The gastrointestinal tract Upper gastrointestinal tract
General considerations
Many authorities now advocate flexible oesophago-gastro-duodenoscopy (OGD) as the primary imaging modality in patients with upper gastrointestinal symptoms. In locations where endoscopy is freely available there has been a decline in the number of contrast studies performed. While some radiologists may strive to maintain their erstwhile role in the luminal GI tract, it is more appropriate to define strategies for the investigation of upper GI symptoms based on the relative strengths of radiology and endoscopy in given clinical situations. Moreover, it must be realised that in many parts of the world - both" developing" and "developed" - such pragmatic considerations as cost and availability will be the predominant factors in the choice of primary investigation. The advent of endoscopy has had the desirable side-effect of encouraging radiologists to optimize their own techniques with the development of double-contrast and then biphasic barium studies. There has also been a shift among GI radiologists towards functional or dynamic studies (for example videofluoroscopy of swallowing disorders) and imaging modalities such as CT and US that can de fine extramural disease.
In an attempt to best reflect the relative strengths of OGD and barium studies in patients presenting with various symptom complexes, Table 1 provides a suggested policy for primary investigation, the reasons for which are given in the appropriate sections of the following text.
Table 1.
Suggested primary imaging modality
Symptom complex BA OGD
| DYSPEPSIA * | | |
| "Simple" | + | |
| "Complicated" | | + |
| REFLUX OESOPHAGITIS | + | |
| DYSPHAGIA | + | |
| HAEMA TEMESIS/MELAENA | | + |
| PREVIOUS GASTRIC SURGERY | | |
| - for recurrent disease | | + |
| - for anatomy / emptying | + | |
Notes:
BA = barium study; OGD = oesophagogastroduodenoscopy
* Complicated dyspepsia is used here to indicate features which, when one or more are present, may be expected to be associated with a high prevalence of gastric pathology (thus requiring biopsy) and it is therefore rational for OGD to be the primary imaging modality. These features are:
Age> 40-45 years
Constant daily pain
Weight loss
Vomiting
Past history of gastric ulcer Previous gastric surgery
Absence of these features is denoted as "simple" dyspepsia.
Investigation of dysphagia
Dysphagia may be due to abnormalities of function (neuromuscular) or structure. Endoscopy and radiology are complementary investigations but a contrast swallow is the investigation of first choice since it allows dynamic study of neuromuscular function, as well as the detection of structural abnormalities in the pharyngo-oesophageal segment such as webs, that may be missed endoscopically, and diverticula that may present a hazard to endoscopy. In addition, mild strictures and Schatzki rings can be overlooked by modem thin-calibre fibrescopes. Radiology is often able to define the length of an endoscopically impassable stenosing lesion and to provide information about extrinsic compressions. Endoscopy will usually be required for biopsy of radiologcally demonstrated strictures and for radiologically negative dysphagia.
Although it is useful to distinguish abnormalities of the oropharyngeal and oesophageal phases of swallowing, it is recognized that the level of obstruction cannot reliably be determined by the patient's subjective site of "sticking". Up to one third of patients with oesophageal causes of dysphagia have symptoms referred to the neck. In addition, hypopharyngeal and oesophageal abnormalities often co-exist. Prominence of the cricopharyngeus (cricopharyngeal bars) and Zenker's diverticula are associated with gastro-oesophageal reflux and other distal abnormalities such as Schatzki rings and hiatus hernia; reflux may present with globus sensation, sore throat and hoarseness. A significant proportion of patients with gastro-oesophageal reflux present with pharhyngeal symptoms. Radiological examination therefore should include all phases of swallowing, although in practice the study is tailored to the patient's symptoms with emphasis on a particular region. In addition, gastric fundal lesions and even gastric outlet obstruction should be excluded, since these may present as "dysphagia".
Oropharyngeal swallowing - examination techniques
Ideally the examination should be recorded dynamically with cineradiography or videofluoroscopy, since the examination may then be replayed, frame by frame, to assess oropharyngeal function. In addition, subtle abnormalities such as webs may only transiently be visible during the passage of a liquid bolus. The use of a 105 mm camera is much less satisfactory; a frame rate of only 6 per second is usually obtainable.
