 1995; 165: 1437-1439.

29. Yamamoto K, Ishii Y, Furudate M et al. Phase 3 multicenter clinical study of 111In-DTPA-D-octreotide (MP-1727)
in patients with gastrointestinal hormone producing tumors. Jpn J Nuclear Med 1995; 32: 1269-1280.

30. Buetow PC, Parrino TV, Buck JL et al. Islet cell tumors of the pancreas: pathologic-imaging correlation among size,
necrosis and cysts, calcification, malignant behavior, and fuctional status. AJR 1995; 164: 1175-1179.

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9
The Kidney, Bladder, Prostate and Testes

Walter Curati and Gordon Williams

Renal tumours

Bladder tumours

Prostate tumours

Testicular tumours

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Over the last 10 years medical imaging has considerably improved the diagnosis and staging of renal, bladder, prostate
and testicular tumours. For the kidney alone, the incidental discovery of a solid space-occupying lesion during an
abdominal ultrasound investigation amounts to approximately one-third of all renal cell carcinomas. 1, 2

The `classic' presentation of haematuria, pain and mass is rare and only occurs in large tumours.3 In up to 50% of cases
two symptoms are present. Haematuria alone is present in 33% of cases and means that the neoplastic lesion extends
into the pelvicalyceal system.

In a patient found to have a renal mass, ultrasound will differentiate a cyst from a solid tumour much more reliably than
CT. The smaller the cyst, the more difficult the assessment is by CT. If ultrasound rules out a simple cyst, Doppler
studies, in particular power Doppler, and more recently ultrasound contrast agents, can assess its vascularity as
consistently as a contrast-enhanced CT. CT has a role in staging as statistically 85% of all solid renal tumours are renal
cell carcinomas and almost all tumours of the pelvicalyceal system are malignant.

This chapter focuses on imaging techniques for the renal tract and establishes algorithms for a logical investigative
process.

Renal Tumours

Renal tumours represent approximately 3% of all malignancies in the adult population. Males between the ages of 50
and 70 are most likely to develop such a tumour. Renal cell carcinoma (adenocarcinoma, hypernephroma) is responsible
for approximately 90% of all primary renal tumours and the transitional renal cell carcinoma of the pelvicalyceal system
for approximately 10%.

Renal Cell Carcinoma

Renal cell carcinoma has an incidence of 3.5 per 100 000 population per year. It is a tumour found in adults with a M:F
sex ratio of approximately 2:1. It is a solitary tumour in 80% of cases. Multiple primaries are commonly linked with the
von Hipple-Lindau hereditary syndrome. The renal cell carcinoma presents genetically with a DNA alteration (a
deletion) on chromosome 3. This is also found in patients with von Hipple-Lindau syndrome. In about half of these
cases an additional deletion occurs on chromosome 5.

Renal cell carcinoma most commonly develops within the renal cortex. The more peripheral it is, the more the outline of
the organ is distorted. The vascularity of the tumour involves enlarged feeding arteries and draining veins. These
characteristics are obviously valuable diagnostic features for Doppler ultrasound (power Doppler, in particular, with
contrast-enhancing agents), contrast-enhanced CT and angiography. Part of the course of these tumours is frequent
necroses and haemorrhages leading to cystic spaces. Some tumours, however, are initially cystic4 with thick, irregular
walls comprising one or more mural nodules.

There are three other types of renal cell carcinoma:

Chromophobe cell carcinoma (renal `C' adenocarcinoma)

Tubulo-papillary carcinoma (renal `TP' adenocarcinoma)

Collecting tubule carcinoma (renal `B' adenocarcinoma)

which together represent approximately 15% of all renal cell carcinomas.

The TNM classification for staging renal cell carcinoma is:

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T0: No evidence of tumour

T1: Less than 2.5 cm, intrarenal

T2: More than 2.5 cm, still intrarenal

T3a: Tumour invades the adrenal or the fat within Gerota's fascia

T3b: Tumour invades the inferior vena cava still under the diaphragm

T3c: Tumour invades the inferior vena cava above the diaphragm

T4: Tumour extends beyond Gerota's fascia

Carcinosarcomas, as the name suggests, are poorly differentiated and invasive and have a poor prognosis.

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Figure 9.1
Right renal cell carcinoma diagnosed and resected during pregnancy in a 24-year-old patient.
a) and b) MRI contiguous T1-weighted SE coronal sections demonstrating a 5 cm intermediate
signal mass at the right lower pole. c) and d) MRI contiguous STIR coronal sections: same lesion with
lower signal return than the rest of the kidney. e) and f) US mixed echoic pattern within a 5 cm mass of
the lower pole of the right kidney (arrows delineate the mass).

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Figure 9.2
MRI scans of the brain. a) Post contrast enhanced
T1-weighted SE axial image above the lateral
ventricles: multiple small high signal lesions are
identified. b) 2 months later the disappearance of the
metastases is demonstrated.

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Figure 9.3
Metastatic renal cell carcinoma in a
64-year-old female patient. a) Postero-anterior
(PA) chest radiograph: widening of the right upper
mediastinum (arrow) and right hilum (open arrows)
and metastatic lymph nodes are seen. b) Frontal
and c) oblique views of the right humerus. Internal
fixation to prevent patholgical fracture
secondary to a large osteolytic metastasis of the
mid-diaphysis with periosteal reaction and soft
tissue involvement (arrows).

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Figure 9.4
Renal cell carcinoma in a 60-year-old male patient. CT a) pre- and b) post-contrast images at the level of the
hilum of the left kidney. CT c) pre- and d) post-contrast images at the lower pole. An enhancing mass with
a large area of necrosis (small arrows) extends beyond the capsule and accesses the Gerota's fascia. The left
renal vein is invaded by tumour (large arrow).

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Figure 9.5
Metastatic renal cell carcinoma in a 51-year-old female patient. a) Chest X-ray showing multiple large
pulmonary and hilar metastases. b) Contrast-enhanced CT of the brain showing small right
frontal metastasis (arrow).

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Figure 9.6
A 63-year-old male patient with a complicated cyst in the left kidney and simple cysts in the right kidney.
a) and b) Contrast-enhanced CT at 1 cm intervals. Contiguous section at the interpolar region of the left
kidney showing irregular system and soft tissue posteriorly. c) and d) Ultrasound coronal section with
magnified area detailing a thick septum. On colour Doppler the vascular signal is returned.

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Figure 9.7
see caption overleaf

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Figure 9.7
Metastatic renal cell carcinoma in a 20-year-old male patient. a) Intravenous urogram showing
deformity of the right pelvicalyceal system with mass effect (arrows). b) Chest X-ray showing nodoreticular
pattern which is consistent with lymphangitis. (c) & (d) US: 5 cm mixed echoic mass in axial and coronal
planes. (e) & (f) Contrast enhanced CT: Contiguous scans. Mixed attenuation 5 cm mass at the level of
right hilum large retroperitoneal nodes (large arrows) displacing renal veins and right renal artery (small
arrows).

Less malignant renal tumours are:

1. Oncocytomas are characterized by masses containing exclusively cells with eosinophilic cytoplasm. They are usually unique but
can be found in kidneys presenting with renal cell carcinoma. 5 Oncocytomas are well circumscribed, partly encapsulated tumours
and can grow up to 10 cm in diameter. They rarely recur or metastasize.6

2. Renal adenomas are, as far as imaging is concerned, a very artificial subdivision of renal cell carcinomas as they are small but can
metastasize. However, it is true that genetically they present a trisomy 7 or 17 and the alteration of chromosome 3 is absent. They are
very commonly small (< 1 cm) and well circumscribed.

3. Angiomyolipomas occur in 80% of patients presenting with tuberous sclerosis. They are single in 80% of the cases. Middle-aged
females are more frequently affected with a F:M sex ratio of 2:1. In total they represent only 1% of all operated renal tumours.
Angiomyolipomas are lobulated and by definition contain blood vessels, muscular bundles and fat tissue in variable proportions.
They are benign but of high morbidity if more than 4 cm in diameter8, 9 as they bleed repeatedly.

Transitional Cell Carcinoma

These urothelial tumours are histologically identical to urothelial bladder tumours. They represent 7% of all malignant tumours of the
kidney. Macroscopically and radiologically they grow within the pelvicalyceal system and ultimately tend to occupy it entirely. They
can also infiltrate the renal parenchyma.

They can be classified as follows:

Grade 1: well differentiated cells

Grade 2: moderately differentiated cells

Grade 3: poorly differentiated cells.

The majority of the transitional cell carcinomas are Grade 2.10

In one-third of patients, the tumours are multiple. The multiplicity rate is highest for Grade 3. As demonstrated in cases of simple
nephrectomy, further tumours can develop down the ureter in approximately 50% of cases. Transitional cell carcinomas are bilateral
in 10% of patients. Metastases to bone, lung and liver (one-third each) occur in less than 20% of patients and usually relate to Grade
3 tumours.

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There are several interesting epidemiological aspects of transitional cell carcinomas. Its incidence is 100 times higher in patients with
Balkan nephropathy (along the Danube River, south of Belgrade).11 Risk factors include tobacco (a 6-fold increase in male smokers
and 8-fold in females12), chemicals (aniline, benzidine, solvents) and phenacetin (above a cumulative dose of 1 kg). The
chromosomal abnormality is directly related to carcinogen exposure: urothelial abnormalities are more sensitive to carcinogens.13

The TNM staging for transitional cell carcinoma is:

T0: No evidence of tumour

Ta: Non-invasive papillary carcinoma

Tb: Carcinoma in situ

T1: Tumour infiltrating the submucosa

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T2: Tumour infiltrating the muscular wall

T3: Tumour infiltrating the renal pelvic fat or the kidney

T4: Tumour extending through the kidney into the perirenal fat or adjacent organs

Squamous Cell Carcinoma, Cholesteatoma and Mucinous Adenocarcinoma

Squamous cell carcinoma of the renal pelvis is a rare tumour of the kidney. It is very infiltrative and commonly presents
with metastases. Chronic infections and calculi are predisposing factors with calculi present in more than 50% of cases.

Cholesteatoma (or squamous metaplasia) is related to infected stones and presents as irregular filling defects of the
collecting system.

Mucinous adenocarcinoma is a variant of adenocarcinoma and is rarely encountered.

Metastases

According to large autopsy series, renal metastases are three times more common than primary tumours. Bilateral
involvement is demonstrated in 50% of cases. The percentage of primary tumours presenting with renal metastases is
shown in Table 9.1.

At autopsy the kidneys are involved in 60% of cases of non-Hodgkin's lymphomas, 15% of Hodgkin's lymphomas and
20-60% of various leukaemias (according to type).

Bladder Tumours

Bladder carcinoma is the most frequent malignant neoplasm of the urinary tract. Carcinoma of the bladder is most
prevalent in the 50-70 year age group and is more

Table 9.1 Percentage of primary tumours presenting with rental

metastases.
Primary tumour Renal deposits (% of cases)
Bronchus
20
Breast
15
Pancreas
12
Colon
12
Ovaries
8
Rectum
6

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Prostate
4
Melanoma
2

Figure 9.8
Large transitional cell carcinoma of the bladder in a
49-year-old patient. Contrast-enhanced CT section at
the midpelvic level. Note the marked irregular thickening
of the bladder walls. The tumour remains confined to the
pelvic fat with strands of soft tissues surrounding the
bladder.

common in men than in women with a M:F sex ratio of 3:1. 14 Transitional cell carcinomas represent approximately
90% of all bladder tumours and develop as papillary or sessile growth. Amongst the other tumours (10% in total),
adenocarcinomas, leiomyomas, fibromas (non-malignant) and leiomyosarcomas and fibrosarcomas (malignant) are
classical. Metastases from other organs are rare. It should be remembered that the pheochromocytomas (endocrine),
endometriosis (endocrine-sensitive) and haemangiomas of the benign type are very symptomatic and are therefore
worth mentioning here.

The TNM classification for staging bladder cancer:

Ta: Confined to mucosa

T1: Invades the submucosa (lamina propria)

T2: Invades superficial muscle

T3a: Invades deep muscle

T3b: Invades perivesical fat

T4: Invades pelvic organs.

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Prostate Tumours

Benign prostatic hypertrophy is mentioned here as it should be included in the differential diagnosis for carcinoma of
the prostate. Benign prostatic hypertrophy with intravesical enlargement causes elevation of the trigone resulting in a `J'
or fish-hook deformity of the ureters. Bladder outlet obstruction produces trabeculations of the bladder with in some
cases diverticular formation.

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Carcinoma of the Prostate

Carcinoma of the prostate is the commonest cancer identified at autopsy from the age of 50 (30%) to 90 (90%) with a
linear progression. More than 95% of all tumours are adenocarcinomas. The clinical presentation varies from frequent
micturition (most commonly without haematuria) to symptoms of bone or low back pain secondary to bone metastases
and less commonly to renal failure due to ureteric obstruction by tumour infiltration or haemorrhages due to the release
of prostatic fibrinolysin in the systemic circulation. The diagnosis is established by histological confirmation following
biopsy.

The zonal model describes three main zones within the prostate:

peripheral zone (70% of all cancers)

central zone (10%)

transitional zone (20%).

Staging is particularly important for prostate cancer as in recent years nerve sparing radical prostatectomy techniques
have been developed and can cure the patient. The Jewitt & Whitmore classification 15 for prostate cancer staging is
shown in Table 9.2,

Prostatic specific antigen (PSA) assays and increased awareness of symptoms and signs lead to earlier diagnosis of
prostatic cancer and improved long-term outcome.

Transrectal ultrasound (TRUS) has the advantage of allowing precise assessment of the capsular integrity or penetration
(the most relevant parameter as mentioned above). Ultrasound-guided biopsies of sites of possible extension also allow
assessment of degree of tissue differentiation (stages T1a or A1) and are key to accurate staging.

CT scanning is used for the staging of prostate cancer but not for the primary localization of the tumour as direct
visualization is not possible (which also means that stages T1 and T2 (TNM) or A and B (Jewitt & Witmore) are not
seen on CT examination). CT is used for the evaluation of suspected direct periprostatic extension: pelvic soft tissues
(fat planes) or organs such as seminal vesicles, bladder and rectum, and local or distant adenopathies. The further
problem when using CT for staging is the lack of definition of internal architecture in normal sized nodes (<1 cm)
potentially containing small areas of metatases and in enlarged nodes with fibrotic changes only and thought to be
metastatic. CT, however, allows precise targetting of enlarged nodes for biopsies.

Table 9.2 Jewitt & Witmore classification 15 fro prostate cancer staging.
TNM Stage Definition
A Non-palpable cancer
T1a A1 < 5% of tissue (well differentiated tissue)
T1b A2 > 5% of tissue (or poorly differentiated tissue)
T1c
B Palpable nodule confined within the prostatic capsule
T2a B1 Palpable nodule < 1.5 cm in diameter
T2b B2 Palpable nodule > 1.5 cm in diameter
T3-T4 C Extension beyond the prostatic capsule without distant metastases
D Metastases

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N D1 Metastases to regional lymph nodes

M D2 Metastases to bone or viscera

MRI is the imaging modality of choice for the anatomical assessment of the lobes of the prostate and the seminal
vesicles: the outline of the tumour is a clear interface between its low signal (on T2-weighted images) and the high
signal of the normal gland, the periprostatic venous plexus and the seminal vesicles. The invasion of the adjacent organs
and the metastatic lymph node involvement is also seen more clearly with MRI than CT due to the multiplanar
capability of MRI: primary acquisitions in

Figure 9.9
Metastatic adenocarcinoma of the prostate in an
82-year-old patient. The nuclear medicine bone scan
shows multiple areas of focal increased uptake which
is consistent with metastases.

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coronal and sagittal planes improve the assessment of integrity of neighbouring structures. These considerations apply
both to body coil and endorectal coil MRI. The conventional body coil technique provides a broad field of view for the
pelvis whereas the endorectal coil technique provides high resolution imaging for the accurate preoperative staging of
localized prostate cancer. 16

Testicular Tumours

Testicular tumours normally present with a painless lump in the testicle. The practice of testicular self-examination with
increased awareness of testicular neoplasm has led to patients presenting at an earlier stage of the disease. This positive
trend is somewhat offset by the increased incidence of testicular cancer in the second half of this century.17

Of all testicular tumours, 90% arise from germ cells and are malignant. They can be divided into two groups:
seminomas and non-seminomatous tumours. The former are the most frequent and they present around the age of 40
and are highly radiosensitive. The non-semi-nomatous group presents during the teenage years. The staging for
testicular cancer is shown in Table 9.3.

The non-seminomatous tumours include:

Type Incidence Age Prognosis

20% 30yrs Poor

Embryonal carcinoma (metastases +)

Teratomas 10% 10-30yrs Good

Choriocarcinoma rare 20-30yrs Poor

(metastases ++)

rare < 10yrs Poor

Yolk sac carcinoma (metastases ++)

30% Variable Variable

Mixed pattern teratocarcinoma

Spread occurs via the regional lymphatics (except for choriocarcinoma and yolk sac carcinoma) along the spermatic
vein to sentinel nodes lateral to the paralumbar nodes on the left in the renal perihilar region at the level of L1/L2 and on
the right in the paracaval region below the renal artery and vein (L1-L3). From the retroperitoneal level the lymphatic
spread extends via the thoracic duct into the mediastinum and lungs. (Choriocarcinoma and yolk sac carcinoma present
with hematogenous spread).

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Table 9.3 Staging for tesicular cancer

AJC TNM UICC TNM
(American Joint (Union Internationale Centre le Cancer)
Committee)
Stage I T1 : Tumour occupying less than half of testis
surrounded by palpably normal gland
T2 : Tumour occupying half or more of testis
with no enlargement or deformity
T3 : Tumour confined to testis, causing
enlargement or deformity
T4a : Tumour extending to epididymis
Stage II T4b : Tumour invading other local structures
N0 : No deformity of regional lymph nodes on
lymphangiography
N1 : Regional lymph nodes deformed on
lymphangiography
N2 : Fixed, palpable lymph nodes
Stage III N1 : Metastases to nodes outside the abdomen
or to viscera
Stage IV Metastases to lung and liver

Lymphangiography, CT and MRI can all assess the retroperitoneum. Lymphangiography, the earliest technique,
demonstrates involvement even in non-enlarged lymph nodes but is invasive and time consuming (up to fours hours for
the initial phase of the investigation). Its success rate is similar to that of CT. CT has advantages over
lymphangiography in that it is non-invasive (except for intravenous administration of contrast), can assess the viscera
and the non-opacified lymph nodes and in particular screens the liver and the lungs. CT is also the routine modality for
follow-ups. MRI is as sensitive as CT in imaging the pelvis, retroperitoneum and liver but is of little value in the chest.
CT should still therefore be performed for the lungs.

References

1. Nakano E, Iwasaki A and Seguchi T. Incidentally diagnosed renal cell carcinoma. Eur Urol 1992; 21: 294-298.

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2. Özen H, Colowick A and Freiha FS. Incidentally discovered solid renal masses: what are they? Br J Urol 1993; 72:
274-276.

3. Chisolm GD. Nephrogenic ridge tumours and their syndromes. Ann NY Acad Sci 1974; 230: 402-423.

4. Davidson AJ, Hartman DS and Choyke PL. Radiographic assessment of renal masses: Implications for patient care.
Radiology 1997; 207: 297-305.

5. Lense E, Siegel R and Hewan-Lowe K. In situ oncocytic change is association with multiple renal cell
adenocarcinomas. Arch Pathol Lab Med 1991; 115: 1067-1069.

6. Licht MR, Novick AC and Tubbs RR. Renal oncocytoma: Clinical and biological correlates. J Urol 1993; 150:
1380-1383.

7. Kovacs G. Application of molecular cytogenetic techniques to the evaluation of renal parenchymal tumours. J Cancer
Res Clin Oncol 1990; 116: 318-323.

8. Blute ML. Angiomyolipoma: Clinical metamorphosis and concepts for management. J Urol 1988; 139: 20-24.

9. Wills JS. Management of small renal neoplasm and angiomyolipoma: a growing problem. Radiology 1995; 197:
583-586.

10. Guinan P, Vogelzang NJ and Randazzo R. Renal pelvic cancer: a review of 611 patients in Illinois 1975-1985.
Urology 1992; 40: 393-399.

11. Cukuranovic R, Ignjatovic M and Stefanovic V. Urinary tract tumours and Balkan nephropathy in the south Moravia
River basin. Kidney Int 1991; 40: 580-584.

12. McLaughlin JK, Silverman DT and Hsing AW. Cigarette smoking and cancers of the renal pelvis and ureter. Cancer
Res 1992; 52: 254-257.

13. Greenland JE, Weston PM and Wallace DM. Familial transitional cell carcinoma and the Lynch syndrome II. Br J
Urol 1993; 72: 177-180.

14. Heiken JP, Forman HP and Brown JJ. Neoplasms of the prostate, bladder and testis. Radiol Clin N Am 1994; 32:
81-98.

15. Whitmore WF Jr. Natural history staging of prostate cancer. Urol Clin North Am 1984; 11: 205-220.

16. Cavanagh PM. Staging of prostate cancer: the role of MRI. Clin MRI 1997; 7: 4-10.

17. Richie JP. Neoplasms of the testis. In: Walsh PC, Retik AB, Stamey TA, and Vaughan ED (eds) Campbell's
Urology, 6th Edition. Philadelphia 1992, WB Saunders, vol.2, pp 1222-1263.

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10
The Endocrine System

Daniel A Darko and Karim Meeran

Pituitary gland

Thyroid gland

Adrenals

Gut hormone tumours

Testicular tumours

Ovarian tumours

Bone

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Endocrine cells produce and secrete specific substances which act as messengers to cells at different sites. In addition,
many produce receptors for other hormones, such as somatostatin. Techniques that visualize these unique features make
endocrine malignancy amenable to imaging. In addition, the fact that some endocrine malignancies secrete large amount
of hormones enables angiography to be combined with selective venous sampling and assay of the samples for
particular hormones. However, before considering the more specialist imaging methods, it is important to remember
that plain radiology is extremely important in many endocrine diagnoses.

As well as the classical endocrine system, which includes the pituitary, thyroid, adrenal glands, ovaries, testes,
parathyroid and pancreas, the gut and bone are also recognized as important endocrine organs. Many of the neoplasms
in endocrine disease are benign histologically but can be life threatening because of the hormones they produce. In
addition, there are some inheritable neoplasias and these have been classified with eponymous names, e.g. multiple
endocrine neoplasia (MEN) type 1 (Sipple syndrome), MEN 2 and Von Hippel Lindau syndrome. In MEN 1, there is an
autosomal dominant risk of individuals developing parathyroid adenomata or hyperplasia (causing hypercalcaemia),
pituitary adenomata (causing prolactinomas, acromegaly or Cushing's disease) or pancreatic neoplasia. The gene for
MEN 1 is coded for on chromosome 11. It has recently been cloned 1, 2 and the gene product has been labelled
`MENIN' but, remarkably, the function of this protein is unknown. In von Hippel Lindau syndrome, patients have an
autosomal dominant risk of phaeochromocytomas, cerebellar and spinal haemangioblastomas, retinal haemangiomas
and renal cell carcinoma. The gene for this condition is coded for on chromosome 3 and the protein product is a tumour
suppressor gene. Patients known to have any of the inherited endocrine neoplasias are regularly screened for the
development of the relevant tumours, usually by imaging the appropriate area.

Pituitary Gland

The pituitary gland sits in the pituitary fossa of the sphenoid bone of the skull. A plain lateral X-ray can show
destruction of either of the clinoid processes or an enlarged fossa in pituitary adenomas. In addition, specific pituitary
tumours can produce particular changes in the lateral skull X-ray. Acromegaly, for example, causes thickening of the
skull vault and enlargement of the sinuses as well as a large pituitary fossa. Other pituitary adenomas tend to be small
and hence do not produce changes in a lateral skull X-ray. More than 90% of prolactinomas and almost all
corticotrophinomas (Cushing's disease) are microadenomas (i.e. <1 cm in diameter) and those as small as 1 mm in
diameter can be visualized using both CT and MRI scanning. It is also important to look for deviation of the stalk as this
may be the only evidence of a microadenoma.

Occasionally, pituitary tumours outgrow their blood supply and hence autoinfarct. At the time of infarction, patients
may present with headache, visual disturbance and diplopia, a condition known as pituitary apoplexy. This may be the
first sign of any pituitary abnormality. Often, however, even the infarction goes undiagnosed and patients may have
normal pituitary function. Imaging of such a patient may show no obvious pituitary tissue or an empty sella. Normal
pituitary cells may be distributed at the edge of the fossa. The term `empty sella syndrome' has been used to describe the
presence of an empty sella in patients with headache who may be obese.3

Suspected Cushing's Disease

In patients with suspected Cushing's disease (who by definition have a pituitary tumour secreting ACTH, also known as
a `corticotrophinoma'), inferior petrosal sinus sampling (IPSS) and assay of the samples for ACTH has become routine
before transsphenoidal hypophysectomy. Otherwise hypophysectomy may be erroneously carried out in patients with
another cause of Cushing's syndrome, such as ectopic ACTH or adrenal adenomas. IPSS is generally performed by
interventional radiologists and serves to confirm not only that the pituitary adenoma is the source of the problem, but
also the side on which it lies.4

One catheter is inserted into each femoral vein, and threaded up under X-ray control into the inferior petrosal sinuses.
As both lines traverse the inferior vena cava, where the two lines may cross over, it is important to be sure of which side
each catheter is placed by injecting contrast into each line immediately before the start of the procedure.

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Once each line is correctly placed, blood must be allowed to flow freely and collected drop by drop from the end of the
catheter. Aspiration, if required, must be performed very slowly, as fast aspiration will draw blood from surrounding
structures and may artificially lower ACTH concentrations in the samples. To ensure the catheters are correctly placed,
other pituitary hormones (thyrotropin

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(TSH) and prolactin) are usually measured. Two baseline samples are drawn at 5 min intervals from each inferior
petrosal sinus. Peripheral samples are also drawn and are essential for final interpretation of the results and to confirm
that the catheters are correctly placed. After the second baseline sample has been drawn, an intravenous bolus of
corticotrophin releasing factor (CRF) is administered, and three further samples are taken at 5 min intervals. A typical
set of results, confirming a left-sided pituitary adenoma, is shown in Table 10.1. 4

Occasionally, excess ACTH comes not from the pituitary but from an ectopic source, such as a bronchial carcinoma or
adenoma, or from the pancreas. Patients with ectopic ACTH usually present with profound hypokalaemia, weakness,
and, if they have malignant neoplasms, classical truncal obesity may not be obvious because of weight loss. In such
patients, cortisol levels usually do not suppress with either low- or high-dose dexamethasone, but occasionally
suppression does occur. If IPSS is performed in these patients, the peripheral sample will have a similar (or higher)
ACTH than the central ones.

Acromegaly

These tumours are often large and can threaten nearby structures, including the optic chiasm. As stated previously, a
lateral skull X-ray may show destruction of bone locally. In addition, the skull vault may be thickened and the sinuses
large. A CT or MRI scan will show the size of the tumour more accurately and will indicate whether there is pressure on
the optic chiasm. Hand X-rays will show spade-like hands with soft tissue enlargement and tufting of the distal
phalanges (Fig. 10.1). Because these patients often have diabetes, lateral foot X-rays may show calcification of the
dorsalis

Table 10.1 Typical ACTH levels for a left-sided pituitary

corticotrophinoma.
ACTH level
Inferior petrosal sinus
samples
Time* Peripheral sample Left Right
-5
25 95 25
0
27 93 30
+5
85 4560 140
+ 10
125 2990 155
* Time from CRF bolus (min)

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Figure 10.1
Hand X-ray of patient with acromegaly.

pedis and the heel pad may be thickened. Visceral organomegaly also occurs and scanning of the abdomen may show
this. Importantly, acromegalics are at risk of colonic carcinoma,5, 6 and because of their very long colon, colonoscopy
may be difficult. In these instances, barium enemas need to be performed every 3-5 years. Any adenomata must be
colonoscopically removed.

Prolactinomas

Microadenomas account for 90% of prolactinomas. In women, they often present with amennorrhoea or galactorrhoea
in women. In men, microadenomas go undetected because the male breast is not oestrogenized and men present either
with loss of libido, or later with features of a macroadenoma, such as visual loss or seizures. The belief that men have
macroadenomas while women have microadenomas may therefore be due to reporting bias, although there is some
evidence that prolactinomas in males are more aggressive and less responsive to medical therapy.7, 8 CT or MRI of the
pituitary may confirm the adenoma, and if very small, often the only feature is deviation of the pituitary stalk.
Prolactinomas often respond to dopamine agonists such as bromocriptine or cabergoline. Prolactin levels fall and the
tumour shrinks. Rescanning after a year of dopamine agonist treatment is useful to confirm this. Patients whose tumours
grow despite dopamine agonists may require surgery or radiotherapy.

Thyroid Gland

The thyroid gland is unique in that normal thyroid cells as well as differentiated thyroid tumours usually take up iodine.
Cold iodine has a molecular weight of 127. Two

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isotopes of iodine, 131I and 123I, have a relatively short half-life and can therefore be used in vivo, both in the
diagnosis and treatment of thyroid dysfunction. In addition, thyroid C-cells (which are embryologically derived from
neural crest cell that migrate into the 3rd and 4th branchial arches amongst others to form the amine precursor uptake
and decarboxylation (APUD) cell series take up metaiodobenzylguanidine (MIBG) and patients with medullary thyroid
carcinoma have a high uptake of this compound. Adrenal medullary chromaffin cells (classical APUD cells), which are
also of neural crest origin, take up MIBG and high adrenal uptake is seen in patients with phaeochromocytomas (see
below). The MEN 2 syndrome is an autosomal dominant disorder and is secondary to a mutation of the specific
proto-oncogene RET, which codes for a tyrosine kinase on chromosome 10. There are three subtypes of MEN 2 (Table
10.2). 9

Thyrotoxicosis

This is caused by an excess of thyroid hormone in the circulation. It can occur either because of a toxic hypersecreting
thyroid nodule within a normally suppressed thyroid gland, or because of Graves' disease, where an autoantibody may
stimulate the entire gland to become overactive. Radioactive iodine uptake can also be quantified and gives a measure
of thyroid activity. It can be particularly useful in distinguishing viral (`De Quervain's') thyroiditis from Graves disease'.
Both can cause hyperthyroidism but radioactive iodine uptake is suppressed in viral thyroiditis (Fig. 10.2) and increased
in Graves' disease (Fig. 10.3). In patients with hyperthyroidism, 99mTc-pertechnetate is used to distinguish a toxic
nodule (Fig. 10.4) from Graves' disease (Fig. 10.3). Fig. 10.5 shows a normal 99mTc-pertechnetate scan from the same
patient as shown in Fig. 10.4 but after a therapeutic dose of radioiodine.

