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Neuroimaging in Patients With Dysphagia 363
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Fig. 5 Axial computed tomography images of two different
patients. a A large cerebral infarct (dark area) involving the
whole left middle cerebral artery territory. The patient
complained of aphasia, hemianopia, right-sided hemiplegia,
and sensory loss. b A large cerebral hemorrhage in the left
frontal and parietal lobes with blood in the subarachnoid space
different cranial nerve nuclei involved in the swallowing are located. MRI provides more detailed
anatomical and morphological information than CT
especially in pathological conditions of the skull base
and posterior cranial fossa, including the brain stem.
In the last decade new MRI modalities have been
introduced enabling functional evaluation of different
CNS structures involved in swallowing using functional MRI. Structural evaluation of different tracts
involved in the swallowing connecting the motor
cortex with swallowing centers of the brain stem is
now possible by using diffusion tensor imaging and
tractography.
4 Dysphagia Following Stroke
Stroke affects 2,000 people per million worldwide
each year (Thorvaldsen et al. 1995); 80–85% of
strokes are ischemic and 15–20% are hemorrhagic.
Up to 35–50% of patients with stroke develop
and the left lateral ventricle. The patient complained of aphasia
and sensory and motor deficit. The hemorrhage affects the
cortical representation of the face and the tongue, resulting in
swallowing difficulties primarily due to impairment of the oral
phase of swallowing. Both patients needed long-standing tube
feeding
dysphagia (Paciaroni et al. 2004; Gordon et al. 1987).
In a systematic review of published literature concerning dysphagia after stroke, the incidence of stroke
was about 50% using clinical testing and about 75%
using instrumental testing. Dysphagia tends to be less
severe compared with brain stem stroke (Martino
et al. 2005). Among patients with middle cerebral
artery ischemic stroke, the size of the infarct plays a
more important role than the location of the ischemic
injury (Paciaroni et al. 2004; Fig. 5). Cortical and
subcortical supratentorial lacunar infarcts as well as
brain stem infarcts may result in dysphagia (Fig. 6).
Cerebral infarctions affect all three phases of swallowing with subsequently increased risk of aspiration
of liquid or solid food and development of pneumonia, which is one of the life-threatening complications
of stroke (Miller 1999). Cerebral infarctions may be
classified as either large-vessel infarcts or smallvessel infarcts. Patients with large-vessel infarcts
affecting the middle cerebral artery territory present
with hemiplegia, sensory loss, aphasia, neglect, and
364 K. Abul-Kasim
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Fig. 6 Axial T2 fluid-attenuated inversion recovery (FLAIR)
MRI of two different patients. a A small infarct affecting the
frontal lobe operculum responsible for speech and the anterior
part of the insular cortex. The patient had complained of
visual disturbance (hemianopia). Patients with
bilateral infarcts involving the frontoparietal operculum develop severe dysphagia (Foix–Chavany–
Marie syndrome). The clinical presentation of largevessel infarcts affecting the brain stem differs
depending on the structures affected, often with
evidence of involvement of different cranial nerves,
dysarthria, dysphagia, syncope, and ataxia as well
as motor and sensory deficit (Fig. 7). Large-vessel
infarcts affecting the middle cerebral artery territory
induce dysphagia by affecting the cortical structures
responsible for the processing of the swallowing,
whereas large-vessel infarcts affecting the vertebrobasilar circulation result in infarcts affecting
different cranial nerve nuclei and fibers as well as
the reticular formation and solitary tract. There are
several vascular syndromes affecting different parts
of the brain stem and medulla oblongata that can
potentially result in dysphagia. One specific syndrome is Wallenberg’s syndrome (posterolateral
medullary syndrome). Patients with this syndrome
present with Horner’s syndrome (ptosis, mitosis,
and anhydrosis of the ipsilateral side of the face),
sensory loss of temperature, and pain in the ipsilateral side of the face and in the contralateral side
expressive aphasia and swallowing difficulties. b Multiple
lacunar cortical and subcortical infarcts. The infarct marked
with an arrow affects the precentral gyrus
Fig. 7 Apparent diffusion coefficient of magnetic resonance
diffusion showing a large infarct of the left side of the upper
pons and mesencephalon (dark area of restricted diffusion
indicating acute infarction). Among other neurological deficits,
the patient complained of dysphagia due to affection of cranial
nerve nuclei, primarily those of the trigeminal nerve
Neuroimaging in Patients With Dysphagia 365
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Fig. 8 MRI diffusion showing a small infarct (bright lesion
marked with a long arrow) in the right posterolateral part of the
medulla oblongata. The patient presented with symptoms and
signs consistent with Wallenberg’s syndrome. Dysphagia
was primarily caused by involvement of the solitary tract.
