Stricture is commonly the result of acute oesophagitis followed by chronic transmural oesophagitis and subsequent fibrosis. Reflux of gastric juices is responsible for 90 per cent of benign strictures of the oesophagus. Less frequent causes include infection, trauma, and congenital malformations.

Painless dysphagia is the typical presenting symptom of oesophageal strictures. Diagnostic dilemmas are frequent because of the similarity in the signs, symptoms, and radiological findings for benign and malignant oesophageal disease. Once a benign stricture is diagnosed, treatment selection must be made from an array of medical and surgical therapies. With most reports identifying the mean age of a stricture patient as 75 years, appropriate treatment must weigh the benign nature of the disease against the symptomatic impairment, general health, and estimated longevity of the patient.

Reflux or peptic strictures are a complication of severe gastro-oesophageal reflux disease (Fig. 1) 900. Three factors influence the severity of this process: a mechanically defective lower oesophageal sphincter, inefficient oesophageal clearance of refluxed acid, and abnormal gastric emptying resulting in an excess of acid available for reflux. Reflux strictures occur just above the squamocolumnar junction, the anatomical location of which varies depending on the presence or absence of Barrett's epithelium. Strictures may arise in 35 per cent of patients with Barrett's epithelium (Allison-Johnstone stricture) or may result from night-time pooling of gastric acid below the cricopharyngeus muscle (cricopharyngeal web).

Peptic stricture does not occur in all cases of gastro-oesophageal reflux disease. Strictures arise in 10 per cent of adults treated for reflux symptoms and 12 per cent of paediatric patients having antireflux surgery. When stricture occurs during medical treatment of gastro-oesophageal reflux disease, it signifies failure of conservative therapy. Symptoms of gastro-oesophageal reflux disease typically precede symptoms of stricture by months to years. The spontaneous resolution of previously severe reflux symptoms may signify the development of a stricture. However, 50 per cent of patients with reflux strictures may present themselves with only dysphagia and no prior history of reflux. In a small fraction of cases, adults enter urgently with an acute food bolus impaction.

The Schatzki–Inglefinger ring is a sharply defined fibrous narrowing of the distal oesophagus at the squamocolumnar junction, forming the proximal edge of a sliding hiatal hernia. The ring consists only of mucosa and submucosa and is well treated with bougie dilatation. Surgery is warranted only if intractable reflux becomes evident after dilatation.

Scleroderma may cause a particularly difficult reflux stricture. The fibrous replacement of oesophageal smooth muscle in scleroderma results both in inefficient oesophageal peristalsis and a decreased resting pressure of the lower oesophageal sphincter. Fewer than 50 per cent of patients with scleroderma-related strictures obtain relief when treated conservatively. Frequently, early resection and intestinal interposition are required.

Infections are rare causes of oesophageal stricture, but may be increasing because of the prevalence of immunosuppressed patients with the AIDS virus. Candida albicans is the most frequent pathogen, accounting for nearly half the cases. Also cited are infections with Herpes simplex virus (HSV) and cytomegalovirus (CMV), mucormycosis, histoplasmosis, and tuberculosis.

Initial treatment is directed at the underlying pathogen. Intravenous fluconazole and amphotericin have been recommended for severe candidal infections. Intravenous gancyclovir is advised for HSV or CMV infections. Additional treatment such as bougie dilatation should be delayed to allow resolution of the underlying infection. Dilatation may be unnecessary when acute inflammatory oedema mimics a stricture. Furthermore, the acute nature of these infections makes dilatation more dangerous. The oesophagus lacks the chronic thickening of peptic strictures and is more apt to rupture during dilatation. Exceptions to this rule are the strictures caused by mucormycosis, histoplasmosis, and tuberculosis. These strictures are less likely to respond to antimicrobial drugs or dilation and may require resectional therapy.