Table 10.2 Characterization of three types of the multiple endocrine

neoplasia (MEN) syndrome type 2.
MEN MEN FMTC
2a 2b

Parathyroid hyperplasia

Phaeochromocytoma
medullary thyroid carcinoma (MTC)

Marfanoid habitus

Bowel ganglioneuromatosis
FMTC = familial medullary thyroid carcinoma.

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Figure 10.2
99m Tc-pertechnetate scan in patient
with De Quervain's thyroiditis.

Thyroid Carcinoma

Plain X-rays rarely provide useful information in the management of thyroid neoplasms but on occasion may show bony
or lung secondaries.

For many patients with a thyroid mass, an ultrasound scan is often the first evaluative test they have. A high-resolution
ultrasound in the hands of a good operator can assess nodules as small as 5 mm in diameter. Malignant thyroid nodules
are often poorly defined with irregular margins and are hyperechoic,10 while benign thyroid cysts have a typical smooth
wall with no internal echoes, although they occasionally contain some debris. Calcification within or around a cyst is
associated with neoplasia and invasion of neck muscles or vasculature is highly suggestive of malignacy.11 Finally,
ultrasound can be used for the localization and biopsy of small tumours and local recurrent disease.

CT provides high-definition images of the thyroid, especially any retrosternal extension. It poorly differentiates benign
from malignant masses and its main use is to define the anatomy of the neck region prior to surgery. Spiral CT is
superior to conventional CT in this respect because it collates images faster and thereby eliminates movement artifact.
MRI is similar to CT for imaging the thyroid but is more expensive. It has been described in combination with proton
spectroscopy to distinguish follicular adenomas from carcinomas.12

Thyroglobulin assays are the mainstay for the detection of recurrence or metastases. However, imaging in addition to
clinical examination provides useful information. Radioiodine is trapped and organified by the thyroid and aberrant
thyroid tissue or metastases,

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Figure 10.3
99m Tc-pertechnetate scan in patient with Graves' disease.

Figure 10.4
99m Tc-pertechnetate scan in patient with a toxic nodule.

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Figure 10.5
Normal 99m Tc-pertechnetate scan in patient
after therapeutic iodine.

making it a highly specific test. The sensitivity of radioiodine is influenced by diet, drugs (especially amiodarone) and
tumour histology.

123I has a short half-life (13 hours) and releases short-energy γ-rays. It is the ideal isotope for thyroid imaging. 131 I
has a longer half-life (8 days) and emits a high-energy γ-ray and a β particle, making it best suited for treatment, but
because it is cheaper, easier to obtain and can be stored for longer before use than 123I, it is widely used for imaging as
well as treatment. Use of 131I in imaging requires knowledge of the the physiological sites of iodine concentration and
the causes of artifacts, in order to avoid potential suppression of active thyroid tissue during diagnostic scanning
(thyroid stunning). Many centres limit the amount of radioiodine administered to 74-111 Mbq. 13 To maximize TSH
stimulation of the remaining thyroid tissue, thyroxine therapy should be stopped 4-6 weeks before radioiodine body
scanning. In patients unable to tolerate the hypothyroidism that this induces, a switch to tri-iodothyronine (T3) for 3-4
weeks after thyroxine is discontinued is advised. T3 is then stopped 8 days before scanning. As amiodarone has a
half-life of 30 days and a large excess of cold iodine (127I), patients on amiodarone cannot be imaged with radioiodine.
Patients must discontinue amiodarone for at least 6 months if radioiodine scanning is required. Alternatively, thallium
scans may be used for the detection of local and cervical metastatic disease. These are less sensitive than 131I in
therapeutic doses but may show up metastases that are not seen with any other modality.14

Anaplastic carcinoma of the thyroid poorly concentrates iodine and often does not express thyroglobulin. For this reason
nuclear scanning with radioiodine for diagnosis or treatment is not used. Debulking surgery or radiotherapy may be
carried out to relieve tracheal or airway obstuction.

For well-differentiated thyroid carcinoma, current common practice for surveillence involves radioiodine scanning after
surgery at 6-9 months and then yearly for the next 3 years and a repeat scan at 5 years.15

Parathyroid Disease

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Primary hyperparathyroidism is a common condition affecting about 1% of the population. It is often is discovered
incidentally. The diagnosis is made by the combination of a high calcium with a non-suppressed parathyroid hormone
(PTH). Asymptomatic cases are often observed for a number of years, but the only successful treatment is removal of
the offending parathyroid. Multiple adenomata are present in 20% of cases and imaging of the parathyroids before
surgery is useful.

Simple imaging such as ultrasound can be used to demonstrate lesions. Thallium scanning shows total blood flow to the
thyroid and parathyroid, and the parathyroids can thus be visualized using digital subtraction of 99Tc (which shows the
thyroid) from thallium. 99Tc-sestamibi scanning (Fig. 10.6) is more sensitive and specific for the diagnosis of primary
hyperparathyroidism than thallium-technetium subtraction scanning16 or CT or MRI scanning.17

Medullary thyroid carcinoma (MTC) often presents with a neck mass or raised calcitonin or CEA levels. Ultrasound and
CT are efficient at picking up tumours > 1 cm in diameter. MIBG has been used in the same way as for the detection of
phaeochromocytomas but has a low specificity.18 Newer compounds being evaluated for visualization of MTC include
octreotide.

Adrenals

Phaeochromocytomas

These are usually (90%) benign and come from adrenal chromaffin cells and are hence APUD cells and take up MIBG.
Fig. 10.7 shows an MIBG scan from a patient with bilateral phaeochromocytomas. The diag-

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Figure 10.6
Sestamibi scan in patient with parathyroid adenoma (arrow).

nosis is made when there are high urinary catecholamines and patients often present with episodic hypertension. Adrenal
phaeochromocytomas usually secrete adrenaline whereas extra-adrenal phaeochromocytomas may secrete more noradrenaline.
Ninety per cent of phaeochromocytomas occur in the adrenals with 10% being extra-adrenal (Fig. 10.8). Phaeocromocytomas are
associated with the MEN 2 syndrome, von Hippel-Lindau syndrome and neurofibromastosis. Approximately 10% of these tumours
are malignant and metastatic lesions often deposit along the skeletal axis. The natural history of malignant phaeochromcytoma is
variable and there are several case reports in the literature of > 5-year survival with medical treatment.

Patients with phaeochromocytomas need imaging before surgery to localize the lesion. Plain chest X-rays are useful and provide
information about metastases and any degree of heart failure. Flush aortography is an invasive technique that carries the real risk of
provoking a hypertensive crisis and is now rarely used.

Ultrasound may be useful to investigate large masses within the adrenal gland. MIBG scanning combined with CT scanning of any
hot areas (Fig. 10.9) is now the major method for imaging phaechromocytomas.

Figure 10.7
MIBG scan in patient with bilateral
phaeochromocytomas.

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Figure 10.8
Metastatic phaeochromocytoma.

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Figure 10.9
CT scan from same patient as in Fig. 10.7.

Following intravenous administration, MIBG is actively concentrated in chromaffin cell granules and scintinography is considered to
have >95% specificity for the detection of phaeochromocytomas. 131I and 123I have both been used for radiolabelling and the latter
isotope allows the operator to combine MIBG scaning with single photon emission tomography (SPECT) to provide clearer definition
and anatomy. Our approach to initial imaging is to scan the whole body using MIBG, followed by high-resolution (spiral) CT of areas
with abnormally high uptake. Fig. 10.9 shows the CT scan of the patient with bilateral phaeochromocytomas whose MIBG scan is
shown in Fig. 10.7.

Conn's Syndrome

Primary hyperaldosteronism accounts for < 2% of cases of hypertension. The diagnosis should be suspected in all hypertensive
patients with a low serum potassium but, to confirm the diagnosis, plasma aldosterone levels must be high and renin levels sampled at
the same time must be low. The temptation to scan patients with unexplained hypokalaemia but no biochemical evidence of Conn's
syndrome should be avoided because up to 5% of abdominal CT scans detect incidental masses in the adrenal glands. CT can detect
adrenal masses < 1 cm in diameter. Adrenal hyperplasia is always bilateral and both glands are enlarged. Adrenocortical carcinoma,
which is very rare (1% of cases), is commoner in tumours >3 cm. The commoner adrenocortical adenoma is often smaller.

Iodocholesterol Scintinography

6-131Iodomethyl-19-norcholesterol (iodocholestrerol) is widely employed in the imaging of Conn's syndrome. Patients are prepared
by the ingestion of dexamethasone for a week prior to adminstering iodocholesterol in order to suppress cortisol production from the
normal gland. They are also given saturated solution of iodine or potassium iodide (60 mg tds) to protect the thyroid from radioactive
iodine in the tracer. Adrenal adenomas show up as early unilateral uptake in the affected gland (Fig. 10.10). In hyperplasia there is
bilateral uptake after

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Figure 10.10
Iodocholesterol scan in patient with Conn's syndrome.

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an average 3-5 days. Adrenocortical carcinomas typically show reduced uptake on the side of the tumour.

Selective Adrenal Vein Sampling

This method is the `gold standard' for tumour localization but is technically difficult because of frequent failure to
cannulate the right adrenal vein. It is undertaken in cases where iodocholesterol and CT scanning fail to localize the
tumour adequately. Throughout the procedure a continuous infusion of ACTH is maintained to stimulate a fixed cortisol
production rate from both adrenals. Cortisol and aldosterone are measured from both adrenal veins, which enables
correction in the case of inaccurate placement of adrenal vein cannulae.

Gut Hormone Tumours

The gastrointestinal tract has an important endocrine role and many neurotransmitters are involved in signalling
nutritional status: insulin (stimulates peripheral glucose utilization), gastrin (stimulates gastric acid production),
vasoactive intestinal polypeptide (stimulates colonic secretions), and many other hormones. Tumours of endocrine cells
of the gut are rare but can result in specific syndromes. They can form in any part of the gastrointestinal system but the
commonest areas include gastrin cells of the duodenum, serotonin-secreting enterochromaffin cells commonly found in
the small intestine and oxyntic cell tumours of the stomach. Commonly recognized syndromes secondary to excess
secretion of hormones include Zollinger-Ellison, carcinoid and Verner-Morrison syndrome.

The carcinoid syndrome occurs with excess secretion of serotonin (5-hydroxy tryptamine) and results in increased
urinary excretion of 5-hydroxy indolacetic acid (5-HIAA). Such tumours need to be localized before surgery.
Ultrasound, CT and MRI, which are relatively non-invasive, are often useful. However, these modalities give no
functional data and angiography with intra-arterial provocation provides functional as well as anatomical localization in
some tumours. 19, 20

The liver is a common port for metastatic disease from gut endocrine tumours. Unlike other malignancies, such
metastases do not herald imminent death. They are very slow growing and obtain their blood supply from the hepatic
artery. The normal liver has a dual blood supply from portal triads. If the blood supply via the hepatic artery is cut off
therefore, the tumour will infarct in preference to the liver hepatocytes which can survive on the portal circulation. This
is the basis of hepatic embolization as a therapeutic modality. Inert plastic microspheres are injected selectively into the
hepatic arterioles supplying the metastases in order to infarct them. After embolization, tumour load is reduced and
often the symptoms of flushing, diarrhoea and headache resolve.

Patients with Zollinger-Ellison syndrome present with multiple ulcers of the small bowel, which are caused by a tumour
of the pancreas secreting gastrin. Gastrinomas can also be localized using intra-arterial injection of secretin21, 22 or
calcium. This invasive method currently is the most sensitive technique available.

In 1958 the first case report of Verner-Morrison syndrome concerned 2 patients with hypokalaemia, a profuse watery
diarrhoea and achlorhydria associated with non-β cell adenocarcinoma of the pancreas. It was not until 1973 when
Bloom et al reported raised VIP levels in plasma from patients with this syndrome.23 Vipomas are predominantly
pancreatic, although 10% are found in extrapancreatic sites such as the adrenal medulla or autonomic nervous system.
Vipomas have been localized using ultrasound. Gut endocrine tumours can express octreotide receptors and radioactive
octreotide or analogues can be used to demonstrate the distribution of such tumours.

Insulinomas are usually located in the tail of the pancreas. Patients present with hypoglycaemia relieved by food and the
diagnosis is confirmed when inappropriately high insulin levels occur in the face of hypoglycaemia (glucose <2.2 mM).
Such patients require removal of the tumour, but the lesions are often too small to be seen by ultrasound, CT or MRI
scanning. In addition, non-secreting incidentalomas of no consequence are often found on CT and MRI scanning. For
this reason, the source of insulin needs to be determined. The most sensitive and specific test for localizing a functional
insulinoma is intra-arterial calcium injection and portal venous sampling.19

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Glucagonomas present with a necrolytic migratory erythema, usually to dermatologists who may recognize the
condition from the skin lesions alone. Some patients have diabetes. The incidence of glucagonomas is about 1 per 10
million per annum. Diagnosis is confirmed by measuring a fasting plasma glucagon. The treatment is usually
symptomatic with octreotide and zinc creams for the rash. Hepatic metastases can be treated with embolization (see
above)

Octreotide Scanning

The first report of the use of somatostatin (SST) receptor analogues in scanning endocrine tumours

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was in 1989. 24 Further work lead to the development of 111In-DTPA-D-Phe1-octreotide (also known as 111Inpentreatide), the
standard somatostatin receptor (SSTR) radioligand which binds to SSTR2 and SSTR5.

Several gut tumours show cross-reactivity to VIP and SST analogues25 and the high level of expression by tumour cells of peptide
receptors by carcinoid, neuroendocrine tumours, melanoma and lymphomas allows them to be localized by these analogues.
Vasoactive intestinal peptide (VIP) receptor scintinography is a more recent development26 and early work in small series suggests it
may have a high sensitivity for vipomas. 111In-DTPA-D-Phe1-octreotide has a high sensitivity for the visualization of gastrinomas,
carcinoid tumours (primary and secondary disease), glucagonomas and APUDomas.27 It has also been applied in the imaging of
MTC.28 Fig. 10.11 shows an octreotide scan in a patient with a pancreatic gastrinoma.

Testicular Tumours

Tumours of the testes rarely present to the endocrinologist but occasionally the rare referral for gynaecomastia could have a testicular
cancer since androgens may be isomerized to oestrogens. Germinal cell tumours, in particular of embryological type, which are
commonest in children, may secrete gonadotrophins which are commonly used as tumour markers (e.g. human chorionic
gonadotrophin). The primary approach to localization before surgical resection consists of a chest radiograph and ultrasound. Pelvic
CT to stage disease

Figure 10.11
Octreotide scan in patient with gastrinoma.

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prior to surgery is being advocated to detect early nodal metastasis. 29 Post-surgery patients typically undergo life-long
follow-up with regular clinical examination, chest X-ray and tumour marker profiling.

Ovarian Tumours

Ovarian cancer remains a common cause of cancer-related death in the UK. Survival largely depends on early detection
and nationally there are studies to detect the efficacy of screening in large populations. Ultrasound scanning using
Doppler flow techniques are utilized to detect abnormal flow patterns (secondary to neovascularization) characteristic of
malignancy. Further imaging with CT is occasionally carried out, but the common approach once the diagnosis is
suspected is surgical visualization using laparoscopy. In disease greater than stage I (FIGO classification), postoperative
abdomino-pelvic CT scanning is advocated30 to guide adjuvant therapy. MRI in a few series has both been described as
oversensitive31 and superior32 to ultrasound in its diagnostic value.

Bone

Paget's Disease

The incidence and prevalence of Paget's disease is difficult to quantify since only 1% of patients with the condition have
symptoms. The prevalence, however, is very low under the age of 40 years. It rises after this from about 3% of people
over 40 years old to over 10% in people over 80 years of age. Geographical differences in its prevalance also exist; it is
rare in Japan and the Nordic countries. The aetiology is as yet unknown, but its epidemiology and ultrastructural
features33 suggest an infectious origin.34

The bone in Paget's disease has a highly disorganized architecture. The typical X-ray findings are areas of focal bone
resorption and a disordered trabecular pattern, seen as areas of lysis and sclerosis. Overall bone size appears enlarged
and the cortices are thickened (Fig. 10.12). The sclerosis may be so extensive that it may be confused with metastatic
disease from prostate, breast, lung, thyroid or pancreas associated with sclerotic bony metastases. Classically, Paget's
disease presents with involvement from one end of the bone to the other. Although the risk of transformation to
osteosarcoma is now judged to be about 1%, it is important to remember that Paget's disease and malignancy may
coexist.

Figure 10.12
Pagets skull.

Bone in Malignant Disease

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The bone is a common site for metastatic disease and bronchus, breast, kidney, thyroid and prostatic carcinoma in
particular target bone. In addition, multiple myeolma can cause lytic lesions of the bone. Prostatic carcinoma can cause
sclerotic lesions and most other malignancies cause lytic lesions.

Bone involvement in multiple myeloma classically produces extensive bone destruction with pain and susceptibility to
fracture. Skeletal X-rays reveal osteoporosis, lytic lesions and fractures. Characteristic skeletal lesions are punched-out
lytic areas which are sharply circumscribed. The vertebrae, skull, thoracic cage and pelvis are the commonest sites of
involvement. Pathological fractures are common and should suggest the possibility of multiple myeloma. In contrast to
patients with metastatic carcinoma, the vertebral pedicles are rarely involved in myeloma.

Summary

Imaging in endocrinological malignancy has a particularly useful role because tumours often express receptors that
enable them to be localized with particular ligands, they may secrete hormones that can be measured at the time of
angiography and, when they spread to the liver, hepatic embolization is a useful therapeutic option. The prognosis in
most endocrine tumours is far better than it is for most other solid tumours and for this reason the role of the
interventional radiologist is particularly valuable.

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Acknowledgement

The authors would like to thank Dr R Jewkes who supplied most of the figures used to illustrate this chapter.

References

1. Chandrasekharappa SC, Guru SC, Manickam P et al. Positional cloning of the gene for multiple endocrine
neoplasia-type 1. Science 1997; 276: 404-407.

2. Lemmens I, Van de Ven WJ, Kas K et al. Identification of the multiple endocrine neoplasia type 1 (MEN1) gene. The
European Consortium on MEN1. Hum Mol Genet 1997; 6: 1177-1183.

3. Catarci T, Fiacco F, Bozzao L, Pati M, Magiar AV, Cerbo R. Empty sella and headache. Headache 1994; 34:
583-586.

4. Oldfield EH, Doppman JL, Nieman LK et al. Petrosal sinus sampling with and without corticotropin-releasing
hormone for the differential diagnosis of Cushing's syndrome. N Engl J Med 1991; 325: 897-905.

5. Ituarte EM, Petrini J, Hershman JM. Acromegaly and colon cancer. Ann Intern Med 1984; 101: 627-628.

6. Sharma S, Longo WE, Baniadam B, Vernava AM. Colorectal manifestations of endocrine disease. Dis Colon Rectum
1995; 38: 318-323.

7. Daunt N, Mowat P. Computed tomographic appearances and clinical features of prolactin-secreting pituitary
adenomas in young male patients. Clin Radiol 1985; 36: 227-231.

8. Delgrange E, Trouillas J, Maiter D, Donckier J, Tourniaire J. Sexrelated difference in the growth of prolactinomas: a
clinical and proliferation marker study. J Clin Endocrinol Metab 1997; 82: 2102-2107.

9. Eng C, Clayton D, Schuffenecker I et al. The relationship between specific RET proto-oncogene mutations and
disease phenotype in multiple endocrine neoplasia type 2. International RET mutation consortium analysis. JAMA 1996;
276: 1575-1579.

10. Simeone JF, Daniels GH, Mueller PR et al. High-resolution realtime sonography of the thyroid. Radiology 1982;
145: 431-435.

11. Solbiati L, Cioffi V, Ballarati E. Ultrasonography of the neck. Radiol Clin North Am 1992; 30: 941-954.

12. Mackinnon WB, Delbridge L, Russell P et al. Two-dimensional proton magnetic resonance spectroscopy for tissue
characterization of thyroid neoplasms. Diagnosis of follicular thyroid lesions by proton magnetic resonance on fine
needle biopsy. World J Surg 1995; 80: 1306-1311.

13. Cavalieri RR. Nuclear imaging in the management of thyroid carcinoma. Thyroid 1996; 6: 485-492.

14. Brendel AJ, Guyot M, Jeandot R, Lefort G, Manciet G. Thallium-201 imaging in the follow-up of differentiated
thyroid carcinoma. J Nucl Med 1988; 29: 1515-1520.

15. Singer PA, Cooper DS, Daniels GH et al. Treatment guidelines for patients with thyroid nodules and
well-differentiated thyroid cancer. American Thyroid Association. Arch Intern Med 1996; 156: 2165-2172.

16. Rauth JD, Sessions RB, Shupe SC, Ziessman HA. Comparison of Tc-99m MIBI and TI-201/Tc-99m pertechnetate
for diagnosis of primary hyperparathyroidism. Clin Nucl Med 1996; 21: 602-608.

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17. Peeler BB, Martin WH, Sandler MP, Goldstein RE. Sestamibi parathyroid scanning and preoperative localization
studies for patients with recurrent/persistent hyperparathyroidism or significant comorbid conditions: development of an
optimal localization strategy. Am Surg 1997; 63: 37-46.

18. Skowsky WR, Wilf LH. Iodine 131 metaiodobenzylguanidine scintigraphy of medullary carcinoma of the thyroid.
South Med J 1991; 84: 636-641.

19. O'Shea D, Rohrer Theurs AW, Lynn JA, Jackson JE, Bloom SR. Localization of insulinomas by selective
intraarterial calcium injection. J Clin Endocrinol Metab 1996; 81: 1623-1627.

20. Hammond PJ, Bloom SR. Searching for gastrinomas. Br Med J 1993; 307: 4-5.

21. Doppman JL, Miller DL, Chang R et al. Gastrinomas: localization by means of selective intraarterial injection of
secretin. Radiology 1990; 174: 25-29.

22. Gibril F, Doppman JL, Chang R, Weber HC, Termanini B, Jensen RT. Metastatic gastrinomas: localization with
selective arterial injection of secretin. Radiology 1996; 198: 77-84.

23. Bloom SR, Polak JM, Pearse AG. Vasoactive intestinal peptide and watery-diarrhoea syndrome. Lancet 1973; 2:
14-16.

24. Krenning EP, Bakker WH, Breeman WA et al. Localisation of endocrine-related tumours with radioiodinated
analogue of somatostatin. Lancet 1989; 1: 242-244.

25. Virgolini I, Yang Q, Li S et al Cross-competition between vasoactive intestinal peptide and somatostatin for binding
to tumor cell membrane receptors. Cancer Res 1994; 54: 690-700.

26. Virgolini I, Raderer M, Kurtaran A et al. Vasoactive intestinal peptide-receptor imaging for the localization of
intestinal adenocarcinomas and endocrine tumors. N Engl J Med 1994; 331: 1116-1121.

27. Hammond PJ, Arka A, Peters AM, Bloom SR, Gilbey SG. Localization of metastatic gastroenteropancreatic
tumours by somatostatin receptor scintigraphy with [111In-DTPA-D-Phe 1]-octreotide. QJ Med 1994; 87: 83-88.

28. Lamberts SW, Reubi JC, Krenning EP. Validation of somatostatin receptor scintigraphy in the localization of
neuroendocrine tumors. Acta Oncol 1993; 32: 167-170.

29. White PM, Howard GC, Best JJ, Wright AR. The role of computed tomographic examination of the pelvis in the
management of testicular germ cell tumours. Clin Radiol 1997; 52: 124-129.

30. Dobson M, Carrington BM, Radford JA, Buckley CH, Crowther D. The role of computed tomography in the
management of ovarian tumours of borderline malignancy. Clin Radiol 1997; 52: 280-283.

31. Mascaretti G, Carta G, Renzi E et al. Transvaginal ultrasonography and nuclear magnetic resonance. Comparison of
techniques in the evaluation of ovarian lesions. Minerva Ginecol 1994; 46: 591-595.

32. Acar B, Posaci C, Dicle O, Topuz A, Erten O. Diagnostic value of magnetic resonance imaging in gynaecology.
Aust N Z J Obstet Gynaecol 1992; 32: 252-255.

33. Rebel A, Basle M, Pouplard A, Malkani K, Filmon R, Lepatezour A. Bone tissue in Paget's disease of bone.
Ultrastructure and immunocytology. Arthritis Rheum 1980; 23: 1104-1114.

34. Holdaway IM, Ibbertson HK, Wattie D, Scragg R, Graham P. Previous pet ownership and Paget's disease. Bone
Miner 1990; 8: 53-58.

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11
The Ovaries, Endometrium and Cervix

N M deSouza and W P Soutter

Imaging techniques

The ovaries

The uterus

Cervical cancer

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Imaging Techniques

Cross-sectional imaging plays a crucial role in the detection, assessment and follow-up of gynaecological malignancy.
Ultrasound, X-ray, computed tomography (CT) and magnetic resonance imaging (MRI) are all widely used and can
offer complementary information depending on the clinical situation.

For transabdominal ultrasound a 3.5-5 MHz transducer is used, while for endovaginal sonography a 5.0-7.5 MHz probe
is appropriate. Endovaginal ultrasound is superior for near field lesions but its field of view and penetration are limited.
Transabdominal ultrasound may be used for assessment of abdominal and pelvic lymphadenopathy, renal obstruction or
liver metastases. Colour flow and duplex Doppler imaging may be used with either probe: the former allows
identification of vascularity and the latter can be used to characterize arterial waveform patterns and resistive indices.

With CT a meticulous scanning technique is essential to look for metastases. The complete scanned field ranges from
the dome of the diaphragm to the inguinal region. Contrast opacification of the bowel is mandatory and 8-10 mm thick
slices through the abdomen and 5 mm slices through the pelvis are optimal. Intravenous contrast opacification aids
differentiation between iliac vessels and lymph nodes. In general, CT scanning of the pelvis is not as helpful as in the
upper abdomen and ultrasound and MRI are preferred.

Similar imaging volumes to include the abdomen and pelvis are required when using MRI. With this modality multiple
imaging planes for lesion visualization are a distinct advantage. In the pelvis T2-weighted images provide maximal
tissue contrast. Fat-suppressed or short T1 inversion recovery (STIR) sequences in the coronal plane show pelvic
lymphadenopathy to best advantage. To reduce bowel motion the patient is advised to remain nil by mouth for 6 hours
prior to scanning. In addition, glucagon or buscopan may be administered intramuscularly. The use of a phased array
multicoil wrapped around the lower abdomen markedly improves signal to noise ratios and hence image quality.
Respiratory motion may be controlled with respiratory gating and vascular motion with the use of pre-saturation bands.

The Ovaries

Normal Anatomy and Variations

The ovaries vary in appearances with their functional status. Infantile ovaries are small (except in the neonate when
hypertrophy and follicular growth stimulated by maternal hormones may surprise the inexperienced) and they enlarge
before puberty. They are ovoid in shape, approximately 2.5-4 cm long and can be anywhere within the true pelvis.
Follicular development begins before menstruation but cycles in young women and perimenopausal women are often
imperfect, so that follicles may persist and continue enlarging for several months. Normally ovulation occurs at a
follicle size of 20-25 mm diameter and the echo-free follicle is replaced by a corpus luteum which can be cystic or solid.
Corpora lutea produce a confusing variety of appearances, whose only consistent feature is their relative transience. In
doubtful cases, repeated scans after an interval of several weeks may be needed to resolve the question.

On MRI normal ovaries are often difficult to define but they may be recognized on STIR sequences as very high signal
ovoid structures.

Ovarian Carcinoma

The risk of ovarian cancer increases with age and becomes significant after the menopause. (Serov et al, 1973): 15.7 of
100 000 women aged 40-44 years and 54 of 100 000 women aged 75-79 years will develop ovarian cancer. 2
Nulliparous women are at increased risk for developing ovarian cancer.3 Early menopause and long-term oral
contraception appear to protect against ovarian cancer possibly because of the reduced frequency of ovulation.4
Familial ovarian cancer is responsible for 3-5% of cases. Environmental factors, both dietary1, 2 and chemical such as
herbicides,5 asbestos and talc6 have all been linked with an increased risk of ovarian cancer.

Screening

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Ovarian cancer is diagnosed late because of a lack of symptoms and the intraperitoneal location of the ovaries. The
overall 5-year survival is 30%7 and the majority of patients have extrapelvic spread at initial presentation.2 The goal of
screening is to detect the cancer at a curable stage and to improve ovarian disease specific survival. To this end
screening programmes with bimanual rectovaginal pelvic examination, CA125 testing and transabdominal as well as
transvaginal sonography have all been advocated for high risk patients such as close relative with ovarian cancer.

Campbell et al8 screened 5479 females aged 18-19 years with transabdominal sonography and found 326 to have
persistently abnormal ovaries. Only 9 of these cases had tumours: 5 had Stage I ovarian cancer and 4 metastatic lesions
to the ovaries. Van Nagell et al9 screened 3220

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postmenopausal women and detected 1.4% of morphologic ovarian abnormalities. Only 2 cases had Stage I ovarian
cancer, 1 had more advanced disease and the other lesions were benign. Attention should therefore focus on high risk
groups to improve the risk: benefit ratio.

