Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Mucosa
 The
 Esophagogastric  Junction
 Barrett's
 Esophagus

  Browse by Author
  Browse by Movies
OESO©2015
 
Volume: Barrett's Esophagus
Chapter: Pathophysiology
 

What can be concluded from 24-hour pH studies in patients with achalasia?

J.M. Streitz, F.H. Ellis (Duluth, Boston)

Patients with achalasia, both before and after treatment, may display evidence of abnormal gastroesophageal reflux (GER) during 24-hour pH monitoring. Since an increasing severity of GER leads to an increasing incidence of Barrett's esophagus, such data is useful in speculating upon the incidence and etiology of Barrett's esophagus in such patients.

Untreated achalasia

GER would be unexpected in a patient with untreated esophageal achalasia, whose lower esophageal sphincter (LES) Barrett's esophagus is hypertensive and relaxes incompletely with swallowing. Nonetheless, abnormal distal esophageal acid exposure is well documented in such patients, occurring in 2.5% to 20% of patients tested [1, 2]. Explanations for this low esophageal pH include:
- transient LES relaxation,
- slow esophageal clearance of refluxed acid due to an aperistaltic esophageal body,
- fermentation of retained food.

The first mechanism is poorly documented but seems likely in light of 24-hour pH recording data. The second mechanism is unequivocally documented, and the third is theoretically possible but seems unlikely to provide a major contribution to esophageal acidification.

Twenty-four hour pH recordings in patients with untreated achalasia demonstrate three distinct patterns in our experience:
- absence of reflux events,
- episodic reflux with slow clearance,
- prolonged acid exposure with failure to clear or neutralize refluxed acid.

Most patients show no evidence of acid reflux, a pattern exemplified by Figure 1a. In those patients with abnormal acid exposure, abrupt drops in pH, consistent with GER, are

Figure 1. A. 24 hour pH monitor tracing in a patient with untreated achalasia demonstrating absence of acid reflux. B. The same patient following limited esophagomyotomy, showing the usual absence of acid reflux.

evident and suggest transient LES relaxation, although the mechanism is poorly understood. Acid reflux events are often followed by slow clearance and a gradual restoration of a normal pH value. Acid clearance is appreciably worsened by the supine position, and nocturnal acid reflux events may result in extended periods of low pH in the distal esophagus (Figure 2).

It has been proposed that food retained in the esophagus may ferment and cause a gradual drop in esophageal pH, which could account for some of the observed acid exposure. Shoenut et al. [1] performed an in vitro simulation with lactobacillus which showed a pH drop from 7 to 5 over six hours. This gradual, downward trend was readily distinguishable from an abrupt reflux event due to GER.

Crookes et al. [3] performed an in vitro incubation of chewed, bland food with saliva at 37 degrees C. This resulted in a gradual drop over 24 hours to a median pH of 4.0. The authors concluded that patients demonstrating a similarly declining pH tracing had fermentation of retained food, rather than GER, as the cause of acidification. They also concluded that an acidic pH of 3 to 4, in the absence of pepsin, was not injurious to the esophageal mucosa. This would make esophageal acidification due to food fermentation an unlikely etiology of Barrett's esophagus. Interestingly, Shoenut et al. [1] found that of those patients who demonstrated abnormal esophageal acid exposure, none had retained food evident at endoscopy, and they concluded that food fermentation was an infrequent contributor to low esophageal pH.

Figure 2. 24 hour pH tracings in two patients with untreated achalasia demonstrating slow clearance (A) and prolonged, supine depression of esophageal pH (A and B).

Treated achalasia

Treatment of achalasia in order to disable the hypertensive LES, either by forceful dilation or surgical myotomy, can occasionally lead to incompetence of the LES and subsequent GER. A properly performed, limited esophagomyotomy results in a low rate of GER in our experience [4]. We examined 14 patients following limited esophagomyotomy, using 24hour pH monitoring and esophageal manometry. Thirteen of the 14 patients had fewer than 29 reflux episodes (normal < 49), and 10 patients demonstrated normal acid exposure, with a mean% time of pH < 4.0 of 0.9% (normal < 4.5%) (Figure 1b). Of those 4 patients with acid exposure times > 4.5%, only one had symptomatic reflux, and none had endoscopic evidence of esophagitis. This insensitivity of patients with achalasia to acid reflux has been noted by others [5]. The 24-hour pH tracings in these four patients showed slow clearance of a relatively few reflux events (Figure 3).

Figure 3. Two patients following limited esophagomyotomy demonstrating slow clearance of infrequent acid reflux events.

Conclusions

Abnormal GER may occur in both treated and untreated achalasia patients, most of whom do not exhibit symptoms. The evidence of 24 hour pH data indicated that acid reflux occurs in sufficient severity in some patients both before and after treatment for achalasia that Barrett's esophagus could develop following acid-induced mucosal injury.

It is well documented that the incidence of Barrett's esophagus increases with increasing severity of GER. In most patients with achalasia, 24-hour pH data indicate no GER whatsoever, making acquisition of Barrett's esophagus unlikely. In those with GER, acid exposure times may be lengthy owing to poor clearance and allow for squamous epithelial damage and the development of glandular metaplasia.

Abnormal esophageal acid exposure does occur in some patients with untreated achalasia and is usually due to GER. Fermentation of retained food is probably an unusual cause of significant esophageal acidity.

Prolonged acid exposure seen in some patients following esophagomyotomy is usually due to slow clearance of a relatively few acid reflux events.

References

1. Shoenut JP, Micflikier AB, Yaffe CS, Den Boer B, Teskey JM. Reflux in untreated achalasia patients. J Clin Gastroenterol 1995;20:6-11.

2. Patti MG, Arcerito M, Tong J, De Pinto M, de Bellis M, Wang A, Feo CV, Mulvihill SJ, Way LW. Importance of preoperative and postoperative pH monitoring in patients with esophageal achalasia. J Gastrointestinal Surg 1997;6:505510.

3. Crookes PF, Corkill S, DeMeester TR. Gastroesophageal reflux in achalasia. Dig Dis Sci 1997;42:1354-1361.

4. Streitz JM Jr, Ellis FH Jr, Williamson WA, Glick ME, Aas JA, Tilden RL. Objective assessment of gastroesophageal reflux after short esophagomyotomy for achalasia with the use of manometry and pH monitoring. J Thor CV Surg 1996;111:107-113.

5. Shoenut JP, Duerksen D, Yaffe CS. A prospective assessment of gastroesophageal reflux before and after treatment of achalasia patients: pneumatic dilation vs. transthoracic limited myotomy. Am J Gastro 1997;92:1109-1112.


Publication date: August 2003 OESO©2015