Wall thickening can arise from corrosives, Crohn’s disease, reflux, infection, intubation, epidermolysis bullosa, and radiation (Fig. 7) [2]. In addition, eosinophilic oesophagitis is a less common but growing aetiology (rising in incidence along with other autoimmune diseases, asthma, and food allergies) of oesophageal thickening [19, 20]. It is thought that foreign antigens are introduced (through food or pollen) and induce eosinophilic infiltration leading to inflammation. The morbidity of the disease relates to the degree of inflammation which leads to scarring and formation of excessive fibrous tissue in the lining of the oesophagus. While it does typically respond well to steroids, some cases may require interventional dilatation or even esophagectomy.Fig. 7

Oesophagitis. CT angiogram of the chest in soft tissue window shows circumferential oesophageal wall thickening in a patient who presented with chest pain. Please note the contrast enhancement of the mucosa which creates a hyperdense inner layer contrasting with the rest of the wall; this is an imaging feature that can be observed in gastrointestinal inflammatory diseases

Another aetiology of oesophageal wall thickening is benign tumours [21, 22]. These tumours are rare (represent less than 1% of oesophageal neoplasms) and include leiomyomas, granular cell tumours, hemangiomas, and fibroepithelial polyps. Leiomyomas are the most common benign tumour of the oesophagus. Imaging typically shows an oval-shaped intramural mass; calcifications are highly characteristic (Fig. 8) [23]. Granular cell tumours are benign tumours appearing in the gastrointestinal tract, most commonly occurring in the oesophagus (representing about a third of all such tumours). They are neural in origin and most commonly located in the distal oesophagus. Grossly, these tumours are sessile submucosal structures covered with normal mucosa [24]. Another benign tumour of the oesophagus is hemangioma. It is very rare in the oesophagus (representing only ∼3% of all benign oesophageal tumours), but when it does occur, it tends to be in the lower oesophagus. CT imaging typically shows a well-defined soft tissue mass within the oesophageal wall and phleboliths are characteristic (Fig. 9) [25].Fig. 8

Leiomyoma. Esophagram in AP projection demonstrates a smooth, lobulated filling defect within the mid-thoracic oesophagus at the level of the carina. Notice the filling defect makes an acute angle to the oesophageal wall, suggesting that this lesion is intrinsic to the oesophagus

Oesophageal varices can be categorised as uphill (ascending from the intra-abdominal oesophagus), which are more common, or downhill (descending from the upper thoracic oesophagus) (venous anatomy reviewed in Table 1). Uphill varices are typically caused by portal hypertension, which results in collateral blood flow through the gastric and lower oesophageal veins. Uphill varices can extend superiorly to the level of the azygos vein. Downhill varices result from obstruction of the superior vena cava leading to collateral blood flow through the oesophageal veins. If the SVC obstruction is above the level of the azygos vein, the varices will extend inferiorly to the level of the carina, after which blood will drain into the azygos system. However, if the obstruction occurs below the level of the azygos vein, the varices can extend more inferiorly. Varices produce serpiginous filing defects on fluoroscopic barium studies. On CT, varices can give the appearance of a thickened oesophageal wall and phleboliths can mimic oesophageal wall calcifications, however the dilated vessels are easily identified on intravenous contrast-enhanced images (Fig. 10) [26]. Chest x-ray can show oesophageal varices as a lobular retrocardiac mass [27]. Despite their appearance, varices typically do not produce obstructive symptoms.Fig. 10

Varices. Maximum intensity projection of a CT angiogram of the chest in soft tissue window shows numerous calcifications along the oesophageal wall and portal collateral vessels in this patient with extensive uphill oesophageal varices

In addition to spontaneous and iatrogenic hematoma formation, the many possible aetiologies of intramural hematoma include trauma, caustic oesophageal injury, and vomiting [28]. Intramural hematoma due to blunt trauma is uncommon due to the protected positioning of the oesophagus [29]. The issue in these cases is often satisfaction of search and delineating vascular, spinal cord, pulmonary (especially tracheal), pleural, and musculoskeletal abnormalities. Trauma in the oesophagus is very important since it may have implications for positioning of enteric tubes and nonspecific complaints of chest pain. Imaging will typically show an intramural fluid collection distending the walls of the oesophageal lumen which will be of intermediate density but higher than the blood pool on non-contrast imaging and will be hypodense on post-contrast imaging (Fig. 11). In addition, areas of active contrast extravasation may be present within the wall of the oesophagus or seen filling the oesophageal lumen. Patients chronically anticoagulated on warfarin are at increased risk of hematoma formation. As patients with this condition typically present with chest pain, this condition must be differentiated from acute cardiovascular disease related to the aorta, pulmonary arteries, or coronary arteries, all of which may cause bleeding in the mediastinum. Identifying the centre of the hematoma mass and knowledge of acute aortic injury can help differentiate oesophageal injury from vascular injury (Fig. 11) [30]. Intramural hematoma typically resolves in a few days or weeks without intervention, however follow-up imaging is indicated in these patients.Fig. 11

Intramural Hematoma. CT angiogram of the chest in soft tissue window shows a markedly thickened oesophageal wall that is slightly higher in density than soft tissue. The oesophageal wall partly surrounds the aorta. This patient was found to have a large intramural hematoma

This is the most common diverticulum in the oesophagus and results from herniation of the mucosa through a weak area of the cricopharyngeus muscle. Patients with these diverticula can be asymptomatic or suffer a range of symptoms including dysphagia, chronic cough, and regurgitation of food [32]. On barium esophagram, a Zenker diverticulum will present as a midline posterior oesophageal outpouching which will pool oral contrast. It is best seen in the lateral projection (Fig. 12a and b).Fig. 12