Other early detection studies coupled conventional ultrasound techniques with colour Doppler imaging in an attempt to
visualize early physiologic changes, such as angiogenesis, 10 that occur before morphologic changes in ovarian
architecture can be detected. Colour Doppler imaging (CDI) is based on the principal that fast growing tumours contain
many new blood vessels that have relatively little smooth muscle in their walls. The resistance to blood flow within
these vessels is therefore less than the resistance to flow within vessels of benign lesions. In practice, however, clinical
studies of CDI have revealed that normal physiologic changes in the premenopausal ovary at the time of ovulation have
low impedance flow characteristics similar to those seen in malignancy.11 Carter et al12 examined 123 women with
suspected pelvic masses using both conventional transvaginal sonography and CDI. A comparison of findings between
the benign and malignant tumours was made by analysing different thresholds of the intratumoral pulsatility and
resistance index values by means of receiver-operator characteristic curves. The area under the curve indicated the
efficiency of the pulsatility and resistance index values at predicting malignancy. Malignant tumours were generally
larger and had a complex or solid pattern. Absent colour flow was found equally among benign and malignant tumours.
There was no difference in systolic, diastolic or mean velocities between benign and malignant tumours. No significant
difference existed in performance of either the pulsatility or resistance index in predicting malignancy, although the best
thresholds for predicting malignancy were obtained with a pulsatility index of 1.0 and a resistance index of 0.6. This
relatively poor specificity, difficulties in reproducibility and subjectivity of results have limited the usefulness of CDI in
ovarian cancer screening.

CA125 is elevated (> 35 U/ml) in ~ 80% of patients with epithelial ovarian cancer but is also elevated in hepatic
cirrhosis, endometriosis, the first trimester of pregnancy and advanced intra-abdominal malignancy.3 Only 50% of
patients with Stage I disease have elevated CA125 levels,3 indicating that half the patients would not be detected by
CA125 levels at a potentially curable stage.

The National Cancer Institute's consensus conference on ovarian cancer14 concluded that `there is no evidence available
yet that the current screening modalities of CA125 and transvaginal sonography can be used effectively for widespread
screening to reduce mortality from ovarian cancer nor that their use will result in decreased rather than increased
morbidity and mortality'. Women from a family with a hereditary cancer syndrome should be referred to a specialist to
discuss the appropriate use of diagnostic testing and prophylactic surgery. The optimal interval for screening
interventions also remains unknown.

Clinical Presentation

Ovarian cancer presents with nausea, dyspepsia and abdominal discomfort: in the later stages abdominal distension and
an abdominal mass may be noted by the patient.

Staging

Staging is based on the disease site and extent at exploratory laparotomy. (Table 11.1) Definitive staging requires
abdominal hysterectomy with bilateral salpingooophorectomy, excision of omentum, biopsy of pelvic and abdominal
nodes and cytological examination of effusions. Without rigorous staging, patients are generally understaged. Spread is
by surface shedding and seeding to other organs, the subphrenic space and diaphragm. Lymphatic dissemination and
obstruction produce omental implants and `caking' and result in ascites. All peritoneal surfaces are involved including
the bowel wall. Haematogenous spread to liver, lungs and bone is rare.

The dramatic difference in cure rates between patients with local disease (80-90%) and those with distant disease
(15-25%), means that imaging to detect ovarian cancer early is desirable.

Imaging

Primary Site

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Imaging is used to assess tumour size, wall thickness, internal architecture, including septations, calcifications, cystic
and solid components and papillary nodules. Thin-walled unilocular cysts with few septations and no papillary
projections suggest a benign lesion.15,16,17 Papillary projections are highly indicative of malignancy.15, 16, 18 The
findings of thick walls and septa > 3 mm (Fig 11.1) are less reliable signs of malignancy.19 In addition, pelvic, omental
and mesenteric involvement may be noted. Ascites is non-specific and is found in 40% of patients without metastases.1

The probability of malignancy is also related to tumour size.20, 21 Goldstein et al21 did not find any cancer among 52
postmenopausal women with thin-walled unilocular

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Table 11.1 FIGO staging for primary ovarian carcinoma

Stage FIGO definition
I Growth limited to ovaries
Ia Growth limited to one ovary no ascites; no tumour on external surface;
capsule intact
Ib Growth limited to both ovaries no ascites; no tumour on external surfaces;
capsule intact
Ic Tumour either Stage Ia or Ib but tumour on surface of one or both ovaries;
or with capsule ruptured; or with ascites present containing malignant
cells; or with positive peritoneal washings
II Growth involving one or both ovaries with pelvic extension
IIa Extension and/or metastases to the uterus or tubes
IIb Extension to other pelvic tissues
IIc Tumour either Stage IIa or IIb but tumour on surface of one or both
ovaries; or with capsule ruptured; or with ascites present containing
malignant cells; or with positive peritoneal washings
III Growth involving one or both ovaries with peritoneal implants outside the
pelvis or positive retroperitoneal or inguinal nodes. Superficial liver metastases
equals Stage III
IIIa Tumour grossly limited to the true pelvis with negative nodes but with
histologically confirmed microscopic seeding of abdominal peritoneal
surfaces
IIIb Tumour with histologically confirmed implants on abdominal peritoneal
surfaces none exceeding 2 cm in diameter. Nodes are negative
IIIc Abdominal implants greater than 2 cm in diameter or positive
retroperitoneal or inguinal nodes
IV Growth involving one or both ovaries with distant metastases. If pleural
effusion is present there must be positive cytology to allot a case to Stage IV.
Parenchymal liver metastasis equals Stage IV

ovarian lesions of < 5 cm in diameter. Rulin & Preston 20 found that in 150 postmenopausal patients the malignancy
rate was 3% for lesions < 5 cm, 11% for lesions 5-10 cm in diameter and 63% for lesions > 10 cm. Haemorrhage in a
unilocular cyst is typical of benign lesions. On US however, a clot may look like papillary projections and fibrous
strands may be misread as septa.

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Figure 11.1
Ovarian cancer: Transabdominal ultrasound image
in longitudinal section showing a large cystic mass
(arrows) with multiple septations within it (arrowhead)
typical of a cystic ovarian neoplasm. BL = bladder.

A scoring system has evolved which results in false positives because of confusion between unusual appearing corpora
lutea and benign tumours. Benign lesions are unilocular or multilocular with thin septa and no nodules, whereas
malignant lesions are often multilocular with thick septa and nodules (Fig. 11.2). Uniformly echogenic lesions are less
likely to be malignant than those of mixed echogenicity. In postmenopausal women, anechoic lesions < 5 cm in
diameter are unlikely to be malignant but those > 5 cm carry a 10% chance of malignancy.22 However, Campbell et al8
were unable to identify any morphological characteristics to differentiate reliably between ovarian tumour-like
conditions, benign ovarian tumours and early malignant tumours. Bourne et al23 proposed that the false positive rate
may be reduced by the use of transvaginal colour flow imaging but these studies have been reported as both
disappointing24 and useful.25 Initially, a low resistance index (< 0.4) was advocated as the best discriminator but this
has proved unreliable and a high peak velocity may be a better feature.

As a tumour arising from a non-essential organ that remains primarily confined to the peritoneal cavity, ovarian cancer
makes an attractive target for monoclonal antibodies. In the last decade progressive improvement in tumour imaging has
been observed when one compares the best examples of early studies performed with 131I heterosera to the best of
modern images obtained with 123I, 99mTc or 111In labelled monosera. However, these antibodies are limited by
problems that include antibody specificity, detectability and the immunoreactivity of the patient to the antibodies used.

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Figure 11.2
MR images through the pelvis using an external
phased array multicoil. a) Sagittal and b) transverse
T2-weighted spin-echo (2500/80 ms [TR/TE]) images
show a large cystic mass (long arrow). Irregular
septations (arrowhead) and papillary projections (short
arrow) are seen and are indicative of malignancy.

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Methods have therefore been developed to 198Au-label a human monoclonal antibody (TC5) developed against an
ovarian cell surface antigen, 26 which has a high sensitivity and specificity for detecting ovarian cancer. Antibodies
coupled to drugs or biological toxins are also under investigation. Some antibodies may have direct antitumour effects
through binding to biologically active receptors or through immune receptor functions. The use of antibody fragments,
chimeric antibodies and genetically engineered antibodies is also under active investigation.27 Monoclonal antibodies
have great potential for improving the diagnosis and for treatment of ovarian cancer.

The potential of positron emission tomography (PET) is being evaluated to distinguish benign from malignant tumours
by comparing the results of 18F fluoro-2-deoxyglucose (18F FDG) PET scans with surgical findings. The positive
predictive value from one such study was 86% and, more importantly, the negative predictive value was 76%.28 It may
be possible using such techniques to identify metabolically active tumours that are not clearly seen on morphological
studies.

Pelvic and Abdominal Spread

CT is the most useful imaging modality to demonstrate macroscopic recurrence but may fail to show even quite large
tumour masses. A variety of manifestations can be seen with CT, each of which can have a spectrum of appearances
including ascites, peritoneal seeding and visceral and nodal metastases.29 Ultrasound may also be used to detect ascites
and liver metastases, although it may be difficult to differentiate benign from malignant cystic masses. MRI should be
performed in women with questionable macroscopic recurrent tumour in the pelvis and negative CT examination.
Although in a small study, it has been shown that MRI is at least equivalent and may be superior to CT in the evaluation
of ovarian malignancy.30 Neither CT nor MRI can exclude microscopic disease.31

In a correlative imaging study, Peltier et al32 found that using Fab'2 fragments of 111In labelled monoclonal antibody
CA125, a positive immunoscintigram, even with a negative CT and ultrasound, was highly suggestive of recurrence in
the abdomen and pelvis. 111In CYT 103 immunoscintigraphy detected occult disease in 20 of 71 patients with
surgically documented ovarian adenocarcinoma33 and this approach may be a valuable addition to the presurgical
evaluation in patients with suspected, persistent or recurrent pelvic tumour.

The Uterus

Normal Anatomy and Variations

The uterus is a pear-shaped structure with an expanded fundus narrowing to a cylindrical cervix. The normal uterine
cavity is triangular with the cornua and the internal cervical os as the corners.

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The morphology of the normal uterus is best defined on MRI where the zonal architecture of the uterus may be
recognized. 34 On T2-weighted images the endometrium is seen as a central high signal stripe which increases in
thickness in the secretory phase of the menstrual cycle. The inner myometrium (junctional zone) is of lower signal
intensity than the outer myometrium on T2-weighting and histologically correlates with a layer of more densely packed
smooth muscle.

Fluid may be present within the cavity at menstruation. Persistent fluid or fluid in a non-menstruating woman is
abnormal. In adolescence, it may be caused by vaginal atresia whilst in postmenopausal women cervical stenosis, either
fibrotic or malignant, must be considered.

Endometrial Cancer

The median age of patients with endometrial cancer is 61 years, with 75-80% of women being postmenopausal and 3%
being less than 40 years old. In women under 40, there is a higher incidence in those who are obese and anovulatory,
e.g. in polycystic ovarian disease. The major risk factor for the development of this cancer is excessive unopposed
oestrogen stimulation of the endometrium. In postmenopausal women this is caused by a circulating oestrone derived
from the conversion of 4-androstenedione in fat and muscle. A marked increase in body weight thus increases
circulating oestrone, promoting endometrial proliferation. Administration of exogenous unopposed oestrogens in
hormone replacement therapy increases the risk of developing endometrial cancer to 7-10 times that of the general
population.35 Addition of progestagen lowers the risk to below that of the general population.

Although it reduces the death rate in women with breast cancer, tamoxifen increases the annual incidence of
endometrial cancer from 0.2/1000 women to 1.6/1000 women.36 Although the relative risk is large, the absolute risk of
endometrial cancer is still very small in tamoxifen-treated women.

Screening

There are no immediate prospects for mass screening. A number of tests such as endometrial biopsy, curettage,
brushings, lavage, aspiration and progestagen challenge tests are available but no data support their value in reducing
the morbidity and mortality of this disease.

Clinical Presentation

Postmenopausal bleeding is the presenting symptom in 75-80% of cases. The remainder present with discharge, pain or
an abnormal cervical smear test. In premenopausal patients bleeding is usually irregular but can be regular and heavy.

Although curettage is mandatory in all patients with postmenopausal or irregular bleeding, imaging at this point helps
establish the diagnosis and assess the extent of disease.

Staging

The current FIGO staging criteria are shown in Table 11.2. The overall 5-year survival is 65% and is similar to
carcinoma of the cervix of an equivalent stage.

Imaging

Primary Site

Thickening of the endometrium is characteristic of endometrial carcinoma and is well demonstrated on transvaginal
ultrasound. However, specificity is low and Doppler has been suggested as a way to distinguish hormonal causes of
thickening (weak signals) and malignancy which gives marked colour and spectral Doppler signals. Endometrial cancer
is very rare if the endometrium is < 4 mm thick.

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In patients already proven to have endometrial cancer, the presence and depth of myometrial extension has important
prognostic and therapeutic implications. Myometrial invasion may be classified as absent, superficial or deep. It may be
possible to assess the depth of myometrial invasion with high resolution ultrasound probes. In a study of 20 patients,
70% of ultrasound estimations of invasion depth were within

Table 11.2 FIGO surgical staging of endometrial carcinoma.

Stage Description
IaG123 Tumour limited to endometrium
IbG123 Invasion < 1/2 myometrium
Ic123 Invasion > 1/2 myometrium
IIaG123 Endocervical glandular involvement only
IIbG123 Cervical stromal invasion
IIIaG123 Tumour invades serosa anod/or adnexae and/or positive peritoneal
cytology
IIIbG123 Vaginal metastases
IIIcG123 Metastases to pelvic and/or para-aortic lymph nodes
IVa Tumour invades bladder and/or bowel mucosa
IVb Distant metastases including intraabdominal and/or inguinal
lymph nodes

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10% of the actual pathological measurement. 37 Errors in estimation occurred when the tumour was exophytic and had
significant extension into the uterine cavity. False positives also occur if the uterine cavity is over distended with pus or
blood when a subendometrial hypoechoic halo may be demonstrated. Ultrasound assessment of the integrity of the
hypoechoic layer can be improved by the use of transvaginal or transrectal sonography.

Changes in uterine blood flow have been used to detect endometrial cancer using endometrial thickness (including
tumour) and pulsatility index (PI) derived from flow velocity waveforms recorded from both uterine arteries and from
within the tumour. Bourne et al38 found an overlap in endometrial thickness between women with and without
endometrial cancer but the PI was invariably lower in women with postmenopausal bleeding due to endometrial cancer
than in those with other reasons for blood loss. Blood flow impedance is inversely related to the stage of cancer. PI
values in healthy women increase slightly with age but decrease with oestrogen replacement therapy. Therefore,
although Doppler studies may be helpful in the detection of endometrial cancer, allowance must be made for oestrogen
replacement therapy.

CT may also be used to stage endometrial cancer. It depicts endometrial cancer as a hypodense lesion in the uterine
parenchyma39 or as a fluid-filled uterus due to tumour obstruction of the endocervical canal or vagina. These findings,
however, are non-specific and are easily confused with leiomyomata, intrauterine fluid collections and extension of a
cervical carcinoma into the uterine body. In addition, a central lucency may occur in normal postmenopausal women.

MRI appears to represent a unique method of assessing a patient with an endometrial cancer, possessing advantages
over other radiological techniques in stage I and II disease, but probably equal to CT in a patient with a more advanced
tumour.40 On T2-weighted MRI, endometrial cancer has an intermediate high signal intensity, similar to that of normal
endometrium, but shows some degree of variability (Fig. 11.3). The high signal makes the tumour quite distinct from
the surrounding myometrium which possesses an intermediate signal intensity. In a premenopausal uterus, however, it
may be difficult to differentiate tumour from adenomatous hyperplasia or indeed from the high signal of normal
endometrium. Contrast-enhanced T1-weighted MRI improves the ability to assess the depth

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Figure 11.3
Endometrial cancer: Sagittal MR image through the
pelvis using an external phased array multicoil.
T2-weighted spin-echo (2500/80 ms [TR/TE])
images show an intermediate signal-intensity mass
(arrow) within the endometrium that is expanding the
cavity. A break in the low signal stripe of the junctional
zone (arrowheads) indicates myometrial invasion.

of myometrial invasion by endometrial tumour.41 MRI has been found to have a sensitivity of 57% and a specificity of
96% for tumour confined to the endometrium, 74% and 74% for superficial invasion and 88% and 85% respectively for
deep penetration.42 However, the degree of invasion may be overestimated by exophytic polypoid tumours with
significant extraluminal extension. Powell et al40 found the low signal band of inner myometrium to be thinned or
absent in those patients with deeply invasive tumours (Fig. 11.4) and this correlated well with the pathological
measurement of myometrial invasion.

The sagittal plane is the most appropriate for examination of a patient with primary endometrial cancer as this provides
a longitudinal view of the uterus which will include both corpus and cervix. The sagittal plane also provides the
opportunity to assess anterior invasion of the tumour into the bladder and posteriorly to the rectum.

Recurrence

Transrectal sonography has been investigated in cases where recurrent endometrial cancer is suspected.45 Physical
examination may be difficult because of postsurgical fibrosis. Infiltration to the surrounding connective tissues and
organs such as the rectum and bladder can be identified and transrectal ultrasound can

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Figure 11.4
Advanced endometrial cancer: Sagittal MR image
through the pelvis using an external phased array
multicoil. T2-weighted spin-echo (2500/80 ms [TR/TE])
images show a very large intermediate signal-intensity
mass (arrow) within the endometrium, expanding the
uterine cavity and breaching the junctional zone in
several places (arrowheads). Well-defined low
signal-intensity masses within the endometrium
represent incidental fibroids (open arrows). There is a
large clot in the vagina (curved arrow).

be used to guide transvaginal or transperineal fine-needle biopsy. CT 46 or MRI may also be used to detect recurrent
disease and metastatic carcinoma to omentum or lymph nodes.

Cervical Cancer

There is a wealth of epidemiological evidence to suggest that the risk of developing cervical neoplasia is associated with
sexual behaviour. This may be due to a sexually transmitted agent, in particular human papilloma virus, as well as
immunosuppressive agents present in seminal fluid which may alter the local immune response to viral infections.
However, definitive evidence for these risk factors is not yet available.

Screening

The use of cervical cytology to identify precancerous lesions in asymptomatic healthy women is well established. The
cellular atypia detectable by cervical cytology are graded as mild (I), moderate (II) or severe (III). An international
study by the IARC47 clearly indicated that screening every 3 years is as effective as screening every year. However, in
patients with treated CIN, annual screening cytology is recommended because of a 5% risk of recurrent CIN.48

Clinical Presentation

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Intermenstrual or postcoital bleeding are the most common presenting symptoms. A foul smelling vaginal discharge
may occur. Pelvic and leg pain occur in the later stages of the disease due to pelvic sidewall involvement and invasion
of the lumbosacral plexus. Bladder invasion causes haematuria and urinary frequency while rectal invasion causes
tenesmus and bleeding.

Staging

This is done by bimanual examination under anaesthesia using the FIGO system (Table 11.3). Imaging does not alter
the FIGO staging of the disease but its use is vital in the assessment of disease extent. MRI is the modality of choice for
assessing the primary tumour and pelvic organs.

CT, transabdominal ultrasound and lymphangiography have all been used to assess nodal involvement, but none is
sufficiently accurate to advocate routine use. Lymphangiography correctly identifies only 61% of women with positive
nodes,50 while CT had a false negative rate of 34%.51

Imaging

Primary Site

Transabdominal ultrasound is of little value in the assessment of patient with cervical cancer.52 Poor image quality and
difficulty in interpretation are the major problems. Transrectal ultrasound produces clearer views of the cervix but
differentiation of tumour from normal cervix is still poor. The same difficulty limits the value of CT since both the
normal cervix and cervical carcinoma have similar attenuation values so that the primary tumour can only be recognized
if it alters the size and contours of the normal cervix.

Several studies have now confirmed the accuracy of MRI in the staging of early cervical cancer in comparison to the
surgical stage.53, 54 Patients are best assessed using T2-weighted MRI of the primary tumour which is superior to CT
in tumour detection (sensitivity 75% vs. 51%, p < 0.005) and in overall tumour staging (accuracy 75-77% vs. 32-69%, p
< 0.025).55, 56

The resolution of MRI of the primary tumour (Fig. 11.3) may be further improved by using intracavi-

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Table 11.3 FIGO staging classification for cervical cancer.49

Stage Description
0 Preinvasive carcinoma (carcinoma in situ, CIN)
I Carcinoma confined to the cervix (corpus extension should be disregarded)
Ia Invasive cancer identified only microscopically. All gross lesions, even with superficial invasion, are stage Ib cancers. Depth of
measured stromal invasion should not be >5 mm and no wider than 7 mm*
Ia1 Measured invasion no >3 mm in depth and no wider than 7 mm
Ia2 Measured depth of invasion >3 mm and no >5 mm and no wider than 7 mm
Ib Clinical lesions confined to the cervix or preclinical lesions greater than Ia
Ib1 Clinical lesions no >4 cm in size
Ib2 Clinical lesions >4 cm in size
II Carcinoma extending beyond the cervix and involving the vagina (but not the lower third) and/or infiltrating the parametrium (but not
reaching the pelvic side wall)
IIa Carcinoma involving the vagina
IIb Carcinoma has infiltrated the parametrium
III Carcinoma involving the lower third of the vagina and/or extending to the pelvic side wall (there is no free space between the tumour
and the pelvic side wall)
IIIa Carcinoma involving the lower third of the vagina
IIIb Carcinoma extending to the pelvic wall and/or hydronephrosis or non-functioning kidney due to ureterostenosis caused by tumour
IVa Carcinoma involving the mucosa of the bladder or rectum and/or extending beyond the true pelvis
IVb Spread to distant organs
*The depth of invasion should not be >5 mm from the base of the epithelium, either surface or glandular, from which it originates. Vascular
space involvement, either venous or lymphatic, should not alter the staging.

tary receiver coils. Endorectal coils give high resolution images of the posterior cervix but the anterior margin of the tumour and its relation to
the bladder base is often difficult to define because of drop-off in signal. Endovaginal coils give very high resolution images of the cervix and
adjacent parametrium. 57 The distortion of the low signal ring of inner stroma may be apparent and any breaks in the ring representing
tumour extension may be identified (Fig. 11.5).

With MRI, the invasion of cervical cancer may be assessed in three planes: the coronal and axial planes may be used to determine parametrial
invasion, the axial plane for extension into the bladder and rectum and the sagittal plane for extension into the uterine body, bladder and
rectum.58 The use of 3D volume imaging also provides the necessary information to calculate tumour volumes, which is of prognostic
significance. Volumes obtained with MRI correlate well with those obtained by histomorphometric methods but only weakly with clinical
stage.59 The volumetry of the tumour also permits more accurate judgement of the histological findings of parametrial invasion, vascular
involvement and lymph node involvement.60

Parametrium

Transrectal ultrasound, CT and MRI have all been used to assess parametrial spread. In a series of 180

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Figure 11.5
Cervical carcinoma: Transverse T2-weighted MR
image (2500/80 ms [TR/TE]) image of the cervix using
an endovaginal receiver coil. A high signal intensity
mass (short arrow) is seen expanding the cervix on the
right with a rim of normal low signal stroma around it
(arrowheads). This indicates that the tumour is
confined to the cervix at this level. Normal looking low
signal-intensity cervical stroma is present on the left
(long arrow).

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patients, good correlation was found between ultrasound and surgical findings, but significant problems arose in
distinguishing between inflammatory or fibrotic change and tumour invasion. 61 Similarly, false positive diagnosis may
arise from misinterpreting normal inflammatory parametrial soft tissue strands as tumour invasion on both CT and MRI.
A comparison of the assessment by these modalities with histological findings after radical hysterectomy showed an
accuracy rate for parametrial involvement of 87-90% for MRI, 55-80% for CT and 82.5% for examination under
anaesthesia.54, 56 Extracervical extension on MRI is best defined using contrast enhancement and varied pulse
sequences. MRI therefore yields valuable information for treatment planning62 and should be used routinely in
conjunction with clinical staging to determine the appropriate therapy in patients with cervical carcinoma. An
intravenous urogram (IVU) may sometimes be useful in estimating the pelvic extent of cervical carcinoma by
demonstrating partial or complete ureteric obstruction and/or displacement and distortion of the bladder outline. The
IVU is abnormal in 2.1% of stage I cases, in 5.1% of stage II, in 26.8% of stage III and in 48.9% of stage IV.63 The
presence of a hydronephrosis or nonfunctioning kidney due to stenosis from tumour invasion of the ureter puts the
patient into stage III even if, according to the other findings, the case should be allotted to an earlier stage.

Barium enema abnormalities are rare in cervical cancer and proctoscopy is also positive if an abnormality is observed
on the enema.

Nodal Involvement

The role of lymphangiography in the staging of cervical cancer is controversial with up to 71% false positives and 16%
false negatives. Percutaneous fine-needle aspiration biopsy of nodes may improve the results obtained with pelvic
lymphangiography. CT has proved to be a reliable method for staging and following lymph node disease in patients
with lymphoma but the major drawback for epithelial tumours is that the nodes must be enlarged to be detected. Thus
metastases <2 cm will not be identified.

MRI is superior to CT in pelvic lymph node evaluation (accuracy 88% vs. 83%, p < 0.01).55 However, like CT it relies
on changes in the size of the lymph nodes since the tumour deposits themselves are not highlighted (Fig. 11.6).
Although an in vitro study has shown that lymph nodes containing metastases have a significantly longer T2 than
normal or hyperplastic nodes, in vivo tissue characterization based on relaxation times or signal intensities does not
support this data.

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Figure 11.6
Advanced cervical carcinoma: Transverse proton
density-weighted MR image (2500/20 ms [TR/TE])
image of the cervix using a whole body receiver coil.
The cervix is expanded with a centrally situated tumour
(arrowhead). Large intermediate signal-intensity lymph
node masses are seen bilaterally at the pelvic
side-walls (arrows).

A small patient study suggested that 123I-labelled epidermal growth factor may be used to recognize cervical cancer
lymph node metastases because these tumours express high levels of the receptor.65

Distant Spread

Even in advanced pelvic spread, involvement of distant sites is the exception rather than the rule. In only 1 of 160
patients was bone scan positive and this patient had stage 4 disease with liver metastases.66 Patients with stage I and
stage II cervical cancer do not need to have bone scans.

A chest X-ray is a routine pretreatment investigation but the yield of lung metastases at first presentation is likely to be
no more than 2%.

Response and Recurrence

In conjunction with clinical examination, MRI may provide a more objective comparison of surgery and radiotherapy.
Serial MRI may be used before and after primary radiation therapy to assess tumour response.67 Primary tumours with
a volume of >50 cm3 are likely to have no response or a delayed response.67 An early (2-3 months) and significant
decrease in the signal intensity and volume of tumour indicates a favourable response.

With the increased use of new cytotoxic regimes for primary tumours and increased use of surgery, accurate imaging
techniques become more important. Early detection of recurrent cervical cancer in order to institute cytotoxic therapy
may be of value. CT and ultra-

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sound have limited ability to differentiate between fibrosis and tumour recurrence. Although isolated reports promote
MRI in distinguishing post-treatment fibrosis and recurrent pelvic neoplasm by measuring signal intensities from the
different tissues on T2-weighted pulse sequences, 68 in individual cases fibrosis is often impossible to differentiate from
recurrence.

Conclusion

Until recently, management of gynaecological malignancy relied heavily on clinical findings. Newer imaging methods,
particularly MRI has pushed imaging to the forefront in the assessment of gynaecological tumours. Such detailed
images of the pelvis provide important information to the gynaecological oncologist in planning treatment.

References

1. Serov SF, Scully RE, Sobin LH. International Classification of Tumours no. 9. Histological Typing of Ovarian
Tumours. Geneva: World Health Organization, 1973.

2. Young RC, Perez CA, Hoskins WJ. Cancer of the ovary. In: De Vita VT, Hellman S, Rosenberg SA (eds). Cancer.
Principles and Practices of Oncology. Philadelphia: JB Lippincott Company, 1993, vol. 1, pp. 1226-1263.

3. Smith LH, Oi RH. Detection of malignant ovarian neoplasm. A review of literature. 1. Detection of patient at risk:
Clinical, radiological and cytological detection. Obstet Gynecol Surv 1984; 39: 313-328.

4. Cramer DW, Hutchinson GE, Welch WR, Scully RE, Knapp RC. Factors affecting the association of oral
contraceptives and ovarian cancer. N Engl J Med 1982; 307: 1047-1051.

5. Donna A, Crosignani B, Robutti F et al. Triazine herbicides and ovarian epithelial neoplasm. Scand J Work Environ
Health 1989; 15: 47-53.

6. Longo DL, Young RC. Cosmetic talc and ovarian carcinoma. Lancet 1979; 2: 349-351.

7. Webb MJ. Screening for ovarian cancer. Br Med J 1993; 306: 1015-1016.

8. Campbell S, Bhan V, Royston P, Whitehead MI, Collins WP. Transabdominal ultrasound screening for early ovarian
cancer. Br Med J 1989; 299: 1363-1366.

9. Van Nagell JR Jr, DePriest PD, Puls LE et al. Ovarian cancer screening in asymptomatic postmenopausal women by
transvaginal sonography. Cancer 1991; 68: 458-462.

10. Folkman J, Watson K, Ingber D, Hanahan D. Induction of angiogenesis during the transition from hyperplasia to
neoplasia. Nature 1989; 339: 58-61.

11. Karlan BY, Platt LD The current status of ultrasound and color Doppler imaging in screening for ovarian cancer.
Gynecol Oncol 1994; 55: S28-33.

12. Carter J, Saltzman A, Hartenbach E, Fowler J, Carson L, Twiggs LB. Flow characteristics in benign and malignant
gynecologic tumors using transvaginal color flow Doppler. Obstet Gynecol 1994; 83: 125-130.

13. Johnson RJ. Radiology in the management of ovarian cancer. Clin Rad 1993; 48: 75-82.

14. Trimble EL. The NIH Consensus Conference on Ovarian Cancer: screening, treatment, and follow-up. Gynecol
Oncol 1994; 55: S1-3.