The image shows also a larger infarct in the right adjacent part
of the cerebellum (marked with a short arrow)
Fig. 10 Axial T2 FLAIR MRI showing a small bright lesion in
the lateral dorsal pons. Dysphagia in this case was due to
involvement of motor and sensory nuclei of the trigeminal
nerve
Fig. 9 Axial T2 FLAIR MRI of a patient with vascular
dementia with widespread signal abnormalities in the white
matter (confluent bright area) and multiple small infarcts
(black lesions). The patient had hypertension, cognitive
impairment, and dysphagia
of the extremities. Dysphagia is always present due
to involvement of the solitary tract (vagus and
glossopharyngeal nerve nuclei) (Fig. 8).
In the acute phase of the stroke, CT is the
method of choice to detect early signs of largevessel infarcts and cerebral hemorrhage. When the
CT findings are normal on admission of the patient
and when the patient complains of dysphagia and/or
the presence of other neurological deficits, MRI is
usually performed to visualize small supratentorial
cortical and subcortical infarcts as well as brain
stem infarcts that have failed to be detected by CT.
Special attention should be paid to small infarcts in
the medulla oblongata, brain stem, anterior insula,
lateral portion of the precentral gyrus, posterior
portion of the inferior frontal gyrus, basal ganglia,
and internal capsule. MRI enables detection of
small infarcts and helps to determine their age by
demonstrating restricted diffusion on diffusionweighted images in the acute phase of ischemia and
showing contrast enhancement in the subacute
stage. Evidence of chronic ischemic changes in the
white matter of the brain stem or the supratentorial
white matter as in cases of vascular dementia may
explain the occurrence of dysphagia among these
patients (Fig. 9).
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Fig. 11 Axial T2 FLAIR and postcontrast T1-weighted MRI,
respectively. a A large glial tumor (histopathologically proven
to be grade II astrocytoma) in the right frontal lobe in a patient
with epilepsy, and slowly progressive speech and swallowing
5 Other Neurological Disorders
Causing Dysphagia
In trauma, CT is the method of choice as it can detect
brain contusions, hemorrhages, and brain swelling.
However, small cortical and subcortical hemorrhages,
brain stem hemorrhages, and nonhemorrhagic lesions
that usually occur in patients with deep axonal injury
are not commonly to detected by CT. These patients
usually have dysphagia, and the establishment of this
diagnosis by performing MRI is essential from a
therapeutic and prognostic point of view.
MS is believed to be an autoimmune disease
resulting in inflammation of the myelin sheaths
around the axons of the brain and spinal cord with
subsequent demyelination, damage, and scarring of
the affected brain tissue. MS often affects young
adults, is more common in women than in men, and
has a prevalence ranging between 2 and 150 per
100,000 individuals (Rosati 2001). The clinical presentation of MS differs depending on the site of the
MS lesions. Optic neuritis is a common clinical
difficulties. b Contrast-enhanced tumor in the left side of the
pons in a patient with right-sided sensory loss and dysphagia
due to involvement of the lateral spinothalamic tract and
trigeminal and facial nerve nuclei
Fig. 12 Coronal T2-weighted MRI of a patient with amyo-
trophic lateral sclerosis showing high signal intensity along the
corticospinal tract (arrows)
Neuroimaging in Patients With Dysphagia 367
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presentation and in many patients is the presenting
feature. MS has the predilection to affect the brain
References
stem, the cerebellar peduncles, the corpus callosum,
and the periventricular white matter (Fig. 10). However, at least one subcortical lesion should be present
to establish the diagnosis according to McDonald’s
four radiological criteria for the diagnosis of MS.
