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J Thorac Cardiovasc Surg 1994;107:1244-1250
© 1994 Mosby, Inc.
GENERAL THORACIC SURGERY |
Los Angeles, Calif.
From the University of Southern California School of Medicine, Department of Surgery, Los Angeles, Calif.
Address for reprints: Tom R. DeMeester, MD, University of Southern California School of Medicine, Department of Surgery, 1510 San Pablo St., Suite 514, Los Angeles, CA 90033-4612.
Abstract
The outcome of Nissen fundoplication in patients with a nonspecific motility abnormality compared with the outcome in patients with normal motility is unknown. One hundred consecutive patients who underwent primary Nissen fundoplication were evaluated before and a median of 50 months after operation, with emphasis on the presence of a preoperative motility disorder and its relationship to preoperative and postoperative symptoms. Compared with patients who had normal motility, patients with a nonspecific motility abnormality had a greater prevalence and severity of heartburn and regurgitation before operation. These patients also had a greater esophageal exposure to gastric juice on pH monitoring as a result of poorer esophageal clearance function. The prevalence and severity of preoperative dysphagia was not related to the presence of a motility disorder. A 90% or a 95% actuarial success rate was achieved in the relief of heartburn and regurgitation over a 96-month period in patients with and without a motility abnormality. The overall actuarial success rate was 93%. Dysphagia was rarely caused or made more severe by the procedure; if present before the operation, it was relieved in most patients. The prevalence of persistent postoperative dysphagia was similar in patients with and without a motility abnormality. The success of Nissen fundoplication in properly selected patients is not affected by the presence of a nonspecific motility disorder. (J THORACCARDIOVASCSURG1994;107:1244-50)
The Nissen fundoplication has been maligned by a reported prevalence of dysphagia after the operation. 
1,2 Indeed, studies have shown that persistent dysphagia after the operation can occur from errors in technique such as misplacing the fundoplication around the stomach or making the fundoplication too long or too tight. 3,4 Further, it has been suggested that Nissen fundoplication done in patients with poor contractility from advanced reflux disease results in dysphagia by adding too much outflow resistance. 5 Although a nonspecific motility disorder can be associated with gastroesophageal reflux disease, its prevalence and how it affects the symptoms of the disease or the outcome of a Nissen fundoplication is not known. To answer these questions, we studied 100 consecutive patients who underwent a primary Nissen fundoplication for gastroesophageal reflux disease.
PATIENTS AND METHODS
Study population
The study population consisted of 58 men and 42 women who had a primary antireflux repair for gastroesophageal reflux disease by the same surgeon (T.R.D.). The median age was 55 years, with a range of 20 to 86 years. Patients were selected for the operation according to previously published criteria, 6-8 which are summarized in Table I. All patients had 24-hour esophageal pH monitoring to document an increased esophageal exposure to gastric juice. Two patients with achlorhydria were included on the basis of a positive result on a standard acid reflux test. Standard manometry was used to determine the presence of a mechanically defective sphincter and evaluate the motility of the esophageal body. Patients with a contraction amplitude less than 20 mm Hg, in the distal three fifths of the esophagus, or with a named motility disorder such as achalasia, scleroderma, or diffuse esophageal spasm, were excluded.
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Questionnaire
Before the operation patients completed a detailed questionnaire regarding the symptoms of heartburn, regurgitation, and dysphagia. The severity of each symptom was graded from 0 to 3 (Table II). After operation, a similar grading of symptoms was done with a specific focus on the recurrence of heartburn, regurgitation, and persistent dysphagia; that is, symptoms lasting longer than 3 months after the operation. The median follow-up was 50 months, with a range of 3 to 96 months.
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(Table III).
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8 All patients had increased esophageal exposure to acid as defined by the total time of esophageal acid exposure or a DeMeester score greater than the 95th percentile of the results in normal subjects (>4.5% or >16.7, respectively).
Operation
Nissen fundoplication was done in a similar manner in each patient, with the use of modifications designed to overcome the side effect of persistent dysphagia. 6 Briefly, the fundoplication was constructed by dividing the short gastric vessels to mobilize the gastric fundus, sizing the fundoplication with a 60F Maloney bougie, enveloping the lower esophagus with the anterior and posterior gastric fundic walls over a distance of 1 to 1.5 cm, and properly positioning the fundoplication by placing its right lip between the right vagus nerve and the body of the esophagus. The only modification of the previously published method was the use of pledgets on the outside of the fundoplication and not between the fundus and the esophagus.