15. Outwater EK, Mitchell DG. Magnetic resonance imaging techniques in the pelvis. MRI Clin N Am 1994; 2: 161-188.

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16. Outwater EK, Dunton CJ. Imaging of the ovary and adnexa: Clinical issues and applications of MR imaging.
Radiology 1995; 194: 1-18.

17. Buy JN, Ghossain MA, Sciot C et al. Epithelial tumors of the ovary: CT findings and correlation with US.
Radiology 1991; 178: 811-818.

18. Granberg S, Wikland M, Jansson I. Macroscopic characterization of ovarian tumors and the relation to the
histological diagnosis. Criteria to be used for ultrasound evaluation. Gynecol Oncol 1989; 33: 139-144.

19. Stevens SK, Hricak H, Stern JL. Ovarian lesions. Detection and characterization with gadolinium-enhanced MR
imaging at 1.5T. Radiology 1991; 181: 481-488.

20. Rulin MC, Preston AL. Adnexal masses in postmenopausal women. Obstet Gynecol 1987; 70: 578-581.

21. Goldstein SR, Subramanyan B, Synder JR, Beller U, Raghavendra BN, Beckman EM. The postmenopausal cystic
adnexal mass: the potential role of ultrasound in conservative management. Obstet Gynecol 1989; 73: 8-10.

22. Andolf E, Jorgensen C. Cystic lesions in elderly women, diagnosed by ultrasound. Br J Obstet Gynaecol 1989; 96:
1076-1079.

23. Bourne T, Campbell S, Steer C, Whitehead MI, Collins WP. Transvaginal colour flow imaging: a possible new
screening technique for ovarian cancer. Br Med J 1989; 299: 1367-1370.

24. Hata K, Hata T, Manabe A, Sugimura K, Kitao M. A critical evaluation of transvaginal Doppler studies,
transvaginal sonography, magnetic resonance imaging and CA 125 in detecting ovarian cancer. Obstet Gynecol 1992;
80: 922-926.

25. Kawai M, Kano T, Kikkawa F, Maeda O, Ogichi H, Tomoda Y. Transvaginal Doppler ultrasound with colour flow
imaging in the diagnosis of ovarian cancer. Obstet Gynecol 1992; 79: 163-167.

26. Chaudhuri TR, Zinn KR, Morris JS, McDonald GA, Llorens AS, Chaudhuri TK. Detection of ovarian cancer by
198Au-labelled human monoclonal antibody. Cancer 1994; 73: 878-883.

27. Rubin SC. Monoclonal antibodies in the management of ovarian cancer. A clinical perspective. Cancer 1993; 71:
1602-1612.

28. Hubner KF, McDonald TW, Niethammer JG, Smith GT, Gould HE, Buonocore E. Assessment of primary and
metastatic ovarian cancer by positron emission tomography (PET) using 2-[18F] deoxyglucose (2-[18F]FDG). Gynecol
Oncol 1993; 51: 197-204.

29. Lee MJ, Munk PL, Poon PY, Hassell P. Ovarian cancer: computed tomography findings. Can Assoc Radiol J 1994;
45: 185-192.

30. Smelka RC, Lawrence PH, Shoenut JP, Heywood M, Kroeker MA, Lotocki R. Primary ovarian cancer: prospective
comparison

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of contrast enhanced CT and pre and post contrast, fat suppressed MR imaging, with histological correlation. J
Mag Res Imag 1993; 3: 99-106

31. Prayer L, Kainz C, Kramer J et al. CT and MR accuracy in the detection of tumour recurrence in patients treatment
for ovarian cancer. J Comput Assist Tomogr 1993; 17: 626-632.

32. Peltier P, Wiharto K, Dutin JP et al. Correlative imaging study in the diagnosis of ovarian cancer recurrences. Eur J
Nucl Med 1992; 19: 1006-1110.

33. Surwit EA, Childers JM, Krag DN et al. Clinical assessment of 111In-CYT-103 immunoscintigraphy in ovarian
cancer. Gynecol Oncol 1993; 48: 283-284.

34. Hricak H, Alpers C, Crooks LE, Sheldon PE. Magnetic resonance imaging of the female pelvis: initial experience.
AJR 1983; 141: 1119-1128.

35. Mack T M, Pike M C, Henderson B et al. Estrogens and endometrial cancer in a retirement community. N Eng J of
Med. 1976; 294: 1262-1267.

36. Fisher B, Costantino JP, Redmond CK, Fisher ER, Wickerham DL, Cronin WM. Endometrial cancer in tamoxifen
treated breast cancer patients: findings from the National Surgical Adjuvant Breast and Bowel Project (NSABP) B-14. J
Natl Cancer Inst 1994; 86: 527-537.

37. Fleisher AC, Dudley SB, Entman SS, Baxter JW, Kalemeris GE, Everette JA. Myometrial invasion by endometrial
carcinoma: sonographic assessment. Radiology 1987; 162: 307-310.

38. Bourne TH, Campbell S, Steer CV, Royston P, Whitehead MI, Collins WP. Detection of endometrial cancer by
transvaginal ultrasonography with colour flow imaging and blood flow analysis: a preliminary report. Gynecol Oncol
1991; 40: 253-259.

39. Suzuki M. Role of x-ray, CT and magnetic resonance imaging in the diagnosis of gynecological malignant tumour.
Nippon Sanka Fujinka Gakkai Zasshi 1989; 41: 942-952.

40. Powell MC, Womack C, Buckley JH, Worthington BS, Symonds EM. Pre-operative magnetic resonance imaging of
stage 1 endometrial adenocarcinoma. Br J Obstet Gynaecol 1986; 93: 353-350.

41. Sironi S, Colombo E, Villa G et al. Myometrial invasion by endometrial carcinoma: assessment with plain and
gadoliniumenhanced MR imaging. Radiology 1992; 185: 207-212.

42. Sironi S, Taccagni G, Garancini P, Belloni C, DelMaschio A. Myometrial invasion by endometrial carcinoma:
assessment by MR imaging. AJR 1992; 158: 565-569.

43. Lien HH, Blomlie V, Trope C, Kaern J, Abeler VM. Cancer of the endometrium: value of MR imaging in
determining depth of invasion into the myometrium. AJR 1991; 157: 1221-1223.

44. Gordon AN, Fleischer AC, Dudley BS et al. Preoperative assessment of myometrial invasion of endometrial
adenocarcinoma by sonography (US) and magnetic resonance imaging (MRI). Gynecol Oncol 1989; 34: 175-179.

45. Squillaci E, Salzani MC, Grandinetti M et al. Recurrence of ovarian and uterine neoplasms: diagnosis with
transrectal US. Radiology 1988; 169: 355-358.

46. Balfe DM, Heiken JP, McClennan BL. Oncologic imaging of carcinoma of the cervix, ovary and endometrium. In:
Bragg DG, Rubin P, Youker JE (eds) Oncologic Imaging. Oxford: Pergamon Press, 1986, pp. 437-477.

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47. IARC Working Group on Evaluation of Cervical Cancer Screening Programmes. Screening for cervical squamous
cancer: duration of low risk after negative results of cervical cytology and its implication for screening policies. Br Med
J 1986; 293: 659-664.

48. Soutter WP, Wisdom S, Brough JK, Monaghan JM. Should patients with a mild atypia in a cervical smear be
referred for colposcopy? Br J Obstet Gynaecol 1986; 93: 70-74.

49. Shepherd JH. Staging announcement FIGO staging of gynaecological cancers; cervical and vulval. Int J Gynecol
Cancer 1995; 5: 319.

50. Lagasse LD, Ballon SC, Berman ML, Watring WG. Pretreatment lymphangiography and operative evaluation in
carcinoma of the cervix. Trans Pac Coast Obstet Gynecol Soc 1979; 46: 123-128.

51. Pectasides D, Kayianni H, Facou A et al. Correlation of abdominal computed tomography scanning and second-look
operation findings in ovarian cancer patients. Am J Clin Oncol 1991; 14: 457-462.

52. Levenback C, Dershaw DD, Rubin SC. Endoluminal ultrasound staging of cervical cancer. Gynecol Oncol 1992; 46:
186-190.

53. Powell MC, Buckley JH, Wasti M, Worthington BS, Sokal M, Symonds WM. The application of magnetic
resonance imaging to cervical carcinoma. Br J Obstet Gynaecol 1986; 93: 1276-1285.

54. Togashi K, Nishimura K, Itoh K. Uterine cervical cancer: assessment with high field MR imaging. Radiology 1987;
160: 431-435.

55. Kim SH, Choi BI, Han JK et al. Preoperative staging of uterine cervical carcinoma: comparison of CT and MRI in
99 patients. J Comput Assist Tomogr 1993; 17: 633-640.

56. Ho CM, Chien TY, Jeng CM, Tsang YM, Shih BY, Chang SC. Staging of cervical cancer: comparison between
magnetic resonance imaging, computed tomography and pelvic examination under anaesthesia. J Formas Med Assoc
1992; 91: 982-990.

57. deSouza NM, Scoones DJ, Krausz T, Gilderdale DJ, Soutter WP. High-resolution MR imaging of stage I cervical
neoplasia, using a dedicated endovaginal coil: MR features and correlation of imaging and pathologic findings AJR
1996; 166: 553-559.

58. Goto M, Okamura S, Ueki M, Sugimoto O. Evaluation of magnetic resonance imaging in the diagnosis of extension
in uterine cervical cancer cases with special attention to imaging planes. Nippon Sanka Fujinka Gakki Zasshi 1990; 42:
1627-1633.

59. Burghardt E, Hofmann HM, Ebner F, Haas J, Tamussino K, Justich E. Magnetic resonance imaging in cervical
cancer: a basis for objective classification. Gynecol Oncol 1989; 33: 61-67.

60. Burghardt E, Baltzer J, Tulusan AH, Haas J. Results of surgical treatment on 1028 cervical cancers studied with
volumetry. Cancer 1992; 70: 648-655.

61. Yuhara A, Akamatsu N, Sekiba K. Use of transrectal radial scan ultrasonography in evaluating the extent of uterine
cervical cancer. J Clin Ultrasound 1987; 15: 507-517.

62. Sironi S, Belloni C, Taccagni GL, DelMaschio A. Carcinoma of the cervix: value of MR imaging in detecting
parametrial involvement. AJR 1991; 156: 753-756.

63. Griffin JW, Parker RG, Taylor WJ. An evaluation of procedures used in staging carcinoma of the cervix. AJR 1976;
127: 825-827.

64. Weiner JL, Chako AC, Merton CW, Gross S, Coffey EL, Stein HL. Breast and axillary tissue MR imaging
correlation of signal intensities and relaxation times with pathologic findings. Radiology 1986; 160: 229-305.

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65. Scotian C, Pateisky N, Vavra N et al. Lymphoscintigraphy with 123I-marked epidermal growth factor in cervix
cancer. Gynakol Geburtshilfliche Rundsch 1992; 32: 17-21.

66. Hirule P, Mattman KP, Schmidt B, Pfiefter KH. Indications for radioisotope bone scanning in staging of cervical
cancer. Arch Gynaecol Obstet 1990; 248: 21-23.

67. Flueckiger F, Ebner F, Poschauko H, Tamussino K, Einspieler R, Ranner G. Cervical cancer: serial MR imaging
before and after primary radiation therapy a two year follow up study. Radiology 1992; 184: 89-93.

68. Ebner F, Kressel HY, Mintz MC et al. Tumour recurrence versus fibrosis in the female pelvis: differentiation with
MR imaging at 1.5T. Radiology 1988; 166: 333-340.

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12
The Lymphatic System

Walter Curati

Pathology and classification

Imaging strategies

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In the study of tumours, the lymphatic system has a dual role: per se it presents with its own diseases (Hodgkin's disease (HD) and
non-Hodgkin's lymphoma (NHL)) and it is also involved in the metastatic spread of tumours. This `dual role' constitutes the mainframe
of pathology and classification.

The lymphatic system has two functions:

provision of immunity-related cells (lymphocytes and macrophages) and sera to fight antigens of various sorts;

clearance of circulating micro-organisms and cells identified as undesirable.

This combination of functions explains either the successful clearance of small clones of mutant cells or the passive acceptance and
proliferation of exogenous micro-organisms carrying infections or endogenous mutants in the initial stages of tumour development.

The following are required to implement these functions:

factories to produce cells and sera (thymus, spleen, liver and bone marrow);

distribution network (lymphatic channels).

The same lymphatic channels plus interconnected nodes also act as collectors and filters for interstitial fluids and cells.

Pathology and Classification

Lymphomas account for 5-6% of adult tumours in the UK. 1 The incidence of HD peaks in the third and sixth decades, whereas that of
NHL increases from the fifth decade onwards.2 Men are affected more than women (1.4: 1 for HD and 1.1: 1 for NHL).3

At the time of its clinical manifestation a lymphoma is commonly implanted in two or more sites. In such cases, staging plays a key part
in the diagnostic process as it determines treatment strategy. The Rye classification for HD is shown in Table 12.1.4

HD spreads along contiguous groups of nodes: cervical, thoracic, abdominal and the involvement by vicinity extension motivates the
diagnostic and treatment strategies. NHL covers a broader spectrum of cell types (lymphocytes, histioytes or mixed) and of nodal and
extranodal involvement and spread. Over the last 15 years, AIDS-related NHL has been described and approximately 10% of AIDS
patients develop this complication and ultimately die from it.

Post-transplant lymphomaproliferative disorders are usually NHL and have a polymorphous histological appearance. They can remain
limited to the allograft.

Imaging Strategies

Diagnosis

Lymphoma can be suspected from a combination of clinical symptoms: long-standing weakness, malaise and/or fever and signs:
lymphadenopathy and weight loss, or as an incidental finding of an enlarged mediastinum and/or hilar on a plain chest X-ray. How is
imaging used in confirming diagnosis? Filly et al5 studied 300 untreated HD and NHL and found 2/3 HD and 1/3-1/2 NHL patients to
have thoracic nodes. The most useful imaging technique is then the one that allows local-

Table 12.1 Rye classification of Hodgkin's disease.4

Histology Distinctive features Relative frequency in adults (%)
Lymphocytic Abundant stroma of mature lymphocytes and/or histiocytes; no necrosis. 10-15
Reed-Sternberg cells may be sparse
Nodular stenosis Nodules of lymphoid tissue separated by bands of doubly refractile 20-50
collagen: atypical `lacunar' Hodgkin's cells in clear spaces within the
lymphoid nodules
Mixed cellularity Usually numberous Reed-Sternberg cells and mononuclear Hodgkin's 20-40
cells in a pleomorphic stroma of eosinophils, plasma cells, fibroblasts and
necrotic fat

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Lymphocytic Reed-Sternberg cells usually, although not always, abundant; marked 5-15
paucity of lymphocytes; diffuse, non-refractile fibrosis and necrosis may
be present

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Figure 12.1
Pathways for diagnosis of Hodgkin's disease and
non-Hodgkin's lymphoma.

ization of a lymph node for needle biopsy and histological assessment. In most cases, CT can localize the node and
guide the biopsy. Alternatively, for the abdomen and pelvis, ultrasound can be used.

Staging

Sensitivity (detection of disease without false negatives), specificity (confirmation of absence of disease wihout false
positives) and accuracy (total sum of sensitivity and specificity) are the best criteria by which to assess the performance
of staging techniques. Tolerance and compliance are additional parameters.

Table 12.2 Staging and monitoring techniques

Staging Monitoring
Whole body techniques
CT +++ +++
MRI ++ ++
PET (+ + +) +++
Organ techniques
Ultrasound ++ ++
Lymphography +++ +++
Plain X-rays + ++

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Modalities

CT is the best technique for assessing the thorax, abdomen and pelvis. It:

delineates the anatomy: assesses infiltration and extension;

visualizes the lymph nodes: isolated or in groups.

Once high resolution fast imaging becomes widely available in terms of costs and technology, MRI may be even better
than CT. At present it is limited to the pelvis and abdomen (principally the retroperitoneum) in view of the limited
motion artefacts, the coronal plane acquisition and the fat tissue background which is easy to suppress by means of
various sequences (STIR etc.) and locally, to the brain, spinal cord, etc. by using highly sensitive sequences to suppress
the CNF signal and raising the T2-weighting (FLAIR etc.).

Positron emission tomography (PET) localizes functional abnormalities with reasonable spatial resolution. Local
metabolic hyperactivity is identified and quantified by excessive consumption of metabolites, which permits both
accurate staging and monitoring but requires multidisciplinary expertise.

Ultrasound is restricted to areas where the presence of air or gas does not restrict anatomical view, i.e. the upper
adomen (often without retroperitoneum), lower pelvis and thoracic wall. Locally it can be used to assess renal (ureteric)
obstruction.

Lymphography was the first accurate (and universally used in oncologic centres) imaging technique for lymphomas and
in particular HD. It achieves superb and long-lasting opacification of lymph nodes and allows identification of disease
spread and response to treatment. The technique has two drawbacks: 1) visualization is limited to the para-aortic and
iliac groups of nodes (in the case of bipedal injection) and 2) it is necessary to dissect and cannulate the superficial
lymphatics with very fine needles which requires considerable expertise. Lymphography has been widely superceded by
CT.

Chest X-ray reveal lymph nodes only in the hilar and mediastinum providing they alter the outline of these regions at a
soft tissue-air interface or stand out in an area normally occupied by fat only and not obscured by bone. It is effective
and simple as a method of monitoring the reduction or increase in size of groups of nodes in the hilar or mediastinal
outline. Plain abdominal X-rays can monitor the size of the liver and spleen objectively and at a fraction of the cost of
CT. Skeletal surveys

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Figure 12.2
Non-Hodgkin's lymphoma type T in a 72-year-old male patient. Contrast-enhanced CT of the
chest at different levels with soft tissue and lung windows showing anterior and middle mediastinums.

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Figure 12.3
Large mediastinal nodes, adrenal glands and liver in a 66-year-old male patient with metastatic right
upper lobe bronchial carcinoma. Contrast-enhanced CT of the chest and upper abdomen at different levels.
a)-d) Right upper lobe atelectasis, pleural effusion and mediastinal nodes (arrows). e) and f) Metastatic liver
disease and enlarged right adrenal glands (open arrows).

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are not required as bone involvement at presentation is rare (HD 4% and NHL 1%).+6

Metastatic involvement of the lymphatic system is only mentioned here as it is described in the organ-specific chapters
of this book. The following rule of thumb for nodal size in relation to metastatic spread is useful in all situations:

well-defined lymph nodes < 1 cm: normal

well-defined lymph nodes 1-1.5 cm: questionably malignant

any lymph node > 1.5 cm: abnormal.

Conclusion

The single most important contribution of imaging for HD and NHL is the localization of a node for biospy. CT is the
most accurate and effective imaging technique for staging and monitoring of HD and NHL.

References

1. Bunch C, Gatter KC. The lymphomas. In: Weatherall DJ, Leadingham JC and Warrell DA (eds). Oxford Textbook of
Medicine, 3rd Edition. Oxford: Oxford University Press, 1996, Section 22.5.3, pp. 3568-3587.

2. Bragg DG. Radiology of the lymphomas. Curr Prob Diag Radiol 1987; 16: 183-206.

3. Sandrasegaran K, Robinson PJ, Selby P. Staging of lymphoma in adults. Clin Radiol 1994; 49: 149-161.

4. Lukes RJ, Butler JJ. The pathology and nomenclature of Hodgkin's disease. Cancer Res 1966; 26: 1063-1081.

5. Filly R, Blank N, Castellino RA. Radiographic distribution of intrathoracic disease in previously untreated patients
with Hodgkin's disease and non-Hodgkin's lymphoma. Radiology 1976; 120: 277-281.

6. Vanrenterghem Y. Lymphoproliferative disorders in organ transplant recipients. Eur. Radiol. 1997; 7: 665-667.

7. Bonnadonna G, Santoro A. Clinical evaluation and treatment of Hodgkins' disease. In: Wiernick PH, Canellos GP,
Kyle RA, Schiffer CA (eds) Neoplastic Diseases of the Blood. New York: Churchill Livingstone, 1985, vol II, pp.
789-790 and 794-795.

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13
The Bone and Soft Tissue

Asif Saifuddin

Primary bone tumours

Skeletal metastases and myeloma

Primary soft-tissue tumours

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Neoplasms of bone and soft tissues may be divided into primary (benign and malignant) and secondary (metastatic). Primary bone and
soft-tissue tumours are rare but the skeleton is one of the commonest sites of metastatic disease. This chapter covers primary and metastatic
disease of bones and soft tissues as separate entities, highlighting important clinical features and aspects of treatment but emphasizing the
role played by imaging in the management of patients presenting with such diseases.

Primary Bone Tumours

Classification and Incidence

Table 13.1 gives a classification of bone tumours and an indication of their relative frequencies based on referrals to the Mayo Clinic. 1 Primary
bone neoplasms are rare. It has been estimated that 1500 new malignant bone tumours are recorded in the United States per year, compared to
93 000 new cases of lung carcinoma and 88 000 new cases of breast carcinoma.1 There is no reason to believe that this ratio is different in the
United Kingdom. However, sarcomas of bone account for a significant proportion of cancers occurring in childhood and adolescence. In the
0-14 year age group, they have a recorded incidence of 6.1 per million caucasian children. After the age of 14 years, they are the fifth
commonest childhood malignancy, after leukaemia, CNS tumours, lymphoma and soft-tissue sarcomas.2

Osteosarcoma and Ewing's sarcoma are the commonest malignant bone tumours in children and adolescents. In adults, apart from multiple
myeloma, chondrosarcoma is the commonest primary bone malignancy.1

Benign bone tumours account for just under one-quarter of all primary bone neoplasms.1 This does not include benign tumour-like conditions,
such as fibrous dysplasia, simple bone cyst (SBC) and aneurysmal bone cyst (ABC). The commonest benign neoplasms are osteochondroma,
giant-cell tumour (GCT), enchondroma and osteoid osteoma.1

Table 13.1 Classification and relative frequency of primary bone tumours (excluding myeloma) (Adapted from Mayo Clinic data (total 7338
cases)1
Benign Malignant
Cartilaginous
Chondrosarcoma* 1049 (14.3%)
Osteochondroma 872 (11.9%)
Enchondroma 335 (4.6%)
Chondroblastoma 119 (1.6%)
Chondromyxoid fibroma 45 (0.6%)
Osseous
Osteosarcoma** 1718 (23.4%)
Osteoid osteoma 331 (4.5%)
Osteoblastoma 87 (1.2%)
Round cell
Ewing's sarcoma 512 (7.0%)
Lymphoma 694 (9.5%)
Fibrous
Benign fibrous Malignant fibrous
histiocytoma 9 (0.12%) histiocytoma 338 (4.6%)
Desmoplastic fibroma 12 (0.16%)
Vascular
Haemangioma 108 (1.5%) Haemangioendothelioma 80 (1.1%)
Haemangiopericytoma 13 (0.18%)
Others
Giant-cell tumour 568 (7.7%)
Chordoma 356 (4.9%)
Lipoma 1 (0.1%) Liposarcoma 1 (0.01%)
*Includes secondary, dedifferentiated and mesenchymal cs
** Includes central (conventional and low-grade), surface (parosteal, periosteal and high-grade), Paget's and post-irradiation os

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Clinical Features

Primary bone neoplasms most commonly present with bone pain and/or a palpable mass. Alternatively, they may
produce pathological fracture or may be incidental findings on radiographs obtained for other reasons. 3 Tumours of the
spine not uncommonly present with neurological symptoms and signs due to neural compression.4,5 Sciatica is also a
common presentation of malignant tumours arising from the iliac bone and sacrum, while painful scoliosis is a classical
presentation of spinal osteoid osteoma or osteoblastoma.6

Constitutional symptoms such as fever and weight loss are often seen with Ewing's sarcoma which is classically
associated with a very large mass. A raised ESR is also a feature.

Age, Sex and Race

Ewing's sarcoma and osteosarcoma have highest incidence in the first two decades of life, with Ewing's sarcoma having
an earlier peak incidence. Osteosarcoma in older age groups occurs following Paget's disease or radiotherapy.
Chondrosarcoma has its greatest incidence in the fourth to seventh decades, as do primary bone lymphoma, chordoma
and malignant fibrous histiocytoma (MFH).1 As regards benign bone tumours, the majority have their highest incidence
in the second to fourth decades of life.

Some tumours, such as osteoid osteoma and osteosarcoma, show an increased incidence in males, but this is not a
striking feature. Ewing's sarcoma has an extremely low incidence in children of Afro-Caribbean and Chinese origin.2

Site

Most primary bone tumours arise in the distal femur, proximal tibia and proximal humerus.7 This is particularly the
case for osteosarcoma. However, there are many exceptions, such as chondrosarcoma, which is most commonly located
in the pelvis or proximal femur, and Ewing's sarcoma, which has a propensity for the diaphyses of long bones and the
pelvis.1 GCT characteristically occurs in a subarticular site, whereas chondroblastoma is typically located within an
epiphysis.

Primary tumours of the small bones of the hands and feet are extremely rare and are usually enchondromas. Similarly,
primary tumours rarely affect the skull, mandible or sinuses.1

Primary malignant neoplasms are rare in the spine and tend to involve the vertebral body. Chordomas arise centrally,
usually within the sacrum or clivus.1 Conversely, benign spinal tumours, particularly osteoid osteoma and
osteoblastoma, tend to involve the neural arch.6

Mortality

The introduction of chemotherapy in the management of patients with conventional osteosarcoma has resulted in a
dramatic increase in 5-year survival rates in tumour centres from approximately 15% to 60%.8 Chemotherapy also
facilitates tumour resection, allowing the majority of patients with extremity osteosarcoma to benefit from limb-salvage
surgery. Reported 5-year survival rates for Ewing's sarcoma are in the range of 50-70%.9

Approximately 20% of patients will have detectable pulmonary metastases at presentation. This, and the presence of
bony metastases, are poor prognostic signs. Although pulmonary metastatectomy increases disease-free survival, it
rarely results in increased long-term survival.10

The prognosis for patients with low-grade malignant tumours such as chondrosarcoma and chordoma is much better.
These tumours are rarely associated with metastatic disease and chemotherapy is not used in their management. Death is
usually due to local recurrence.

Imaging

The aims of imaging in the initial assessment of primary bone lesions are to try and answer the following questions:

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What is the most likely diagnosis?

What is the local extent of disease (local staging)?

If the lesion is malignant, has it metastasized (distant staging)?

Diagnosis

The first investigation for a patient presenting with a suspected primary bone tumour is the plain radiograph.7, 11
Despite the introduction of bone scintigraphy, computed tomography (CT) and more recently magnetic resonance
imaging (MRI), the plain radiograph remains the most valuable investigation in formulating an initial differential
diagnosis. With the combination of radiographic appearance, site of the

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lesion and age of the patient, a correct diagnosis can be achieved in the majority of cases.

The plain radiographic features that need to be assessed include the following:

Site of Lesion

Many tumours have a predilection for various parts of the skeleton. It is therefore important to ascertain the precise site
of the lesion, not only within the skeleton but also within the individual bone. In a long bone, the lesion may be
epiphyseal, metaphyseal, metadiaphyseal or diaphyseal. It may also arise within the medullary canal, the cortex or from
the surface of the bone. In the spine, it may arise solely within the vertebral body or the neural arch or may involve both
of these structures. In the long bones, the site of the lesion can usually be accurately determined by the combination of
good quality anteroposterior (AP) and lateral radiographs. In the spine or pelvis, CT is of additional value for precise
localization.

Margin of Lesion and Pattern of Bone Destruction

Assessment of these two factors results in an accurate assessment of the rate of growth (and therefore aggressiveness) of
a solitary bone lesion. Radiographic patterns of bone destruction have been graded by Lodwick et al 12 as being either
geographic (Grade IA, B or C), moth-eaten (Grade II) or permeative (Grade III). A Grade IA lesion represents the
appearance produced by the most benign (or non-aggressive) of bone lesions (Fig. 13.1), whereas a Grade III lesion
indicates a rapid rate of growth seen with the most malignant (or aggressive) of bone lesions (Fig. 13.2).

The type of periosteal reaction produced by the lesion also gives clues as to its activity. A thick, well-formed periosteal
reaction indicates a slow rate of growth, whereas a rapidly growing tumour may produce no identifiable periosteal
reaction at all, since the periosteum only becomes visible radiographically once it has had time to produce bone on its
inner surface. Aggressive bone neoplasms may also break through the cortex of the bone, producing an extraosseous
mass. This feature is generally indicative of a malignant lesion.

Matrix of the Lesion

The matrix of a tumour refers to the extracellular tissue produced by the tumour and within which the tumour cells lie.
Tumours of cartilaginous or osseous origin may produce characteristic patterns of matrix mineralization which can be
recognized radiographically (Figs 13.1 and 13.2).

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Figure 13.1
Anteroposterior radiograph of a patient with an
enchondroma of the little finger metacarpal,
appearing as a well defined expanding lesion with a
sclerotic margin and matrix calcification typical of a
cartilaginous tumour.

Figure 13.2
Anteroposterior (left) and lateral (right) radiographs
of the distal femur of an 11-year-old boy with
osteosarcoma, appearing as a destructive
bone-forming lesion in the metaphysis.

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Bone scintigraphy, CT and MRI play little role in the diagnosis of primary bone lesions. Although these techniques are
more sensitive than plain radiography in the identification of medullary pathology, they lack specificity. Exceptions
include the ability of CT and MRI to demonstrate lesions containing fat, such as lipomas, and scintigraphy and CT to
detect and characterize osteoid osteoma and osteoblastoma, particularly in the spine (Fig. 13.3). CT and MRI can also
demonstrate fluid-fluid levels, most commonly seen in aneurysmal bone cysts (Fig. 13.4). MRI may suggest a lesion to
be much more aggressive than it actually is, due to the demonstration of reactive peritumoural oedema. 13

Following the initial imaging assessment, several situations may arise. First, the radiological or imaging appearances
may be pathognomonic of a non-progressive benign tumour or tumour-like lesion which needs no active treatment.
Examples include non-ossifying fibroma, asymptomatic osteochondroma or enchondroma, fibrous dysplasia and some
traumatic conditions, such as myositis ossificans and stress fracture.7 A confident diagnosis of these latter two
conditions is particularly important since biopsy of such lesions may result in a misdiagnosis of osteosarcoma by an
inexperienced pathologist, with tragic consequences for the patient.