Lesions affecting the brain stem and the subcortical
white matter may produce dysphagia in patients with
MS. In advanced and late-stage MS, dysphagia and
the requirement of tube feeding are not uncommon. In
patients with MS, MRI is the method of choice to
establish the diagnosis, help the clinicoradiological
correlation, and depict lesions with ongoing activity
by showing restricted diffusion and/or contrast
enhancement. Patients with MS might exhibit plenty
of lesions in their white matter, and MRI helps to
detect lesions that are responsible for the symptoms,
including dysphagia.
In patients with brain tumors, both CT and MRI are
suitable methods in the workup of these diseases,
although MRI is more sensitive to show the accurate
extent ofthe tumor(Fig. 11), theperifocal edema, or to
detect subtle contrast enhancement that might affect
regions responsiblefor swallowing not depicted byCT.
MRI is also the method of choice in the workup of
diseases such as ALS (showing increased signal along
the corticospinal tract; Fig. 12), Wilson’s disease
(showing bilateral symmetrical low T1 signal and
high T2 signal in basal ganglia, especially putamen),
and pontocerbellar atrophy.
Barritt AW, Smithard DG (2009) Role of cerebral cortex
plasticity in the recovery of swallowing function following
dysphagic stroke. Dysphagia 24:83–90
Daniels SK (2006) Neurological disorders affecting oral,
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esophagus. GI Motil Online. doi: 10.1038/gimo34
Daniels SK, Foundas AL (1997) The role of the insular cortex
in dysphagia. Dysphagia 12:146–156
Gordon C, Hewer RL, Wade DT (1987) Dysphagia in acute
stroke. Br Med J 295:411–414
Hamdy S, Aziz Q, Rothwell JC, Singh KD, Barlow J,
Hughes DG, Tallis RC, Thompson DG (1996) The cortical
topography of human swallowing musculature in health and
disease. Nat Med 2:1217–1224
Logemann JA, Veis S, Rademaker AW, Huang CW (1999)
Early recovery of swallowing post-CVA. Paper presented at
the eighth annual meeting of the Dysphagia Research
Society, Burlington, VT
Martino R, Foley N, Bhogal S, Diamant N, Speechley M,
Teasell R (2005) Dysphagia after stroke: incidence, diagnosis, and pulmonary complications. Stroke 36:2756–2763
Miller AJ (1999) The neuroscientific principles of swallowing
and dysphagia. Singular, San Diego
Paciaroni M, Mazzotta G, Corea F, Caso V, Venti M,
Milia P, Silvestrelli G, Palmerini F, Parnetti L, Gallai V
(2004) Dysphagia following stroke. Eur Neurol 51:
162–167
Rosati G (2001) The prevalence of multiple sclerosis in the
world: an update. Neurol Sci 22:117–139
Thorvaldsen P, Asplund K, Kuulasmaa K, Rajakangas AM,
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Cross-Sectional Imaging of the Oesophagus
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Using CT and PET/Techniques
Ahmed Ba-Ssalamah, Barbara J. Fueger,
and Wolfgang Schima
Contents
1 Introduction.............................................................. 370
2 CT and PET/CT Technique ................................... 370
3 Oesophageal Cancer ................................................ 371
4 CT, PET/CT Imaging of the Oesophagus ............ 372
4.1 Tumour Detection and Classification ....................... 372
4.2 Follow-Up After Oesophagectomy........................... 377
5 Other Oesophageal Malignancies .......................... 378
5.1 Oesophageal Lymphoma ........................................... 378
5.2 Leiomyoma and GIST............................................... 379
5.3 Fibrovascular Polyps ................................................. 380
5.4 Oesophageal Fistula................................................... 381
5.5 Oesophageal Perforation ........................................... 381
6 Other Conditions ..................................................... 382
6.1 Achalasia.................................................................... 382
6.2 Diverticula ................................................................. 383
6.3 Duplication Cyst ........................................................ 384
6.4 Hiatal Hernia ............................................................. 384
6.5 Oesophagitis............................................................... 385
6.6 Oesophageal Varices ................................................. 385
6.7 Dysphagia Lusoria and Aortic Disease .................... 386
7 Clinical Value of Multi-Detector CT .................... 387
References.......................................................................... 388
A. Ba-Ssalamah (&) B. J. Fueger
Department of Radiology,
Medical University of Vienna, Vienna, Austria
e-mail: ahmed.ba-ssalamah@meduniwien.ac.at
W. Schima
Department of Radiology, KH Göttlicher Heiland, KH der
Barmherzigen Schwestern Wien,
and Sankt Josef-Krankenhaus, Vienna, Austria
Abstract
Multidetector computed tomograpy (MDCT) is the
most frequent imaging modality in the diagnostic
work-up of oncologic diseases of the abdomen.
