An oesophageal stricture refers to a narrowing of the oesophageal lumen (Fig. 1). Narrowing may be due to intrinsic disease of the oesophagus or extrinsic compression. Causes of intrinsic disease can include inflammation, fibrosis, and neoplasia, whereas extrinsic compression may be due to an enlarged lymph node, extra-luminal cancer, or adjacent organ [1]. Benign peptic strictures occurring secondary to gastro-oesophageal reflux disease (GORD) account for up to 80% of all benign strictures [2]. The cardinal symptom of an oesophageal stricture is dysphagia, which occurs when there is >50% narrowing of the oesophageal lumen [3]. Other symptoms depend on the aetiology and can include heartburn, regurgitation, weight loss, abdominal pain, food bolus, and aspiration pneumonia.

The presence of dysphagia is concerning and usually prompts urgent assessment. Gastroscopy is the first-line investigation that allows direct oesophageal visualisation. This enables an accurate diagnosis of intrinsic oesophageal disease, location of oesophageal narrowing, acquirement of oesophageal tissue, and exclusion of malignancy. A severe stricture is one that does not allow passage of a standard gastroscope (≤10mm). Barium swallow can also be used in suspected oesophageal strictures. This helps identify the location, length, diameter, and number of strictures. The British Society of Gastroenterology (BSG) guidelines recommend that barium swallow is performed for all suspected complex strictures [4]. In addition, barium swallow has been shown to be more sensitive in the detection of oesophageal strictures compared to conventional gastroscopy, especially in milder strictures [5].

The goal of treatment is to maintain adequate and durable patency of the oesophageal lumen. The choice of treatment depends on multiple factors including aetiology and stricture complexity. In case of oesophageal inflammatory strictures, it is essential to optimise medications such as proton pump inhibitors to control any oesophageal inflammation, which limits success of endoscopic therapy [6,7]. Endoscopic dilatation is the principal treatment that is usually successful in up to 90% of cases within five sessions [8]. The aim of endoscopic intervention is to achieve an oesophageal lumen ≥15mm, although this is a largely arbitrary cut-off without an evidence base. The optimum size will vary between patients and should be individualised. Strictures that are refractory to endoscopic therapy and significantly impacting life may require surgical intervention. However, with the growing number of endoscopic options, surgery is rarely needed [9].

In this review, we provide a global overview on the endoscopic management of oesophageal strictures that is essential for gastroenterologists and endoscopists involved in their management. In section 2, we provide a technical overview of the current therapeutic options available. In sections 3 Endoscopic management of malignant strictures, 4 Endoscopic management of benign strictures, 5 Endoscopic management of iatrogenic strictures, we discuss the evidence for these choices in both malignant and benign strictures according to aetiology.

The aetiology of an oesophageal stricture is broadly divided into benign or malignant. The two most common malignancies are adenocarcinoma and squamous cell carcinoma. Benign aetiologies may be due to intrinsic oesophageal disease (e.g. peptic stricture) or secondary to an iatrogenic or accidental event (e.g. post-endotherapy). Certain causes are more likely to lead to refractory strictures, which include caustic ingestion, post-surgery or endotherapy, and following radiotherapy [10]. Table 1 summaries the main causes of benign oesophageal strictures.

Motility disorders of the oesophagus may also lead to oesophageal narrowing, particularly at the upper and lower oesophageal sphincters. This can lead to a similar presentation with dysphagia, regurgitation, and weight loss. The most prominent of these are achalasia and cricopharyngeal dysfunction, but a whole range of motility disorders can affect the oesophagus. Their management wlll not be discussed, but we point the reader to an excellent overview article [11].

Benign oesophageal strictures may be broadly defined as simple or complex. This depends on the stricture length, location, diameter, and underlying aetiology [12].

Simple: <2cm, straight, able to pass a standard gastroscope, low-risk aetiologies (e.g. peptic, eosinophilic oesophagitis).

Complex: ≥2cm, tortuous, inability to pass a standard gastroscope, high-risk aetiologies (e.g. caustic, post-radiotherapy, anastomotic).

Simple strictures are more likely to respond to conventional endoscopic therapy, whereas complex strictures are difficult to treat. Complex strictures usually need fluoroscopy and may require more advanced endoscopic techniques because they are high-risk of becoming refractory or recurring [9].

When a stricture dose not respond to endoscopic therapy it may be classified as refractory or recurrent. The basis of the definition for a refractory or recurrent stricture was coined in 2005, and broadly refers to oesophageal luminal narrowing causing dysphagia in the absence of inflammation where the oesophageal lumen cannot be maintained to a diameter of 14mm [13].

Refractory: inability to maintain oesophageal diameter at 14mm over 5 sessions of dilatation at 2 weekly intervals.

Recurrent: inability to maintain oesophageal diameter at 14mm for 4 weeks once a diameter of 14mm has been achieved.

Strictures secondary to radiotherapy, caustic injury, or surgical anastomoses are most likely to lead to a refractory stricture [10]. This often leads to use of more complex endoscopic methods to treat luminal narrowing including stenting, stricturotomy, or injection therapy with corticosteroids.