Many centres have set up "dysphagia groups" - multidisciplinary special interest groups, comprising radiologists, speech pathologists, dieticians, neurologists, laryngologists, gastroenterologists, etc. - to assess patients with oropharyngeal swallowing difficulties. This is of particular importance where aspiration is a problem, not only in determining the cause and degree of dysfunction but, by testing the patient with various consistencies of bolus and assessing compensatory mechanisms, therapeutic and dietary manoeuvres can be instituted to minimise the problem.
A "routine" examination in a patient with dysphagia likely to be of oropharyngeal origin may be as follows:
1) If there is no history to suggest aspiration, anteroposterior and lateral
views of the pharynx at rest are obtained after coating with high-density barium. A lateral view is also taken with phonation of "eeee" or during a Valsalva manoeuvre to distend the pharynx. In certain patients vocal cord movement should be observed in frontal projection during phonation of "ee".
2) If the study is to particularly assess aspiration, the patient can be examined sitting in a special chair in front of the fluoroscopy table. Varying consistencies of bolus are used ranging from non-ionic iodinated contrast (ionic contrast such as Gastrografin must never be used if there is a risk of aspiration), through low-density barium, varying thicknesses of puree mixed with barium, to barium "cookies". Solid boluses are given with extreme caution if aspiration is seen with thinner liquids. The latter are more likely to be associated with aspiration. Some workers start with thicker and then gradually decreasing consistencies until the patient is seen to aspirate. The effect of head and/or body position and the use of ice may also be tested. In such a way it is possible to assess the type of dietary manipulation required in, for example, a stroke patient with swallowing difficulties, to allow discontinuation of nasogastric tube feeding while minimizing the risk of aspiration.
Videofluoroscopic recording allows review of:
- tongue movement and bolus formation
- palatal dysfunction which may result in posterior leakage into the pharynx from the mouth and nasal regurgitation-epiglottis and laryngeal movement during swallowing, particularly laryngeal elevation and closure and epiglottic tilt thus preventing laryngeal penetration and aspiration
- pooling and retention of contrast in the valleculae and/or pyriform fossae
- whether laryngeal penetration/aspiration is detected and cleared by the patient
- the temporal relationship of aspiration to swallowing (before, during or after)
- the function of the pharyngo-oesophageal segment which includes the cricopharyngeal sphincter - this must open completely in time with the passage of the bolus
Compensatory mechanisms employed by the patient should be observed, such as abnormal palatal descent to prevent posterior leakage and enlargement of Passavant's cushion.
3) Where the clinical features point to an oesophageal cause of dysphagia and the study is not specifically directed to assessing the oropharyngeal phase of swallowing, initial inspection of this phase prior to examining the oesophagus may be modified by asking the patient to take a small sip of high-density barium under fluoroscopy to exclude aspiration or major or high obstruction. As this results in coating of the oropharynx, frontal and lateral views of the pharynx may be obtained at this time. Detailed assessment of the oesophagus (see below) is then of ten best performed before returning to the examination of the pharyngo-oesophageal segment for functional and structural abnormalities with videofluoroscopy and/or rapid-sequence camera, since the lower density barium (100% w/v or less) used for the pharyngo-oesophageal segment sometimes interferes with coating by the high-density barium used for the double-contrast oesophagram. The pharyngo-oesophageal segment is examined in lateral, frontal and oblique projections with liquid boluses. Evidence of cricopharyngeal dysfunction is looked for, as well as structural abnormalities such as webs and diverticula. Sometimes solid boluses (marshmallows or barium-soaked bread, for example) may be indicated to show hold-up due to subtle strictures or webs.
Oropharyngeal dysphagia: pathologic conditions
Neuromuscular diseaseMany patients requiring assessment have been victims of stroke or head injuries. Bulbar palsy leads to a lower motor neurone lesion resulting in abnormality of the pharyngeal phase of swallowing. Pseudobulbar palsy affects the upper motor neurons and primarily causes problems with oral initiation of swallowing. Disorders of deglutition affect 20-40% of patients with unilateral stroke.
