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
CT in T and N staging, but is of limited availability. The accuracy of EUS in T staging is due to the fine detail achievable in imaging the 5-layer structure of the wall. This structure is a constant finding in the normal upper GI tract (Fig. 8).
A review of several studies showed EUS to be 85% and 75% accurate and CT to be 60% and 74 % accurate in the T and N staging, respectively, of oesophageal carcinoma (although there is an indication that improved equipment and techniques may be leading to better CT results). There are two major drawbacks to EUS staging. Firstly, stenosing lesions can
 | Figure 8. Normal endoscopic ultrasound appearance of stomach wall, showing 5 layer structures; b=wall of waterdistended balloon used for acoustic coupling. Concentric rings are scanning artefacts from endoluminal transducer. 1 and 2=mucosal layers; 3=hyperechoic submucosa; 4=hypoechoic muscularis propria; 5=adventitia/serosa. (Reproduced with permission of Australasian Radiology). |
not be passed by the EUS endoscope in up to about 50% of patients. Although this can be a problem, often in practice staging of only the proximal aspect of these stenosing tumours is not associated with much inaccuracy, since the advanced nature of these lesions can still be discerned. "Miniprobes" are now available which can be passed through the
biopsy channel of a conventional flexible endoscope and thence through a stenotic oesophageal
lesion, but experience with these is as yet relatively limited. The second problem with EUS is the difficulty in distinguishing
benign from
malignant nodes, thus reducing the
specificity of N staging.
Specificity for nodal malignancy ranges from 54 to 72 %. With the exception of coeliac
lymph nodes, which are classified as distant metastases in oesophageal
carcinoma, M staging with EUS is not possible, only limited views of the liver being obtained. A combination of EUS and
CT is thus required for complete TNM staging. EUS may also be used to monitor response to chemo/
radiotherapy of oesophageal
carcinoma and the detection of submucosal recurrence following surgery.
Oesophageal bolus obstruction
In adults, bolus obstruction is usually related to a lump of meat or ingested bones but there is often an underlying motility disturbance or stricture. The impacted material is obvious on a contrast swallow. Water-soluble contrast medium should be used initially if perforation is suspected. Even when this is not the case it is probably best to use non-ionic water soluble contrast, since if there is complete obstruction the patient is at risk for aspiration. In addition, endoscopy is usually required to remove the bolus, and the presence of barium in the oesophagus obscures endoscopic view. Various "radiological" manoeuvres have been attempted to facilitate onward passage of the bolus. A hypotonic agent may be given to relax the oesphagus combined with an effervescent agent. Although Glucagon has been most of ten used, some authors advocate Buscopan since this relaxes the oesophageal body as well as the LOS. There is a potential danger to this technique as overdistension may lead to oesophageal laceration. Once the acute episode is over and spasm and oedema have settled the patient should be investigated for underlying oesophageal pathology.
Gastro-oesophageal reflux (GOR) disease
Most patients with symptoms of GOR disease do not require investigation. Indications for investigation include: if the diagnosis is in doubt; for exclusion of co-existent gastro-duodenal disease; failure of response to conventional medical treatment; imaging of complications. Since each of the various modalities available tends not to address all of the aspects of GOR disease, patients who do require investigation often are subjected to a combination of complementary tests. Investigations are directed towards answering several interrelated questions.
Is reflux present? Is there oesophageal dysmotility?
The gold-standard for assessment of reflux episodes is ambulatory pH monitoring. However, this is not universally available. Scintigraphy using 99mTechnetium sulphur colloid provides a test of acceptable sensitivity and specificity compared with pH monitoring and is superior to contrast radiography in this aspect, although some authors have expressed doubts regarding its specificity. Assessment of reflux at barium studies should be directed not only towards the identification of reflux, but also towards the rate and efficiency of clearing of the refluxate from the oesophagus, abnormality of which may point to an associated motility disorder. All individuals have episodes of reflux associated with transient falls in LOS pressure but are able to clear the refluxate rapidly. Most
 | Figure 9.
Relatively mild reflux oesophagitis. Note "smudged" appearance of mucosa and thickened longitudinal folds. In this patient there is a small hiatus hernia and mild stricture (arrowed). |
patients with symptomatic reflux have normal LOS pressure but exhibit diminished clearance. There is controversy as to whether this represents a primary oesophageal motor disorder (for which there is recent evidence) or is secondary to associated oesophagitis. A proportion of symptomatic refluxers have reduced gastric emptying. Other oesophageal motility disorders seen in GOR include an increase in frequency of tertiary contractions - usually non-segmenting, but occasionally segmenting, in which case differentiation from
diffuse oesophageal
spasm must be made in older patients - and transient contractions of the muscularis mucosae leading to
transverse striations, so- called oesophageal "shivers" or "feline"
oesophagus.