Secondly, the imaging features may be pathognomonic for a benign lesion following which definitive treatment can be
instituted. A typical example of this is osteoid osteoma. It is now common practice to excise such lesions
percutaneously using CT guidance.14

Thirdly, the imaging features may be characteristic of a locally aggressive benign lesion, such as a giant-cell tumour, or
a malignant lesion, such as an osteosarcoma or Ewing's sarcoma. Such lesions need further imaging for local staging
and, in the case of malignant tumours, for distant staging. Following these staging procedures, biopsy is undertaken in
order to obtain histological confirmation of the diagnosis.

Finally, the imaging features may not be characteristic of any lesion. In this situation, biopsy is required to make a
histological diagnosis, following which the appropriate treatment can be planned.

Local Staging

Clear identification of the local extent of a focal bone lesion is vital so that complete excision can be achieved at the
first attempt. For tumours arising within the appendicular skeleton, the surgeon needs to know:

the extent of tumour within the medullary cavity (the intraosseous extent);

whether the tumour has extended through the cortex to form an extraosseous mass, as is usually the case with
osteosarcoma;

the relationship of extraosseous tumour to adjacent structures (the extraosseous extent), in particular the neurovascular
bundle and adjacent joint.

If the neurovascular bundle is encased by tumour, then amputation will usually be necessary. The primary amputation
rate for osteosarcoma is approximately 8%. If there is no involvement of the neurovascular bundle, limb salvage surgery
becomes possible. Involvement of the adjacent joint (usually the knee) will alter management, such that an
extra-articular resection must be performed followed by arthrodesis. This results in a poorer functioning limb.

With regard to the spine, the extension of tumour into the paravertebral and extradural space and the relationship of
tumour to the thecal sac must be identified.

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Figure 13.3
A 14-year-old boy with osteoblastoma of L4. A) The bone scan
shows a focal region of increased activity related to the pedicle of L4. B)
CT shows an expanded lytic lesion with matrix mineralization (arrow).

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Figure 13.4
A 12-year-old girl with an aneurysmal bone cyst of the proximal
fibula. A) Anteroposterior radiograph demonstrates an expansile
lytic lesion. B) Axial MRI shows characteristic fluid fluid levels
within the lesion.

MRI is ideally suited to local staging of an aggressive benign or primary malignant bone neoplasm for several reasons.
MRI can be performed in any desired plane, typically sagittal, coronal and axial. MRI is the most sensitive technique for
imaging the marrow cavity and soft tissues, with the exception of tendons where ultrasound is extremely valuable.
However, the latter situation is not of particular relevance to tumour imaging. The large variety of MRI sequences
allows clear differentiation between intraosseous tumour and normal marrow tissue, and between extraosseous tumour,
muscle and the neurovascular bundle (Fig. 13.5). 7, 11 MRI can also identify `skip' metastases (metastases to the same
bone), which are a rare occurrence in appendicular osteosarcoma. Also, MRI is not associated with potentially harmful
ionizing radiation, which is of importance in the young patient population that presents with primary malignant bone
tumours.

MRI has some disadvantages. Infants and young children need general anaesthesia, as movement will degrade image
quality. Contraindications to MRI include patients with cardiac pacemakers, aneurysm clips and cochlear implants. A
small proportion of patients suffer claustrophobia, but this can usually be overcome with sedation.

The local extent of the tumour will determine whether limb-salvage surgery is possible. The MR images together with
measurement films (plain radiographs of the whole limb) are then used to design an endoprosthesis.

MRI is also of established value in assessing malignant tumours of the spine, clearly demonstrating the extent of tumour
within the body and neural arch, as well as extension into the epidural space. Infiltration of the dura, however, is
difficult to identify. MRI will also demonstrate normality of the adjacent vertebral bodies, which is important if they are
to be the site of spinal fixation following tumour excision. Benign tumours of the spine are still better imaged with CT,
which allows

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Figure 13.5
An 11-year-old girl with osteosarcoma of the distal femur. A)
Sagittal MRI sequence identifies the intraosseous extension of
tumour. B) Axial MRI sequence demonstrates the relationship of
tumour (arrowheads) to the neurovascular bundle (long arrow).

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a clearer definition of tumour margins, particularly for lesions arising in the neural arch (Fig. 13.3B). As regards
tumours of the bony pelvis, important points in the intraosseous staging of the lesion are the relationship to the
sacroiliac joint and acetabulum.

Scintigraphy no longer plays any role in the local staging of bone neoplasms. Arteriography may still be of occasional
value when it is not clear from MRI if local vessels are involved. Arteriography and preoperative embolization is
occasionally performed for vascular tumours around the pelvis [11].

Distant Staging

Primary bone tumours most commonly metastasize to the lungs and skeleton. 15 Spread to regional lymph nodes is rare
but occasionally seen with osteosarcoma. Metastases to the liver occur with Ewing's sarcoma once tumour has spread to
the lungs. All patients presenting with primary malignant bone tumours therefore require a chest radiograph and CT of
the lungs and mediastinum.15 Chest CT is far more sensitive than plain radiography for the identification of pulmonary
metastases. Metastases from bone sarcomas have a predilection for the subpleural region of the lungs, where they may
produce spontaneous pneumothorax.

The major role for bone scintigraphy is the identification of metastatic disease to the skeleton.15 Bone scintigraphy is a
sensitive technique for identification of skeletal pathology,16, 17 but is relatively non-specific and cannot clearly
distinguish infection or trauma from neoplastic disease. Furthermore, the differentiation of benign and malignant
neoplasms is unreliable. Therefore, scintigraphy has a limited role in assessment of the primary tumour other than
osteoid osteoma and osteoblastoma (Fig. 13.3A). More skeletal metastases can be identified by MRI than by bone
scintigraphy. However, it is not practical to image the whole skeleton with MRI in order to identify metastatic
disease.18 MRI is used as an adjunct to scintigraphy, when the appearances of the bone scan are not typical or if there is
persistent focal bone pain in the presence of normal plain radiography and scintigraphy.

The identification of metastatic bone disease in patients with osteosarcoma is of particular importance since this
virtually excludes the possibility of cure. This is not the case with Ewing's sarcoma.

Biopsy

Biopsy is the next step in the investigation of primary bone neoplasms once all staging examinations have been
performed. Biopsy is performed by either the surgeon or the radiologist, and may be either open (through a small
surgical incision) or closed (by a percutaneous needle technique).19 It is of overriding importance that the biopsy takes
place in the institution where definitive surgical treatment is to be performed. An inappropriate biopsy site may preclude
limb-salvage surgery.20

The practice of the London Bone Tumour Service is to utilize percutaneous needle biopsy, usually by a radiologist in
the X-ray department. There are several advantages to this method. With the aid of the plain radiographs and MR
images, the radiologist will be able to target the biopsy to the part of the tumour that is most likely to give a positive
diagnosis. The biopsy may be guided either by fluoroscopy, ultrasound or CT. A short general anaesthetic is used for
children, whereas the vast majority of adults tolerate the procedure as outpatients under local anaesthesia.

When examined by an experienced bone tumour pathologist, needle biopsy has a diagnostic accuracy of over 95%.21
Histological examination of the biopsy specimen not only enables a definitive diagnosis, but also establishes the grade
of malignancy, which is one of the criteria for surgical staging of the tumour.

Surgical Staging

The combination of local extent, metastatic spread and histological grade allows the tumour to be graded according to
one of the several surgical staging systems available.22 Correct surgical staging is important for predicting prognosis
and for planning treatment.

Treatment

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With the establishment of a definitive diagnosis, local and distant staging of the lesion, an appropriate treatment plan
can be formulated. This will include a variety of surgical procedures for benign neoplasms and some malignant
tumours, such as low-grade chondrosarcoma or parosteal osteosarcoma. High-grade malignant tumours of the long
bones, including osteosarcoma and Ewing's sarcoma, will be treated initially by neoadjuvant chemotherapy followed by
endoprosthetic replacement where appropriate (Fig. 13.6). Radiotherapy may also be used for patients presenting with
pathological fracture.

During the period of chemotherapy, the radiologist's role is to assess the response of the tumour to chemotherapy. This
is usually attempted by serial MRI,23, 24 but Doppler ultrasound may be of value by demonstrating reduced vascularity
within the tumour.25

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Figure 13.6
A 38-year-old man with distal femoral Ewing
sarcoma. Anteroposterior and lateral radiographs
showing appearances of an endoprosthetic
replacement.

While the patient is undergoing chemotherapy, the endoprosthesis is designed and manufactured. This takes 4-6 weeks.

Following surgery for high-grade malignant neoplasms, pathological examination of the excised specimen allows an
assessment of the degree of tumour necrosis. Based on this, decisions are made as to the choice of post-operative
(adjuvant) chemotherapy.

Radiological Follow-Up

The purpose of postoperative radiological follow-up of primary bone tumours is essentially two-fold; first, to assess the
effects of surgery and, secondly, to identify tumour recurrence.

Many benign neoplasms are treated by local excision with or without filling of the surgical defect by bone graft or
cement. Serial radiography will demonstrate adequate healing of surgical defects and satisfactory incorporation of bone
grafts. Recurrence of tumours treated by curettage and methyl methacrylate cement installation (cementoma) can be
identified radiologically several months prior to recurrence of symptoms. 26

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Potential complications of endoprosthetic replacement include mechanical loosening and infection. Both of these can be
identified by plain radiography. Swelling at the site of an endoprosthesis can be due to either chronic infection or
tumour recurrence. The presence of a metallic implant makes assessment with CT and MRI difficult, although not
impossible (Fig. 13.7). Ultrasound, which is not subject to metal artefact, can be very useful in this situation.
Identification of any mass lesion adjacent to a prosthesis can be followed by ultrasound-guided needle biopsy.

Where endoprosthetic replacements have not been used, possible tumour recurrence is best investigated by MRI. MRI is
effective at distinguishing between recurrent tumour, postoperative fibrosis and radiotherapy changes. If recurrent
tumour is suspected, needle biopsy is usually performed for histological confirmation prior to further treatment.

Follow-up of patients with osteosarcoma and Ewing's sarcoma also requires serial chest radiography and CT to assess
the response of pulmonary metastatic disease to chemotherapy or to identify new metastatic disease.

The development of any new bone pain should be investigated with plain radiography and whole-body bone
scintigraphy. MRI may be performed if these two investigations are normal. It should be remembered that bone pain
does not necessarily indicate skeletal metastatic disease but may be a consequence of treatment. Osteonecrosis is a well
recognized complication of radiotherapy and can be differentiated from metastasis by MRI.

Skeletal Metastases and Myeloma

Skeletal metastases and myeloma are considered together since they occur in the same age group and are the two major
differential diagnoses in patients presenting with multifocal destructive bone lesions.

Metastases are the commonest tumours to occur in the skeleton and the skeleton is one of the commonest sites of
metastatic disease. The reported incidence of skeletal metastases from postmortem studies in patients dying of cancer is
12-70%.27 Skeletal metastases are estimated to be 25 times more common than primary bone tumours and
approximately 9% are solitary.28 Therefore, in a patient over the age of 40, a solitary metastasis is more common-

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Figure 13.7
A 52-year-old man with recurrent pain and swelling
after endoprosthetic replacement for proximal tibial
chondrosarcoma. A) Lateral radiograph shows
satisfactory appearances of the endoprosthesis. B)
Sagittal MRI sequence demonstrates the recurrent
tumour (arrows).

ly encountered than a primary bone tumour. The commonest cancers to metastasize to bone are prostate, breast, lung,
renal and thyroid. Occasionally, patients present with metastatic disease to bone of unknown origin. 15

Skeletal metastases may occur in any bone but the spine, pelvis, proximal femur, ribs and skull are the commonest
sites.27 Over 80% of metastatic deposits occur in the axial skeleton.16

Multiple myeloma is the commonest primary bone malignancy.1 The condition is commoner in males and the peak
incidence is in the sixth to seventh decades of life. The sites of occurrence in the skeleton mirror those of metastatic
disease. Patients may also present with a solitary lesion, termed plasmacytoma, which usually progresses to multiple
myeloma.

Clinical Features

Pain is the commonest symptom in patients with either skeletal metastases or myeloma. However, 30-50% of patients
with skeletal metastases have no pain.29

Pathological fracture is also a common presentation. When this involves a vertebral body, it is frequently associated
with spinal cord compression. Asymptomatic skeletal metastases may also be identified by bone scintigraphy as part of
the staging process of patients with known cancer.16, 17

Imaging

Initial Assessment

The initial imaging investigation in any patient presenting with a possible metastatic lesion or myeloma is the plain
radiograph, which may show a variety of appearances (lytic, sclerotic or mixed).

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In a patient over 40 years of age presenting with focal bone pain and a destructive lesion on plain radiography, the
working diagnosis is metastasis or myeloma. The next step in the diagnostic pathway is the demonstration of multiple
lesions, which is best achieved by whole body bone scintigraphy (Fig. 13.8). Metastases typically appear as multiple
asymmetric areas of increased activity located predominantly in the axial skeleton. Occasionally, lesions appear as focal
areas of reduced activity, usually seen with renal carcinoma metastases. Another well recognized pattern is the
`superscan'. This occurs when there is widespread osteoblastic metastatic disease involving the skeleton and is most
often seen in prostatic and breast cancer.16

In patients presenting with metastatic disease of unknown origin, the lung and kidney are the most likely primary
sites.15 The bone scan should be followed by chest radiography and ultrasound or CT of the abdomen. If a primary site
is not identified, needle biopsy of the presenting lesion is indicated.

The further imaging of a skeletal metastasis depends upon the effects it is producing. Surgical intervention is indicated
in several circumstances. First, in patients presenting with vertebral lesions causing spinal cord

Figure 13.8
Bone scan in a
patient with
metastatic
prostatic cancer.
Metastases
typically appear
as multiple areas
of increased activity
in the axial skeleton.

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compression, either due to pathological collapse or extradural extension, MRI is indicated to determine the exact local
extent of tumour so that surgical resection can be planned (Fig. 13.9). MRI is also of value in the differentiation of
osteoporotic and malignant collapse. 18 Secondly, in a patient presenting with a solitary extremity metastasis, treatment
may be by wide excision and endoprosthetic replacement. Local staging with MRI is then required, as for a primary
malignant bone neoplasm. Thirdly, surgery may be required either prophylactically or for an established pathological
fracture. This risk of pathological fracture is proportional to the extent of cortical destruction.29

In contrast to skeletal metastases, the bone scan is less sensitive than plain radiography in the detection of myeloma
deposits.16, 17 The diagnosis is usually established by a combination of laboratory tests and bone marrow aspirate.
Needle biopsy is indicated for plasmacytoma, in which case the typical serum protein abnormalities may not be
present.1 As with metastatic disease, further imaging with MRI is indicated for local staging prior to spinal cord
decompression or excision of solitary lesions. Plain radiographs of painful lesions should be obtained to assess the
likelihood of pathological fracture.

Following Treatment

The treatment of skeletal metastases is primarily palliative, the aims being to relieve pain, prevent pathological fracture,
improve mobility and function and, if possible,

Figure 13.9
A 70-year-old man with prostatic cancer. Sagittal
MRI sequences showing metastasis to the thoracic
spine with spinal cord compression.

prolong survival. Treatment options, apart from pain relief, include endocrine therapy, chemotherapy, targeted
radiotherapy, biphosphonates and external beam radiotherapy,30 in addition to surgery, as described above.

Treatment response can be assessed, although not very accurately, by serial radiography or scintigraphy. As yet, MRI is
not a sensitive technique for identifying response since abnormal appearances may remain despite successful medical
treatment.18

Primary Soft-Tissue Tumours

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Primary soft-tissue tumours are a highly heterogeneous group of tumours that may arise from muscle, fat, fibrous tissue,
vessels and nerves. They may be benign or malignant (in which case they are termed sarcomas). It is estimated that
benign tumours are 100 times commoner than malignant tumours.31 Soft-tissue sarcomas account for approximately
1% of cancers in the United States and 2% of cancer deaths. The lower limbs are the commonest site of occurrence
(40%), followed by the upper limbs (20%), head and neck (10%) and trunk or retroperitoneum (30%).32

The commonest soft-tissue sarcomas are malignant fibrous histiocytoma (MFH), liposarcoma and synovial sarcoma.
The commonest benign soft-tissue tumours are intramuscular lipoma, fibromatosis, haemangioma and nerve-sheath
tumours.15 However, it should also be remembered that metastatic disease and lymphoma, as well as non-neoplastic
lesions, such as ganglion cyst, abscess and post-traumatic ossification or aneurysm, can present as soft-tissue masses.

Clinical Features

Soft-tissue tumours most commonly present as painless masses. Features that suggest malignancy include pain and
rapid enlargement.33 Also, extremity masses arising deep to the fascia and that are larger than 5 cm in diameter, are
more likely to be malignant. However, almost one-third of sarcomas are subcutaneous and smaller than 5 cm.15

Imaging

Initial Assessment

The aims of initial imaging of soft-tissue masses are diagnosis and staging. The initial assessment is with plain
radiography which, however, is not as valuable a diagnostic aid for soft-tissue tumours as it is for bone lesions. Most
soft-tissue tumours are isodense to mus-

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cle. A mass with fat density indicates a diagnosis of lipoma or liposarcoma. Phleboliths (small rounded calcifications)
are characteristic of soft-tissue haemangioma. The plain radiograph may also show extrinsic pressure erosion of bone or
periosteal reaction. 15

Ultrasound is of value in differentiating solid and cystic masses and can give some indication of tumour size. If the mass
is completely cystic (especially if related to a joint), superficial and less than 5 cm in diameter, it is probably benign.
Larger solid masses are more likely to be sarcomas, in which case it is advisable to refer the patient to a specialist
centre.15

MRI has a greater diagnostic capability for soft-tissue masses than for bone lesions. Benign soft-tissue tumours that can
be diagnosed include lipoma, haemangioma, fibromatosis, myxoma and nerve sheath tumours (based on their
relationship to major nerves). Non-neoplastic masses identifiable by MRI include ganglion cyst, enlarged bursa and
haematoma.34

MRI is of less value in allowing a pre-biopsy diagnosis for soft-tissue sarcoma. Characteristic features are seen with
well-differentiated liposarcoma (Fig. 13.10), myxoid sarcomas and malignant peripheral nerve sheath tumours.
However, the majority of soft-tissue sarcomas show an indeterminate pattern (Fig. 13.11).35 The differentiation
between benign and malignant lesions on MRI is not clear-cut, although masses showing marked heterogeneity and
internal septation appear more likely to be malignant.36

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Figure 13.10
A 50-year-old man with low-grade
liposarcoma of the left thigh. A) Coronal
and B) axial MRI sequences show a
large mass in the medial aspect of the
thigh with the signal characteristics of fat.

Figure 13.11
A 68-year-old man with a
high-grade liposarcoma of the
left thigh. A) Coronal and B)
axial MRI sequences show a
mass in the medial aspect of the
thigh. The lesion has no characteristic
features but the relationship to the
neurovascular bundle (arrow) is
clearly shown.

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MRI is the technique of choice for local staging of soft-tissue sarcomas, 15, 32 allowing the clearest identification of
tumour margins and the relationship to the neurovascular bundle and adjacent bone (Fig. 13.11). Patients with
soft-tissue sarcomas also require distant staging as for malignant bone tumours.15

Following staging, biopsy is indicated for those masses which are indeterminate in nature based on clinical and imaging
findings. Percutaneous needle biopsy with ultrasound-guidance is usually a successful technique. Biopsy of deep lesions
that are not identified by ultrasound can be guided with CT.

Assessment of Recurrence

Surgery is the mainstay of treatment for primary soft-tissue sarcoma. Wide local excision may be combined with
radiotherapy. The role of neoadjuvant chemotherapy for soft-tissue sarcomas is unclear,37 although it is beneficial for
rhabdomyosarcoma and synovial sarcoma. The evaluation of potential tumour recurrence (estimated to occur in 10-20%
of cases) is therefore hampered by changes resulting from the surgical procedure and radiotherapy. Local recurrence
will usually occur within 2 years of therapy and since it can be effectively treated with further surgical excision or
radiotherapy, early detection with MRI is important. MRI can also characterize benign masses at the resection site such
as seromas, abscesses and chronic haematomas.37

Radiotherapy produces characteristic changes limited to the radiation portal within subcutaneous tissues and muscle.
Recurrent tumour typically appears as a relatively well-defined nodule or mass which can be differentiated from
postoperative fibrosis by dynamic enhanced MRI techniques.38 Where any doubt persists, further needle biopsy is
indicated.

Conclusion

The successful treatment of a patient with a suspected primary bone or soft-tissue neoplasm requires close cooperation
between surgeons, radiologists and pathologists, as well as radiotherapists, oncologists and paramedical staff. Because
of their relative rarity, such tumours are best treated in specialist centres. Therefore, as soon as the diagnosis of a
potential primary bone tumour or soft-tissue sarcoma has been made by clinical and initial radiographic findings, and
ideally prior to biopsy, the patient should be referred to a tumour unit for further management.

Acknowledgements

The author would like to thank Mr Stephen Cannon, FRCS and Dr Jane Edge for their helpful comments, Ms Veronika
Aurens for typing the manuscript and Mr Dirk de Camp, Department of Medical Photography, Institute of Orthopaedics,
UCL, for the illustrations.

References

1. Unni KK. Dahlin's Bone Tumors. General Aspects and Data on 11,087 Cases, 5th edn. Philadelphia:
Lippincott-Raven, 1996.

2. Souhami R. Incidence and aetiology of malignant primary bone tumours. Clin Oncol 1987; 1: 1-20.

3. Letson GD, Greenfield GB, Heinrich SD. Evaluation of the child with a bone or soft-tissue neoplasm. Orthop Clin N
Am 1996; 27: 431-451

4. Weinstein JN, McLain D, McLain RF. Primary tumors of the spine. Spine 1987; 12: 843-851.

5. Dreghorn CR, Newman RJ, Hardy GJ et al. Primary tumours of the axial skeleton. Experience of the Leeds Regional
Bone Tumour Registry. Spine 1990; 156: 137-140.

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6. Pettine KA, Klassen RA. Osteoid osteoma and osteoblastoma of the spine. J Bone Joint Surg (Am) 1986; 68-A:
354-361.

7. Stoker DJ. The place of radiology in diagnosis and management. Clin Oncol 1987; 1: 65-96.

8. Bramwell VH, Burgers M, Sneath R et al. A comparison of two short intensive chemotherapy regimens in operable
osteosarcoma of limbs in children and young adults: the first study of the European Osteosarcoma Intergroup. J Clin
Oncol 1992; 10: 1579-1591.

9. Jurgens H, Exner U, Gadner H et al. Multidisciplinary treatment of primary Ewing's sarcoma of bone: a 6-year
experience of a European cooperative trial. Cancer 1988; 61: 23-32.

10. Bloem JL, Kroon HM. Osseous lesions. Radiol Clin N Am 1993; 31: 261-278.

11. Stoker DJ. Management of bone tumours the radiologist's role. Clin Radiol 1989; 40: 233-239.

12. Lodwick GS, Wilson AJ, Farrell C et al. Determining growth rates of focal lesions of bone from radiographs.
Radiology 1980; 134: 577-583.

13. Seeger LL, Durgan DH, Eckardt JJ, Bassett LW, Gold RH. Nonspecific findings on MR imaging. The importance of
correlative studies and clinical information. Clin Orthop 1991; 270: 306-312.

14. Bemard R, Berlin M-F, Wiolard M, Grenier P. Osteoid osteoma: CT-guided percutaneous excision confirmed with
immediate follow-up scintigraphy in 16 outpatients. Radiology 1996; 201: 239-242.

15. Simon MA, Finn HA. Diagnostic strategy for bone and soft-tissue tumours. J Bone Joint Surg (Am) 1993; 75-A:
622-631.

16. Brown ML. Bone scintigraphy in benign and malignant tumours. Radiol Clin N Am 1993; 31: 731-738.

17. Brown ML, Collier D, Fogleman 1. Bone scintigraphy: part 1. Oncology and infection. J Nud Med 1993; 34:
2236-2240.

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18. Traill Z, Richards MA, Moore NR. Magnetic resonance imaging of metastatic bone disease. Clin Orthop 1995; 312:
76-88.

19. Simon MA, Biermann JS. Biopsy of bone and soft-tissue lesions. J Bone Joint Surg (Am) 1993; 75-A: 616-621.

20. Springfield DS, Rosenberg A. Biopsy: complicated and risky (editorial). J Bone Joint Surg (Am) 1996; 78-A:
639-643.

21. Stoker DJ, Cobb JP, Pringle JAS. Needle biopsy of musculoskeletal lesions. A review of 208 procedures. J Bone
Joint Surg (Br) 1991; 73-B: 498-500.

22. Finn HA, Simon MA. Staging systems for musculoskeletal neoplasms. Orthopedics 1989; 12: 1365-1371.

23. Fletcher BD. Response of osteosarcoma and Ewing's sarcoma to chemotherapy: imaging evaluation. Am J
Roentgenol 1991; 157: 825-833.

24. Erlemann R, Sciuk J, Bosse A et al. Response of osteosarcoma and Ewing's sarcoma to preoperative chemotherapy:
assessment with dynamic and static MR imaging. Radiology 1990; 175: 791-796.

25. Van der Woude H-J, Bloem JL, Schipper J et al. Changes in tumor perfusion induced by chemotherapy in bone
sarcomas: color Doppler flow imaging compared with contrast-enhanced MR imaging and three-phase bone
scintigraphy. Radiology 1994; 191: 421-431.

26. Remedios D, Saifuddin A, Pringle JAS, Giant-cell tumour of bone: radiological versus clinical recurrence following
cementation. J Bone Joint Surg (Br) 1997 79-B: 26-30.

27. Brage ME, Simon MA. Metastatic bone disease. Evaluation, prognosis and medical treatment considerations of
metastatic bone tumours. Orthopedics 1992; 15: 589-596.

28. Stoker DJ. Bone tumours: malignant lesions. In: Grainger R, Allison DJ (eds) Diagnostic Radiology An Anglo
American Textbook of Imaging, 2nd edn. Edinburgh: Churchill Livingstone. 1992: 1527-1554.

29. Galasko CSB. Diagnosis of skeletal metastases and assessment of response to treatment. Clin Orthop 1995; 312:
64-75.

30. Houston SJ. The systemic treatment of bone metastases. Clin Orthop 1995; 312: 95-104.

31. Enzinger FM, Weiss SW. Soft-Tissue Tumors, 3rd edn. St. Louis: Mosby Year Book. 1995.

32. Moreau G, Bush CH, Scarborough MT, Enneking WF. Surgical considerations in the diagnostic imaging evaluation
of musculoskeletal masses. MRI Clin N Am 1995; 3: 577-590.

33. Frassica FJ, Thompson RC. Evaluation, diagnosis and classification of benign soft-tissue tumours. J Bone Joint Surg
(Am) 1996; 78-A: 126-140.

34. Sundaram M, Sharafuddin MJA. MR imaging of benign soft-tissue masses. MRI Clin N Am 1995; 3: 609-628.

35. Hanna SL, Fletcher BD. MR imaging of malignant soft-tissue tumours. MRI Clin N Am 1995; 3: 629-650.

36. Weatherall PT. Benign and malignant masses: MR imaging differentiation. MRI Clin N Am 1995; 3: 669-694.

37. Varma DGK, Jackson EF, Bullock RE, Benjamin RS. Soft-tissue sarcoma of the extremities. MR appearances of
post-treatment changes and local recurrence. MRI Clin N Am 1995; 3: 695-712.

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38. Vanel D, Shapeero L, De Baere T et al. MR imaging in the followup of malignant and aggressive soft-tissue tumors:
results of 511 examinations. Radiology 1994; 190: 263-268.

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14
The Cardiovascular System

Craig A Hackworth and Martin J Lipton

Nature and incidence of cardiac neoplasia

Mechanisms of tumour extension

Clinical manifestations of neoplastic heart disease

Primary tumours of the heart

Malignancy and the great vessels

Differential diagnosis of cardiac tumours

Future impact of digital imaging on tumour diagnosis

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Nature and Incidence of Cardiac Neoplasia

Primary tumours of the heart are rare, with an incidence of 1 in 2000 autopsies. 1 Approximately 75% of these primary
cardiac neoplasms are benign. Cardiac metastases on the other hand, are 20-40 times more frequent. However, any
benign or malignant cardiac lesion may produce a range of symptoms and mimic a wide spectrum of heart disease.
Early diagnosis of primary cardiac tumours permits the opportunity for a complete cure by surgical resection. The
success of surgery depends on diagnostic imaging studies, which define the site and nature of a tumour as well as its
relationship to cardiac, pericardial and other adjacent structures. Therefore, early diagnosis is critical as it may avoid
serious complications and even prevent sudden death.

Since the diagnostic approach is similar for any suspected cardiac neoplasm, a solid understanding of the wide spectrum
of pathology encountered is essential. The heart is involved in approximately 10% of all patients with malignancies, and
of these, tumour is present in the pericardium in 85%. Pericardial infiltration accounts for both cardiac dysfunction and
symptoms which are found in nearly all patients. The physiological effect is usually secondary to pericardial thickening
with or without effusion. Frequently a malignant effusion is haemorrhagic, as compared to the serous type seen
commonly with other forms of heart disease. Pericardial effusion associated with malignancy may be secondary to
hypoalbuminaemia, chemotherapy response and radiation therapy. Almost any tumour, except neurogenic neoplasms
can metastasize to the heart.2 However, the most common sources of cardiac metastases are lung carcinoma in men and
breast cancer in women. Approximately 10% of these patients will develop metastases to the heart. Melanoma is a much
less common tumour, but has the highest incidence of metastases to the myocardium, followed by leukaemia and
lymphoma.