It is seldom possible to diagnose specific diseases from the radiographically observed dysfunction of swallowing, but one can of ten determine the pathophysiological mechanisms involved. Some specific neuromuscular disorders and the observed signs at videofluoroscopy are shown in Table 2.
Table 2.
Some specific neuromuscular diseases associated with oropharyngeal dysphagia.
Disease Notes/radiographic abnormality
| Motor neurone disease (ALS) |
Oropharyngeal muscle atrophy
Pharyngeal paresis
Nasopharyngeal regurgitation
Airway penetration
Compensatory extension of head/neck |
| Multiple sclerosis |
Dependent on site and extent of demyelination |
| Parkinson's disease |
"Dysphagia" common. Dysfunction of oral initiation i.e. bolus formation; hesitancy and repetitive tongue movement; delayed swallow reflex; vallecula pooling and airway penetration; aspiration may be "silent".
|
| Poliomyelitis (bulbar) |
Pharyngeal muscle paresis; aspiration. Pharyngeal muscle atrophy in "post-polio syndrome".
|
| Myasthenia gravis |
Fatiguing of pharyngeal muscles during repetitive swallowing. |
| Myopathies |
May affect bulbar muscles. Striated muscles of cervical oesophagus may also be affected with reduced peristalsis. Cricopharyngeal "chalasia" in myotonic dystrophy. |
|
Figure 1.
Cricopharyngeal webs extending from the anterior wall at level indicated by large arrow. Note “jet" phenomenon below the webs and prominent cricopharyngeus impression posteriorly (white arrow).
|
|
Figure 2.
Cricopharyngeal diverticulum (arrowed). Note marked associated prominence of cricopharyngeus and luminal narrowing. |
Structural abnormalities
Cricopharyngeal prominence ("pharyngeal bar'')
The posterior indentation at approximately C5/6 level by cricopharyngeus muscle normally effaces as a bolus passes through. Mild persistent indentation may be normal but more obvious prominence may be seen in some patients with dysphagia (Figs. 1, 2). There is association with distal oesophageal disease, especially gastro-oesophageal reflux (GOR), and other pharyngeal abnormalities. A spectrum of cricopharyngeal abnormalities can be seen with GOR. It is likely that acid reflux leads to oedema, spasm and/or hypertrophy of cricopharyngeus; this in turn raises pharyngeal pressure proximal to the upper oesophageal sphincter and hence the association of GOR with a (usually small) pulsion-type Zenker's diverticulum. Other causes of cricopharyngeal prominence include intrinsic cricopharyngeal disease, and neuromuscular diseases affecting the oropharynx.
Cricopharyngeal webs
These mucosal folds occur on the anterior wall at the hypopharynx/oesophagus junction. Often they are thin and asymptomatic, but they may be circumferential and cause luminal narrowing (Figs. 1 and 14). A characteristic "jet effect" may be seen on contrast swallow when a large bolus passes through a web. Differentiation must be made between webs and the submucosal venous plexus which is a normal structure on the anterior wall. The latter causes an impression that is effaced as the bolus distends the lumen. Large boluses and dynamic imaging, such as videofluoroscopy, may be required to detect webs since they may appear transient during a contrast swallow. Sometimes webs are associated with iron-deficiency, glossitis and pharyngeal atrophy (Plummer-Vinson or Paterson-Kelly syndrome). Web-like stenoses may also be seen in various bullous skin diseases, such as epidermolysis bullosa.
Pouches and diverticula
The most significant lesion is the hypopharyngeal (Zenker's ) diverticulum, that occurs at the junction of hypopharynx and oesophagus at Killian's dehiscence between the horizontal and oblique fibres of the cricopharyngeus muscle (Fig. 2). This pulsion diverticulum starts posteriorly and enlarges posterolaterally, usually to the left. Dysphagia occurs as the pouch fills preferentially with food and obstructs the lumen of the oesophagus. There is typically regurgitation of pouch contents and, of ten, aspiration as the pouch overflows. A plain radiograph of the thoracic inlet may show an air-fluid level in the diverticulum. There is usually a prominent cricopharyngeal impression, which may be related to the association with raised pharyngeal pressure which causes the diverticulum. The association with distal oesophageal disease, particularly gastro-oesophageal reflux, has been described above.