Localized injury to the oesophagus can cause transmural inflammation, which results in stricture. Caustic burns from ingested alkali or acids are the most frequent examples of this class of stricture. Other causes include prolonged nasogastric intubation, radiation therapy, or pill impaction. Pill injuries are rare in patients with an otherwise normal oesophagus. The finding of such an injury should prompt a search for an underlying cause such as a neoplasm or a motility disorder. Old age and sustained release pills are additional risk factors for pill induced stricture. Potassium chloride and quinidine are the most common agents. Aspirin, ascorbic acid, phenytoin, and tetracycline have also been cited as causes.

An increasingly frequent problem is post-sclerotherapy stricture, reported in 4 to 50 per cent of patients who have received sclerotherapy for oesophageal varices. Studies reveal no evidence of gastro-oesophageal reflux disease in these cases. Fibrosis caused by the sclerosant is the most likely aetiology.

Congenital causes for oesophageal stenosis such as oesophageal atresia and tracheo-oesophageal fistulae are most frequently identified in neonates and infants. Both of these developmental foregut abnormalities may result in late oesophageal stricture despite initial surgical correction. Tension at the repair site, subclinical anastomotic leaks, acid reflux, and abnormal distal oesophageal motility all predispose for perianastomotic stricture. A related problem is residual tracheobronchial remnants within the oesophagus after correction of congenital tracheo-oesophageal fistula. Surgical intervention is rarely required for anastomotic stricture but may be necessary for tracheobronchial remnants.

Oesophageal webs (thin fibrous membranes in the mid or upper oesophagus) are covered by normal squamous epithelium on both sides and are successfully treated with bougienage.

Rare systemic illnesses have been reported to cause oesophageal stricture including pemphigus, Stevens–Johnson syndrome, toxic epidermonecrolysis, Behçet's syndrome, chronic granulomatous disease of childhood, Crohn's disease, Plummer Vinson syndrome, and epidermolysis bullosa dystrophica recessive. Treatment consists of therapy of the underlying disease and gradual dilation. Resection with oesophageal replacement is required in rare cases in which the strictures do not respond to conservative therapy.

The goals of diagnostic testing are to exclude malignancy, to assess the severity and aetiology of the stricture, and to search for associated underlying conditions. One of the first steps to evaluate the patient with dysphagia is to obtain a barium swallow. Barium oesophagography is a simple, inexpensive examination which can assess the diameter and length of the stenosis as well as provide clues to other causes of dysphagia. A hiatal hernia with free reflux to the level of a short distal oesophageal stricture suggests a diagnosis of peptic stricture. Strictures longer than 20 mm, ‘apple core’ lesions, upper or mid-oesophageal location, and the absence of reflux all raise the suspicion of neoplasm rather than stricture. In either case, the barium swallow serves as a guide to the subsequent endoscopic examination.

Endoscopic biopsy and cytological brushings are essential to exclude malignancy in the early assessment of oesophageal stricture. Endoscopy allows a careful assessment of the length and location of the stricture relative to the squamocolumnar junction, the gastro-oesophageal junction, and the diaphragmatic hiatus. Biopsy and brushings should be taken of the stenosis, and any oesophageal mucosa of abnormal appearance. Initial dilation of the stricture is generally performed at the time of endoscopy.

Pressure manometry is an important step in the evaluation of patients with stricture. Manometry can assess the status of the lower oesophageal sphincter and oesophageal motility. A low or normal lower oesophageal sphincter pressure is typical of gastro-oesophageal reflux disease. Manometry can also facilitate selection of operative therapy. Some authors rely on manometric indications (e.g. mean lower oesophageal sphincter pressure less than 6 mmHg, intra-abdominal length of the lower oesophageal sphincter less than 1 cm, and total length less than 2 cm) to select patients for surgery (Fig. 2) 901. When poor distal motility is noted, a partial fundoplication (i.e. Belsey wrap) would be advised to avoid postoperative dysphagia. This is in contrast to the recommended use of a total fundoplication (i.e. a Nissen wrap) when motility is normal.

