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Ann Thorac Surg 1999;68:1014-1020
© 1999 The Society of Thoracic Surgeons

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Original Articles: General Thoracic

Results of the Collis-Nissen gastroplasty in patients with Barrett’s esophagus

^a Division of Thoracic Surgery, Department of Surgery, Centre Hospitalier de l’Université de Montréal, Montréal, Quebec, Canada
^b Department of Nuclear Medicine, Centre Hospitalier de l’Université de Montréal, Montréal, Quebec, Canada

Presented at the Thirty-fifth Annual Meeting of The Society of Thoracic Surgeons, San Antonio, TX, Jan 25–27, 1999.

Abstract

Background. Barrett’s esophagus (BE) is an advanced stage of gastroesophageal reflux disease. Medical treatment and standard antireflux operations show a high failure rate. An elongated gastroplasty, wrapped by a total fundoplication should provide a tension-free repair with adequate protection against reflux. The aim of this study is to review the operative effects of a Collis-Nissen gastroplasty to treat reflux in Barrett’s esophagus.

Methods. From January 1989 to December 1997, 45 patients with BE (38 men, 7 women) aged 53.5 years, underwent a Collis-Nissen gastroplasty. Mean follow-up is 35.9 months (range, 6 to 110 months). Pre- and postoperative evaluations included symptom assessment, esophagogram, endoscopy, manometry, 24-hour pH study, and esophageal emptying scintigrams.

Results. There were no operative deaths. All reflux symptoms were controlled. Acid reflux was significantly reduced (percent time exposure decreased from 10% to 1%) and lower esophageal sphincter (LES) pressure were restored to normal (LES gradient increased from 4 mm Hg to 11 mm Hg). LES incomplete relaxation was noted in 50% of patients postoperatively. Endoscopically, mucosal damage from reflux healed but the columnar mucosa with intestinal metaplasia persisted.

Conclusions. The Collis-Nissen gastroplasty, in patients with BE, controls reflux disease, its symptoms, and the mucosal damage associated with this condition. It restores the LES gradient but increases the resistance to bolus transit. There is no regression of the abnormal mucosa despite reflux control.

Barrett’s esophagus (BE) is an increasingly frequent condition in which the normal squamous epithelium of the distal esophagus is replaced by a metaplastic columnar mucosa. Combined acid and alkaline refluxates may be responsible for the appearance of more severe mucosal damage [1, 2]. However, pancreato-biliary secretions are seen as an essential reflux component causing a repair pattern that leads to the appearance of intestinal metaplasia [3]. The potential development of carcinoma is known to be associated with this cell lineage [4]. Barrett’s esophagus is seen as an advanced complication of reflux disease. It appears following prolonged exposure to the damaging refluxate, and the first basis for treating Barrett’s esophagus is eliminating pathologic gastroesophageal reflux. In prospective trials, Attwood and colleagues, and Ortiz and coworkers (Table 1) reported that medical treatment fails to control reflux symptoms and damage in 54% to 88% of patients. Standard antireflux operations fail in 15% to 21% of cases. The long-term results reported by Csendes in 1998 show that simple partial or total fundoplication fail in 64% of their operated patients (Table 1). Neither medical nor surgical treatment results in regression of the columnar mucosa. For these reasons, we first deal with the reflux condition in patients with BE, leaving to subsequent follow-up the oncologic problem related to the intestinal metaplasia of its mucosa. We offer patients an elongated gastroplasty wrapped by a total fundoplication to provide a tension-free repair and adequate antireflux protection. The aim of this study is to evaluate the clinical results and the objective effects of a Collis-Nissen gastroplasty on Barrett’s esophagus.

From January 1989 through December 1997, 45 patients (38 men, 7 women) with mean age 53.5 years (range, 35–75 years), with documented intestinal metaplasia in their columnar lined esophagus, underwent a Collis-Nissen gastroplasty. Their average height was 170 cm (5.6 ft) and their mean weight was 75.8 kg (167 lb) at operation. The duration of reflux symptoms ranged from 3 to 37 years, with an average of 13 years. All patients had at least 6 months of acid suppression with proton pump inhibitor and/or anti-H2 medication occasionally in association with prokinetic agents. The mean follow-up is 3.0 years (range, 0.5–9 years). Seven patients had a previous Nissen fundoplication that failed 3 to 19 years following the initial operation. Pre- and postoperative evaluations included symptom assessment, esophagogram and upper gastrointestinal (GI) studies, endoscopy and biopsies, manometry, 24-hour pH studies, and esophageal emptying scintigrams.