Lateral pharyngeal protrusions (pharyngoceles or ears) extend from the tonsillar fossae, valleculae or pyriform sinuses. They are not usually true diverticula, are rarely of significance and are associated with glassblowing and trumpet-playing. True lateral diverticula are rare and may communicate with the lumen by a neck. Lateral diverticula may also arise at the pharyngo-oesophageal junction in a weak triangular area caudal to the transverse portion of cricopharyngeus muscle; this corresponds to the passage for the inferior laryngeal nerve.
Pharyngeal tumours
The large majority are carcinomas. They may be diagnosed endoscopically, but radiographically they are best seen on double contrast pharyngograms as masses within the lumen and/or deformity. Smaller lesions may be demonstrated as irregularities of the mucosa. Multiple projections are needed for optimal demonstration, including distended views as described above. CT is useful for staging.
Pharyngeal foreign bodies
In adults most commonly the problem is one of an impacted fish or chicken bone. A lateral radiograph of the neck taken at soft tissue exposure may show a radio-opaque foreign body, but many such bones are poorly opaque. Evidence of perforation should be sought, including extraluminal gas and widening of the prevertebral soft tissues. A contrast swallow is performed with a small volume of low-density barium, or water-soluble non-ionic contrast if perforation is suspected. If no foreign body is seen, a small cotton ball or marshmallow soaked in barium may show it.
The oesophageal phase of swallowing - examination techniques
Contrast studies
The examination is multiphasic - double-contrast erect views to show mucosal detail; single-contrast distended views to best show strictures, rings and hiatus hernias; single boluses with the patient recumbent to assess motility; occasionally mucosal relief views for varices and oesophagitis. If the examination is part of a study of the stomach and duodenum, it is best to complete the double-contrast views of these organs before returning to the oesophagus to perform the single-contrast phase, since the thinner barium used for the latter will interfere with obtaining the optimum coating of the stomach and duodenum.
Evidence of gastro-oesophageal reflux is also sought. Spontaneous reflux during the examination is noted. If this does not occur, reflux is provoked by tilting the patient head down and then by turning the patient from prone to supine, left-side down to fill the gastric fundus with barium, and then supine LAO to submerge the cardia. If no reflux occurs, a water-siphon test is undertaken. Many normal individuals will reflux a little contrast in this situation, but will rapidly clear the oesophagus again in a swallow or two. True "refluxers" on the other hand tend to have less effective peristalsis and delayed clearance.
Hypotonic drugs commonly used in upper GI barium studies have an effect on oesophageal motility and/or the lower oesophageal sphincter, and should therefore be avoided when the primary purpose of a study is to assess these functions. Hyoscine butylbromide (Buscopan) reduces peristalsis and decreases lower oesophageal sphincter pressure. Glucagon has little effect on oesophageal motility but also reduces sphincter pressure.
Radionuclide scintigraphy
Radionuclide oesophageal transit studies provide a simple, cheap and
Non-invasive method of diagnosing motility disorders as well as unique quantitative information on oesophageal emptying. Boluses of 99mTc-sulphur colloid are given diluted in water, and time-activity curves generated over different segments of the oesophagus and the stomach are obtained. Although good sensitivity and specificity have been reported compared with manometry, some authors have questioned the reliability and reproducibility of the technique.
Oesophageal manometry
This study remains the gold-standard for oesophageal motility disorders, but is not widely available. Contrast studies, performed as outlined above, correlate well with manometry and provide a satisfactory screening examination in most situations.