Spontaneous reflux during a barium study is seen in less than 50% of symptomatic refluxers. When seen it correlates well with symptomatic GOR. However, as stated previously, it can occasionally be se en in normal individuals and, therefore, it is necessary to assess oesophageal clearance when it occurs. The oesophagus should be c1eared in two or three swallows at twenty-second intervals when the patient is slightly headdown. If spontaneous reflux is not seen, a provocation test may be performed. Unfortunately, all such manoeuvres, while increasing sensitivity, also significantly decrease specificity. Many radiologists have ceased using them. The water siphon test is the simplest that may be performed; a small amount of reflux is often seen in normals and once again, volume clearance of any refluxate must be assessed. Recent evidence suggests that combining identification of reflux with abdominal compression with a measurement of the internal calibre of the oesophagus at the cardia of greater than 2.5 cm gives an accuracy of 80% for GOR.
Is there oesophageal injury?
Endoscopy and/or contrast radiography are used to image oesophagitis and the other complications associated with GOR.
Oesophagitis
Endoscopy is superior to radiology in the diagnosis of oesophagitis. Barium studies are accurate for moderate and severe grades of oesophagitis, but are insensitive for mild oesophagitis and also are associated with significant false positives. The technique should be multiphasic, including double- and single-contrast examinations. Although double contrast films best demonstrate ulceration, most false-positives occur due to over-reading of thickened folds and granular mucosa. The mildest changes of oesophagitis (Fig. 9) include a loss of smoothness, or "smudging" of the mucosal surface, a finely nodular or granular mucosal pattern in the distal third of the oesophagus and oedematous longitudinal folds (exceeding 2 mm in thickness in the distended oesophagus or 3 mm on mucosal relief films). The granular pattern must be distinguished from Candida oesophagitis which tends to be better defined, from glycogenic acanthosis (a normal finding manifest as well-defined, usually small nodules, more prominent in the mid-oesophagus) and from undispersed effervescent agent. A characteristic oesophago-gastric fold may be seen, consisting of a prominent gastric fold continuing proximally to the
 | Figure 10.
Reflux oesophagitis showing nodular, mildly narrowed distal oesophagus with sacculation above a hiatus hernia (arrowed). |
squamocolumnar junction where it may appear as a
polypoid lesion. This is inflammatory in nature and probably represents localised
gastritis. However, the appearance is often sufficiently worrying to warrant
endoscopy and
biopsy to exclude
tumour.
More severe changes include restricted distensibility, due to spasm and oedema, and punctate erosions or linear ulcers, often with a radiolucent halo of oedema. Other causes of ulceration, such as opportunistic infections and drugs tend to produce their own patterns (see below). The severest grades of oesophagitis (Figs. 10-12) demonstrate multiple erosions or ulcerations, plaque-like "pseudomembranes" which may mimic candida
 | Figure 11.
Hiatus hernia (diaphragrnatic hiatus arrowed), tapered peptic stricture, and oesophageal ulceration (white arrows). |
 | Figure 12.
Barrett's oesophagus. Stricture above the GOJ with associated moderately large ulcer (arrowed). The oesophagus above the stricture is nodular with thickened folds indicating oesophagitis. Below the stricture there is a reticular rnucosal pattern. |
or infiltrative
carcinoma, nodularity, a severely distorted scarred mucosal pattern and strictures. Scarring may lead to stricturing, sacculations or wall puckering.
Strictures and rings
Radiology can demonstrate subtle strictures and Schatzki rings, which may be missed with modem "skinny" endoscopes. Although symptoms of dysphagia may be due to reflux oesophagitis without stricture formation, such a history without obvious narrowing on the semi-prone single contrast views taken with maximal distension with a liquid bolus, should lead to an examination with marshmallows or a bread bolus. Most reflux-associated strictures occur in the distal oesophagus near the gastrooesophageal junction. A hiatus hernia is almost invariably present. Typically, the stricture is smooth and tapered in appearance (Fig. 11). It is reasonable policy that most strictures should be inspected endoscopically and biopsied to exclude malignancy. This is certainly true if there is asymmetry and irregularity. More proximal strictures should raise the possibility of Barrett's oesophagus (Fig. 12).
