Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Esophagogastric  Junction

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Volume: The Esophagogastric Junction
Chapter: Esophageal columnar metaplasia (Barrett s esophagus)

What are the indications for antireflux surgery in Barrett's esophagus?

H.J. Stein, J.R. Siewert (Munich)

Barrett's esophagus (BE), i.e. specialized columnar epithelial metaplasia in the distal esophagus, develops in up to 20% of patients with gastroesophageal reflux disease. Compared to reflux patients without columnar metaplasia, gastroesophageal reflux in patients with BE has a more severe character and more frequently results in complications such as penetrating ulcers and strictures [1]. In addition, the presence of BE is associated with a markedly increased rate of esophageal adenocarcinoma. The risk for malignant degeneration appears to be largest in patients who have a columnar epithelial lining of the distal esophagus greater than 3 cm in length. Esophageal adenocarcinoma may, however, also arise from very short segments of specialized columnar epithelium [1].

Recent experimental and clinical studies indicate that persistent reflux of gastric acid contaminated with duodenal contents, i.e. bile and pancreatic juice, appears to promote the development of BE and its malignant degeneration [2]. Since a surgical antireflux procedure can effectively abolish reflux of any gastric contents into the esophagus, antireflux surgery should, at least theoretically, halt upward progression, induce a regression and prevent malignant degeneration of the Barrett' epithelium in addition to healing of acute mucosal injury and long-term control of reflux symptoms. Because of the insensitivity of Barrett's mucosa, typical reflux symptoms are, however less prevalent in patients with specialized columnar metaplasia as compared to reflux patients without Barrett's mucosa [1]. The indications for antireflux surgery in patients with benign BE are therefore discussed controversially. While some recommend antireflux surgery in any patient with documented BE, others prefer a more discriminate approach with antireflux surgery only in those with recurrent reflux symptoms and complications requiring chronic medical therapy. An assessment of the outcome of antireflux surgery in patients with BE with respect to symptom control, healing of acute mucosal injury, regression of Barrett's epithelium and prevention of malignant degeneration is therefore essential when objectively evaluating the indications for the procedure.

Does antireflux surgery control symptoms
and esophageal injury in Barrett's esophagus?

Several studies have shown that the results of antireflux surgery in patients with BE are similar to those achieved in patients with gastroesophageal reflux disease and no Barrett's metaplasia. Nissen fundoplication heals esophagitis associated with BE and provides long-term symptom control in 85%-95% of patients [3-8]. Two recent prospective studies convincingly demonstrated that Nissen fundoplication is superior to continuous medical management in the treatment and prevention of strictures and esophageal ulcers [4, 5]. In our experience Nissen fundoplication healed esophagitis, ulcers and strictures and provided excellent long-term reflux control in 88% of 66 patients with BE.

Does antireflux surgery induce regression of Barrett's esophagus?

Spreading of squamous epithelial islands from the top of previously documented BE with partial or even complete regression of of the columnar mucosa has been reported in several patients following antireflux surgery. Progression of the extent of the columnar epithelium despite reflux control by Nissen fundoplication has, however, also been described (Table I).

Reports on regression or progression of the extent of BE after antireflux surgery should be interpreted carefully [12]. Due to methodological problems the extent of Barrett's epithelium after antireflux surgery is difficult to assess. A relocation of the squamo-columnar junction after antireflux surgery may represent altered geometry of the distal esophagus after the surgical procedure or healing of acute esophageal injury rather than true regression of Barrett's mucosa. Technical factors, i.e. the number and site of biopsies obtained and variations in the interpretation of endoscopy and biopsy findings between different investigators may also contribute to these observations. The matter is further complicated by the observation that columnar epithelial metaplasia can persist underneath apparently regenerating squamous epithelium [12]. Taking only superficial biopsies in these patients may result in the erroneous diagnosis of regression.
Table I. Progression and regression of the lengt

Nevertheless, convincing evidence of partial or complete regression of columnar epithelium after antireflux surgery has been presented in several reports (Table I). These studies indicate that regression is more likely to occur in patients with good symptomatic outcome after fundoplication as compared to those with persistent reflux symptoms and mucosal injury. The prevalence and extent of regression of BE after Nissen fundoplication is, however, low and similar to the regression observed with continuous medical aggressive acid suppression.