Normal oesophageal motility
Primary oesophageal peristalsis is induced by a swallow at the pharyngo-oesophageal junction. Caudad progression of a bolus is achieved by a wave of inhibition preceding the bolus and a wave of contraction behind it. This is seen radiographically as a V -shaped stripping wave. Normally all of a liquid bolus is stripped, but some proximal escape may be seen at the level of the aortic arch even in normal individuals, which is then cleared by secondary peristalsis. This phenomenon increases in frequency with age. The lower oesophageal sphincter (LOS) segment is 34 cm in length and is an area of high resting pressure (which aids in the prevention of gastro-oesophageal reflux) that falls prior to the arrival of a bolus to allow its passage. In some normal individuals a little retrograde propulsion of the bolus occurs at the sphincter. As the LOS segment relaxes and distends with the bolus the lower oesophageal ampulla is seen radiographically. Secondary peristalsis is also a propulsive wave that occurs to clear the oesophagus of any retained bolus. This is induced by oesophageal distension and initiates around the level of the aortic arch. Tertiary contractions are non-propulsive and cause a variable degree of narrowing of the lumen. Non-segmenting contractions occur in a significant proportion of swallows in normal individuals, but increase with age and in conditions that increase the irritability of the oesophagus, such as oesophagitis. Segmenting tertiary contractions that obliterate the lumen are almost invariably associated with disorders that significantly affect primary peristalsis.
Oesophageal motility disorders
The barium swallow is a simple and sensitive method of assessment of oesophageal motility and has been shown to correlate very well with the "gold-standard" of oesophageal manometry. Patients with motor disorders of the oesophagus present with dysphagia and/or chest pain. Primary disorders of oesophageal motility include achalasia, diffuse oesophageal spasm, nutcracker oesophagus, and a collection of conditions grouped as a "non-specific oesophageal motility disorder" (NEMD - with which presbyoesophagus may be included). In addition, there is a miscellany of often systemic conditions that cause secondary motility disorders, including systemic sclerosis (CREST syndrome), diabetes and neurological
|
Figure 3.
Longstanding achalasia with complicating squamous oesophageal carcinoma. Note dilated lower oesophagus with beaking of gastro-oesophageal junction and hold-up of barium above. There is an extensive irregular neoplastic mass in the proximal oesophagus causing luminal narrowing and thickened folds, and displacing the trachea anteriorly (arrows). |
disorders, Reflux oesophagitis is associated with disordered motility, including diminished peristalsis, delayed bolus clearance and decreased LOS pressure. Debate continues as to whether this is secondary or whether "refluxers" have a primary oesophageal motor disorder. A significant number of patients with "atypical" non-cardiac chest pain prove to have GOR or oesophageal motility disorders.
Achalasia can present at any age but is commonest in the 30-50 year age group. Dysphagia may initially be intermittent and eventually is persistent. Patients often develop manoeuvres to empty the oesophagus and relieve symptoms. Oesophageal dilatation is mild in the early stages, which may make radiographic diagnosis difficult, but is progressive. On plain radiography there may be an air-fluid level in the oesophagus, the level of which reflects the degree of hold-up above the LOS and thus
 a | Figure 4.
Endoscopic ultrasound images in patient with pseudo-achalasia due to carcinoma at the GOJ. (a) asymmetrical transmural tumour (T). Concentric rings are artefacts from the endoluminal probe within the oesophagus (oe); ao=aorta. (b) peri-oesophageal nodal metastases (N). Note circumferential oesophageal wall thickening due to tumour with loss of normal ultrasonic layers (compare with Fig. 8). |
 b |
severity. A gastric air bubble is often absent. Contrast swallow with the patient erect demonstrates a variable degree of dilatation of the
oesophagus above a beak-like narrowing at the lower oesophageal sphincter. The sphincter opens intermittently under the force of the hydrostatic pressure of the
barium column above it to allow bolus passage. The distal two-thirds of the
oesophagus, which contains smooth muscle, is aperistaltic. The abnormalities of peristalsis and of the sphincter are present even in the early stages of the disease. A variant known as "vigorous achalasia" is described in which there are repetitive tertiary contractions which may be associated with chest pain; the degree of dilatation is typically less with this variant. Some authors dispute its existence as a separate entity. There is an increased incidence of squamous
carcinoma of the
oesophagus in achalasia (Fig. 3).