Oesophageal pH studies, typically 24-h continuous lower oesophageal pH monitoring, have high sensitivity and specificity for diagnosing gastro-oesophageal reflux disease as a cause of oesophageal stricture. It is important that such studies be performed after adequate dilatation of the stricture and temporary discontinuation of H&sub2;-blocking medications.

After a diagnosis of benign oesophageal stricture is made, most patients respond to a course of conservative therapy consisting of intensive medical treatment with concurrent dilation of the stricture.

Standard medical therapy for reflux stricture includes simple measures such as elevation of the head of bed, avoiding eating before bedtime, and the use of antacids. Histamine receptor antagonists (H&sub2;-blockers) such as cimetidine, ranitidine, famotidine, and nizatidine are the mainstays of medical therapy. A 6-week course of H&sub2;-blockers at standard dosages allows healing of oesophagitis and erosions in 50 to 75 per cent of patients. However, maintenance treatment with H&sub2;-blockers has not been shown to prevent recurrence of oesophagitis.

Omeprazole is a potent sodium-potassium ATPase inhibitor that decreases acid production in the stomach. It is very effective against gastro-oesophageal reflux disease, with 75 to 95 per cent healing of oesophagitis at a daily dosing of 20 to 40 mg. Maintenance therapy, however, shows relapse rates of 11 to 26 per cent.

Metoclopramide, domperidone, and cisapride increase the lower oesophageal sphincter pressure and improve gastric emptying, correcting two factors responsible for gastro-oesophageal reflux disease. These agents may be used with H&sub2;-receptor blockers or omeprazole for maximal medical therapy.

Intralesional steroid (triamcinolone acetate) has been used endoscopically to avoid resection of caustic and anastomotic strictures that have failed to improve with other medical therapy. However, controlled trials will be necessary to prove the safety and efficacy of this method.

Dilation plays an important role in stricture management. The primary therapeutic goal of dilation is to break up the fibrous stricture and improve dysphagia and alimentation. Dilatation is frequently required to allow endoscopic inspection and biopsy, manometry, and pH monitoring for diagnosis. When a stricture is non-dilatable, treatment requires stricture resection and oesophageal reconstruction.

Although clinical improvement in some patients may last months or years, objective results of dilation are transient, with manometric improvement lasting less than 12 weeks. Increases in lumen size after dilation are smaller than the subjective improvement in swallowing would suggest, a finding explained by the fact that forceful dilation disrupts the stricture but creates localized muscular spasm.

Many dilators are used for treating benign oesophageal strictures. Axial dilators, or bougies, forcefully break the fibrous stricture as they are passed from proximal to distal. Balloon dilators, on the other hand, are positioned through the stricture prior to inflation and exert a radial force (Fig. 3) 902. No trials have shown a significant difference in the dilating capabilities of axial bougies and radial balloon dilators. Disposable balloon dilators are more expensive than reusable alternatives.

Maloney and Hurst dilators are mercury-filled rubber bougies that are easy, economical, and safe to use. The bougies are passed manually, with topical anaesthesia, but without fluoroscopic control; they are safe enough for selected patients to use them independently at home. Eder–Puestow dilators consist of a flexible guidewire which is passed through the stricture and over which a series of metal olives are passed. The Savary–Gilliard dilator resembles the Eder–Puestow bougie in that it consists of a spring-tipped guidewire over which tapered plastic bougies (6–17 mm diameter) are passed. Trials have described more effective and longer-lasting results when Eder–Puestow style dilators are compared with rubber bougies. Less frequently used axial dilators include the Tucker string-guided dilator which requires a gastrostomy, and Hegar dilators which may be used at laparotomy.

Balloon dilations are performed by positioning the proximal aspect of the balloon at the proximal limit of the stricture. The balloon is inflated to 35–60 mmHg and the inflation is held for 1 min. The use of balloon dilators may be better in selected short strictures. Examples include the Rigiflex TTS system, the Gruentzig balloon, and the Browne–McHardy pneumatic dilator.