Operation and indications
In all patients, indications for operation were mucosal and functional damage. Failed antireflux operation was associated with this type of damage in 7 patients. In addition, 38 patients had gastroesophageal reflux unresponsive to medical therapy. Six patients had bleeding episodes. None of the patients had either primary esophageal motor disorders or scleroderma that was treated beforehand. All patients were operated through a left thoracotomy. Thirty-seven patients had an uncut Collis-Nissen gastroplasty using the technique reported by Bingham, and Pera and coworkers [5, 6]. Eight patients had a cut Collis gastroplasty with a fundoplasty and Nissen fundoplication as modified by Reilly and Jeyasingham [7]: For the cut gastroplasty, the esophagus and proximal stomach are dissected as for an uncut Collis-Nissen gastroplasty. A surgical stapler (TA-30, AutoSuture; Auto Suture, United States Surgical Corporation Norwalk, CT) is applied along the lesser curvature of the stomach while a #50 mercury bougie is positioned in the stomach and held in place along the lesser curvature. The anterior and posterior walls of the stomach are stapled together, forming a 3-cm neo-esophagus with a well-measured and protected lumen diameter. The fundus is divided from the gastroplasty suture line. Transverse closure creates a wider fundus that is wrapped easily around the elongated gastroplasty. The fundic wrap covers the gastroplasty line and the transverse closure of the fundus with healthy gastric wall. This procedure differs from the technique initially described by Henderson, and Orringer and Sloan [8, 9] where the neo-esophagus is wrapped obliquely by the fundus remaining after transection with the GIA surgical stapler (Auto Suture, United States Surgical Corporation Norwalk, CT). The repair is reduced under the diaphragm and fixed in place by three sutures jointing the seromuscular apex of stomach with the apex of the fundoplication, and then passed through the diaphragm from the abdominal site to the thoracic surface and tied in the chest.

Symptom assessment
During the clinical interviews, patients were questioned on the presence or absence of four symptom categories: (1) dysphagia and/or slow emptying; (2) regurgitation and/or heartburn; (3) odynophagia and/or chest pain; (4) oropharyngeal symptoms including oral dysphagia and/or aspiration.

Radiology
Standard barium esophagogram and upper GI evaluation were obtained under fluoroscopic control with four to six frames printed per second. The presence of hiatal hernia, gastroesophageal reflux, and barium stasis were recorded. Other anatomic abnormalities such as esophageal dilatation, strictures, or narrowing were also noted.

Radionuclide esophageal scintiscan
This study was used to assess the emptying capacity of the esophagus. It was performed after a 4 to 6 hour fast. The patient stands upright in front of a large-field-of-view scintillation camera interfaced to a computer and equipped with a low-energy all-purpose parallel-hole collimator. After ingestion of a bolus of 10 mL of water labeled with 1.0 mCi of sulfur colloid Tc-99m, computerized data is acquired at 0.5-second intervals for 2 minutes over the whole esophageal region. Five quantitative parameters were generated: the time for esophageal clearance of 25%, 50%, 75%, and 90% of the ingested radioactive water, and the esophageal stasis at 2 minutes. The esophageal emptying time is interpreted as the time needed to clear 90% of the ingested bolus.

Manometry
Fasting patients were assessed using a four-lumen polyvinyl motility catheter (Mui Scientific, Mississauga, Canada). The technique was detailed in our previous publication [6].

24-hour pH recording
Esophageal pH was recorded using the Sandhill ambulatory pH recorder (Littleton, CO), and the technique was also described previously [6].

Control group
Esophageal nuclide transit studies, esophageal manometric and pH metric recordings were compared to those of a normal patient population (mean age 50.5 years, male:female = 9:11) who underwent a full esophageal investigation for unrelated symptoms (atypical epigastric or chest pain). These patients had no evidence of esophageal disease or upper GI pathology following their evaluations.

Endoscopy
Endoscopic examinations were performed using a video-monitoring system (Olympus, GIF-130, Olympus Canada, Toronto). Mucosal lesions were classified using Armstrong and colleagues’ MUSE system in which metaplasia, ulcer, stricture, and erosion are quantified [10]. The distance of the proximal limit of the columnar mucosa from the incisors was recorded. The level at which the tubular esophagus joins the regular rugal folds of the gastric cavity is recorded second. The crural impression of the hiatus is recorded third. After the operation, the top of the fundoplication is interpreted as the distal end of the esophagus at diaphragmatic level. The length of the columnar lined mucosa is computed from these observations. The diagnosis of Barrett’s esophagus is based on the presence of intestinal-type goblet cells in at least one biopsy from the abnormal mucosa in the lower esophagus, irrespective of its length [11]. The diagnosis of dysplasia followed Riddle’s criteria [37] and was recorded separately.