Mechanisms of Tumour Extension

The route of tumour spread is dependent on the site of the primary malignancy. Carcinoma of lung, breast and
oesophagus usually reach the heart by direct extension. However, approximately 50% of patients with lung and breast
carcinoma develop cardiac metastases without evidence of direct extension. These isolated cardiac metastases exhibit
retrograde tumour spread via lymphatics with microscopic nodules deposited throughout the myocardium.

Another well known route of spread is by venous extension. Renal cell carcinoma and hepatoma are notorious for
metastasizing in this fashion. Tumour thrombus exits a major draining vein and classically grows along the inferior vena
cava (IVC). These tumour thrombi may extend into the right atrium.

Finally, haematogenous spread is the main route of dissemination in the case of sarcoma, lymphoma, leukemia and
melanoma. Chapter 4 deals with tumours involving the lungs and mediastinum.

McAllister and Fenoglio1 reviewed 533 cases of primary tumours and cysts of the heart and pericardium at the Armed
Forces Institute of Pathology in Washington, DC. The incidence of various cardiac tumours found in their series is
given in Table 14.1.

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Table 14.1 Tumours and cysts of the heart and pericardium1 (reproduced with
permission).
Type Number Percentage
Benign
Myxoma
130 24.2
Lipoma
45 8.4
Papillary fibroelastoma
42 7.9
Rhabdomyoma
36 6.8
Fibroma
17 3.2
Hemangioma
15 2.8
Teratoma
14 2.6
Mesothelioma of the AV node
12 2.3
Granular cell tumour
3
Neurofibroma
3
Lymphangioma
2
Subtotal 319 59.8
Pericardial cyst
82 15.4
Bronchogenic cyst
7 1.3
Subtotal 89 16.7
Malignant
Angiosarcoma
39 7.3
Rhabdomyosarcoma
26 4.9
Mesothelioma
19 3.6
Fibrosarcoma
14 2.6
Malignant lymphoma
7 1.3
Extraskeletal osteosarcoma
5

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Neurogenic sarcoma
4
Malignant teratoma
4
Thymoma
1
Leiomyosarcoma
1
Liposarcoma
1
Synovial sarcoma
1
Subtotal 125 23.5
TOTAL
533 100.0

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Clinical Manifestations of Neoplastic Heart Disease

It is important to recognize that any space occupying lesion in the heart carries a risk of functional cardiac impairment,
embolism or sudden death. Neoplastic disease of the heart, whether primary or secondary, can only present with a
limited number of signs and symptoms (Table 14.2). Modern surgical techniques may allow complete resection of a
tumour and offer the potential for a cure. Therefore, the physician is obligated to make the diagnosis early and to define
as precisely as possible the extent and nature of the tumour. Recent radiological techniques, as discussed below, provide
improved diagnosis and tissue characterization as well as 3D imaging and display.

Primary Tumours of the Heart

Cardiac Myxomas

Cardiac myxomas represent one-half of all primary myocardial neoplasms. These lesions are intracardiac and are
normally attached by a pedicle. Myxomas usually, but not exclusively, lie near the foramen ovale. Over 75% arise in the
left atrium, 20% occur in the right atrium and the remainder in either ventricle. 3 Myxomas have a gelatinous
consistency and range in size from 1 to 15 cm (average 5 cm). Tumours may contain haemorrhage, thrombus or
calcification.

Patients may be asymptomatic, or exhibit a triad of embolic, obstructive and constitutional symptoms. Indeed, systemic
illness occurred in 90% of patients in some series.4, 5 The typical patient is between 30 and 60 years old. The clinical
presentation may mimic that of mitral valve disease. However, atypical symptoms including syncope, weight loss,
fatigue, fever, anemia, elevated sedimentation rate and abnormal serum proteins may occur. Haemolytic anaemia is
typically associated with calcified myxomas, especially in a right atrial location. Atrioventricular valve obstruction
secondary to prolapse of the tumour may produce stenosis of the atrioventricular valve and/or regurgitation resulting in
the `wrecking ball' phenomenon. A syndrome myxoma is also described. This is characterized by skin pigmentation and
the presence of endocrine neoplasms in addition to the myxoma.6, 7 Tumour embolism occurs in approximately 50% of
myxomas. Surgical embolectomy is usually necessary, since these emboli are resistant to percutaneous interventional

Table 14.2 General manifestations of neoplastic heart disease1 (reproduced with

permission).
Pericardial involvement
Pericarditis, pain
Pericardial effusion
Radiographic enlargement
Arrhythmia, predominantly atrial
Tamponade
Constriction
Myocardial involvement
Arrhythmias, ventricular and atrial
Electrocardiographic changes
Radiographic enlargement: generalized, localized
Conduction disturbances and heart block
Congestive heart failure
Coronary involvement: angina, infarction
Intracavitary tumour
Cavity obliteration
Valve obstruction and valve damage
Embolic phenomena: systemic, neurologic, coronary
Constitutional manifestations

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techniques. Histopathologic evaluation of the embolus often provides the first evidence of a cardiac myxoma.

The clinicopathological features of 107 atrial myxomas were reviewed at the Armed Forces Institute of Pathology.8
Table 14.3 illustrates the wide spectrum of symptoms. It is noteworthy that local recurrence may occur after myxoma
excision. Even more remarkable is that neurological symptoms may progress and even appear after resection. Numerous
reports emphasize that late diagnosis is common, especially when symptoms are remote from the heart.8, 9 Therefore, it
is essential to have a high index of suspicion and be vigilant in considering this diagnosis, since appropriate diagnostic
studies will otherwise not be requested. The diagnostic procedures now available to identify cardiac tumours are listed
in Table 14.4.

Most patients with a suspected myxoma are referred to a cardiologist, who usually performs a 2D echocardiogram that
reveals the tumour. Doppler assessment of mitral valve flow provides haemodynamic evaluation. The plain chest
radiograph is usually normal, but may reveal left atrial enlargement, elevated pulmonary venous pressure and
pulmonary arterial hypertension. CT and MRI are newer, equally non-invasive techniques that frequently offer more
information. MRI is an excellent technique for displaying, not only the cardiac chamber cavities, but also the
myocardial wall (Fig. 14.1a and b). Both these relatively new imaging tech-

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Table 14.3 Presenting symptoms in 107 patients with cardiac myxoma8 (reproduced with permission).
All sites Left atrium Right atrium Other sites
Embolic symptoms*
22 21 0 1
Asymptomatic
19 12 5 2
Constitutional
19 14 2 3
Dyspnoea
18 16 1 1
Syncope
8 3 5 0
Palpitations
7 6 1 0
Chest pain
4 3 1 0
Haemoptysis
3 1 0 2
Sudden death
3 3 0 0
Ankle oedema
2 0 2 0
Mean duration of symptoms (mo) 16.6 (n=30) 17.7 (23) 13.6 (5) 12.5 (n=2)
Values are no. of cases.
* Cerebrovascular accident, 10; cerebrovascular accident with other peripheral emboli. 4; haemaniopsia. 2; leg weakness,
pulselessness or gangrene, 4; Lariche's syndrome, 1; flank pain and haematuria (renal artery embolism), 1.
In 19 cases the presenting symptoms included malaise, sudden vertigo, fever of unknown origin (2 related to bacterial
endocarditis), weight loss, and combination of non-specific constitutional symptoms.
Precise length of symptoms was known in 30 cases only.

niques are continually being refined and applied more widely. Myxomas can also be diagnosed by ECG-gated radionuclide scan
using technitium-99m labelled red blood cells.

Differential Diagnosis

The location, appearance and mobility of myxomas is characteristically diagnostic. However, large vegetations on the mitral or
tricuspid valve, thrombus and other tumours must be excluded (Fig. 14.2). Neither echocardiography nor MRI are tissue specific.
However, MRI may be advantageous when the 2D echocardiogram cannot delineate the extent of cardiac chamber wall involvement.
Spin echo and gradient echo MRI imaging techniques can survey the whole heart in unrestricted multiple planes. Both MRI and
electron beam or conventional CT scanning made the correct diagnosis and were more precise in lesion characterization in 30 of 107
myxomas evaluated by Burke & Virmani. 8

Myxoma may also be diagnosed by angiography. Coronary arteriography may demonstrate a tumour

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Figure 14.1
a) Axial T1-weighted MRI. A round mass as identified in the right atrium immediately opposite to the
tricuspic valve. This represents a surgically proven right atrial myxoma. b) Axial gradient echo MRI.
The round mass in the right atrium appears as a low signal defect. Flowing blood in the right atrium,
right ventricle and left atrium appears as high signal in these flow sensitive images. (Courtesy
of Murray Baron, MD.)

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Table 14.4 Diagnostic cardiac imaging methods

Clinical examination
Electrocardiogram
Chest radiograph
Echocardiography and Doppler ultrasound
Computer tomography
Magnetic resonance imaging and angiography
Nuclear medicine studies
Invasive angiocardiography

blush. Ventriculography invariably can demonstrate the mass and its motion, including atrio-ventricular prolapse.
However, invasive catheterization carries the risk of tumour embolism 10 and should now be replaced by safer
non-invasive studies.

A thrombus within a cardiac chamber can usually be distinguished by its shape and location. Most thrombi are not
mobile. CT may be helpful in differentiating a thrombus from other tissues on the basis of density (Hounsfield Units).11
CT can identify clot in the atrial appendage of patients with mitral stenosis with excellent reliability. MRI interpretation
can be more difficult. Slow blood flow around a thrombus, most often related to a hypokinetic myocardial segment near
the ventricular septum or free wall, may produce indeterminate MRI signal, which makes interpretation difficult.
However, gradient echo and other MRI pulse sequences may resolve this question.

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Figure 14.2
Contrast-enhanced CT. A heavily calcified mass
is identified within the left atrium immediately adjacent
to the atrioventricular junction. A large calcified mitral
valve vegetation was recovered at surgery.

Other Benign Cardiac Tumours

Lipomas occur throughout the heart and pericardium. Lesions reside in the myocardial free wall or the septae. They are
frequently round in appearance and vary in size from 2 to 8 cm. Lipomas are easily recognized with MRI because they
have such high signal intensity, due to their short T1 relaxation time and a long T2 consistent with fat.12 Recent studies
have shown that transoesophageal echocardiography can provide more diagnostic information than transthoracic
echocardiography when evaluating lipomas.13 Patients with cardiac lipomas may present with pericardial effusion,
supraventricular tachycardia and sudden death. Other lesions, such as pericardial and parasitic cysts, must be
differentiated from lipomas. However, the clinical presentation is often helpful in distinguishing these other entities.

Rhabdomyoma is the most common cardiac tumour in infants and children. It is considered to be a hamartoma rather
than a true neoplasm.14,15,16,17,18 Multiple lesions are usually present. These masses tend to be pedunculated and are
most frequently found in the left ventricle. Conduction problems or obstruction produce the symptoms which bring most
patients to their physicians. Hypoxic episodes, similar to those associated with tetralogy of Fallot, have also been
reported. Rhabdomyomas may be diagnosed during the evaluation of children with tuberous sclerosis, 30% of whom
will manifest lesions. The diagnosis is frequently made by cross-sectional imaging. Intrauterine echocardiography has
also been successful in identifying rhabdomyomas. Currently, surgery is performed for multiple tumours only.

Paragangliomas and Other Infrequent Neoplasms

Phaeochromocytoma, or chemodectomas, arise in the thorax from neuroectodermal elements. These tumours are
exceedingly uncommon and only 2% of all phaeochromocytomas occur in the chest. Lesions may or may not be visible
by plain radiograph. Recently 131I-MIBG (iodine-131 metaiodobenzylguanidine) radionuclide scanning followed by
CT and MRI has shown promise in the diagnosis of cardiac paragangliomas.19, 20 This dual modality approach may
greatly benefit diagnosis and exact tumour localization which will aid patient care and surgical planning.

A number of other rare benign tumours occur in the heart. Case reports of fibroma, mesothelioma of the atrioventricular
node and haemangiomas are described.1, 2

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Malignant Primary Tumours of the Heart

Sarcomas account for nearly all primary malignant cardiac neoplasms. These tumours exhibit a strong male prevalence.
The right atrium or pericardium are the predominant sites of origin (Fig. 14.3). 21 One-quarter of these neoplasms are
intracavitary. Patients may present with obstructive symptoms, heart failure and/or a haemorrhagic pericardial effusion.
Diagnosis is usually made by echocardiography. Coronary arteriography can demonstrate angiomotous vasculature. CT
and MRI both provide more global anatomic information of these rare tumours. The clinical course is rapid, often with
widespread metastases.

True rhabdomyosarcoma is the second most frequent primary malignant cardiac tumour. This tumour also exhibits a
male preponderance. No single chamber is affected more frequently. The prognosis for cardiac rhabdomyosarcoma is
also dismal.

Extremely rare primary cardiac involvement by fibrosarcoma, liposarcoma, haemangiopericytoma and primary
lymphoma have been reported (Fig. 14.4a and b). Fibrous histiocytoma has been identified in the left atrium also. This
specific tumour has an association with Dacron vascular grafts which raises the question of a carcinogenic link to this
material.22

Pericardial Tumours

The commonest pericardial mass lesions are cysts. These benign lesions are often discovered incidentally on a chest
radiograph in patients aged 40-60 years, with

Figure 14.3
Contrast-enhanced CT. Diffuse pericardial thickening
with effusion is noted. Encasement and deformation
of the superior vena cava is also present. This process
extended caudad to involve the right ventricle. Open
biopsy revealed aggressive spindle cell sarcoma of
ventricular origin.

no particular sex predilection. The right costophrenic angle and upper mediastinum are their most frequent locations.
Communication into the pericardial cavity is rare. Occasionally, these cysts may become symptomatic, producing chest
pain, cough and dyspnoea. Surgical excision, if required, is usually curative.

Teratoma

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Teratomas occur most frequently in infants and children. Females are affected more often than males. Most tumours are
intrapericardial, but extracardiac. Teratomas are rarely intracardiac. These tumours can be very large, occasionally
reaching 15 cm in diameter. They routinely derive their blood supply either from the root of the aorta or the pulmonary
arteries. Recurrent pericardial effusions in children should suggest the diagnosis.23, 24 Surgery is usually curative since
cardiac teratomas are rarely malignant. The classical chest radiograph finding of radiopaque cartilage or a tooth remnant
is uncommon. Cross-sectional imaging is extremely useful in tumour localization for surgical resection.

Mesothelioma

Mesothelioma is the third most common primary malignant tumour involving the heart and pericardium. Most patients
are males in their fourth to sixth decade.25 This locally aggressive tumour may produce constrictive physiology or limit
venous return secondary to IVC obstruction. Radiographic findings of associated asbestosis exposure should be sought
in the chest. However, mesotheliomas often occur in the absence of this history. Treatment is usually palliative and the
prognosis is poor.

Metastatic Disease to the Heart

Secondary malignant tumours of the heart are usually carcinomas rather than sarcomas. Cardiac metastases eventually
occur in 2-21% of all cancer patients.26,27,28 Improved patient treatment with increased survival appears to account for
an increasing incidence of cardiac metastases. Numerous cell lines including those from primary carcinomas, sarcomas,
leukaemia and lymphoma may metastasize to the heart. However, only melanoma has a predilection for the
myocardium. Cardiac metastases have been reported in up to 50% of patients with melanoma.29

Finally, direct cardiac invasion can occur. Mediastinal tumours are frequently responsible. This direct extension is
thought to be related to the proximity of the cardiac lymphatic channels. Carcinoma of the lung and

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Figure 14.4
a) Contrast-enhanced CT. A mixed large attenuation mass involves the right atrium. Single level region
of interest (ROI) evaluation of the mass by time density curves showed pronounced vascularity. This
prompted coronary arteriography. b) Right coronary arteriogram reveals a massive coronary artery supply to
the mass with neovascularity and abnormal `pooling' of contrast medium. Surgery revealed a
haemangiosarcoma of the pericardim.

breast are most notorious for cardiac invasion. Involvement of the great vessels by local tumours may also occur. 30

Isolated metastases to the pericardium are infrequent. Patients may present with pericardial effusion, constriction and tamponade.
Diagnosis is normally made by cross-sectional imaging with echocardiography, CT and MRI.

Transplantation

Patients who have undergone heart transplantation are at risk from infection, rejection and malignant tumours. Cyclosporin-induced
tumours were discussed in a series reported by Penn.31, 32 Malignant tumours developed in 33 (5%) of 721 recipients after organ
transplantation. Eight of 10 malignant tumours occurring in cyclosporin-treated recipients were malignant lymphomas. The mechanism
of neoplasia in these circumstances has been well described. Cyclosporin, a fungal metabolite, inhibits suppressor T-cells, which
control overproduction of B cells. Although this helps suppress the rejection of transplanted organs, it also depresses the defense
system and allows unrestricted proliferation of B cells infected by the Epstein-Barr virus. The malignant tumours occurring in
transplant recipients treated with cyclosporin are characterized by their relatively early appearance after transplantation (in Penn's two
series the latent period in untreated cases averaged 54 months, while in treated cases it was only 4 months), by their widespread
involvement at the time of diagnosis and by their regression or complete resolution after the reduction of immunosuppression
specifically by lowering the dose of cyclosporin. The occurrence of tumours is often, but not always, related to cyclosporin treatment.
Lesions are usually clearly seen with ultrasound and CT (Fig. 14.5a and b). These neoplasms may differ from those occurring in
non-transplant patients in that they are more homogeneous, solid, and can lack the low density appearance of lymphomas in the
latter.33

Carcinoid Heart Disease

Carcinoid primary tumours do not arise in the heart, although rarely they metastasize to the myocardium.34,35,36 Tumours producing
the carcinoid syndrome usually originate in the gastrointestinal tract. Carcinoid tumours in the bronchus, testes and ovary have also
been implicated. The morphology and chemical staining differ, depending on the location of the primary, but the carcinoid syndrome
itself results from the secretion and release of humoral substances (5-HT) into the systemic circulation. These circulating vasoactive
amines produce flushing of the skin, hyperactivity of the gut, bronchial and rarely, coronary artery spasm and unusual lesions in the
heart.37,38,39 The right side of the heart is predominantly affected.40 Pulmonary and tricuspid valve stenosis results from the
endocardial

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Figure 14.5
Oblique long axis echocardiogram of right atrium and ventricle in an 8-year-old liver transplant
recipient. A lobulated mixed reflectivity mass is demonstrated in the right atrium (arrows).
Contrast-enhanced CT of the same child performed to assess for additional adenopathy reveals that the
mass (m) also involves the atrial septum and left atrium. Open biopsy of a mediastinal component of this
mass yielded B-cell lymphoma.

deposition of a shiny yellow fibrous material. This process may also result in mitral valve regurgitation.

The treatment of carcinoid syndrome primarily involves systemic chemotherapy. Symptomatic control with α-adrenergic blockers,
5-HT antogonists and somatostatin analogues is routinely employed. However, response is variable. 41, 42 Catheter-directed
chemoembolic therapy may be considered in symptomatic patients with substantial hepatic tumour burden. Surgery with pulmonary
and tricuspid valve excision is performed infrequently. Recurrent deposition of carcinoid plaque may occur on a valve prosthesis
within a year. More recently, balloon valvuloplasty has been employed for treatment of carcinoid heart lesions.43

Malignancy and the Great Vessels

Superior Vena Cava Syndrome

Superior vena cava syndrome (SVCS) occurs in approximately 5% of patients with malignancy and is a significant clinical problem.
Patients most frequently present with dyspnoea, often exacerbated by supine posture. Oedema of the upper extremity and face as well
as cyanosis occur. Bronchogenic carcinoma produces approximately 80% of all cases of SVCS. Lymphoma is the next most common
cause. Metastatic lesions to the superior mediastinal lymph nodes and locally aggressive tumours of breast, thyroid, thymus and germ
cell origin account for the remaining 9% of patients.44

Clinicians rely heavily on imaging, not only to provide a precise diagnosis, but also to guide and expedite therapy in these clinically
tenuous patients. Routine chest radiographs are frequently available and approximately 60% reveal a superior mediastinal mass.45
Ultrasound, scintigraphy and direct venography can all be used to confirm the presence of SVC obstruction, but cross-sectional
imaging such as CT and MRI have greater importance early in therapy.46,47,48 These cross-sectional imaging modalities can
determine the exact position of the offending obstruction. The same modalities are then used to guide the biopsy approach optimally
which can decrease patient morbidity and mortality.49

The majority of patients with SVCS are treated with radiation therapy, with or without chemotherapy, and this usually relieves their
symptoms. However, approximately one-third of this group either will not respond to the treatment or develop recurrent SVCS.
Percutaneous techniques using thrombolytic infusions, angioplasty and stents have been reported. The early experience is promising
and technical success in stent deployment is possible in greater than 80% of these patients. These techniques produce faster relief of
symptoms and do not appear hampered by the effects of radiation therapy. The greatest problem with these percutaneous methods is
recurrence of SVCS in up to 45% of patients. Tumour progression or stent thrombosis represent the two major problems. However,
these can be addressed effectively with repeat stent placement, thrombolytics and long-term oral anticoagulation.50,51,52

Vascular Invasion and Resectability

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Imaging plays an important role in the evaluation of vascular invasion by tumour. This is especially true in the treatment of tumours
affecting the IVC and aorta.

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Direct vascular invasion of the IVC is most frequently due to malignancy arising from the kidneys. Five to 15% of renal
tumours exhibit direct caval extension, which may involve the right atrium. Although less common, direct tumour
spread from the liver, adrenal glands, pelvic organs, retroperitoneal masses and lymph nodes can also involve the IVC
(Fig. 14.6a and b). 53,54,55 Detection of IVC involvement has been greatly advanced over the past two decades by the
routine use of cross-sectional imaging (ultrasound, CT and MRI) in the evaluation of the abdomen and pelvis. Surgeons
are now capitalizing on these improvements in imaging, which allow them to perform their operations more precisely
and with far greater confidence. Individuals previously deemed unresectable are now surgical candidates, with
acceptable morbidity and mortality from exceedingly complex procedures.56, 57 Imaging has, therefore, made a
significant contribution to patient care in this aspect of oncology.

Advances in imaging also permit a better understanding of aortic invasion in patients with lung and oesophageal
carcinoma. Determination of invasion of the aorta has been based on the extent of tumour contact on conventional CT.
Recent applications of cine CT may better define whether tumour-aorta contact is significant through respiratory or
cardiac motion studies.58 Advances in intravascular ultrasound may better grade the importance of tumour-vessel
contact also. Imaging with an intra-aortic probe was recently used in a small series of oesophageal tumours and allowed
direct aortic wall characterization. This allowed the authors to identify adventitial tumour spread, preoperatively, in 3
patients who would have been graded as having no tumour invasion by standard CT guidelines.59 The application of
direct imaging of vessel walls appears to be the logical next step to cancer staging and planning. This approach is
valuable for evaluating other tumours which involve the mediastinum such as superior sulcus tumours.60

Differential Diagnosis of Cardiac Tumours

A number of disorders must be considered in the differential diagnosis of cardiac tumours. Modern diagnostic imaging
methods are not only able to display and characterize cardiac wall and chamber anatomy, but also they can evaluate
cardiac function and flow, and these techniques may be able to distinguish between such mass lesions.61,62,63,64
There are a number of infiltrative diseases which may mimic cardiac tumours. Cardiomyopathy is the commonest and
causes difficulty when there is asymmetrical myocardial involvement.

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Figure 14.6
a) Contrast-enhanced CT in an elderly male with
metastatic prostate carcinoma. A mixed attenuation
mass arises in the right adrenal bed (arrow). This process
extends into the inferior vena cava (arrowhead). b) Digital
subtraction inferior vena cavogram. A polylobulated
mass (arrows) produces near occlusion of the inferior
vena cava. At the time of this exam, the patient had
developed new bilateral lower extremity oedema.

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Cross-sectional imaging provides the best diagnostic approach in these patients and has been discussed in the literature
for MRI and for CT. 65, 66 Sarcoidosis, amyloidosis and tuberculosis may also produce masses, often impinging upon
the right heart, and these lesions may produce symptoms of pericardial constriction.67,68,69 Both MRI and CT provide
excellent diagnostic capability in these patients.70,71,72 Tumours of the pericardium such as mesothelioma can produce
a similar clinical picture.73 Pseudotumours due to a variety of other uncommon lesions also occur, such as parasitic
echinococcal cysts. However, a thorough history and physical examination will often suggest the diagnosis.

Involvement of the great vessels may occur either by direct invasion or by propagation of tumour along the great veins
and this may extend into the right heart chambers. Pulmonary embolism can also occur and be safely identified by these
non-invasive studies.74, 75

Future Impact of Digital Imaging on Tumour Diagnosis

The revolution in microprocessors in terms of speed, size and reduced cost has led to rapid and more sophisticated
medical imaging equipment with faster image acquisition with CT, MRI, ultrasound, positron emission tomography
(PET) and single photon emission tomography (SPECT). However, of equal importance and perhaps even more exciting
is the development of 3D displays, including the use of colour Doppler, reproducible quantitation, integration of images
from different modalities, and most recently, the presentation of this data in virtual reality. This area has particular
relevance to an organ as complex in structure and function as the beating heart. It also has special implications for
radiation therapy planning using modern computerized linear accelerators with `beam's eye view' treatment ports. Both
CT and MRI offer 3D displays of the vascular tree as well as high spatial and contrast resolution of adjacent soft
tissues.76, 77 Echocardiography has recently become a digital imaging modality with advanced 3D imaging capability.
These technologies are continually being refined and improved. Furthermore, the ability to measure organ tissue
perfusion appears closer to clinical application as the pharmaceutical industry has started to develop new contrast media
for all of these modalities. MRI spectroscopy has the capability to study tumour chemistry and also to identify anatomic
structure and function. Measurements of tumour oxygen consumption and the patterns of tumour blood flow are also
being explored by several research teams and this area appears to be promising.78

Technological advances have not been solely confined to high profile imaging modalities such as CT, ultrasound, MRI,
PET and SPECT. Digital radiography using photostimulable phosphor technology is being employed increasingly and
will have a significant impact by converting all conventional radiography to digital media, which accounts for
approximately 80% of the total radiology workload in a general hospital. Computer-aided diagnosis in conjunction with
digital radiography has the potential for improved diagnosis and treatment of cancer patients. Computer programs have
been developed that can identify abnormalities such as nodules, interstitial infiltrates and cardiomegaly by automated
analysis of a digital radiograph. Though the accuracy of these programs still falls short of that of an experienced
radiologist, these techniques have been shown to improve the ability of most observers to detect subtle abnormalities in
simulated clinical situations. Temporal subtraction is a digital technique that registers and subtracts a previous from a
current chest radiograph to enhance detection of interval change. Energy subtraction, on the other hand, exploits the
differential absorption of specific components of the X-ray beam to produce separate `bone' and `soft tissue' images
from a single exposure (Fig. 14.7a and b). As image interpretation migrates from the viewbox to the computer
workstation in the future, the increasingly more powerful computer programs are likely to play an important role.

Conclusion

Although cardiac tumours are rare, they nevertheless represent an important subgroup, the diagnosis of which is
challenging for the primary care physician. Symptoms are not characteristic and serious complications including stroke,
myocardial infarction and even sudden death from arrhythmia may be the first signs of the tumour.

The most common primary cardiac neoplasm is the benign myxoma and the most frequent primary malignant lesion is
sarcoma. Cardiac metastases from distant primary carcinomas are now frequently encountered. Echocardiography until
the past decade was the only consistently reliable and available non-invasive diagnostic tool. New non-invasive CT and
MRI exams now exist and have greatly limited the use of echocardiography and angiocardiography with or without
coronary arteriography in the evaluation of cardiac neo-

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Figure 14.7
a) Routine chest radiograph: Increased cardiac size
has developed in this woman with known breast
carcinoma since the previous chest radiograph. (Courtesy
of Heber MacMahon, MD) b) Temporal subtraction
image, obtained by automated digital registration and
subtraction of the previous from the current radiograph
shows a change in the cardiac silhouette due to
pericardial effusion, indicated by a black halo
surrounding the heart. Areas of new opacity appear
dark while unchanged areas are light grey in the
subtraction image.

plasms. 79,80,81,82,83,84 These techniques provide additional diagnostic information and are regarded as essential for
adequate treatment planning, particularly when surgical resection is being considered.

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79. Cassidy MM, Schiller NB, Lipton MJ, Higgins CB: Interaction of echocardiography with recent noninvasive
cardiovascular imaging modalities. Cardiology, Sept/Oct: 29-47, 1987.

80. Higgins CB, Lipton MJ. Computed tomography and magnetic resonance imaging of cardiac and paracardiac
tumours. In: Taveras JM, Ferucci JT Jr (eds) Radiology: Diagnosis/Imaging/Intervention. Philadelphia: JB Lippincott
Company. 1984 Vol 2, Section 59, pp 1-4.

81. Lipton MJ. The thorax: heart and mediastinum. In: Burgener F, Kormano M (eds) Differential Diagnosis in CT.
Stuttgart: Georg Thieme, 1996, pp. 222-245.

82. Baron M. MRI of pericardium, cardiomyopathy and cardiac masses. In: Casarella WJ (ed) Syllabus for the
Categorical Course on Cardiovascular Imaging. American Roentgen Ray Society, 1990.

83. Carrol CL, Higgins CB, Caputo GR. Magnetic resonance imaging of acquired cardiac disease. Texas Heart Inst J
1996; 23: 144-154.