Secondary or pseudo-achalasia is a syndrome similar to achalasia due to tumours at or around the gastro-oesophageal junction and is related to destruction of the intramural myenteric plexus. The commonest cause is adenocarcinoma of the stomach. A mass may be detected on imaging by endoscopic ultrasound (Fig. 4) or computed tomography. Amyl nitrite inhalation may also distinguish true from pseudo-achalasia, having no effect on the sphincter in the latter. Rarely other tumours may cause secondary achalasia as a non-metastatic manifestation of malignancy. Infestation with Trypanosoma cruzi (Chagas' disease) causes a disorder identical to idiopathic achalasia.
Diffuse oesophageal spasm presents with intermittent dysphagia and/or chest pain. Radiographically there are segmenting tertiary contractions ("corkscrew" oesophagus; Fig. 5) interspersed with normal peristaltic waves (c.f. vigorous achalasia). The diagnosis should only be made in the absence of gastro-oesophageal reflux, since this can lead to a similar pattern of contractions. Also, it should be noted that similar appearances can be seen in asymptomatic elderly patients (presbyoesophagus).
Nutcracker oesophagus is not a radiological diagnosis. There are supernormal high amplitude primary peristaltic contractions seen on manometry which have no radiological correlate; patients present with atypical chest pain. Presbyoesophagus is a term best reserved for asymptomatic elderly patients with abnormalities of motility which include diminished primary peristalsis, tertiary contractions and delayed transit.
Non-specific oesophageal motility disorder (NEMD) is a miscellany of abnormalities of oesophageal contractions and LOS behaviour seen in patients with dysphagia and/or atypical chest pain which cannot be easily categorised into any of the above disorders.
Systemic sclerosis/CREST syndrome involves the oesophagus and is associated with LOS incompetence allowing free reflux and resultant oesophagitis. There is absent peristalsis in the smooth muscle part of the oesophagus and often mild oesophageal dilatation. As a consequence of the severe oesophagitis, strictures occur frequently associated with Barrett's mucosa. Sacculation may be seen in the region of the stricture
 | Figure 5.
Multiple tertiary segmenting oesophageal contractions - "corkscrew oesophagus". |
Structural causes of oesophageal dysphagia
Benign stricturesCommoner causes of oesophageal strictures are listed in Table 3. Varieties of peptic strictures are dealt with under
Gastro-oesophageal Reflux Disease. Radiation, caustic and post-infective strictures are described in the relevant sections. BuIlous skin diseases, especially epidermolysis buIlosa and pemphigoid, are associated with proximal oesophageal strictures or web-like narrowing.
Table 3.Causes of oesophageal strictures
Benign Site Features, comments
| Peptic | | |
| reflux oesophagitis | distal, near GOJ, above hernia | smooth tapering |
| Barrett's oesophagus | more proximal | deep ulcer; reticular mucosa |
| Nasogastric intubation | distal | long strictures; history |
| Schatzki ring | GOJ | symmetrical 2-4 mm long
|
| Caustic | single or multiple, long | history |
| Radiation | related to portal | tapered, history |
| Skin diseases | high
| strictures or webs; bullous diseases
|
| above left atrium | history, enteric KC1 especially |
| Post-infective | usually mid | Candida, TB |
| Benign tumours | variable
| submucosal lesion;
smooth muscle
tumours commonest |
MalignantCarcinoma Leiomyosarcoma
Extrinsic
Lymphoma
Benign tumours
Benign mucosal tumours do not cause luminal narrowing. The commonest are squamous papillomas seen as small polypoid lesions on double contrast radiography. Submucosal benign tumours are much more common; the vast majority of the se are leiomyomas. Unlike their counterparts elsewhere in the GI tract, oesophageal smooth muscle tumours are hardly ever malignant, nor do they ulcerate. They may be an incidental finding or cause dysphagia. Being of smooth muscle origin they occur in the mid or distal oesophagus. In profile they appear radiographically as smooth filling defects with right angle or slightly obtuse re-entrant angles at their borders. En face, the tumour appears to widen the lumen. Endoscopic ultrasound is useful in confirming the diagnosis. Other benign submucosal tumours (fibromas, neural tumours, duplication and retention cysts, lipomas) are rare.
 | Figure 6.