A typically long distal oesophageal stricture may be seen in patients who have had a nasogastric tube in situ. While this usually occurs after relatively prolonged intubation, and is probably due to reflux, sometimes stricturing is seen after a short episode.
Schatzki rings are mucosal rings at the gastro-oesophageal junction. Although recent evidence suggests that these rings may not be associated with GOR, it is convenient to consider them here. They have a characteristic appearance, being symmetrical with a longitudinal extent of no more than a few millimetres, and they will be missed radiologically if only erect double contrast views are obtained. Full column semi-prone head-down views are required (Fig. 13); an examination with a solid bolus may be needed. They may be asymptomatic or be associated with intermittent bolus obstruction. As a general rule, rings with a calibre of 13 mm or less tend to be symptomatic. Oesophageal webs, occurring more proximal than Schatzki rings, may also be associated with GOR.
Barrett's (columnar-lined) oesophagus
In Barrett's oesphagus there is progressive columnar metaplasia of the distal oesophagus associated with chronic GOR and oesophagitis. Its importance is in its malignant potential; dysplastic change is the precursor
 | Figure 13.
Schatzki ring at the GOJ shown on single contrast fuli-column view with patient semiprone. The lesion was not visible on a double contrast erect oesophagogram. |
of oesophageal adenocarcinoma. This usually occurs around the squamocolumnar junction.
Endoscopic surveillance, with multiple biopsies, is increasingly recommended to detect severe dysplasia and early neoplastic change. Barrett's
oesophagus has been more frequently recognised in recent years. A prevalence of about 10% is reported in patients investigated for GOR. Contrast oesophagography is insensitive in the diagnosis, but there are features which may be identified which put the patient in a high risk group, and should be reported as such. These features are: a "high" stricture, i.e. 5 cm or more proximal to the
gastro-oesophageal junction; u1ceration (especially deep) in the body of the
oesophagus; a reticular mucosal pattern, especially when located immediately distal to a stricture (Fig. 12). The last sign was originally reported as highly specific for Barrett's
oesophagus, but this has been questioned; it is also an insensitive sign, being present in 5-30%. The presence of a distal peptic stricture and/or reflux oesophagitis p1aces the patient in a moderate risk category for Barrett's
oesophagus, one study reporting a 16% incidence in this group.
Oesophageal intramural pseudodiverticulosis
This is an uncommon condition of somewhat obscure aetiology which is probably part of the spectrum of GOR disease. Multiple tiny flask-like outpouchings are seen in the wall of the oesophagus which represents dilated ducts of mucus glands (Fig. 14). They may be diffuse or segmental and may only be seen on single-contrast, only entry of the thinner barium into the invaginations being possible. The great majority of cases are associated with strictures, of ten of the proximal oesophagus. Outpouchings may be localised to the area of the stricture. A case of perioesophageal abscess has been reported in this condition.
Is there a hiatus hernia?
The presence or absence of a hiatus hernia is really only relevant in two respects. Firstly, if surgery is contemplated for GOR disease. Secondly, it is unusual for the more severe grades of oesophagitis to be present in the absence of a hiatus hernia. The exact relationship of hernias to GOR disease is uncertain. The presence of a hernia appears to facilitate reflux. On the other hand, when severe oesophagitis has been present for some time, longitudinal scarring of the oesophagus may lead to shortening and the appearance of a hernia. Radiology is more sensitive than endoscopy for the demonstration of hiatus hernia. However, a small hernia can be demonstrated in a large number of normal individuals, especially in the semiprone head-down position. Oesophagitis is present in only a small number of subjects with hiatus hernias. It has been suggested that hiatus hernias should be ignored unless they are present at rest in the supine position.
Are the symptoms due to reflux?
This largely lies outside the ambit of the radiologist. Oesophageal pH monitoring can correlate symptoms with objective episodes of reflux, and may pinpoint the cause of symptoms in patients without overt oesophageal lesions. A Bernstein test can be performed, when the response of the patient can be assessed to the instillation into the oesophagus of dilute hydrochloric acid. Acidified barium can occasionally be used, and
 | Figure 14.
Intramural pseudodiverticulosis of the upper oesophagus (arrows) with associated stricture. Note also cricopharyngeal web (arrowheads). |
 | Figure 15.
Candida oesophagitis (HIV positive patient). Multiple linear punctate and comma-shaped plaques are shown in longitudinal orientation. |
is sometimes useful in patients with globus pharyngeus; observed reflux of acidified
barium may mimic the patient's symptoms.