The results of conservative treatment combining medications and dilation have been reported by numerous investigators. Overall, conservative therapy results in relief of dysphagia, satisfactory alimentation, and an infrequent need for maintenance dilations in 60 to 75 per cent of patients. In one large series, 46 per cent needed one dilation, while 75 per cent needed three or less to achieve long-term relief from dysphagia. Perforations occur in 1 per cent of procedures and in 3 per cent of patients over a prolonged course of dilations.

Patients receiving conservative therapy include a selected population of patients who would fare poorly with surgery because of their age or underlying conditions. Selecting non-surgical therapy means accepting the attendant risks of repeated dilations for an indefinite time. There is controversy regarding the appropriateness of prolonged conservative therapy, particularly for patients with Barrett's epithelium.

Surgical therapy for benign oesophageal strictures is reserved for the patient who fails to improve with conservative management or who suffers complications from dilations. Table 2 291 lists the indications for referring a patient with stricture to surgery. The choice of operation is best made with consideration of the ability to dilate the stricture preoperatively as well as knowledge of the propulsive force of the oesophagus and the degree of anatomical shortening that has occurred.

Commonly performed operations are listed in Table 3 292. In a patient with a dilatable stricture and minimal shortening of the oesophagus, a satisfactory result may be obtained by performing preoperative and intraoperative dilations together with a standard antireflux procedure. Severe shortening of the oesophagus may require a gastroplasty in conjunction with the antireflux procedure to maintain a length of intra-abdominal oesophagus and to minimize the chance of a slipped antireflux wrap. Non-dilatable strictures, severe primary oesophageal dysmotility syndromes, and failed antireflux procedures require resection of part or all of the oesophagus. Reconstruction with jejunum, colon, or stomach is performed at the time of resection to restore the continuity of the upper gastrointestinal tract.

The first level of surgical intervention is dilation in conjunction with a standard antireflux procedure such as a Nissen, Belsey, or Hill repair. With some variations depending on the type of operation being performed, the gastro-oesophageal junction is placed intra-abdominally and may be wrapped with gastric fundus. ( Figs. 4 903, 5 904, 6 905) These operations create good or excellent results in 70 to 85 per cent of patients with less morbidity and mortality than is seen with resection. Dilation and an antireflux procedure should be reserved for patients with abnormal 24-h oesophageal pH monitoring, diminished lower oesophageal sphincter tone on manometry, proven relief of dysphagia after dilation, and evidence of adequate peristalsis in the distal oesophagus.

For patients with a reflux stricture and a shortened oesophagus, gastroplasty combined with dilation and fundoplication is indicated. The so-called Collis–Belsey or Collis–Nissen operations consist of a Collis gastroplasty to lengthen the shortened oesophagus and a partial or complete antireflux wrap of the neo-oesophagus with gastric fundus (Fig. 7) 906. One study described 93 per cent of patients experiencing good long-term results. In patients with motility disorders, the results are less dramatic, with only 54 per cent experiencing good results. A Nissen 360° wrap has also been used in conjunction with gastroplasty, but may be complicated by recurrent dysphagia if distal oesophageal motility is suboptimal.

There are instances in which oesophageal resection and reconstruction for benign stricture is advisable despite the greater risk attendant with this procedure. Patients who have undergone one or more previous antireflux operations, patients with severe reflux stricture and a primary dysmotility syndrome, and patients with non-dilatable strictures are candidates for resection.

Resection of the strictured oesophagus allows several alternatives for reconstruction: jejunal interpostion, colon interposition, or gastric pull-up. If resection can be limited to a short distal segment, jejunal interpostion grafting can provide a safe and effective conduit. Jejunal grafts are based on more reliable blood supply than are colonic grafts, especially in the elderly. Furthermore, jejunal grafting avoids the necessity for vagotomy and gastric drainage which is required when a gastric pull-up is used for reconstruction. When jejunum is not suitable for oesophageal reconstruction, isoperistaltic left colon may be successfully employed in the same fashion. The stomach remains a suitable substitute for resected oesophagus, but reflux and postvagotomy complications make it less desirable than other alternatives.

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