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Index

Abscesses, brain, 9, 14

Acinar cell carcinoma, pancreas, 122

Acinar cell cystadenocarcinoma, pancreas, 122

Acoustic Schwannoma, 17, 19

Acromegaly, 20-21, 141, 142

ACTH

assay, 141

ectopic secretion, 142

Adenocarcinomas

bladder, 135

bronchus, 49

ethmoid sinus, 41 (Fig.)

gallbladder, 120, 120 (Table)

metastases to brain, 14

nasosinusal, 40

oesophagus, 81

small intestine, 90

transpyloric spread, 88

see also Renal cell carcinoma

Adenoid cystic carcinoma, 44

Adenomas

colon, 101-102

(see also Familial adenomatous polyposis)

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gallbladder, 119-120

liver, 114, 116-117

Adenopathy

bronchial carcinomas, 49

hilar, 121

neck, 39-40

pelvis, MRI, 155

Adjuvant chemotherapy

colorectal cancer, 104

primary bone tumours, 183

Adrenal glands, 145-148

Adrenal vein sampling, 148

Adrenocortical adenomas, 147-148

Adrenocortical carcinoma, vs adenoma, 147

Aerodigestive tract, upper, head and neck tumours, 35-40

AIDS

lymphoma, 169

CNS, 14

thorax, 56

tissue characterization of lesions, 30

see also Kaposi's sarcoma

Air contrast see Double contrast

Airway mucosa, head and neck tumours, 35

AJC (American Joint Committee), testicular cancer staging, 137

Aldosterone, Conn's syndrome, 147

Algorithms, 3-4

A-fetoprotein

hepatocarcinoma, 117

liver adenomas, 116

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American Joint Committee, testicular cancer staging, 137

Amiodarone, thyroid scintigraphy, 145

Ampulla of Vater, carcinoma, 87

Amputation, osteosarcoma, 180

Amyloidosis, vs cardiac tumours, 199

Anaplastic astrocytoma, 9, 11 (Fig.)

Anaplastic carcinoma of thyroid, 145

Androgenic steroids, liver adenoma, 116

Aneurysmal bone cysts, 177

Angiocardiography, 199-200

Angiography

cardiac myxoma, 193-194

hepatocarcinoma, 118

primary bone tumours, 182

small intestine, 90

see also CT arteriography; Flush aortography

Angiography (magnetic resonance), 17, 30

Angiomyolipoma, kidneys, 134

Angioplasty, superior vena cava syndrome, 197

Angiosarcoma, heart, 191 (Table)

Anterior cranial fossa, 40

Anterior craniofacial resection, 42

Aorta, tumour invasion, 197-198

oesophageal carcinoma, 82

Aortography, and phaeochromocytoma, 146

Apical tumours, 53-54

APUD cell tumours, 143

SST analogue scintigraphy, 149

Arsenal diagnostique, 3

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Arterial waveform patterns, duplex

Doppler ultrasound, 155

Arteriography see Angiography; CT arteriography; Flush aortography

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Asbestos workers, mesothelioma, 59-60, 195

Ascites, 93

liver metastases, 118

ovarian carcinoma, 158

Astrocytomas, 9-11

vs central neurocytoma, 12

spinal cord, 25

Atrial myxoma, 192-194

Audit, 4

Balkan nephropathy, 134

Balloon valvuloplasty, carcinoid

syndrome, 197

Barium enemas

acromegaly, 142

cervical carcinoma, 163

double contrast, 101-102, 103

Barium meals, 85

Barium studies, small intestine, 89-90

Barium swallows, 81

Basioccipital region, 23

BCRA1, BCRA2 genes, 65

Benign prostatic hypertrophy, 135

Bile duct tumours, 119-121

Biliary cystadeno(carcino)mas, 119

Biliary cysts, 113

Biopsy

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bone tumours, 180, 182

breast, 67, 68

ductal adenocarcinoma of pancreas, 122

haemangioma, 114

hepatocarcinoma, 118

liver adenoma, 117

liver metastases, 119

lymph nodes, ovarian carcinoma staging, 156

neck masses, 44

pleura, 60

soft-tissue sarcomas, 187

Biphasic helical computed tomography, carcinoid tumours, 108

Bladder tumours, 135

Bleomycin toxicity, 58 (Fig.)

Blood flow impedance, endometrial cancer, 160

Blood vessels, tumour spread along, 37

Body coil vs endorectal coil MRI, prostate cancer, 137

Bone, 150

invasion, head and neck tumours, 37-38

metastases, 183-185

colorectal cancer, 105

treatment, 185

pain, 183

primary tumours, 177-183

benign, 178

biopsy, 182

closed, 182

needle, 182

open, 182

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distant staging, 182

local staging, 180-182

scintigraphy, 178, 180, 182

metastases, 184

breast cancer, 75, 76

Brainstem gliomas, 15

Brain tumours

bronchial carcinoma metastases, 49

extra-axial, 15-19

intra-axial, 9-15

Branchial cleft cysts, 43

Breast

symptomatic, 65-66, 67

tumours, 65-77

heart involvement, 191, 196

male breast, 73-74

from mammography, 67-68

small intestine, 94

stomach, 87

Bronchi, oesophageal carcinoma spread, 82

Bronchial adenoma, ectopic ACTH secretion, 142

Bronchial carcinomas, 49-51

ectopic ACTH secretion, 142

heart

invasion, 195-196

metastases, 191

pleura, 60

small intestine, 95

solitary pulmonary nodules, 52

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superior sulcus tumours, 53-54

superior vena cava syndrome, 197

Bronchiectasis, 51

Bronchiolo-alveolar carcinoma, 49

Bronchogenic cysts, heart, 191 (Table)

Bull's eye appearance, gastric melanoma, 87

CA125 testing, ovarian carcinoma screening, 155, 156

Caecal carcinoma, 93

Calcification

islet cell tumours of pancreas, 123

liver metastases, 106

meningioma, 17

oligodendroglioma, 11

Paget's disease of breast, 73

solitary pulmonary nodules, 53

thyroid masses, 143

Calcium injection, intra-arterial, portal venous sampling, 148

Calculi, squamous cell carcinoma of kidneys, 135

Candida albicans pneumonia, 57

Carcinoid syndrome, 148

heart, 196-197

Carcinoid tumours

colorectal, 108

peptide receptors, 149

small intestine, 91-92

stomach, 86-87

Carcinoma in situ, 162 (Fig.)

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Carcinomas

choroid plexus, 20

skull base, 23

see also Specific types and sites

Carcinosarcoma

kidneys, 127

oesophagus, 83

Cardiac tumours, 191-197, 198-200

Cardiomyopathy, 198-199

Cartilage invasion, head and neck tumours, 37-38

Cavernoma, brain, 9

C-cells, thyroid, 143

Central nervous system, 9-32

see also Brain tumours

Central neurocytoma, 12

Central scar, focal nodular hyperplasia, 114

Cerebellar haemangioma, von Hippel Lindau syndrome, 141

Cerebellopontine angle tumours, 17, 19

Cerebrospinal fluid seeding, 15

ependymoma, 13

pineal teratoma, 23

Cervical adenopathy, metastases, 39-40

Cervix uteri

carcinoma, 161-164

vs endometrial cancer, 160

stenosis, 159

Chemicals, transitional cell carcinoma, 134

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Chemotherapy

bone scintigraphy, 75

breast cancer response, MRI, 69

lung toxicity, 57

primary bone tumours, 182-183

soft-tissue sarcomas, 187

see also Adjuvant chemotherapy

Chest radiography, gastric carcinoma staging, 85

Children

neck masses, 43

primary bone tumours, 177

Cholangiocarcinoma, 120-121

Cholangiography, 121

Cholesteatoma, kidney, 135

Chondroblastoma, 178

Chondrosarcoma

incidence, 177

prognosis, 178

skull, 23

Chordoma, 178

skull, 23, 24 (Fig.)

Choriocarcinoma

metastases to brain, 14

testes, 137

Choristoma, 20

see also Granular cell tumours

Choroid plexus papilloma, 20

vs meningioma, 17

Chromaffin cells see Phaeochromocytoma

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Chromophobe cell carcinoma, kidney, 127

Cirrhosis

CA125 elevation, 156

hepatocarcinoma, 117

Classifications

Dukes, colorectal cancer, 101, 104

Eggel's, hepatocarcinoma, 117

Jewitt & Whitmore, prostate cancer, 136

primary bone tumours, 177

Rye, Hodgkin's disease, 169 (Table)

see also Staging; TNM classification

Collecting tubule carcinoma, kidney, 127

Colloid scintigraphy, focal nodular hyperplasia of liver, 114

Colography, computed tomography, 103

Colon, 108

hydrosonography, 104

Colonoscopy, 101, 103

acromegaly, 142

Colorectal cancer, 101-109

acromegaly, 142

caecum, 93

duodenal spread, 88

metastases, surgery and lymphadenectomy, 119

Colour Doppler ultrasound

breast, 68

gynaecology, 155, 156

transvaginal, 157

Computed tomography

bone lesion excision guidance, 180

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bone tumour needle biopsy, 182

bronchial carcinomas, 51

staging, 50

colorectal cancer, 102-103

densitometry, solitary pulmonary nodules, 53

gastric carcinoma, 85

gynaecology, 155

myelography, 25

see also CT arteriography; Spiral computed tomography

Computer-aided diagnosis, 199

Congenital cysts, pancreas, 122

Conn's syndrome, 147-148

Contraceptives, oral, liver adenoma, 114, 116

Contrast media

bowel opacification, 155

injection for CT

bronchial carcinoma staging, 50

colorectal cancer, 103

focal nodular hyperplasia of liver, 114

hepatocarcinoma, 127

liver metastases, 119

solitary pulmonary nodules, 53

see also Ultrasound contrast media

Cord compression see Spinal cord compression

Core biopsy, breast, 67

Coronary arteriography, 199-200

cardiac myxoma, 193-194

cardiac sarcomas, 195

Corpora lutea, 155

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Corticotrophinoma, 141

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Corticotrophin releasing factor, for inferior petrosal sinus sampling, 142

Cost vs benefit, 3-4

Craniofacial resection, anterior, 42

Craniopharyngioma, 20, 22

Cribriform plate, 42

CT arteriography, liver metastases, 106-107

Cushing's disease, 141-142

Cushing's syndrome, 20-21, 21

Cyclosporin, tumours, 196

Cystadeno(carcino)mas, biliary, 119

Cystadenoma, bile ducts, 120 (Table)

Cystic tumours of pancreas, 122-123

Cysts

biliary, 113

in brain tumours, 9

bronchogenic, heart, 191 (Table)

intramedullary, 25

kidneys, 127, 132-133 (Fig.)

liver, 113, 114

ovaries, 156-157

papillary carcinoma of breast, 73

pericardial, 191 (Table), 194, 195

pineal, 23

thyroid, 143

Cytomegalovirus pneumonia, 57

Dacron grafts, and fibrous histiocytoma, 195

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DCIS see Ductal carcinoma, in situ

Decision analysis, 3

Deep cervical fascia, 43

Demyelination, 9

Densitometry, CT, solitary pulmonary nodules, 53

De Quervain's thyroiditis, 143

Dermoid tumours, 17, 19, 20

Diabetes insipidus, 22

Dietary factors, ovarian carcinoma, 155

Diffusion imaging, functional MRI, 30

Digital mammography, 68

Digital radiography, 199

Digital subtraction inferior vena cavogram, 198 (Fig.)

Doppler ultrasound

focal nodular hyperplasia of liver, 114

gynaecology, 155

primary bone tumours, 182

see also Colour Doppler ultrasound; Pulsed Doppler ultrasound

Double contrast

barium enema, 101-102, 103

barium swallow, 81

Double duct sign, 122

Double reading examinations, radiology, 102

Ductal adenocarcinoma, pancreas, 121-122

Ductal carcinoma

infiltrating, 73

in situ, 65, 72

microcalcifications, 68, 69, 72

invasive, 70-72

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Duct cell adenocarcinoma, pancreas, 122

Ductography, breast, 70

Dukes classification, colorectal cancer, 101, 104

Duodenum, 87-88

carcinoma, 87-88, 120

gastric carcinoma spread, 85, 88

gastric lymphoma spread, 86, 88

intubation, 90

Duplex Doppler ultrasound, gynaecology, 155

Dural tail, meningioma, 17

Dura mater, ethmoid roof, 42

Dye injections, breast cancer surgery, 75

Dysembryoplastic neuroepithelial tumours, 12-13

vs oligodendroglioma, 11

Dysphagia, 81

Dysplasia, colon adenomas, 101

Dyspnoea, 49

Early gastric cancer, 85

Echinococcal infection, 113

heart, 199

liver, 113

Echocardiography, 192, 194

Ectopic ACTH secretion, 142

Eggel's classification, hepatocarcinoma, 117

Emboli, cardiac myxoma, 192

Embolization, hepatic, carcinoid syndrome, 148, 197

Embryonal carcinoma, testes, 137

Embryonal rhabdomyosarcoma, bile ducts, 120 (Table)

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Embryonic cell carcinoma, mediastinum, 58-59

Empty sella syndrome, 141

Enchondroma, 177, 178, 179 (Fig.), 180

Endocrine tumours, 141-151

and cardiac myxoma, 192

pituitary, 20-22

Endometrial cancer, 159-161

Endometriosis

bladder, 135

CA125 elevation, 156

Endoprostheses, primary bone tumour management, 182, 183

magnetic resonance imaging, 181

Endorectal coils, MRI, 137

cervical carcinoma, 162

Endoscopic retrograde cholangiography, 121

Endoscopic retrograde pancreatography, 122

Endoscopic sonography

colorectal cancer, 104

oesophagus, 82-83

(see also Transoesophageal echocardiography)

Endoscopy, 35

gastric carcinoma, 85

nasosinusal tumours, 40

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Endovaginal coils, MRI, cervical carcinoma, 162

Endovaginal ultrasound, 155, 156

colour flow, 157

Energy subtraction, 199

Enteroclysis, 89-90

Ependymoma, 13, 16 (Fig.)

vs central neurocytoma, 12

cerebellopontine angle, 19

infratentorial, 15

spinal cord, 25

Epidermoid tumours, 17, 19, 20

Epiglottis, 37

Epithelial neoplasms, pancreas, 122

Epstein-Barr virus, cyclosporin-induced tumours, 196

Esthesioneuroblastoma, 23

Ethmoid sinus, adenocarcinoma, 41 (Fig.)

Ewing's sarcoma, 178

5-year survival rates, 178

follow-up, 183

incidence, 177

metastases, 182

treatment, 182-183

Extranodal spread, 40

Extraosseous bone tumours, magnetic resonance imaging, 181

Extrathoracic metastases, bronchial carcinomas, 49

Fab'2 antibody fragments, ovarian carcinoma imaging, 158

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Familial adenomatous polyposis, 107-108

Familial ovarian carcinoma, 155

Family history, colorectal cancer, 107-108

Fetus, cardiac rhabdomyoma, 194

Fibre-optic bronchoscopy, 49-50, 51

Fibrillary astrocytoma, 9

Fibroadenoma, breast, 65, 68

Fibroma

bladder, 135

cardiac, 191 (Table)

Fibromatosis, 185, 186

Fibrosarcoma

bladder, 135

heart, 191 (Table), 195

Fibrous dysplasia, 177, 180

Fibrous histiocytoma see Malignant fibrous histiocytoma

FIGO staging

cervical carcinoma, 162 (Fig.)

endometrial carcinoma, 159

ovarian carcinoma, 157 (Table)

Fine needle aspiration cytology

breast masses, 66

bronchial carcinomas, 50, 53 (Fig.)

neck masses, 43, 44

recurrent endometrial cancer, 161

5-year survival rates, primary bone tumours, 178

Flat adenoma, 107-108

Flexible sigmoidoscopy, 102

Fluorodeoxyglucose-PET, 30

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breast cancer, 69, 76

ovarian carcinoma, 158

Fluoroscopy, bone tumour needle biopsy, 182

Flush aortography, and phaeochromocytoma, 146

Focal nodular hyperplasia, liver, 114

vs adenoma, 116-117

Foetus, cardiac rhabdomyoma, 194

Follicular adenoma, vs thyroid carcinomas, 143

Follow-up

breast cancer, 75-76

colorectal cancer, 107-108

Foramen of Monro, compression, 9

Fractures

pathological, 184

stress fractures, 180

Frameless MR stereotaxy, 30

Frostberg, reverse `3' sign, 88

Functional magnetic resonance imaging, 30

radiation effects vs recurrent tumours, 29

Gadolinium enhancement, MRI, 13, 14, 17

breast, 69

Gallbladder

adenocarcinoma, 120

adenoma, 119-120

Gallium scintigraphy, hepatocarcinoma, 117

Gangliocytoma, 11-12

Ganglioglioma, 11-12

Gastrinoma, 148

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pancreas, 122, 123

SST analogue scintigraphy, 149

Gastrointestinal tract, gut hormone tumours, 148-149

Germ cell tumours

mediastinum, 58-59

testes, 149-150

Germinoma

pineal, 23

metastases, 29 (Fig.)

pituitary, 20

Giant-cell astrocytoma, subependymal, 11

Giant-cell tumours of bone, 177, 178, 180

Giant haemangioma, 114

Glioblastoma, vs oligodendroglioma, 11

Glioblastoma multiforme, 9

Gliomas

brainstem, 15

cerebellopontine angle, 19

vs dysembryoplastic neuroepithelial tumours, 13

optic pathway, 20

orbit, 20

pituitary gland, 20

from radiotherapy, 30

spinal cord, 25

Gliomatosis cerebri, 9, 14

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Glomus jugulare tumours, 23

Glomus tympanicum tumours, 23

Glosso-tonsillar squamous cell carcinoma, 36 (Fig.)

Glottis, squamous cell carcinoma, 37 (Fig.)

Glucagonoma, 148

pancreas, 122, 123

SST analogue scintigraphy, 149

Glycogenosis, liver adenoma, 116

Gradient echo imaging, MRI, bronchial carcinoma staging, 50

Grading, radiographic, primary bone tumours, 179

Grafts, vascular, and fibrous histiocytoma, 195

Granular cell tumours

bile ducts, 120 (Table)

gallbladder, 120 (Table)

heart, 191 (Table)

see also Choristoma

Granulomas, lung, 52, 53

Graves' disease, 143

Gut hormone tumours, 148-149

Gynaecology, 155-166

Gynaecomastia, 73

Haemangioblastoma

brain, 13

spinal cord, 25

von Hippel Lindau syndrome, 141

Haemangioma, 185, 186

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bladder, 135

cardiac, 191 (Table)

liver, 113-114

vertebral, 27

von Hippel Lindau syndrome, 141

Haemangiopericytoma

heart, 195

vs meningioma, 17

Haematuria, 127

Haemolytic anaemia, cardiac myxoma, 192-194

Haemoperitoneum, hepatocarcinoma, 117

Haemoptysis, 49, 50-51

Haemorrhage

brain tumours, 9, 15

endometrial cancer, 159

leptomeningeal, 15

ovarian cysts, 157

pituitary gland, 22

Hamartoma

cardiac rhabdomyoma, 194

lung, 52, 53

Hands, acromegaly, 142

Head and neck, 35-45

Heart see Cardiac tumours

Helical computed tomography

biphasic, carcinoid tumours, 108

colorectal cancer, 102

see also Spiral computed tomography

Hemilaryngectomies, planning, 36-37

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Hepatic artery blood flow, vs portal vein blood flow, 106

Hepatic embolization, carcinoid syndrome, 148, 197

Hepatic lymph nodes, colorectal cancer metastases, 105

Hepatic metastases see under Liver

Hepatic reserve, metastases, 118

Hepatocarcinoma, 117

Hepatoma, venous extension, 191

Herbicides, ovarian carcinoma, 155

Hereditary non-polyposis colorectal cancer, 107-108

Heterotopic gastric mucosa, bile ducts, 120 (Table)

High-resolution ultrasound

breast cancer staging, 74

thyroid carcinoma, 143

Hilar adenopathy, 121

Histiocytoma see Malignant fibrous histiocytoma

Hodgkin's disease, 169-173

kidneys, 135

thorax, 55, 56

Hormone replacement therapy, and endometrial cancer, 159, 160

Hormones

gastrointestinal tract, 148

sampling, 141

Horner's syndrome, 54

Hydrocephalus, brain tumours, 9

Hydronephrosis, cervical carcinoma, 163

Hydrosonography, colonic, 104

Hypernephroma see Renal cell carcinoma

Hyperostosis, meningioma, 17

Hyperparathyroidism, primary, 145

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Hypoalbuminaemia, pericardial effusion, 191

Hypophysectomy, investigations, 141

Hypopituitarism, 22

Hypoxia, cardiac rhabdomyoma, 194

Hysterectomy, cervical carcinoma histology, 163

Imaging strategies, 3-4

Immunoimaging, 39

Immunoscintigraphy

colorectal cancer, 105

ovarian carcinoma, 158

see also Monoclonal antibodies

Immunosuppression, cyclosporin-induced tumours, 196

Incidentaloma, pancreas, 148

Infections

endoprostheses, 183

thoracic lymphoma therapy, 57-58

Inferior petrosal sinus sampling, 141-142

Inferior vena cava, tumour invasion, 197-198

Infiltrating ductal carcinoma, 73

Inflammatory disease, vs tumours, 30

facial structures, 42

Infrared light, breast imaging, 70

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Insulinoma, pancreas, 122, 123, 148

Interval cancers, breast, 65

Intestinal obstruction, 93

Intra-arterial calcium injection, portal venous sampling, 148

Intracavitary coils, MRI, cervical carcinoma, 161-162

Intradural tumours, spine, 25-27

Intramedullary tumours, 25

Intramuscular lipoma, 185

Intraoperative ultrasound, liver metastases, 106, 119

Intraosseous bone tumours, magnetic resonance imaging, 181

Intrauterine echocardiography, cardiac rhabdomyoma, 194

Intravenous urography, cervical carcinoma, 163

Invasive ductal carcinoma of breast, 70-72

Invasive lobular carcinoma of breast, 72

Invasive pulmonary aspergillosis, 57

In vitro sonography, lymph nodes, colorectal cancer, 104-105

Iodine, isotopes, 142-143, 145

Iodocholesterol scintigraphy, Conn's syndrome, 147-148

Islet cell tumours, pancreas, 123

Jaundice, 113

bile duct tumours, 119

hepatocarcinoma, 117

liver metastases, 118

ultrasound, 120-121

Jejunum, carcinomas, 87

Jewitt & Whitmore classification, prostate cancer, 136

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Juvenile angiofibroma, 23

Juvenile pilocytic astrocytoma, 15

Kaposi's sarcoma

colon, 108

small intestine, 92

Kidneys, tumours, 127-135

vascular invasion, 198

Klatskin's tumour, 120

Krukenberg tumour, 85

Laminated calcification, solitary pulmonary nodules, 53

Laparoscopy, ovarian tumours, 150

Laparotomy, ovarian carcinoma staging, 156

Large cell carcinoma, bronchus, 49

Laryngeal cartilages

proton density SE magnetic resonance imaging, 38

tumour spread, 37

Laryngectomies, planning, 36-37

Larynx, tumour spread, 35, 36-37

Laser spectroscopy, breast masses, 70

Laser therapy, colorectal cancer, 104

Left atrial enlargement, myxoma, 192

Leiomyomata

bladder, 135

vs endometrial cancer, 160

Leiomyosarcoma

bladder, 135

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colorectal, 108

duodenum, 88

heart, 191 (Table)

oesophagus, 83

small intestine, 92

Leptomeningeal haemorrhage, 15

Leukaemias

heart involvement, 191

kidneys, 135

Limb salvage surgery

magnetic resonance imaging, 181

osteosarcoma, 180

Lingual septum, tongue neoplasms, 36

Linitis plastica, 85, 87

Lipiodol, hepatocarcinoma, 117

Lipoma, 186

cardiac, 191 (Table), 194

intramuscular, 185

neck, 44

Liposarcoma, 185, 186

heart, 191 (Table), 195

Liver

cirrhosis, CA125 elevation, 156

embolization, carcinoid syndrome, 148, 197

metastases, 118-119

breast cancer, 75, 76

colorectal cancer, 105, 106-107

resection for, 105

ovarian carcinoma, 158

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transplantation, hepatocarcinoma, 118

tumours, 113-119

Lobular carcinomas

in situ, 65, 72-73

invasive, 72

Lodwick grading, primary bone tumours, 179

Logic in medicine, 4

Loosening, endoprostheses, 183

Lungs

metastases, 54-55

colorectal cancer, 105

primary bone tumours, 178, 183

tumours, 49-55

Lymphadenectomy, and surgery for colorectal cancer metastases, 119

Lymphadenitis, neck, 43

Lymphangiography

cervical carcinoma, 163

staging, 161

lymphomas, 170

testicular tumours, 137

Lymphangioma

cardiac, 191 (Table)

neck, 43

Lymphangitis carcinomatosa, 55

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pleura, 60

Lymphatic spread

gastric cancer, 85

oesophageal carcinoma, 81

to small intestine, 93

testicular tumours, 137

Lymphatic system, 169-173

colon, 101

Lymph nodes

breast cancer staging, 74-75

cervical carcinoma, 163

colorectal cancer staging, 104-105

gastric cancer, 85

hepatic, colorectal cancer metastases, 105

metastases, 173

neck, 43

oesophageal carcinoma, 81, 82

oesophageal compression, 84

ovarian carcinoma, 158

staging biopsy, 156

see also Adenopathy

Lymphoedema

breast, 69

breast cancer treatment, 75

Lymphomas, 169-173

bone, age incidence, 178

brain, 9, 13-14, 20

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colon, 108

duodenum, 88

head and neck, 43

heart, 191, 195

kidneys, 135

mediastinum, 59

vs meningioma, 17

orbit, 20

peptide receptors, 149

pleura, 60

posterior fossa, 17

small intestine, 90-91

spine, 27

stomach, 86, 88

superior vena cava syndrome, 197

thorax, 55-58

tissue characterization, 30

Lymphopenia, chest infections, 57

Lymphoscintigraphy of breast, 69, 75

Lynch Type I variant, hereditary nonpolyposis colorectal cancer, 107-108

Macroadenomas, pituitary, 21-22, 142

Macrocystic adenoma, pancreas, 122-123

Magnetic resonance angiography, 17, 30

Magnetic resonance cholangiography, 121

Magnetic resonance imaging

acoustic Schwannoma, 17

breast, 69-70

bronchial carcinoma staging, 50

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disadvantages, 181

gynaecology, 155

primary bone tumour follow-up, 182

vs scintigraphy, vertebral metastases, 27

soft-tissue sarcoma recurrence, 187

Magnetic resonance spectroscopy, 30, 199

radiation effects vs recurrent tumours, 29

Malignant fibrous histiocytoma, 185

age incidence, 178

heart, 195

Mammography, 66-68

screening, 65

Masses see Soft tissue masses

Mastectomy, lobular carcinoma in situ, 73

Matrix mineralization, bone tumours, 179, 180 (Fig.)

Maxillary sinus, squamous cell carcinoma, 43 (Fig.)