Non-reflux related oesophagitis
Infectious oesophagitis
Opportunistic infections of the oesophagus usually occur in immunocompromised individuals. They have been increasingly associated in recent years with HIV infection (AIDS). Main causes are Candida, Herpes simplex and Cytomegalovirus (CMV). Candida oesophagitis is of ten associated with oral candidiasis. Double contrast oesophagography demonstrates, with a 90% sensitivity, discrete plaques or small nodules, usually in the proximal or mid-oesophagus. These are typically separated by normal mucosa and may be orientated in the long axis of the oesophagus (Fig. 15). Severe infection, as sometimes seen in HIV patients, manifests as a diffuse "shaggy" oesophageal contour due to plaques and pseudomembranes, especially seen when the lumen is collapsed. Herpex simplex oesophagitis causes discrete superficial ulcers of various shapes, often stellate and often surrounded by a halo of oedema in the mid-oesophagus on a background of normal mucosa. Clustering may occur. This entity may occasionally be seen in immunocompetent patients and requires differentiation from medication-induced oesophagitis (see below). The history will usually help.
CMV oesophagitis is usually associated with AIDS. Although the radiological picture may be indistinguishable from herpes oesophagitis, the appearance in other patients is more typical; flat, large ulcers are seen with associated oedema. Giant ulcers may be present up to several centimetres in size. It is now recognised that the HIV virus itself may cause discrete oesophageal ulceration relatively early in the course of the disease. Tuberculous oesophagitis is rare and is characterised, usually in the proximal half of the oesophagus, by ulceration, wall thickening and sinuses and fistulae to trachea or bronchus. Patients often present with strictures. Radiological appearances may be indistinguishable from carcinoma. Oesophageal involvement may also be related to narrowing or displacement by caseating tuberculous nodes in the mediastinum.
 | Figure 16.
Oesophageal ulceration due to medication (Doxycycline). Note multiple irregular superficial ulcers surrounded by haloes of oedema. |
Drug-induced oesophagitisOesophagitis related to drug ingestion is due to a local irritative effect and therefore usually occurs at the sites of physiological hold-up, such as the aortic arch or the level of crossing of the left main bronchus or, in patients with heart disease, often above a dilated left atrium. The commonest causes of medication oesophagitis are antibiotics, particularly tetracycline and doxycycline, frequently in young patients. The oesophagitis results in odynophagia. Superficial ulcers are seen in the midoesophagus which may be of various configurations (Fig. 16). The ulcers heal on drug withdrawal. Those ulcers that result from slow-release potassium supplements tend to occur in an older age group, are larger and hence may heal with scarring and stricture formation. An apparent stricture may be present in the acute phase due to
spasm and/or oedema. Various other tablets have been reported to cause oesophagitis.
Caustic oesophagitis
Lye (alkalis) are the commonest causes of caustic oesophagitis, usually ingested in the form of drain cleaners, resulting in liquefaction necrosis. While acids can produce oesophageal damage, they tend to predominantly affect the stomach. Chest radiographs and supine and erect or decubitus abdominal films should be performed to detect signs of perforation, such as pneumomediastinum or pneumoperitoneum, as well as evidence of a dilated oesophagus or emphysematous gastritis. Contrast studies may be required. If perforation is suspected, water soluble contrast should initially be used. In the acute phase, abnormal oesophageal motility is seen, either spasm or atony (which may pre sage perforation). Barium studies are not very sensitive for the detection of mild mucosal changes in this condition. Severer forms are se en as oedema, ulceration and sloughing of mucosa. Submucosal contrast may result from the latter. Later, fibrosis occurs which progresses to stricture formation. Strictures are typically long and may be single or multiple.
Radiation-induced oesophagitis
Radiotherapy to the mediastinum can result in acute and chronic effects to the oesophagus; these have been reported following doses of 45-60 Gy over 6-8 weeks. A combination of radiotherapy and chemotherapy is more likely than radiotherapy alone to cause oesophageal injury. Abnormal motility, which may be segmental and related to the radiation portal, with or without mucosal oedema, is seen within 4-12 weeks of radiotherapy. Ulceration, and pseudo-diverticula occur mainly when a mass has been causing extrinsic compression on the oesophagus. Fistulae between oesophagus and airway are uncommon. Oesophageal strictures form some months after completion of radiotherapy and are tapered and occur within the radiotherapy portal.
