Chronic dysphagia
This 59 year-old man presented with a six month history of dysphagia to solids 1. What was seen at his endoscopy? 2. What is the most likely aetiology? 3. How should the patient be investigated and managed?
The endoscopic appearances are those of a benign oesophageal stricture most commonly occurring in
the distal oesophagus as a result of gastro-oesophageal reflux disease (GORD). These strictures are also
occasionally referred to as peptic strictures. Other causes of benign oesophageal stricture include:
Prolonged GORD results in chronic inflammation and fibrosis which in advanced cases can involve the full thickness of the oesophageal wall and can result in oesophageal shortening. Most peptic strictures are however less than 1 cm in length. Between 5 and 10% of patients with GORD will develop a peptic stricture, often having had symptoms for a number of years. The incidence of peptic strictures has decreased in recent years, probably due to the widespread use of acid suppression therapy. In those patients who develop a stricture, the lower oesophageal sphincter pressure, oesophageal motility and gastric emptying are more severely impaired than in those patients with GORD who have not developed this complication. Peptic strictures usually present with dysphagia that is often confined to solids. In advanced cases dysphagia to liquids may occur. Symptoms usually develop slowly and the the degree of weight loss seen in patients with malignant strictures is not often seen. Symptoms of heartburn and regurgitation may improve as a stricture develops and provides a barrier to further reflux episodes. Urgent investigation is required. A barium swallow should initially be performed. It will provide information on the site and extent of any stricture and may give a clue as to the underlying aetiology. This should be followed by endoscopy to determine the cause of the stricture and to allow biopsy of any mucosal lesion. Peptic strictures usually have a smooth mucosal surface. The presence of any irregularity should raise concerns of possible malignancy. Approximately 30% of patients with Barrett's oesophagus will develop a peptic stricture. Treatment of a peptic stricture should be by initial dilatation followed by medical or surgical treatment of the underlying reflux disease. Even small degrees of luminal dilatation can produce significant improvements in symptoms. There are two types of dilators. Axial (Savary-Gilliard) dilators or mercury filled (Maloney) bougies fracture the fibrous narrowing as they are pushed through. Balloon dilators can be positioned across the stricture an inflated. Randomised controlled trials have found no significant difference in the measured relief of dysphagia or need for repeat dilatation between bougie and balloon dilatation. The main complication of dilatation is oesophageal perforation which occurs in approximately 0.5% of procedures. Following dilatation all patients require acid suppression and usually life-long treatment with a proton pump inhibitor. Proton pump inhibitors have been shown to more effective are reducing stricture recurrence than H2 receptor antagonists. After initial dilatation approximately one third of patients will require redilatation within the first 12 months of treatment. If frequent dilatations are required despite acid suppression then surgery should be considered. An antireflux procedure should be performed but because many of these patients have oesophageal shortening, a Collis gastroplasty may be required to restore adequate oesophageal length. Surgery reduces but does not completely abolish the need for stricture dilatation Recent papersRichter J E. Peptic strictures of the oesophagus. Gastroenterol Clin N Am 1999; 28: 875-891.
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