Zenker Diverticulum. Esophagram in AP (a) and oblique (b) projections demonstrates contrast filling a midline posterior outpouching of the cervical oesophageal lumen consistent with a Zenker diverticulum

In contrast to Zenker diverticula, Killian-Jamieson diverticula protrude laterally through the anterolateral wall [32, 33]. They are less common than Zenker diverticula. Barium imaging will demonstrate oral contrast pooling within a lateral outpouching off of the upper oesophagus. It is best seen on the anterior-posterior (AP) projection (Fig. 13a and b).Fig. 13

Killian-Jamieson Diverticulum. Esophagram in AP (a) and oblique (b) projections demonstrates a lateral outpouching of the lumen arising from lower cervical oesophagus consistent with a Killian-Jamieson diverticulum

An epiphrenic diverticulum occurs in the distal third of the oesophagus (within 10 cm of the gastroesophageal junction) (Fig. 14a and b) [34, 35]. It is treated with diverticulectomy. Failure to treat an epiphrenic diverticulum may predispose to bleeding, aspiration, pneumonia, and/or cancer.Fig. 14

Epiphrenic Diverticulum. a Esophagram in oblique projection demonstrates herniation of the lumen within the lower oesophagus centred less than 10 cm from the gastroesophageal junction consistent with an epiphrenic diverticulum. b CT of the chest with IV and oral contrast in soft tissue window shows contrast filling an outpouching located lateral to the lower thoracic oesophagus

Endoscopic procedures, surgical procedures involving adjacent structures, and thermal injury during left atrial ablation can all result in iatrogenic perforation; at least half of all oesophageal perforations are estimated to be iatrogenic in nature (Fig. 15a and b) [28, 36]. Patients with perforation (whether iatrogenic or due to Boerhaave syndrome) present with sudden onset of severe epigastric pain. Typical imaging findings include pneumomediastinum, pleural effusion (left > right), and mediastinal hematoma [30].Fig. 15

Complication of food impaction with tear of oesophagus during chicken bone extraction. a Pre-contrast axial image of the thorax demonstrates a markedly enlarged oesophagus which is high in density (*) when compared to the adjacent blood pool in the aorta (findings consistent with hematoma). b Post-contrast imaging of the same patient demonstrates areas of active contrast extravasation (arrows) within a markedly enlarged and abnormal appearing oesophagus. Clinical note, patient subsequently had multiple episodes of hematemesis

This syndrome involves a spontaneous perforation of the thoracic oesophagus (Fig. 16 a–c). Boerhaave syndrome occurs when incomplete cricopharyngeal relaxation during vomiting results in a sudden increase in intraluminal oesophageal pressure [37]. Rupture is most common in the distal left posterior wall immediately above the diaphragm (representing approximately 90% of ruptures). Treatment is immediate thoracotomy and mortality is very high without prompt intervention.Fig. 16

Boerhaave Syndrome. a AP chest radiograph shows pneumomediastinum (arrow). b Esophagram in AP projection demonstrates contrast extravasating from the distal oesophagus. c CT of the chest with oral contrast in soft tissue window demonstrates extraluminal contrast (white arrowheads), pneumomediastinum (*), and bilateral pleural effusions (arrows) in a patient with Boerhaave Syndrome

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 [28]. Patients commonly presenting with this condition include alcoholics and patients with eating disorders involving vomiting [38]. 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 [30].

Fistulas to the pericardium can occur after radiofrequency (RF) catheter ablation, although the complication rate is less than 5% (Fig. 17) [40]. Patients present with nonspecific signs 1–3 weeks after the procedure and this type of fistula is frequently lethal. Urgent intervention is necessary and may involve stents, pericardial/pleural drains, and antibiotics. RF ablation can also lead to oesophageal thermal injury and ulceration of the oesophagus. Other thoracic complications of RF ablation include oesophageal perforation, pericardial effusion/hematoma, cardiac tamponade, pulmonary vein stenosis, atrioesophageal fistula, and phrenic nerve injury (Fig. 18).Fig. 17

Pericardioesophageal Fistula. CT of the chest in soft tissue window demonstrates fluid and gas (arrow) within the pericardium in a patient with a confirmed pericardioesophageal fistula

Fistulas connecting the oesophagus to the trachea can be congenital or acquired. Approximately 50% of the acquired tracheoesophageal fistulas are secondary to mediastinal malignancy. Among the non-malignant causes, more than 75% are the result of endotracheal cuff-related trauma in patients subject to prolonged mechanical ventilation (Fig. 19) [41].Fig. 19

Tracheoesophageal Fistula. CT of the chest in lung window in axial plane demonstrates communication between the trachea and oesophagus (arrow) secondary to prolonged endotracheal tube intubation

Fistulas between the aorta and oesophagus are rare, although immediately life threatening (Fig. 20a and b) [42]. About two-thirds of these fistulas develop secondary to aortic aneurysm and, in general, this condition is not usually due to an underlying oesophageal abnormality [43]. Although diagnosis is not difficult on imaging, it may not be high on the differential as a cause for hemoptysis in the Emergency Department due to its rarity. Patients usually die from massive haemorrhage. Sepsis can develop from the oesophageal lesion and there can be involvement of surrounding tissues caused by infection [43]. The treatment options are case-dependent but can involve drains, open surgery, and endovascular therapy.Fig. 20

Aortoesophageal Fistula. CT angiogram of the chest in soft tissue window in axial (a) and sagittal (b) planes demonstrates extravasation of contrast from the descending thoracic aorta into the oesophagus. Soft tissue attenuation material within the oesophagus is consistent with clotted blood

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.