Oesophageal diverticula
Most oesophageal diverticula are acquired false diverticula, and so comprise outpouchings of mucosa with or without submucosa. Although there is controversy as to whether those around the level of the carina are due to traction, and thus true diverticula, it is now thought that the majority are of the pulsion variety. Other common sites are at alevel between the aortic arch and the left main bronchus and in the distal oesophagus (epiphrenic). Pulsion diverticula tend to change shape and size and move longitudinally with oesphageal peristalsis. Epiphrenic diverticula may be multiple, are associated with GOR and hiatus hernias and are presumed related to dysmotility. Oesophageal diverticula hardly ever cause symptoms.
 a | Figure 17.
Spontaneous oesophageal perforation. Sudden onset of pain during a meal. (a) Water soluble contrast swallow shows an ovoid filling defect (upper border shown by large arrow) due to intramural haematoma, and linear collection of submucosal contrast (small arrow). (b) CT of same patient shows gas in mediastinum (arrowed) indicating that there has been a transmural perforation. |
 b | |
Oesophageal perforationsPerforations may be transmural or intramural. The great majority are caused by instrumentation or dilatation. Non-iatrogenic causes include vomiting and foreign body impaction. Truly spontaneous transmural perforations (Boerhaave's syndrome) and intramural lacerations or haematomas do occur, but often there is a history of vomiting as a precipitating factor. Intramural haematomas occur in patients on
anticoagulant drugs or with bleeding diatheses. Occasionally, oesophageal injury is a result of penetrating or blunt compression
trauma. Most iatrogenic injuries occur at the cricopharynx or distal
oesophagus. Spontaneous perforations tend to be sited in the distal
oesophagus. Boerhaave's syndrome is usually a dramatic event associated with vomiting, severe chest pain and collapse, but occasionally it is relatively insidious.
Plain chest radiographs will only be abnormal in transmural perforation; signs may include mediastinal widening, pneumomediastinum, surgical emphysema in the neck, loss of the left paraspinal line, a V -shaped lucency at the left base due to air between the left margin of the descending aorta and the left diaphragmatic pleura, an air-fluid level in the mediastinum, and a left pleural effusion or hydropneumothorax. A right pleural effusion may be seen if the perforation is in the more proximal oesophagus. To demonstrate a small transmural perforation a contrast study needs to be performed with meticulous attention to detail. Views are taken with the patient recumbent in supine, and prone-oblique projections, using water-soluble contrast medium. If this is negative, low dens it y barium should be used. Intramural perforations will be demonstrated as submucosal haematomas or dissections (Fig. 17 a); there may be narrowing of the lumen by the mass effect of the haematoma seen as a long smooth filling defect in the mid and lower oesophagus; clot may be present within the lumen if the haematoma has ruptured through the mucosa or there may be a double lumen due to contrast entering the submucosa - so called "double-barrel" appearance.
CT is often useful to examine for mediastinal collections in transmural perforations or to confirm the diagnosis, when contrast studies are equivocal or a small leak has sealed, by demonstrating air or oral contrast within the mediastinum (Fig. 17 b). In addition, there are reports of characteristic findings of submucosal haematomas, including high attenuation blood within the wall of the oesophagus.
Mallory- Weiss lacerations
These are relatively superficial tears occurring in the distal oesophagus around the gastro-oesophageal junction, limited to the mucosa, with or without submucosal involvement, following vomiting and presenting as acute GI haemorrhage. Barium studies are usually negative but in view of the presentation, endoscopy is in any case the investigation of first choice.
Oesophageal varices
Although an optimal barium swallow technique is probably as accurate as endoscopy in the diagnosis of varices, if these are suspected clinically then, even in the patient who is not acutely bleeding, endoscopy is the preferred examination, since it allows assessment of other mucosal lesions related to portal hypertension and also offers the option of injection sclerotherapy. However, if a barium study is used, then a single contrast technique is performed with the oesophagus collapsed - mucosal relief views. Hyoscine butylbromide is given to relax the body of the oesophagus, the mucosa coated with barium and multiple views taken in various supine-oblique and prone-oblique projections, with the patient in a Trendelenburg postion. A Valsalva manoeuvre may be used to distend the varices. The varices are seen as serpiginous filling defects usually along the line of the longitudinal folds in the distal oesophagus. Distinction must be made from the rare varicoid carcinoma; unlike varices the configuration of the latter will not change with oesophageal distension.
Richard M. Mendelson