Does esophageal dysfunction in CLE influence bolus propulsion through the esophagus? Does it differ from that of reflux esophagitis?
HJ. Stein (Munich), T.R. DeMeester (Los Angeles)
Esophageal clearance function is a major determinant of esophageal exposure to gastric juice. Factors important in esophageal clearance include esophageal peristalsis, gravity, salivation and anchoring of the distal esophagus in the abdomen. A defect in any one can prolong esophageal exposure to refluxed gastric content and contribute to the development of mucosal injury. Of the factors mentioned, effective esophageal peristalsis is the most important determinant of esophageal clearance function . In addition, disordered esophageal peristalsis may also hamper propulsion of a swallowed bolus from the negative intrathoracic pressure environment to positive intra-abdominal pressure environment, and thus cause dysphagia .
Using simultaneous manometric and video-fluoroscopic recording of barium swallows, Kahrilas and co-workers have shown that propulsion of a bolus and clearance of refluxed gastric contents depends on peristaltic contractions of sufficient amplitude . In their study nonperistaltic contractions (i.e., simultaneous, interrupted and isolated contractions) and peristaltic contractions of insufficient amplitude resulted in splitting of a swallowed barium suspension and retention of contrast medium in the esophageal body. The minimal contraction amplitude required to occlude the esophageal lumen and propel a liquid bolus was about 30 mmHg in the distal esophagus . This indicates that esophageal clearance function can be assessed by manometry of the esophageal body.
Detailed functional studies of the esophageal body using standard manometry show that the mean amplitude of contractions in the distal half of the esophagus, following 10 wet swallows, is decreased in patients with Barrett's esophagus, as compared to patients with gastroesophageal reflux disease and esophagitis (Fig. 1) [4,5]. A decreased esophageal contraction amplitude in patients with Barrett's esophagus during the upright, supine and meal periods can also be documented with the new technique of ambulatory 24-h esophageal motility monitoring . Ambulatory motility monitoring also shows that, compared to patients with esophagitis, patients with Barrett's esophagus also have an increased frequency of isolated contractions and contractions with an amplitude below 30 mmHg (Fig. 2), resulting in a markedly increased prevalence of contractions that are ineffective for bolus propulsion and clearance of refluxed gastric juice . Combined ambulatory esophageal manometry and pH monitoring confirms that a compromised clearance function results in a prolonged duration of reflux episodes, particularly during the night when the subject is in the supine position and gravity does not aid in clearance of the refluxate . This explains the increased frequency of prolonged reflux episodes in patients with Barrett's esophagus as compared to patients with gastroesophageal reflux and esophagitis (Fig. 3).
Figure 1. .Mean of amplitude of esophageal contractions following 10 wet swallows measured 1,6, 11, 16, and 21 cm below the upper esophageal sphincter (UES) in normal volunteers, patients with esophagitis and patients with Barrett's esophagus. *: p < 0.01 vs. esophagitis and normal volunteers. From , with permission.
These observations have two important implications regarding surgical therapy in patients with Barrett's esophagus. First, the loss of peristaltic function in Barrett's esophagus appears to be, at least in part, secondary to persistent reflux across a mechanically defective lower esophageal sphincter (LES). Since the loss of clearance function further prolongs esophageal exposure to gastric juice, a vicious cycle is initiated. Even with complete suppression of reflux by an antireflux procedure or proton pump inhibitors, esophageal contractility may not recover once fibrosis of the esophageal wall has developed and the mean amplitude of contractions has deteriorated below 30 mmHg [6,7]. Consequently, a correction of the underlying defect, i.e., the mechanically defective LES, should be encouraged early in the course of the disease. Secondly, once esophageal peristalsis has deteriorated, an antireflux repair with little outflow obstruction, i.e., a partial fundoplication, should be considered to avoid induction or accentuation of postoperative dysphagia.
Figure 2. .Mean frequency of isolated and low amplitude contractions (<30 mmHg) on ambulatory 24-h esophageal motility monitoring in normal volunteers, patients with esophagitis and patients with Barrett's esophagus. *: p < 0.01 vs. esophagitis and normal volunteers.
Figure 3. .Frequency of reflux episodes and reflux episodes lasting longer than 5 min (pH < 4) on ambulatory 24-h esophageal pH monitoring in normal volunteers, patients with esophagitis and patients with Barrett's esophagus. *: p < 0.01 vs. esophagitis and normal volunteers. From  with permission.
2. Singh S, Stein HJ, DeMeester TR, Hinder RA. Nonobstructive dysphagia in gastroesophageal reflux disease - a study with combined ambulatory pH and motility monitoring Am J Gastroenterol 1992;87:562-567.
O. Ekberg (Malmo)
The intestinal metaplasia seen in Barrett's esophagus is confined only to the mucosa. It may involve the muscularis mucosa but never reaches into the muscularis propria . Therefore, the mucosal metaplasia does not per se influence esophageal motility. However, Barrett's esophagus is regularly seen together with reflux esophagitis, which might be severe. Areas of squamous epithelium between mucosal metaplasia is therefore regularly, to a more or less advanced degree, altered by reflux esophagitis. Such esophagitis may reach into the muscularis propria, and thereby have an influence on the motility of the esophagus. However, superficial esophagitis, e.g., grade I, is also regularly seen together with abnormal motility, which for instance can be registered during barium swallow and/or manometry. Such dysmotility can be either hypomotility with defective propulsion in the esophagus or hypermotility seen as nonpropulsive vigorous contractions. The mucosal metaplasia as well as esophageal dysmotility are both likely to be secondary to gastroesophageal reflux disease.
Patients with Barrett's esophagus actually have been shown to regularly suffer from severe mechanical dysfunction, both in terms of lower esophageal sphincter dysfunction and also defective clearance of reflux material (both acid and alkaline, from the esophagus) .
It has been shown that the mean amplitude and the propagation rate of the contractile waves in the distal third of the esophageal body in Barrett's esophagus is similar to those found in mild and severe reflux esophagitis . The proportion of abnormal waves are, however, significantly higher in the Barrett's group than in patients with severe esophagitis. In patients with Barrett's esophagus, the manometric esophageal pattern is not different from that found in patients with reflux esophagitis
Figure 1. .Esophageal manometry from mid and distal esophagus before (A) and after (B) fundoplication in a patient with Barrett's esophagus and reflux esophagitis. In (A) there are very weak and simultaneous contractions (arrows) in the distal esophagus and absence of peristalsis in mid esophagus. After surgery (B) peristalsis returned to almost normal (arrow). However, still some simultaneous contractions (open arrow) were registered.
(Fig. 1). The amplitude of esophageal contractions in patients with Barrett's esophagus is proximally normal but regularly markedly reduced in the distal three fifth . There is also a high prevalence of simultaneous, dropped and/or interruptive waves. Such peristaltic abnormalities are found in up to 83% of patients with Barrett's esophagus . The presence of nonpropulsive contractions and pharyngeal swallow not being followed by esophageal peristalsis is not specific for Barrett's esophagus. However, Barrett's esophagus is regularly seen with severe esophagitis and the degree of reflux esophagitis does correlate with motor abnormalities of the esophagus.
2. Stein HJ, Barlow AP, DeMeester TR, Hinder RA. Complications of gastroesophageal reflux disease. Role of the lower esophageal sphincter. Esophageal acid and acid/alkaline exposure, and duodenogastric reflux. Ann Surg 1992;216:35-43.