Does antireflux surgery prevent
malignant degeneration of Barrett's esophagus?

There have been several reports on the development of esophageal adenocarcinoma in patients with known BE between 6 months and 10 years after antireflux surgery (Table II). In addition, up to 11% of patients who present with adenocarcinoma of the esophagus had a previous antireflux procedure (Table III). The estimated risk for developing esophageal adenocarcinoma after antireflux surgery appears to be not different from the risk for malignant degeneration of BE in patients who had no treatment or medical management.

Progression of dysplastic changes in the columnar epithelium and the development of esophageal adenocarcinoma after antireflux surgery must, however, be assessed with caution. Due to the patchy nature of areas of dysplasia and early adenocarcinoma in BE these changes may have already been present and missed on preoperative endoscopy. The efficacy or inefficacy of the antireflux procedure must also be established when the effect of antireflux surgery on malignant degeneration of BE is assessed. Usually the patients who developed an adenocarcinoma after fundoplication had recurrent reflux symptoms prior to the diagnosis of the tumor. Several well documented patients, however, developed adenocarcinoma despite objectively documented reflux suppression by the antireflux procedure.
Table II. Malignant degeneration of Barrett’s mu

What are the indications
for antireflux surgery in patients with Barrett's esophagus?

Since at present there is no well documented proof that antireflux surgery can predictably and reliably induce a regression of Barrett's mucosa or prevent malignant degeneration it can currently not be justified to perform an antireflux procedure in all patients with Barrett's mucosa. Rather, the indications to proceed with antireflux surgery in patients with BE should match those in reflux patients without BE. An antireflux procedure should only be considered in patients, who have persistent or recurrent symptoms and/or complications despite adequate medical management [1, 6]. In patients with good peristaltic activity of the esophageal body a short and floppy Nissen fundoplication effectively controls reflux symptoms, heals acute mucosal injury and prevents stricture formation with minimal side effects. A laparoscopic approach further minimizes the trauma associated with the antireflux procedure. Because the malignant potential of BE persists after antireflux surgery these patients should continue to undergo endoscopic and histologic surveillance.


1. Stein HJ, Siewert JR. Barrett's esophagus: pathogenesis, epidemiology, functional abnormalities, malignant degeneration and surgical management. Dysphagia 1993;8:276-288.

2. Attwood SEA. Alkaline gastroesophageal reflux and esophageal carcinoma: experimental evidence and clinical implications. Dis Esoph 1994;7:87-92.

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6. Stein HJ, Feussner H, Siewert JR. Surgical therapy of gastroesophageal reflux disease: which patient, which procedure, which approach? Dis Esoph 1994;7:239-45.

7. Sagar PM, Ackroyd R, Hosie KB, Patterson JE, Stoddard CJ, Kingsnorth AN. Regression and progression of Barrett's oesophagus after antireflux surgery. Br J Surg 1995;82:806-810.

8. Wellinger J, Ollyo JB, Savary M, Fontolliet C, Chapus G. Le traitement chirurgical de l'endobrachy-oesophage. Helv Chir Acta 1988;55:695-698.

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10. Skinner DB, Walther BC, Riddell RH, Schmidt H, Iascone C, DeMeester TR. Barrett's esophagus. Comparison of benign and malignant cases. Ann Surg 1983;198:554-566.

11. DeMeester TR, Attwood SEA, Smyrk TC, Therkildsen DH, Hinder RA. Surgical therapy in Barrett's esophagus. Ann Surg 199;0212:528-542.

12. Skinner DB. Controversies about Barrett's esophagus. Ann Thor Surg 1990;49:523-524.

13. Streitz JM, Ellis FH, Gibb SP, Balogh K, Watkins E. Adenocarcinoma in Barrett's esophagus. A clinicopathologic study in 65 cases. Ann Surg 1991;213:122-125.

14. Moon MR, Schulte WJ, Haasler GB, Condon RE. Transhiatal and transthoracic esophagectomy for adenocarcinoma of the esophagus. Arch Surg 1992;127:951-955.

15. Menke-Pluymers MBE, Schoute NW, Mulder AH, Hop WCJ, van Blankenstein M, Tilanus HW. Outcome of surgical treatment of adenocarcinoma in Barrett's esophagus. Gut 1992;33:1454-1458.

Publication date: May 1998 OESO©2015