Although CT has been used for preoperative
evaluation of oesophageal cancer, the major role
of CT has been the depiction of lymph nodes,
distant metastases, or both, rather than the evaluation of the local status of oesophageal cancer. The
sensitivity of conventional or helical CT protocols
for the localization of oesophageal cancer, especially early stage cancer, is not satisfactory. This
may be attributed to the fact that conventional or
helical CT cannot offer optimal conspicuity of
oesophageal cancers against the normal oesophageal wall, or because the oesophagus is too long to
be imaged entirely using thin slices during a single
breath-hold on conventional or helical CT scans,
especially in the absence of lumen distension,
since inadequately distended hollow viscera on CT
may hide small lesions and may even mimic
pseudolesions. Thus, optimal distension of the
oesophagus and stomach is important to overcome
this limitation. The combination of the MDCT
technique with thin slice sections and the possibility to obtain high-quality, isotropic, multi-planar
reconstructions and the water filling, or the application of gas-producing effervescent granules to
distend the stomach and the oesophagus are
important factors that may increase the efficacy
of CT for local staging of oesophageal cancer.
Using this technique is not only useful for a
complete preoperative staging of oesophageal
malignancies according to TNM classification but
O. Ekberg (ed.), Dysphagia, Medical Radiology. Diagnostic Imaging, DOI: 10.1007/174_2012_656,
Springer-Verlag Berlin Heidelberg 2012
369
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also clinically relevant for evaluation of a broad
spectrum of inflammatory and traumatic diseases.
The introduction of FDG PET in combination with
MDCT resulted in further optimizing the diagnos-
tic work-up of oesophageal cancer and other
malignant diseases rendering this technique to be
the modality of choice depending on its availabil-
ity. In this book chapter we review the value of the
hydro-MDCT technique and hydro-FDG-PET-CT
technique in the diagnostic work-up of oesopha-
geal diseases.
1 Introduction
Cross-sectional imaging of the oesophagus is challenging due to its pathoanatomical morphology. The
oesophagus is a long tube, and poorly distensible,
with a close relationship to many vital organs. These
factors make the detection and staging of oesophageal
cancer difficult using the cross-sectional modalities.
In addition, the lack of a serosal layer of the
oesophagus facilitates the spread of the tumour into
surrounding organs (Ludeman and Shepherd 2005).
Furthermore, the first symptom of oesophageal cancer
is often dysphagia, which is a late manifestation, and,
at that point, a direct invasion of some vital organs is
almost always present, which renders these patients
inoperable (Smithers et al. 2010).
Using the multi-detector computer tomography
(MDCT) technology covering a large anatomic volume
with thin collimation, imaging of the entire oesophagus
in a single breath hold becomes possible with high
quality multiplanar reformation and three-dimensional
visualisation(Panebiancoet al. 2006; Ba-Ssalamahetal.
2009). Adequate distension of the oesophagus and
stomach, using water and effervescent granulate as a
negativecontrastagent,isaprerequisiteforassessingthe
oesophageal wall and gastrooesophageal junction (BaSsalamah et al. 2009, 2003). Proper contrast material
injection techniques (Mani et al. 2001) enhance further
the differentiation of pathologic tissue from normal
mucosa. Compared to endosonography, multi-detector
CT is able to demonstrate not only the immediate
vicinity of the oesophagus but also the infiltration of the
adjacent organs and the involvement of lymph node
regions or distant metastases (Choi et al. 2010). The
introduction of FDG-PET in combination with MDCT
resulted in further optimising the diagnostic work-up of
oesophageal cancer (Flamen et al. 2000;Koborietal.
