- Pictorial Review
- Open Access
Imaging of the oesophagus: beyond cancer
© The Author(s) 2017
- Received: 12 September 2016
- Accepted: 13 February 2017
- Published: 17 March 2017
Non-malignant oesophageal diseases are critical to recognize, but can be easily overlooked or misdiagnosed radiologically. In this paper, we cover the salient clinical features and imaging findings of non-malignant pathology of the oesophagus. We organize the many non-malignant diseases of the oesophagus into two major categories: luminal disorders and wall disorders. Luminal disorders include dilatation/narrowing (e.g. achalasia, scleroderma, and stricture) and foreign body impaction. Wall disorders include wall thickening (e.g. oesophagitis, benign neoplasms, oesophageal varices, and intramural hematoma), wall thinning/outpouching (e.g. epiphrenic diverticulum, Zenker diverticulum, and Killian-Jamieson diverticulum), wall rupture (e.g. iatrogenic perforation, Boerhaave Syndrome, and Mallory-Weiss Syndrome), and fistula formation (e.g. pericardioesophageal fistula, tracheoesophageal fistula, and aortoesophageal fistula). It is the role of the radiologist to recognize the classic imaging patterns of these non-malignant oesophageal diseases to facilitate the delivery of appropriate and prompt medical treatment.
• Nonmalignant oesophageal disease can be categorised by the imaging appearance of wall and lumen.
• Scleroderma and achalasia both cause lumen dilatation via different pathophysiologic pathways.
• Oesophageal wall thickening can be inflammatory, neoplastic, traumatic, or vascular in aetiology.
Multiple imaging modalities are used in the evaluation of oesophageal pathology, including computed tomography (CT), barium oesophagography, endoscopic ultrasound (EUS), and 18-Fluoro-deoxyglucose positron emission tomography (FDG-PET) [1, 2]. Barium esophagography is a useful initial imaging modality for the diagnosis of patients with dysphagia, reflux, motility disorders, or perforation. For an intact oesophagus, thick and thin barium are used as contrast; however, if perforation is suspected, a diluted water-soluble contrast agent is typically used followed by dilute barium if no perforation is seen .
If pathology is detected during esophagography, CT imaging is often used to clarify findings and define anatomy; it can be particularly helpful in cases of suspected masses as barium esophagography cannot readily define disease extent outside the mucosa. CT imaging can also show wall thickness and evaluate for mediastinal involvement/general extent of disease beyond the mucosa. Importantly, CT imaging can be rapidly performed and is typically well tolerated by patients; this is especially important in patients who are unable to fully participate in a barium swallow study . If oesophageal pathology is suspected, CT should be performed with both intravenous contrast (to assess for enhancing lesions) as well as oral contrast given just prior to imaging (to assist in the evaluation of the oesophageal lumen). If the patient is at high risk for aspiration, water can be used instead of oral contrast to dilate the oesophageal lumen.
If oesophageal pathology is confirmed or highly suspected, endoscopic ultrasound is often utilized to evaluate a specific region of interest as it offers detailed visualization of the layers of the oesophageal wall. In addition, this imaging modality can perform direct biopsy of suspicious lesions, including adjacent lymphadenopathy if present . Limitations of this imaging modality include its operator dependence, the semi-invasive nature of the procedure, and the need to use moderate sedation.
Finally, FDG-PET imaging is typically reserved for cases that are known to be malignant and where evaluation is needed for distant metastasis or to delineate between malignant and nonmalignant aetiologies. It will not be discussed in this paper.
Salient features of oesophageal anatomy
Pharyngoesophageal junction (C6)
Inferior thyroid artery
Diaphragmatic hiatus (T10)
Left gastric and Portal veins
Diaphragmatic hiatus (T10)
Left gastric and Phrenic arteries
Luminal disorders due to dilatation and narrowing
Scleroderma causes dilatation of the oesophagus due to impaired microvasculature leading to a pathological cascade beginning with neuronal injury. In contradistinction to achalasia, neuronal injury in scleroderma leads to denervation muscle atrophy/fibrosis, which in turn causes hypoperistalsis and loss of LES tone . The decreased LES tone results in gastroesophageal reflux which in turn results in reflux oesophagitis, eventually culminating in stricture formation. This is in comparison to achalasia in which the dilatation of the oesophagus is due to increased lower oesophageal sphincter tone. The distended oesophagus and the propensity for reflux predisposes these patients to recurrent aspiration events (Fig. 3a and b). Indeed, patients with fluid within a dilated oesophagus and associated pulmonary parenchymal findings (especially bilateral dependent ground glass opacities and tree-in-bud nodules) should also be diagnosed with chronic aspiration.
Luminal disorders due to foreign body impaction
The oesophagus wall is thin (usually less than 0.3 cm) and made up of mucosa, submucosa, muscularis propria, and adventitia (but no serosa) (Fig. 2) [6, 7]. Of note, the lack of serosa is clinically relevant due to the potential of developing mediastinitis and of facilitating tumour spread. In addition, the thin wall predisposes to wall rupture and fistula formation. Normal oesophageal wall thickness varies based on the anatomic region, the degree of oesophageal dilatation, as well as the gender of the patient (males generally have a slightly thicker oesophageal wall). Pathology involving the oesophageal wall falls into several categories including wall thickening, wall thinning, wall rupture, and fistula formation.
The majority of oesophageal diverticula are cause by herniation of the mucosa and submucosa through the muscularis layer of the oesophagus. Thus, they are actually pseudodiverticula, since not all histological layers are involved. Diverticula are typically categorised as either pulsion or traction. Pulsion diverticula are much more common and are thought to originate due to oesophageal dysmotility. Zenker, Killian-Jamieson, and epiphrenic diverticula are all examples of pulsion diverticula. Less common are traction diverticula, which occur secondary to pulling forces on the oesophagus. They are most common in the middle oesophagus and are often secondary to inflammation (especially in the background of agents such as tuberculosis or histoplasmosis) . Please note that tertiary contractions (those that are non-propulsive) may sometimes mimic traction diverticula, however should not persist over time.
Although it can be due to many causes, a Mallory-Weiss tear refers to a longitudinal mucosal laceration (whereas Boerhaave syndrome involves the entire wall) that typically occurs in the lower oesophagus or at the GE junction . Patients commonly presenting with this condition include alcoholics and patients with eating disorders involving vomiting . The pathogenesis is similar to Boerhaave syndrome. It is important to note that a mucosal laceration without transmural perforation can be radiologically occult. Typical imaging findings may include subtle extraluminal gas or haemorrhage .
As a general principle, the close proximity of the oesophagus to other mediastinal structures predisposes to fistula formation and secondary disease development. As the oesophagus abuts the pericardium, trachea, and aorta, fistulas to all of these structures are possible [30, 39].
Non-malignant oesophageal disease encompasses a large variety of pathology. As discussed, benign tumours, vascular diseases, connective tissue disorders, traumatic injuries, and anatomic variants are all potentially discovered on imaging. Diagnosis of these conditions may be difficult because some of these conditions are uncommon and others may mimic cancer. However, recognizing non-malignant oesophageal diseases can be critical to appropriate and prompt medical treatment, highlighting the essential role of the radiologist in identifying this pathology on imaging.
Compliance with ethical standards
Conflict of interest
The authors declare that they have no conflict of interest.
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