Statistical analysis
Unordered categorical data were analyzed by means of McNemar-test or Fisher’s exact probability test. Wilcoxon or Mann-Whitney U test was used in the comparison between paired or unpaired ordinal categorical data. Parametric data were expressed as median, 15% and 85% percentiles. Kruskal-Wallis test was applied for the multiple comparison, and Newmenyi test was used afterwards for each pair comparison. However, when the data had a normal distribution, analysis of variance (ANOVA) was applied when appropriate. The statistic values were reported. A two-tailed exact p value was provided unless it was greater than 0.2 or less than 0.005. A p value less than 0.05 was considered as statistically significant.

Results

There were no postoperative deaths or major esophageal complications. One patient had bilateral pneumonia with adult respiratory distress syndrome after the operation and recovered eventually after 28 days of intensive therapy. The hospital stay for the remaining patients ranged between 6 and 18 days.

Clinical presentation
Following surgery, all reflux symptoms (regurgitation and heartburn) disappeared (42 of 45 for preop versus 0 of 45 for postop, ² = 42.0, p < 0.005). Pain on swallowing disappeared as well. Dysphagia episodes present in 16 patients before the operation and in 3 patients after operation (² = 11.28, p < 0.005). Oropharyngeal symptoms were rarely present despite the reflux severity. Total body weight, when patients were seen at first consultation was 78.9 kg (174 lb). They had their weight reduced for the operation to 75.8 kg (167 lb). Following surgery, the patients decreased their weight further to 72.7 kg (160 lb) (F = 16.89, p < 0.005).

Radiology
The Collis-Nissen gastroplasty stopped the gastroesophageal reflux (14/45 for preop versus 0/45 for postop, ² = 14.0, p < 0.005) and corrected the hiatal abnormality (26/45 for preop versus 2/43 for postop, T = 1374, p < 0.005). At the same time, it increased the esophageal stasis above the fundoplication (3/45 for preop versus 15/45 for postop, ² = 10.76, p < 0.005) and resulted in a subsequently wider esophagus (5/45 for preop versus 15/45 postop, ² = 6.743, p = 0.009). Pathologic stricture in 11 patients before the operation disappeared on the esophagogram, leaving the fundoplication imprint as the sole narrowing effect evident on postoperative roentgenogram. In 2 patients where a postoperative sliding type I hernia is suggested, the mucosal folds of the columnar mucosa were responsible for this observation.

Radionuclide esophageal scintiscan
Results are detailed in Table 2. Patients with Barrett’s esophagus revealed a significant delay in their esophageal emptying capacity when compared with control group. They showed an increased esophageal stasis at 2 minutes. The Collis-Nissen gastroplasty is seen as further increasing the resistance to emptying. Postoperatively, the esophagus showed a poorer emptying capacity of the radionuclide bolus. Esophageal stasis of the liquid bolus at 2 minutes remained at 4%, significantly higher than the 2% in the control population.

24-hour pH monitoring
Table 2 summarizes our findings. Acid reflux was abolished by the operation with each parameter restored to normal. Ten patients still showed abnormal postoperative esophageal acid exposure (time % was greater than 7%). The acid exposure ranged from 7% to 53% of the time with a median of 13.5%. Eight of these 10 patients had an intact fundoplication with a normal LES gradient (Figs 1A, 1B). Two others showed a flattened but intact repair under the diaphragm with LES gradients respectively at 1 and 6.7 mm Hg (Fig 1C).

View larger version (166K): [in this window] [in a new window]   Fig 1. Endoscopic appearance in patients with Barrett’s esophagus after Collis-Nissen gastroplasty. (A) Normal intragastric view of uncut Collis-Nissen gastroplasty. The remaining gastric fundus wraps the neo-esophagus created from the smaller curvature of the stomach. (B) Intragastric view of cut Collis-Nissen gastroplasty (Jeyasingham modification). The neo-esophagus is wrapped by the same orientation of the wrap as for a standard Nissen fundoplication. (C) Intragastric view of flattened uncut Collis-Nissen gastroplasty. (D) Squamous islands (arrows) appear within the residual columnar lined esophagus following reflux correction by Collis-Nissen gastroplasty.

Barrett’s esophagus is known and seen as an advanced complication of pathological gastroesophageal reflux. The information that led to this affirmation is derived mostly from observations in esophageal function laboratories. Starting in the early 1960s, it was observed that patients with BE had an absent or defective lower esophageal sphincter [12, 13]. Low amplitude contractions in the esophageal body were also observed in association with the deficiencies of the LES [14]. It was in the early 1980s that Ransom and colleagues, Iascone and coworkers (Table 1), and Herlihy and associates [15] suggested that when considering the mucosal damage of reflux esophagitis, Barrett’s esophagus was always associated with the worst functional alteration at the LES level. Kahrilas and coworkers, and Stein and colleagues [16, 17] further strengthened this belief in the late 1980s and early 1990s.