A transthoracic approach was used in patients who had a short esophagus, were obese, or had concomitant pulmonary disease that required definition. A short esophagus was suspected when the distance on endoscopic examination between the crura and gastroesophageal junction was greater than 5 cm and in patients who had a stricture, Barrett's esophagus, or a hiatus hernia that did not reduce on the upright barium roentgenogram. A highly selective vagotomy was done concomitantly through the abdominal or thoracic incision when the patient had documented hypersecretion and an active or confirmed history of duodenal ulcer disease.
Statistical analysis
The Fisher exact test was used to compare proportions. The Mann-Whitney U test was used for comparison of medians. The Kaplan-Meier procedure was used to determine actuarial success of Nissen fundoplication and the Mantel-Cox test was used to compare actuarial success for patients with and without a motility abnormality. Statistical analyses were done with a commercially available statistical package (SAS 6.04, SAS Institute, Inc., Cary, N.C.). Unless otherwise stated, all results are expressed as means ± standard error of the mean.
RESULTS
On the basis of the criteria from 50 normal subjects, 56 patients had normal and 44 patients had abnormal esophageal body motility. There was no significant difference between patients with and those without a motility abnormality for age, sex, height, or weight. Figs. 1 and 2 show the prevalence and severity of symptoms in all patients, those with normal motility, and those with abnormal motility. The prevalence and severity of heartburn and regurgitation in patients with a motility abnormality were significantly greater than in those with normal motility. The prevalence and severity of dysphagia were similar in patients with normal and those with abnormal motility. This similarity remained even when patients with a stricture were excluded.
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After operation 70% of patients were able to belch, and 25% of those who tried were able to vomit. Twenty-three percent of patients admitted on direct questioning to occasional bloating, but only 10% volunteered the symptom as a troublesome complaint. There was no difference in the occurrence of these symptoms in patients with normal and those with abnormal motility. Overall, 48% of patients noticed an increase in flatus after operation but only two considered this a problem. Interestingly, significantly more patients with normal motility noticed this symptom than did those with abnormal motility (60% versus 33%, p < 0.05).
DISCUSSION
The clinical significance of a nonspecific motor abnormality is unclear. The term has been created to classify an abnormality in either contraction amplitude or wave pattern that does not fit the criteria for a named motor disorder, that is, achalasia, diffuse esophageal spasm, nutcracker esophagus, or scleroderma.
In the present study, patients who had study results below the 5th percentile for contraction amplitude, that is, 30 mm Hg, in one or more locations in the lower three fifths of the esophagus, or above the 95th percentile for number of dropped contractions, simultaneous waves, or multipeaked contractions were classified as having a nonspecific motility disorder. They had a greater prevalence and severity of heartburn and regurgitation than those with normal esophageal function. They also had a greater esophageal exposure to gastric juice by virtue of a larger number of reflux episodes that lasted longer than 5 minutes. Kahrilas and associates 9 have attempted to study the effect of nonspecific motility disorders on esophageal function by performing simultaneous manometry and videofluoroscopy. They found that a contraction amplitude of less than 30 to 35 mm Hg in the distal esophagus or the presence of simultaneous waveforms was associated with poor propulsion of liquid barium into the stomach. Both the findings of Kahrilas and associates 9 and our findings show that a nonspecific motor abnormality results in poorer clearance of refluxed gastric juice from the esophagus. This leads to a longer exposure of the esophageal mucosa to gastric juice and sensation of heartburn and regurgitation. Although a nonspecific motility disorder can affect the symptoms of the disease, it does not affect the outcome of a Nissen fundoplication, in that the relief of heartburn and regurgitation was similar in patients with normal motility and those with an abnormal motility. This would indicate that the principal problem in patients with gastroesophageal reflux disease is a defective valve and, once this is corrected, a motility abnormality has minimal effect.
This study showed that dysphagia is a common symptom in gastroesophageal reflux disease, even in the absence of mechanical obstruction from a stricture. This finding has not been fully appreciated. 10,11 Although it is possible that a nonspecific motility abnormality of the esophageal body could interfere with the passage of food and give rise to the sensation of dysphagia, this does not seem to be true, because patients with abnormal motility did not have an increased prevalence of this symptom. Perhaps the assessment of esophageal motility by stationary manometry is not sensitive enough to detect motility abnormalities that can cause dysphagia during eating. Ambulatory esophageal manometry broadens the analysis from 10 to 1000 swallows and evaluates esophageal activity during meals. With this device, we have found that patients with dysphagia do not have an increased percentage of peristaltic waves during meal periods as normal subjects do. Consequently, the dysphagia may be due to the inability of esophageal motor activity to organize into effective peristalsis when the patient eats. 12 It is unlikely that the sensation of dysphagia was due to the presence of mucosal inflammation, because the presence of the symptom was not related to the presence or severity of esophagitis.