1999). Therefore, it can be expected that PET/hydro-
MDCT will furtherincreasethe sensitivityand accuracy
in patients with oesophageal cancer for the initial diagnosis, stratifying patients in the proper therapeutic
options, monitoring during neoadjuvant chemotherapy
and for search of possible recurrence after treatment
(Sharma et al. 2011;Jeganathanetal.2011;Bradley
et al. 2012;Krauseetal.2009). Therefore, FDG-PET/
Hydro-MDCT can be considered as the primary
modality of choice if available.
2 CT and PET/CT Technique
CT examinations of oesophagus should be performed
on at least a 16-detector row CT with a 0.5 s tube
rotation. To acquire a near-isotropic data set, primary
sub millimetre (0.75–0.63 mm) thin collimation raw
data should be performed (Ba-Ssalamah et al. 2009).
For diagnostic viewing, reconstructions of 3–4 mm
thick axial sections directly from the scanning raw
data using the multiplanar reformation function of the
scanner console can be obtained. In addition, routinely coronal and sagittal reformation (with 3-5mm
slice thickness) along the entire oesophagus and the
stomach are performed (Panebianco et al. 2006; BaSsalamah et al. 2003). Contrast material injection for
the oesophagus and stomach is timed in a manner that
ensures capture of the arterial phase for imaging of
the oesophageal and gastric mucosa and evaluation of
possible associated hypervascular focal liver lesions
(Mani et al. 2001; Umeoka et al. 2010; Prokop 2005).
An additional portal venous phase examination of the
whole abdomen is performed for complete staging
purposes as well. In this protocol, the scanning range
includes the cervical region, chest, and the whole
abdomen.
For preparation either for hydro-MDCT as well
as for fused FDG-PET/hydro-MDCT, patients are
instructed to fast for at least 4-6 h prior to the
examination (Ba-Ssalamah et al. 2003). Additionally,
in case of combined FDG-PET/hydro-MDCT blood
glucose levels are measured before the injection of the
FDG tracer (Skehan et al. 2000; Haley et al. 2009).
The scanning starts after a resting period of at least
45 min post injection of the tracer (Kobori et al. 1999;
Weber et al. 2001). During this time period, patients
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are encouraged to drink 1.0-1.5 l of tap water in
order to distend the stomach and oesophagus. HydroMDCT scanning starts immediately after the ingestion of the last portion of tap water (250 ml) and
effervescent gas producing granules. Adequate distension of the oesophagus and stomach, using water
and effervescent granulate as a negative contrast
agent, is a prerequisite for assessing the wall of these
organs (Ba-Ssalamah et al. 2009; Ulla et al. 2010; BaSsalamah et al. 2011).
In case of simultaneous FDG-PET/hydro-MDCT
examinations, the patient remains on the examination
table for both scans. Emission PET-scans last between
3 and 5 min per bed position depending on the body
weight (Halpern et al. 2004; Nagaki et al. 2011;
Talanow and Shrikanthan 2010). Scans are corrected
for decay, scatter and randoms. There are various
reconstruction algorithms for PET images. The most
popular algorithm, ordered subset expected maximisation (OSEM), use CT-derived attenuation correction (Boellaard et al. 2001; Kontaxakis et al. 2002)
Axial and coronal reformatted scans of iodine contrast-enhanced hydro-MDCT are performed to match
the PET section thickness. The examination of hydroMDCT and fused FDG-PET is performed in the
supine position from the top of the head to the midthigh.
The use of FDG-PET yields physiologic information that provides a means for diagnosing cancer
based on altered tissue metabolism enabling co-registration of both anatomic and functional information
obtained by Hydro-MDCT (Bar-Shalom et al. 2005;
Rampin et al. 2005). FDG-PET takes advantage of the
principle that biochemical changes often precede or
are more specific than the structural changes associated with any given disease process (Luketich et al.
1997; Hsu et al. 2009). Therefore, fused FDG-PET/
MDCT offers the potential to show early oesophageal
cancer or small lymph node metastases before any
structural abnormality is detectable, or to exclude the
presence of tumour in an anatomically altered structure. The tumour uptake of FDG, measured as the
maximal standardised uptake value (SUVmax) in
FDG-PET, even provides a quantitative estimate of
tumour aggressiveness (Cerfolio and Bryant 2006).