Maxillonasal tumours, vs nasoethmoidal tumours, 40-41

MDP scanning see Bone, scintigraphy

Mechanical loosening, endoprostheses, 183

Mediastinum

lymphomas, 55

oesophageal carcinoma spread, 82

tumours, 49, 58-59

heart involvement, 195-196

Medullary carcinoma of breast, 71 (Fig.), 73

Medullary thyroid carcinoma, 143, 145

SST analogue scintigraphy, 149

Medulloblastoma, 15

Melanoma

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duodenum, 88

metastases

brain, 14

heart, 191, 195

stomach, 87

peptide receptors, 149

small intestine, 94

Meningeal haemorrhage, 15

Meningioma, 17, 18 (Fig.)

vs acoustic Schwannoma, 19

orbit, 20

pituitary region, 20

from radiotherapy, 30

skull base, 23

spine, 25

Menopause

endometrial cancer, 159

and ovarian carcinoma, 155

MEN syndromes see Multiple endocrine neoplasia syndromes

Mesenchymal sarcoma, gallbladder, 120 (Table)

Mesenchymal tumours

bile ducts, 120 (Table)

gallbladder, 120 (Table)

Mesenteric fibrosis, carcinoid tumours, 92

Mesenteric lymph nodes, computed tomography, 91

Mesorectal excision, total, 105

Mesothelioma, 59-60

AV node, 191 (Table)

heart, 191 (Table), 195, 199

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Metaiodobenzylguanidine scanning

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medullary carcinoma of thyroid, 145

phaeochromocytoma, 145-147, 194

thyroid scintigraphy, 143

Metaplasia, oesophageal carcinoma, 83

Metastases

from bone, 181

to bone, 150

to brain, 9, 14-15

bronchial carcinomas, 49-50

cerebellopontine angle, 19

cervical adenopathy, 39-40

cervical carcinoma, 163

colorectal cancer, 105-107

cranial, extra-axial, 20

to duodenum, 88

gallbladder, 120 (Table)

to heart, 191, 195-196

hepatocarcinoma, 117

intramedullary, 25

to kidneys, 135

liver, 118-119

lungs, 54-55

vs meningioma, 17

oesophageal carcinoma, 81

to oesophagus, 84

ovarian carcinoma, 158

pleura, 60

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posterior fossa, 17

skip, 181

skull

base, 23

extra-axial cranial, 20

to small intestine, 94-95

spine, 23-25, 26 (Fig.), 27, 29 (Fig.)

to stomach, 87

see also Lymph nodes, metastases

Methoxy-iso-butyl-isonitrile scanning, breast, 69

MIBG see Metaiodobenzylguanidine scanning

Microadenomas, pituitary, 20-21, 141, 142

Microcalcifications, breast, 68, 69

ductal carcinoma in situ, 72

invasive ductal carcinoma, 70

Microcystic adenoma, pancreas, 122-123

Micrometastases

breast cancer, 74

colorectal cancer, 105

Mitral valve, cardiac myxoma, 192

Mixed neural/glial cell tumours, 11-12

Mixed pattern teratocarcinoma, testes, 137

Monoclonal antibodies, radiolabelled

breast scanning, 69

ovarian carcinoma, 157-158

at surgery, 108

see also Immunoscintigraphy

Mortality rates, primary bone tumours, 178

Mucinous adenocarcinoma, kidneys, 135

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Mucinous carcinoma of breast, 71 (Fig.), 73

Mucinous cystadenoma, pancreas, 122-123

Mucinous cystic adenoma, pancreas, 122

Mucoceles, paranasal sinuses, 41

Multiple endocrine neoplasia syndromes, 141, 143

phaeochromocytoma, 146

Multiple myeloma, 150, 183-185

Myelography (computed tomography), 25

Myeloma

extradural spinal, 27

multiple, 150, 183-185

Myocardium, cardiac myxoma, 192-193

Myometrium, endometrial cancer invasion, 159-160

Myositis ossificans, 180

Myxoid sarcoma, 186

Myxoma, 186

cardiac, 191 (Table), 192-194

Nasoethmoidal tumours, vs maxillonasal tumours, 40-41

Nasopharyngeal tumours

detection of spread, 37, 38 (Fig.)

skull base, 23

Nasosinusal neoplasms, 40-43

Neck, soft tissue masses, 43-44

Needle aspiration

salivary tumours, 44

thyroid masses, 43

see also Fine needle aspiration cytology

Needle biopsy

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bone metastases, 184

primary bone tumours, 182

Neoadjuvant chemotherapy, primary bone tumours, 182

Nerves, tumour spread along, 37

Nerve sheath tumours, 17-18, 185, 186

skull base, 23

see also Schwannomas

Neural/glial cell tumours, mixed, 11-12

Neuroblastoma, 20

Neuroendocrine tumours, peptide receptors, 149

Neuroepithelial tumours, dysembryoplastic, vs oligodendroglioma, 11

Neurofibroma, 28 (Fig.)

cardiac, 191 (Table)

neck, 44

spine, 25

Neurofibromatosis, 17, 25

phaeochromocytoma, 146

Neurogenic sarcoma, heart, 191 (Table)

Neurogenic tumours, mediastinum, 59

Neurotransmitters, from gastrointestinal tract, 148

Neurovascular bundle

magnetic resonance imaging, 181

osteosarcoma involvement, 180

Neutropenia, chest infections, 57

Nipples

discharge, retraction, 73

Paget's disease of breast, 73

Nodal necrosis, 39

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Non-Hodgkin's lymphoma, 14, 21 (Fig.), 169-173

kidneys, 135

thorax, 55, 56

Non-ossifying fibroma, 180

Non-seminomatous tumours, testes, 137

Non-small cell carcinoma, bronchus, 49

Nulliparity, ovarian carcinoma, 155

Octreotide

gut hormone tumour scintigraphy, 148-149

medullary carcinoma of thyroid, 145

Oesophagus, 81-84

carcinoma, 81-83

gastric carcinoma spread, 85

secondary neoplasms, 83-84

Oestrogens, and endometrial cancer, 159

Olfactory neuroblastoma, skull base, 23

Oligodendroglioma, 9, 11

vs central neurocytoma, 12

Omentum, ovarian carcinoma, 156

Oncocytoma, kidneys, 134

Opportunistic infections, thoracic lymphoma therapy, 57

Optic chiasm, tumours compressing, 20, 142

Oral contraceptives

liver adenoma, 114

ovarian carcinoma protection, 155

Oral tumours, detection of spread, 37

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Orbits, 20

exenteration, 42

nasosinusal tumours, 40

tumour assessment, 41-42

Osteoblastoma, 178, 180, 182

Osteochondroma, 177, 180

Osteoid osteoma, 177, 178, 180, 182

Osteonecrosis, 183

Osteoporosis, multiple myeloma, 150

Osteosarcoma, 178

extraskeletal, heart, 191 (Table)

follow-up, 183

incidence, 177

metastases, 182

to brain, 14

Paget's disease, 150

surgery, 180

treatment, 182-183

Ovarian tumours, 150, 155-158

carcinoma, 155-158

Krukenberg tumour, 85

Paget's disease of bone, 150

Paget's disease of breast, 73

Pancoast's tumours, 53-54

Pancreas

gastrinoma, SST analogue scintigraphy, 149

tumours, 120, 121-123

duodenum, 88

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MEN 1 syndrome, 141

Papilla of Vater, carcinoma, 87

Papillary adenoma, bile ducts, 120 (Table)

Papillary carcinoma of breast, 73

Papillary epithelial neoplasms, pancreas, 122

Papillary fibroelastoma, cardiac, 191 (Table)

Papilloma see Choroid plexus papilloma

Paraganglioma, 23

cardiac, 194

Paraglottic spaces, 35

Paralaryngeal spaces, 37

Parametrium, cervical carcinoma invasion, 162-163

Paranasal sinuses

head and neck tumours, 35

hyperostosis, 17

magnetic resonance imaging, 41

tumours, skull base, 23

see also Nasosinusal neoplasms

Parapharyngeal spaces, salivary tumours, 44

Parasitic cysts

cardiac, 194, 199

see also Echinococcal infection

Parathyroid tumours, 145

MEN syndromes, 141, 143 (Table)

Paravertebral masses, 27

Parinaud's syndrome, 23

Pathological fractures, 184

Pelvis

adenopathy, MRI, 155

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bone tumour assessment, 182

computed tomography, testicular tumours, 149-150

lymphangiography, cervical carcinoma, 163

Periampullary tumours, 120, 121

Pericardial cysts, 191 (Table), 194, 195

Pericardium

cardiac tumours, 191, 195

metastases to, 196

Periorbita, 41

Periosteum

nasosinusal tumours, 41

reaction to bone tumours, 179

Perirectal fascia see Total mesorectal excision

Perirectal lymph nodes, colorectal cancer, 105

Peritoneum

colorectal cancer metastases, 105

gastric carcinoma, 85

ovarian carcinoma, 158

(see also Omentum)

small intestine involvement, 93

Peritumoural reaction, colorectal cancer, 104

Petrous vein sampling, 21

Phaeochromocytoma, 145-147

bladder, 135

heart, 194

MIBG uptake, 143, 194

von Hippel Lindau syndrome, 141

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Phased array multicoil, gynaecology, 155

Phenacetin, transitional cell carcinoma, 134

Phleboliths, 186

Pigmentation, and cardiac myxoma, 192

Pineal cysts, 23

Pinealoblastoma, 23

Pinealocytoma, 23

Pineal tumours, 22-23

Piriform sinus, squamous cell carcinoma, 40 (Fig.)

Pituitary adenomas, 20-22, 141

vs meningioma, 17

Pituitary apoplexy, 22, 141

Pituitary gland, 141-142

Pituitary region, tumours, 20-22

Plasmacytoma, 184

Pleomorphic xanthoastrocytoma, 11

Pleura

effusions, 51, 60

tumours, 49, 59-60

Pneumocystis carinii pneumonia, 57

Pneumonias, 49

thoracic lymphoma therapy, 57

Pneumonitis, radiotherapy, 56-57

Pneumosinus dilatans, 17

Pneumothorax, osteosarcoma metastases, 182

Polycystic kidney disease, 113

Polypoid tumours, endometrial cancer, 160

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Polyposis Registry, 107

Polyps

colon, 101-102

(see also Familial adenomatous polyposis)

lymphomas, 108

gastric carcinoid, 86-87

`Popcorn' calcification, solitary pulmonary nodules, 53

Porcelain gallbladder, 120

Portal circulation, colorectal cancer metastases, 105

Portal vein blood flow, vs hepatic artery blood flow, 106

Portal venous phase, CT arteriography, 106-107

Portal venous sampling, intra-arterial calcium injection, 148

Positron emission tomography, 39-40, 199

lymphomas, 170

see also Fluorodeoxyglucose-PET

Posterior fossa neoplasms, 15

CT vs MRI, 17

Postnecrotic cirrhosis, hepatocarcinoma, 117

Postoperative changes, intracranial tumours, 27

Power Doppler ultrasound, 127

Pre-epiglottic space, 37

Pregnancy, CA125 elevation, 156

Primary treatment, breast cancer, ultrasound, 75

Primitive neuroectodermal tumours, 15, 23

Prolactin, assay, 142

Prolactinoma, 20, 141, 142

Prostate, 135-137

benign hypertrophy, 135

carcinoma, 136-137

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bone metastases, 150

Prostatectomy, radical, 136

Prostatic specific antigens, 136

Prostheses, magnetic resonance imaging, 181

Proton density SE magnetic resonance imaging, laryngeal cartilages, 38

Proton emission tomography, radiation effects vs recurrent tumours, 29

Pseudosarcoma, oesophagus, 83

Pseudotumours, heart, 199

Pterygo-palatine fissure, nasosinusal tumours, 40

Pulmonary aspergillosis, invasive, 57

Pulmonary fibrosis, radiotherapy, 56-57

Pulmonary hypertension, cardiac myxoma, 192

Pulmonary valve, carcinoid syndrome, 196-197

Pulsatility index

endometrial cancer, 160

vs resistance index, ovarian tumour vascularity, 156

Pulsed Doppler ultrasound, hepatocarcinoma, 117

Punctate calcification, liver metastases, 106

Pylorus, gastric tumour spread, 85, 88

Radiation doses, mammography, 67

Radical hysterectomy, cervical carcinoma histology, 163

Radical prostatectomy, 136

Radiographic grading, primary bone tumours, 179

Radiography, digital, 68, 199

Radionuclide scanning see Scintigraphy

Radiosurgery, stereotactic, 15

Radiotherapy

enteritis, 93

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intracranial effects, 27, 29

pneumonitis, 56-57

soft-tissue sarcoma recurrence, 187

Rathke's cleft cysts, 22

Receiver-operator characteristic curves, pulsatility vs resistance index, ovarian tumour vascularity, 156

Rectal carcinoma, 104, 105

Rectal ultrasound, 103-104

Rectovaginal pelvic examination, ovarian carcinoma screening, 155

Recurrence, superior vena cava syndrome, 197

Recurrent tumours

breast cancer, 75-76

cervical carcinoma, 163-164

endometrial cancer, 160

primary bone tumours, 183

vs radiation effects, 29

Regional cerebral blood flow, functional MRI, 30

Renal adenoma, 134

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Renal cell carcinoma, 127, 128-131 (Fig.), 134 (Fig.)

metastases

bone, 184

duodenum, 88

heart, 191

small intestine, 95

von Hippel Lindau syndrome, 141

Resistance index, vs pulsatility index, ovarian tumour vascularity, 156

Retained secretions, vs tumours, facial structures, 42-43

Retromolar trigone, squamous cell carcinomas, 38 (Fig.)

Retropharngeal lymph nodes, 39

Reverse `3' sign of Frostberg, 88

Rhabdomyoma, cardiac, 191 (Table), 194

Rhabdomyosarcoma

chemotherapy, 187

head and neck, 43

heart, 191 (Table), 195

skull base, 23

Risk factors, breast cancer, 65

Rye classification, Hodgkin's disease, 169 (Table)

Salivary glands, head and neck tumours, 35, 44

Salpingo-oophorectomy, ovarian carcinoma staging, 156

Sarcoidosis

vs cardiac tumours, 199

vs lymph node metastases, 56

Sarcomas

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heart

metastatic, 191

primary, 195

soft-tissue, 185-187

Schwannomas

acoustic, 17, 19

neck, 44

spine, 25, 28 (Fig.)

Sciatica, bone tumours, 178

Scintigraphy

breast, 69

cancer metastases, 75, 76

cardiac paraganglioma, 194

gut hormone tumours, 148-149

iodocholesterol, Conn's syndrome, 147-148

liver

focal nodular hyperplasia, 114

haemangioma, 114

and liver metastases, 119

vs magnetic resonance imaging, vertebral metastases, 27

parathyroid disease, 145

phaeochromocytoma, 145-147

small intestine, 90

thyroid masses, 43, 143-145

see also Monoclonal antibodies, radiolabelled

Scirrhous gastric carcinoma, 85

Sclerosis, bone, head and neck tumours, 37

Scoliosis, bone tumours, 178

Screening

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breast cancer, 65, 69

cervical cytology, 161

endometrial cancer, 159

lung cancer, 49

ovarian carcinoma, 155

stomach cancer, 85

Secretions see Retained secretions

Seeding, ovarian carcinoma, 156

Seminal vesicles, 136

Seminoma

mediastinum, 58-59

testes, 137

Sentinel node, breast cancer, 75

Septum pellucidum, central neurocytoma, 12

Seroma, 187

Serotonin, 148

Serous cystadenoma, pancreas, 122-123

Sestamibi scanning, parathyroid disease, 145

Short T1 inversion recovery sequences, MRI, pelvic adenopathy, 155

Sigmoidoscopy, flexible, 102

Silicone breast implants, magnetic resonance imaging, 69

Simple bone cysts, 177

Single photon emission tomography, 39-40, 199

liver metastases, 119

phaeochromocytoma, 147

see also Thallium-SPECT

Sipple syndrome, 141

Skeleton see Bone

Skin pigmentation, and cardiac myxoma, 192

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Skip metastases, 181

Skull base, 23

approach to nasosinusal tumours, 40

Small cell carcinoma, bronchus, 49

Small intestine

barium studies, 89-90

carcinoma, 90

neoplasms, 87, 88-90

secondary neoplasms, 93-95

Small parts tissue imaging, breast ultrasound, 68

Smoking, transitional cell carcinoma, 134

Soft-tissue masses

breast, 65-66

neck, 43-44

Soft-tissue tumours, primary, 185-187

Solid epithelial neoplasms, pancreas, 122

Solitary bone metastasis, 183-184

Solitary pulmonary nodule, 51-53

Somatostatinoma, pancreas, 122, 123

Somatostatin receptor ligand, gut hormone tumour scintigraphy, 149

Spectroscopy, breast masses, 70

Sphenoid region, 23

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Spiculated mass, invasive ductal carcinoma of breast, 70

Spinal cord compression, 27

Spine, 23-27

haemangioma, von Hippel Lindau syndrome, 141

magnetic resonance imaging, 181-182

primary bone tumours, 178

Spiral computed tomography

bronchial carcinoma staging, 50

lung metastases, 54

phaeochromocytoma, 147

thyroid masses, 143

see also Helical computed tomography

Squamous cell carcinomas, 38 (Fig.)

bone invasion, 37

bronchus, 49

head and neck, 35, 36 (Fig.)

kidneys, 135

maxillary sinus, 43 (Fig.)

nasosinusal, 40

oesophagus, 81

piriform sinus, 40 (Fig.)

skull base, 23

Staging

bone tumours, 180-182

breast tumours, 74-75

bronchial carcinomas, 49-50

cervical carcinoma, 161, 162 (Fig.)

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colorectal cancer, 103-105

Dukes classification, 101, 104

endometrial cancer, 159

gastric carcinoma, 85-86

lymphomas, 170-173

thorax, 55-56

nodal, 39 (Table)

oesophageal carcinoma, 81-83

ovarian carcinoma, 156

primary bone tumours, 182

prostate cancer, 136

soft-tissue sarcomas, 187

thoracic tumours, 49

Stents, superior vena cava syndrome, 197

Stereotactic cross-sectional imaging, 30

Stereotactic mammography, 67

Stereotactic radiosurgery, 15

Steroid therapy, chest infections, 57

STIR (short T1 inversion recovery sequences), MRI, pelvic adenopathy, 155

Stomach

lymphoma, spread to duodenum, 86, 88

oesophageal carcinoma spread, 81

primary carcinoma, 84-86

spread to duodenum, 85, 88

secondary neoplasms, 87

Stress fractures, 180

Subependymal giant-cell astrocytoma, 11

Subtraction, digital radiography, 199

Subtraction scanning, parathyroid disease, 145

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Sulphur colloid scintigraphy, hepatocarcinoma, 117

Superior orbital fissure, nasosinusal tumours, 40

Superior sulcus tumours, 53-54

Superior vena cava syndrome, 197

Superscan, bone scintigraphy, 184

Surgery

bone metastases, 184-185

soft-tissue sarcomas, 187

see also Amputation

Surgical staging, primary bone tumours, 182

Synchronous lesions, colorectal cancer, 103

Synovial sarcoma, 185

chemotherapy, 187

heart, 191 (Table)

Talc, ovarian carcinoma, 155

Tamponade, metastases to pericardium, 196

Target lesions, liver ultrasound, 75

Task activation studies, functional MRI, 30

TC5 monoclonal antibody, ovarian carcinoma imaging, 158

Technetium-99m see Scintigraphy

Temporal subtraction, 199

Teratocarcinoma, mixed pattern, testes, 137

Teratodermoids, pituitary region, 20

Teratoma

cardiac, 191 (Table), 195

mediastinum, 58-59

pineal, 23

testes, 137

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Testicular tumours, 137, 149-150

Thallium scintigraphy

breast cancer, 69

parathyroid disease, 145

thyroid masses, 145

Thallium-SPECT, 30, 39

Thermography, breast, 70

Thorax, tumours, 49-61 3D displays, 199

3D volume imaging, cervical carcinoma, 162

Thrombi

hepatocarcinoma, 117

intracardiac, 194

from tumours, 191

Thrombocytopenia, lung haemorrhage, 57

Thrombosis, stents, 197

Thymoma, 58

heart, 191 (Table)

vs lymph node metastases, 56

pleura, 60

Thyroglobulin assays, 143

Thyroglossal duct cysts, 43

Thyroid carcinomas, 143-145

Thyroiditis, De Quervain's, 143

Thyroid masses, 43-44, 142-145

mediastinum, 59

Thyrotoxicosis, 143

Thyrotropin assay, 141-142

Thyroxine therapy, and thyroid scintigraphy, 145

Time factors, imaging strategies, 3-4

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Page 216

Tissue characterization, 30

TNM classification

bladder cancer, 135

bronchial carcinomas, 49, 50 (Table)

colorectal cancer, 103-105

prostate cancer, 136

renal cell carcinoma, 127

testicular cancer, 137

transitional cell carcinoma, 134-135

Tongue

squamous cell carcinoma, 36 (Fig.)

tumour spread from, 35-36, 37

Total mesorectal excision, 105

Toxoplasmosis, vs CNS lymphoma, 14

Trachea, oesophageal carcinoma spread, 82

Transabdominal ultrasound

cervical carcinoma staging, 161

gynaecology, 155

Transhepatic cholangiography, 121

Transitional cell carcinoma

bladder, 135

kidneys, 134-135

Transoesophageal echocardiography, 194

Transplantation

heart, 196

liver, hepatocarcinoma, 118

and lymphomas, 169

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Transrectal ultrasound, 136

cervical carcinoma, 161

recurrent endometrial cancer, 160-161

Transthoracic echocardiography, 194

Transvaginal sonography see Endovaginal ultrasound

Tricuspid valve

carcinoid syndrome, 196-197

cardiac myxoma, 192

Trigeminal nerve, 37

Trigeminal Schwannoma, 19, 23

Tri-iodothyronine therapy, thyroid scintigraphy, 145

Triple assessment, breast masses, 66

Tuberculosis, vs cardiac tumours, 199

Tuberous sclerosis

angiomyolipoma of kidneys, 134

cardiac rhabdomyoma, 194

tumours, 11

Tubular carcinoma of breast, 73

Tubulo-papillary carcinoma, kidney, 127

Tumour rests, rectal cancer, 105

UICC (Union Internationale Contre le Cancer), testicular cancer staging, 137

Ulcers

gastric carcinoma, 85

gastric lymphomas, 86

Ultrasound

bone tumour needle biopsy, 182

breast cancer, 74-76

breast masses, 68-69

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(see also Named tumours)

disappearing haemangioma, 113

gastric carcinoma, 86

gynaecology, 155

intraoperative, liver metastases, 106

jaundice, 120-121

kidneys, 127

liver metastases, 119

neck masses, 43

thyroid tumours, 44

pleural effusion aspiration, 51

rectal, 103-104

soft-tissue sarcoma biopsy, 187

see also Doppler ultrasound; Echocardiography; Endoscopic sonography; High-resolution ultrasound; Transrectal
ultrasound

Ultrasound contrast media, 76, 119

Union Internationale Contre le Cancer, testicular cancer staging, 137

Upper aerodigestive tract, head and neck tumours, 35-40

Ureteric obstruction, cervical carcinoma, 163

Urinogenital system, 127-138

Uterus, 158-164

Vagina

atresia, 159

see also Endovaginal coils; Endovaginal ultrasound

Valve disease

carcinoid syndrome, 196-197

vs cardiac myxoma, 193

Variant carcinomas, pancreas, 122

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Vascular invasion, 197-198

Vasoactive intestinal peptide receptor scintigraphy, 149

Vasogenic oedema, brain tumours, 9, 14

Vasovagal attacks, breast diagnosis, 67, 69

Venography, superior vena cava syndrome, 197

Venous extension, tumours, 191, 197-198

Verner-Morrison syndrome, 148

Vertebrae, 27

see also Spine

Villous adenoma, colorectal, 104

VIPoma, 148

pancreas, 122, 123

VIP receptor scintigraphy, 149

Viral hepatitis, hepatocarcinoma, 117

Virchow-Robin spaces, lymphoma spread, 14

Virtual reality, 199

Visceral metastases, ovarian carcinoma, 158

Vocal cords, 35, 36-37

Volume rendering, colorectal cancer, 102-103

Volumetry, cervical carcinoma, 162

Von Hippel Lindau syndrome, 13, 25, 141

phaeochromocytoma, 146

renal cell carcinoma, 127

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Wrecking ball phenomenon, cardiac myxoma, 192

Xanthoastrocytoma, 11

Yolk sac carcinoma, testes, 137

Zollinger-Ellison syndrome, 148

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Page iii

Imaging in Oncology

Edited by
Walter L. Curati
MD FRCR
Senior Lecturer and Consultant
Department of Imaging
Hammersmith Hospital, London, UK
David O. Cosgrove
MA MSc FRCP FRCR
Department of Imaging
Hammersmith Hospital,
London, UK
Martin J. Lipton
MD
Professor of Radiology and Medicine
Chairman, Department of Radiology
The University of Chicago, Chicago, Illinois,
USA
David J. Allison
BSc MD FRCR FRCP
Director and Professor
Department of Imaging
Hammersmith Hospital, London, UK

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Page iv

© 1998

GREENWICH MEDICAL MEDIA LTD

219 The Linen Hall
162-168 Regent Street
London
W1R 5TB

ISBN 1 900 151030

First Published 1998

Apart from any fair dealing for the purposes of research or private study, or criticism or review, as permitted under the
UK Copyright Designs and Patents Act, 1988, this publication may not be reproduced, stored, or transmitted, in any
form or by any means, without the prior permission in writing of the publishers, or in the case of reprographic
reproduction only in accordance with the terms of the licences issued by the Copyright Licensing Agency in the UK, or
in accordance with the terms of the licences issued by the appropriate Reproduction Rights Organization outside the
UK. Enquiries concerning reproduction outside the terms stated here should be sent to the publishers at the London
address printed above.

The right of W Curati, D Cosgrove, M Lipton & D Allison to be identified as editors of this work has been asserted by
them in accordance with the Copyright Designs and Patents Acts 1988.

The publisher makes no representation, express or implied, with regard to the accuracy of the information contained in
this book and cannot accept any legal responsibility or liability for any errors or omissions that may be made.

British Library Cataloguing in Publication Data

A catalogue record for this book is available from the British Library.

Distributed worldwide by Oxford University Press

Typeset by Saxon Graphics Ltd, Derby

Printed in Great Britain by Ashford Colour Press

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Page ix

Foreword

The key to the successful treatment of most patients with cancer is a detailed understanding of the location of the
primary tumour and its likely routes of spread. Surgery and radical radiotherapy are still the main curative modalities for
cancer although chemotherapy is increasing its potential both in the adjuvant setting and as primary therapy. For the
surgeon and radiotherapist accurate, detailed and comprehensible anatomical information is essential. New technologies
such as minimally invasive organ conservation, tele-surgery, robotics and conformal radiotherapy make such
information even more important.

This book provides a succinct summary of tumour imaging, considering each organ system in turn. It is well illustrated
by good quality clinical images which in themselves provide a useful educational tool. The discussion by well known
experts, helps to guide the clinician to the most appropriate test under different circumstances. As health-care systems
globally become increasingly cost conscious it is vital that carefully selected, high yield investigations are used rather
than the blunderbuss approach with the clinician requesting everything possible. Too often patients with well
documented, essentially untreatable, metastatic disease still linger inappropriately on medical wards being further
investigated rather than being offered appropriate palliative care. And yet accurate tumour staging is essential if the
correct treatment is to be chosen and data from different centres reliably compared. Here you will find excellent
guidance for the most appropriate investigation for many different oncological problems. Useful algorithms for
diagnostic work-up and subsequent management are included for several common clinical scenarios.

Most importantly this book demonstrates the vital need for continual dialogue between those involved in clinical
decision making and the imaging team. In cancer medicine, diagnosis is only useful as a guide to treatment. Constant
interaction and teamwork is an essential component of good patient care in this increasingly important area of medicine.

KAROL SIKORA
CHIEF, WHO CANCER PROGRAMME AND PROFESSOR OF CLINICAL ONCOLOGY,
IMPERIAL COLLEGE SCHOOL OF MEDICINE, HAMMERSMITH HOSPITAL, LONDON
1998

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Page v

Contents

Contributors vii

Forewords ix

Chapter 1 1
Introduction
Walter L. Curati, David O. Cosgrove, Martin J. Lipton and David J. Allison

Chapter 2 7
The Central Nervous System
Lloyd E. Savy and Ivan F. Moseley

Chapter 3 33
The Head and Neck
Antonio Chiesa, Roberto Maroldi, Giuseppe Battaglia, Patrizia Maculotti and Davide Farina

Chapter 4 47
The Lung and Mediastinum
Geraldine Walsh and Christopher D.R. Flower

Chapter 5 63
The Breast
William E. Svensson

Chapter 6 79
The Oesophagus, Stomach, Duodenum and Small Intestine
Daniel J. Nolan

Chapter 7 99
The Colon and Rectum
Clive I. Bartram

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Page vi

Chapter 8 111
The Liver, Biliary System and Pancreas
Michel Lafortune and Luigi Lepanto

Chapter 9 125
The Kidney, Bladder, Prostate and Testes
Walter L. Curati and Gordon Williams

Chapter 10 139
The Endocrine System
Daniel A. Darko and Karim Meeran

Chapter 11 153
The Ovaries, Endometrium and Cervix
Nandita M. deSouza and W.P. Soutter

Chapter 12 167
The Lymphatic System
Walter L. Curati

Chapter 13 175
The Bone and Soft Tissue
Asif Saifuddin

Chapter 14 189
The Cardiovascular System
Craig A. Hackworth and Martin J. Lipton

Index 203

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Page vii

Contributors

David J. Allison
Director and Professor
Department of Imaging
Hammersmith Hospital
London
UK

Clive I. Bartram
Consultant Radiologist
St Mark's Hospital
Northwick Park
Harrow
UK

Giuseppe Battaglia
Assistant
Department of Radiology
University of Brescia
Brescia
Italy

Antonio Chiesa
Professor and Chairman
Department of Radiology
University of Brescia
Brescia
Italy

David O. Cosgrove
Department of Imaging
Hammersmith Hospital
London
UK

Walter L. Curati
Senior Lecturer and Consultant
Department of Imaging
Hammersmith Hospital
London
UK

Daniel A. Darko
Honorary Clinical Research Fellow
Endocrine Unit
Hammersmith Hospital
London
UK

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Nandita M. deSouza
Senior Lecturer and Consultant
The Robert Steiner MRI Unit
Hammersmith Hospital
London
UK

Davide Farina
Resident
Department of Radiology
University of Brescia
Brescia
Italy

Christopher D.R. Flower

Consultant Radiologist
Addenbrooke's Hospital
Cambridge
UK

Craig A. Hackworth
Assistant Professor of Radiology
The University of Chicago
Chicago
Illinois
USA

Michel Lafortune
Professor of Radiology
Centre Hospitalier de l'Université de
Montréal
Quebec
Canada

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Page viii

Luigi Lepanto
Assistant Professor of Radiology
Centre Hospitalier de l'Université de
Montréal
Quebec
Canada

Martin J. Lipton
Professor of Radiology and Medicine
Chairman, Department of Radiology
The University of Chicago
Chicago
Illinois
USA

Patrizia Maculotti
Assistant
Department of Radiology
University of Brescia
Brescia
Italy

Roberto Maroldi
Assistant
Department of Radiology
University of Brescia
Brescia
Italy

Karim Meeran
Consultant Physician and Endocrinologist
Endocrine Unit
Hammersmith Hospital
London
UK

Ivan R. Moseley
Consultant Neuroradiologist
National Hospital, Queen Square &
Moorfield Eye Hospital
London
UK

Daniel J. Nolan
Consultant Radiologist
Department of Radiology
Radcliffe Hospital
Oxford
UK

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Lloyd E. Savy
Consultant Neuroradiologist
Royal Free Hospital & Royal National
Throat Nose and Ear Hospital
London
UK

Asif Siaffudin
Consultant Radiologist
Royal National Orthopaedic Hospital
Stanmore, Middlesex
UK

William E. Svensson
Director of Radiology
Ealing Hospital
Honorary Senior Lecturer
Hammersmith Hospital
London
UK

W.P. Soutter
Reader and Consultant
Gynaecological Oncology
Hammersmith Hospital
London
UK

Geraldine Walsh
Senior Registrar
Addenbrooke's Hospital
Cambridge
UK

Gordon Williams
Consultant and Honorary Senior Lecturer
Urology and Renal Transplant Unit
Hammersmith Hospital
London
UK

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Page xi

Foreword

For a long time imaging has been the province of specialists. This is clearly wrong. Of all branches of medicine surely
imaging is the one where it is easiest to appreciate both the normal and the abnormal. Recent advances have been
dramatic. It is now well within the ken of the average doctor both to appreciate the beauty of normal structure and to
identify a particular abnormality in his patient. This exciting new book is the celebration of those advances and an
opportunity for all clinicians to participate in the action. It sets out in an easy to understand and clear way how to detect
the major human diseases. It has been predicted that once infections are covered by a range of effective antibiotics, a
state that we are close to achieving, and the degenerative arterial diseases, currently the cause of much early mortality
and morbidity, are abolished by new cholesterol lowering agents, our biggest enemy will be cancer. It is thus in the field
of cancer diagnosis that we should focus our attention. This book offers a superb opportunity to get involved personally
and at the cutting edge. The chapters are written by world experts, not only as experts in their field, but as experts in
communication. They have been specifically chosen as good communicators, able to bring to every physician an
understanding of the latest diagnostic techniques and how the reader can personally be able to contribute on behalf of
his patient. Read and enjoy.

STEPHEN BLOOM
CHAIRMAN, DIVISION OF INVESTIGATIVE SCIENCE
IMPERIAL COLLEGE SCHOOL OF MEDICINE
1998

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