The presence of a nonspecific motility disorder before operation appears to have little effect on the outcome in regard to dysphagia, in that the symptom was relieved in as many patients with abnormal motility as in those with normal motility and only three patients free of dysphagia before the operation had dysphagia after the operation. In all of them, dysphagia was scored as grade 1 and was not considered a significant problem by the patient. Of the patients who had dysphagia before operation, in only one was it made more severe, that is, it increased from grade 1 to 2. The remainder were either improved or free of dysphagia after operation. From this experience we conclude that dysphagia lasting longer than 3 months is rarely induced by a properly performed Nissen fundoplication even when a nonspecific motility disorder is present. The exception to this is when there is a marked loss of esophageal function, that is, contraction amplitudes lower than 20 mm Hg throughout the lower three fifths of the esophagus. In this situation, we prefer a partial fundoplication, which is frequently accompanied by a Collis gastroplasty because of esophageal shortening.
It is interesting that all five patients with grade 2 dysphagia after operation had transthoracic repairs. It is our impression that this was due to the manner in which we were constructing the fundoplication when using the transthoracic approach. We were suturing the lips of the wrap posteriorly, which resulted in a long, bulbous anterior fundoplication that probably increased resistance to esophageal emptying. We have since switched to suturing the wrap anteriorly and have alleviated the problem.
The prevalence of mild gastric bloating after operation was 23% and similar to that in our previous report. 6 This symptom has been overemphasized as a surgical side effect, in that a recent multicenter study found that the prevalence of bloating was similar in medically and surgically treated patients. 10 This complaint is probably due to ingested air caused by continuous swallowing, a habit acquired preoperatively to clear the esophagus of refluxed acid.
An increase in flatus occurred in almost half of the patients after operation, but this decreased with time. It is interesting that a higher prevalence of excessive flatus after operation was noted in patients with normal esophageal body motility. It is possible that patients with compromised body motility are less able to pump swallowed air into the stomach, that is, the movement of air, unlike that of food, is unassisted by gravity and is very motility dependent.
In summary, the results show that in properly selected patients a Nissen fundoplication gives excellent relief of regurgitation and heartburn. Preoperative dysphagia is relieved in most patients and rarely occurs as a new symptom after operation. The presence of a nonspecific motility disorder does not affect the outcome of the operation and is of minimal importance in selecting patients for operation.
Appendix: DISCUSSION
Dr. Lucius D. Hill (Seattle, Wash.).
This paper illustrates the futility of trying to correlate symptoms with the lower esophageal sphincter pressure and motility. The reason this is not possible is that these are not the primary barriers to reflux. We now have the technology to look at the gastroesophageal junction with the retroflexed endoscope. In disease-free persons the endoscope would show a beautiful, one-way flap valve on the lesser curvature, which is the primary barrier to reflux. The esophageal junction is anchored down posteriorly to the preaortic fascia. Because it is anchored down, it can generate propulsive peristaltic waves that look good on a tracing. The motility disturbance that the authors describe in this paper is the result of the gastroesophageal junction losing its attachment and not being anchored, as in a hiatal hernia.
The Nissen procedure does not anchor the gastroesophageal junction down so there is no reason to believe that the motility is going to change, as the authors so nicely show in these elegant studies. The motility disorder persists. The authors have picked one parameter, reflux, and claim a 93% success rate over 8 years; but if you read on you see a little bit of a different story. Twenty percent of the patients had dysphagia, 5% had severe postoperative dysphagia (two requiring reoperation and one an esophagectomy in another hospital for persistent stric ture), 30% were unable to belch, 75% unable to vomit, 23% had bloating, and 10% had severe, troublesome, disabling gas bloat.
The reason for this is that the Nissen fundoplication creates an abnormal 360-degree valve rather than the nice 180-degree valve that we would see in disease-free persons. Second, it does not anchor the gastroesophageal junction, so the esophagus has no way to generate peristaltic waves. This is consistent with the findings in the recent report in The New England Journal of Medicine that compared surgical and medical therapy and showed operation was superior to medicine, and yet the 56 patients who comprised the surgical experience had horrendous complications: mediastinal abscess, peritoneal abscess, high degree of gas bloat, and 80% of the patients had one or more surgical complications after operation, and yet we call this good. It is hard to say what is bad.
In a series of nearly 200 repeat Nissen procedures, we have been able to show that by anchoring the gastroesophageal junction down, the motility disorder described by the authors disappears in all but about 5% of cases.