Recent studies demonstrate that FDG-PET can be
used not only for pretreatment staging, but also for the
assessment of treatment response, detection of
recurrence, and prediction of survival in patients with
adenocarcinoma of the oesophagus (Hsu et al. 2009;
Cerfolio and Bryant 2006). FDG-PET/CT more
accurately shows the extent of disease than do other
imaging methods, and this frequently leads to a radical change in patient management.
3 Oesophageal Cancer
Oesophageal cancer is one of deadliest cancers
worldwide and is the sixth leading cause of death
from malignancies (Edwards et al. 2002). Recent
advances in the diagnosis, staging and treatment of
this neoplastic condition have led to small but significant improvements in survival. The lifetime risk of
developing this cancer is 0.8 % for men and 0.3 % for
women. The risk increases with age, the mean age at
diagnosis is 67 years (Edwards et al. 2002; Daly et al.
2000). More than 90 % of oesophageal cancers are
either squamous cell carcinomas or adenocarcinomas
(Edwards et al. 2002). Rarely, carcinomas of other
histologic types, including melanomas, gastrointestinal stroma tumours, carcinoids and lymphomas, may
develop in the oesophagus as well (Barr 2011).
Smoking is associated with an increased risk of both
squamous cell carcinoma and adenocarcinoma of the
oesophagus (Wu et al. 2001; Brown et al. 2001).
Individuals with recurrent symptoms of reflux have an
eightfold increase in risk for oesophageal adenocarcinoma (Lagergren et al. 1999). Barrett’s oesophagus
develops in approximately 5–8 % of patients with
gastrooesophageal reflux disease (Csikos et al. 1985).
The relatively low incidence of oesophageal cancer,
the absence of early symptoms, and the rarity of a
hereditary cause of the disease (Romero et al. 2002)
make prevention, surveillance, and evaluation-based
screening untenable except in certain high-risk areas
(Lagergren et al. 2000) of the world. Patients who are
found to have Barrett’s oesophagus, however, may be
candidates for regular endoscopic surveillance (Yang
et al. 2002).
Over the past 25 years, the nature of oesophageal
cancer has changed from primarily a squamous cell
neoplasm involving the mid-thoracic oesophagus in
50 % of patients, to adenocarcinoma of the gastro
oesophageal junction in nearly two thirds of cases
(Daly et al. 2000;Siewertet al. 2001; Parfittetal. 2006).
Once cancer develops, it may spread rapidly. Only 2 %
of T1 cancers, but 38–60 % of T2 cancers are
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Fig. 1 Hydro-MDCT of the
oesophagus in coronal (a) and
sagittal (b) reformations to
follow the course of the
oesophagus, demonstrating
the normal wall thickening of
the oesophagus (B3mm) and
homogeneous enhancement
(arrows). Note On the sagittal
reformation, the physiologic
angulation caused by the
aortic arch with
pseudothickening (partial
volume) of the oesophageal
wall (arrowhead)
associated with extension of thedisease to lymphnodes
(Siewert et al. 2001; Stein et al. 2005). Therefore an
accurate localstaging in termsof (T staging)has a great
impact on the therapeutic management (Ba-Ssalamah
et al. 2011). At the time ofthe diagnosis of oesophageal
cancer, more than 50 % of patients have either locally
unresectable tumours or radiographically detectable
metastases (Pennathur and Luketich 2008). Thus,
hydro-MDCT and even better combined PET/hydroMDCT (if available)helps to obtainan accurate staging
and consequently to choose the most appropriate
treatment option for those patients in a single examination (Wolf et al. 2011).
4 CT, PET/CT Imaging
of the Oesophagus
4.1 Tumour Detection and Classification
From a morphological point-of-view, oesophageal
carcinoma may manifest as a focal area of mural
thickening with or without ulceration, as a flat or
polypoid lesion, or as generalised mural thickening.