Ulcerating and stricturing squamous carcinoma of the distal oesophagus. Note shouldered margins. |
Oesophageal carcinoma
Radiology has an important role in diagnosis, staging and post-treatment follow-up of this common neoplasm.
Diagnosis
Most neoplasms are squamous carcinomas; the minority are adenocarcinomas arising in Barrett's oesophagus. Most patients present with advanced disease. Tumours are infiltrating (irregular narrowing with nodularity +/- ulceration and shouldered margins), polypoid (intraluminal fungating), ulcerative (relatively flat with ulceration), varicoid (resembling varices, with thickened serpiginous folds due to submucosal spread) or a mixture of any of these types (Figs. 3 and 6). Satellite lesions may be seen due to vertical submucosal spread. Occasionally "early" lesions are seen as small protrusions, plaque-like lesions with or without ulceration, sessile polyps or focal nodules. A superficial spreading variety is also se en, comprising coalescent raised lesions and/or shallow ulceration. In most cases of advanced carcinoma the radiological diagnosis can confidently be made. All lesions, however, should be subjected to endoscopy, biopsies and cytological brushing.
Staging
While surgery remains the mainstay of treatment in resectable carcinoma and arguably provides the best palliation for squamous and adenocarcinoma, palliative surgery is associated with significant morbidity and mortality. Other treatment options are becoming more widely accepted. These include chemo/radiotherapy (which may be used preoperatively or palliatively in combination with endoscopic techniques to provide patency); endoscopic laser treatment and endoscopic stenting, including the use of the new metallic expandable stents. Therefore, the purpose of staging is to assess local resectability and, in those patients treated by non-operative means, to direct therapeutic options and provide baseline information and monitoring. Ideally accurate staging should prevent unnecessary surgery in those patients with unresectable tumours, while not denying surgery to those with potentially curable lesions. Staging is directed to the determination of depth of wall penetration, invasion of adjacent structures (tracheobronchial tree, pericardium or aorta), involvement of regional nodes and distant metastases.
Computed tomography and endoscopic ultrasound are the most accurate methods of staging oesophageal carcinoma. Occasionally the multiplanar imaging potential of MR may be advantageous. Although CT is far more widely available the results for T and N staging have been largely disappointing. This is particularly true for gastro-oesphageal junction carcinomas. Estimation of local spread at CT depends on the identification of transgression of mediastinal fat planes. Unfortunately, these planes are often lacking in these frequently wasted patients. Wall thickening beyond the normal of 3 mm is non-specific, and may represent tumour or benign disease. Demonstration of the depth of wall invasion is not possible at CT. In addition, identification of nodal metatasis is entirely dependent on the visualisation of enlarged nodes, those with a short-axis length greater than 10 mm being taken as abnormal. CT can demonstrate local invasion of the tracheobronchial tree, seen as impingement or bulging of the posterior wall of the carina or left main bronchus; tumour abutment alone is not a specific sign. Identification of aortic involvement is more difficult. Picus showed that if there is an arc
 | Figure 7.
CT at level of carina showing asymmetrical mass (m) of oesophageal wall in contact with descending aorta over arc of approximately 90 % (arrows) indicating tumour invasion is likely. |
of contact of 90° or greater between the
tumour and
aorta, then invasion is very likely (Fig. 7). Less than a 45 degree arc means no invasion. Unfortunately, a large group of tumours are indeterminate. Loss of the triangular fat space between
oesophagus,
aorta and
spine has been reported to be a reasonably accurate predictor of aortic invasion. The
CT protocol should be directed towards local staging and identifying distant metastases. Distention of the
oesophagus with gas is useful as well as, occasionally, decubitus scans. A
dynamic incremental scanning technique with
intravenous contrast is used to detect liver metastases. EUS has been found consistently superior to