I would like to ask the authors three questions. First, did they look at the valve in these patients before and after operation? Second, have they ever considered constructing a normal 180-degree valve that beautifully curtails reflux but does not have the side effects and have they considered anchoring it to the gastroesophageal junction? Finally, why not take these studies and carry the same technology to the operating room? If you do not get the pressure right in the operating room, all those studies do not help the patient very much.
Dr. Bremner.
Thank you very much, Dr. Hill. In this study we did not examine the effect of the operation on the motility abnormalities, as you suggested, but this was looked at in a recent publication of ours. In that study we found that mild abnormalities in contraction amplitude improve after Nissen fundoplication, but when the mean amplitude of the lower two thirds of the esophagus falls below 30 mm Hg there is no improvement in esophageal body function. We interpret this as meaning that once severe impairment in esophageal function occurs, the damage done by long-term reflux is permanent. We suggest that Nissen fundoplication done early in patients with gastroesophageal reflux disease will allow preservation of adequate esophageal body function.
I find your interpretation of our postoperative symptoms somewhat disturbing. Any antireflux procedure is aimed at primarily reducing the symptoms of heartburn and regurgitation. The symptom of dysphagia has not been closely examined previously and has remained somewhat of an enigma in this disease. It was one of the main points of this paper to attempt to shed some light on this area. You are correct in that 19% of our patients had some degree of dysphagia after operation; however, only three of these patients had the symptom as a new symptom and that was mild in all three cases, that is, the patients had an occasional sensation of coarse food sticking for a few seconds but it resolved spontaneously. It did not affect their dietary habits. Only one patient's condition increased from a grade 1 to a grade 2 and this was considered a surgical complication in that the Nissen fundoplication had herniated into the chest. All other patients with some degree of postoperative dysphagia improved somewhat or remained the same. This dysphagia was not related to the presence of a motor disorder as seen on stationary motility study or to the presence of a stricture. Possibly a difference in patient perception exists, or, as I suggested, stationary motility studies may not be sensitive enough to detect subtle motility abnormalities that occur during meal periods and that would account for the symptom of dysphagia during swallowing of food. At any rate, the Nissen fundoplication improved the symptom of dysphagia in most patients.
The postoperative symptom of bloating is probably not related to the surgical procedure as was nicely shown in The New England Journal of Medicine article you referred to. In that study, bloating was as common in medically treated patients as in surgically treated patients. More likely, the symptom reflects habitual air swallowing or a more global foregut disorder, that is, of the stomach and duodenum, in these patients, which is unaffected by either surgical or medical management.
As regards intraoperative pressure monitoring, this is something that we have indeed looked at in the past. We have found, as many others have, that intraoperative pressures bear little relationship to pressures found a few weeks after operation and have little value in assessing the function of a surgically corrected valve. Besides, the Nissen fundoplication works whether complicated intraoperative monitoring is done or not.
Dr. Hill.
Did you look at the valve?
Dr. Bremner.
Yes, we have looked at the valve with the retroflexed endoscope, and more recently with laparoscopes through gastrostomies in animal models. We describe the valve that is seen through the endoscope as a "nipple" and do not conceive of the valve as a "flap" as you describe. In patients with little or no pressure of the lower esophageal sphincter, this valve appears patulous, but after operation, the "nipple," which looks exactly like that seen in disease-free subjects, is restored.
Dr. Hill.
Did you ever consider constructing a 180-degree valve and anchoring it down rather than constructing a 360-degree valve, unanchored?
Dr. Bremner.
Our experience with the Hill procedure you are referring to is limited, and our experience has been mostly with the Nissen fundoplication. By the way, the Nissen procedure is not unanchored, as you say. The diaphragmatic closure and the fundoplication anchor the lower esophageal sphincter in a physiologic way without having to suture the esophagus under tension to the preaortic fascia.
Footnotes
Read at the Nineteenth Annual Meeting of The Western Thoracic Surgical Association, Carlsbad, Calif., June 23-26, 1993. 
References
This article has been cited by other articles:
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  M. Barreca, B. K. Oelschlager, and C. A. Pellegrini Outcomes of Laparoscopic Nissen Fundoplication in Patients With the "Hypercontractile Esophagus" Arch Surg, June 1, 2002; 137(6): 724 - 728. [Abstract] [Full Text] [PDF]
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M. Viljakka, K. Saali, M. Koskinen, L. Karhumaki, J. Kossi, M. Luostarinen, O. Teerenhovi, and J. Isolauri Antireflux Surgery Enhances Gastric Emptying Arch Surg, January 1, 1999; 134(1): 18 - 21. [Abstract] [Full Text] [PDF]
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2 1.29, p = not significant).