Since the thickness of individual layers of the normal oesophageal wall cannot be determined using CT
with certainty because of the variable distensibility of
its lumen, we use 3 mm as the upper limit of normal
(Fig. 1); any increase beyond this is considered
abnormal. Therefore, the following criteria, taken from
the literature (Umeoka et al. 2010; Halvorsen and
Thompson 1984; Moss et al. 1981; Lea et al. 1984;
Picus et al. 1983; Quint et al. 1985; Thompson and
Halvorsen 1994) and recently modified by Ba-Ssalamah et al. (Ba-Ssalamah et al. 2011), are used to
determine the CT-T stage, according to the TNM
classification (pT) adapted by the AJCC 7th edition
(Greene et al. 2002; Sobin and Wittekind 2002; Rice
et al. 2010).
T1: Focal or circumferential wall thickening of [3
and B10 mm and/or intense enhancement of the
oesophageal wall, without stenosis. The outer borders
of the tumour are smooth (Fig. 2).
T2: Focal, polypoid, or diffuse circumferential
thickening of the oesophageal wall [10
and B15 mm, with the possible presence of a mild
stenosis. The outer borders of the tumour are either
smooth or show stranding for less than one-third of
the tumour extension (Fig. 3).
T3: Tumour appears symmetric or asymmetric,
markedly diffuse or circumferential wall thickening
of C15 mm, with mild to severe stenosis, and marked
stranding for over one-third of the tumour extension,
or extensive blurring of the outer border (Fig. 4).
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These structures may be invaded by contiguous
tumour spread. However, it is often difficult to distinguish infiltration into these adjacent organs (T4)
from a broad contact without infiltration. Evaluation
for direct invasion by oesophageal cancer into adjacent vital structures by CT is based on two criteria:
mass effect and loss of fat planes. When the trachea or
bronchial wall is indented or displaced away from the
spine by a tumour mass, then mass effect is present
and invasion is presumed (Lagergren et al. 2000).
Coronal or sagittal reformatted images are best suited
for this purpose and seem to be helpful. The cardia is
directly involved by carcinoma of the distal oesophagus in about 60 % of patients according to the
Siewert classification (AEG I-III) (Fig 6) (Siewert
2007). The depiction of the anatomic location of the
tumour and assessment of the degree of cardia
involvement is crucial for the surgical strategy. This
is a key factor to define gastric fundus involvement,
since the stomach is the organ usually used as the first
choice for reconstruction after esophagectomy.
In case of using fused FDG-PET/hydro-MDCT,
tracer uptake is markedly helpful in the detection of
even a small primary tumour and may be better in the
estimation of its local staging and response to therapy
(Fig 7).
The sensitivity of FDG-PET for detecting primary
oesophageal tumours has been reported to be
91–95 % in prospective studies (Lowe et al. 2005;
Meyers et al. 2007) reported that 75 patients with
oesophageal cancer PET correctly assessed T stage in
43 %, understaged in 29 % and overstaged in 29 %.
Since PET scanners have a limited spatial resolution
of about 5–8 mm, lesions smaller than 1 cm might not
be detected, however, the combination of PET/CT
and hydro technique may improve its efficiency.
N Staging. Lymphatic spread is found in 74–88 %
Fig. 2 Hydro-MDCT of the oesophagus in axial (a) and
coronal (b) reformations shows a small focal polypoid lesion in
the distal third of the oesophagus, with homogeneous enhancement in terms of the T1 tumour (arrows). The outer borders are
smooth
of patients with oesophageal carcinoma because of
the abundant lymphatic vessels in the oesophagus
(Siewert 2007). The frequency of lymphatic metastases is related to the T local staging including the
size and depth of penetration of the tumour (Stein
et al. 2005). The extensive mediastinal lymphatic
T4: Tumour shows invasion into one of the adjacent structures, such as the pericardium, the diaphragm, the pleura (T4a), the tracheobronchial tree,
or the aorta and spine (T4b), using the criteria
described in the literature (Thompson and Halvorsen
1994) (Fig. 5).
drainage of the oesophagus, which communicates
with abdominal and cervical collateral vessels, is
responsible for the findings of mediastinal, supraclavicular, celiac lymph node metastases in at least 75 %
of patients (Thompson et al. 1983). According to the
American Joint Committee on Cancer (Suga et al.
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