In our patient population, symptoms had been present for a mean of 13 years before medication and/or antireflux correction were offered. When compared to a control group, those patients with a well-documented columnar-lined esophagus containing goblet cells revealed a virtually absent LES gradient (4 mm Hg) with esophageal contraction pressures that were altered over the whole esophageal body. Propulsion is similarly affected. This report further documents that BE patients have the most significant functional abnormalities seen in pathologic reflux disease.

An added argument supporting the surgical approach for BE patients is the extremely high failure rate with medical management. Prospective comparison on the effects of therapies in BE patients are available only since the early 1990s. McCallum and colleagues (Table 1) reported to The American Gastroenterology Association the long-term follow-up of 152 medically managed patients. Twenty percent of their group went on to develop dysplasia, suggesting less protection against these changes than for a smaller surgical group they followed in parallel. Attwood and coworkers (Table 1) observed 45 BE patients. In the 26 patients managed medically, 88% had persisting symptoms of heartburn and/or dysphagia, and 38% of their group went on to develop further complications related to reflux. Ortiz and associates [30] (Table 1), in their observations on 59 BE patients randomized to medical or surgical treatment, reported that when managed with medication alone, patients show persisting inflammatory lesions in 54% and develop a stricture in 47%. Katz and coworkers [18] observed endoscopically 102 patients with BE between 1970 and 1994. They found that dysplasia appeared in 23 patients out of 86 treated exclusively with medication. No patient with an antireflux operation revealed these changes. Katzka and Castell [19] documented that symptom suppression with proton pump inhibitor medication did not guarantee acid suppression with normalization of esophageal acid exposure. Furthermore, eradication of bilio-pancreative reflux has not been documented even if acid suppression seems adequate.

Standard antireflux operations have been proposed for many years to manage the pathologic reflux responsible for BE. Table 1 summarizes the experience extracted from the literature when looking specifically at the results of surgical treatment for BE. The assessment of both the surgical and medical publications is rendered difficult because of the changes in definition over the years, when describing what is Barrett’s esophagus. Total or partial fundoplication without elongation results in a high failure rate when trying to control reflux disease. Most of the reported operations are Nissen fundoplication or Belsey and Hill repairs. Objective documentation of reflux events and damage is provided in approximately 50% of reports. When interpreting symptoms, 10% to 60% of standard antireflux operations fail. The frequent presence of a high stricture at the level of the squamocolumnar junction offers one possible explanation for this high failure rate. When Mr Belsey’s experience was reported with the use of his repair, poor results were documented in over 45% of patients when a stricture was present before the operation. Because of the high failure rate in using a standard repair, and because of the frequent association of BE with a stricture, we consider that BE is a pathological condition in which the damaged esophagus is shortened, exposing the operative repair to the same failure risks that were reported with the stricture esophagus by Orringer and Sloan and Belsey and Skinner [9, 20].

The creation of an elongation gastroplasty provides improved intraabdominal length with the neo-esophagus. A good antireflux mechanism is afforded with the total fundoplication. The creation of a total fundoplication gastroplasty may vary in technique and this may influence reflux control. We consider that this operation offers good reflux control but at the same time increases resistance to transit. This is supported by the functional results shown at the LES level where a good resting pressure gradient is restored but at the cost of an incomplete relaxation. The Nissen fundoplication has been shown to produce a similar effect. The functional abnormalities documented in the esophageal body remain unchanged, suggesting permanent functional damage from reflux. The decrease in contraction pressures seen in the proximal esophagus suggests a wider esophageal lumen associated with the obstructive nature of the repair.

Despite good overall control of acid reflux, 10 patients still show abnormal acid presence in their esophagus. At present we cannot say if this acid exposure is due to an operation that fails to control reflux on a definitive basis, or if there is continuous secretion of acid by the intraesophageal epithelium. The abnormal mucosa has not disappeared in any of the treated patients. The presence of goblet cells in the remaining mucosa, as well as under the regenerated squamous epithelium islands, remains an indication for continued endoscopic surveillance. Despite good results for reflux control, there is no evidence that cellular genetic changes have not already occurred, even if preoperatively there is absence of dysplasia. Current recommendations by Williamson and associates and McDonald and colleagues (Table 1) are that endoscopic surveillance remains essential even if a successful antireflux operation has been offered.

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): André C. Duranceau Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chen, L.-Q. Articles by Duranceau, A. C. Search for Related Content PubMed PubMed Citation Articles by Chen, L.-Q. Articles by Duranceau, A. C.