Primary Motility  Disorders of the  Esophagus
 The Esophageal
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 Barrett's
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OESO©2015
 
Volume: Primary Motility Disorders of the Esophagus
Chapter: Diffuse esophageal spasms (Corkscrew esophagus)
 

Are there any studies of DES by 24-hour pH measurement ?

J. Janssens, G. Vantrappen (Leuven)

Symptomatic diffuse esophageal spasm is still an ill-defined condition : intermittent peristalsis, simultaneous contractions, repetitive waves, spontaneous activity, high amplitude contractions, prolonged contractions and abnormal esophageal sphincter function have been accepted by various authors, but in various degrees, in an attempt to refine the manometric criteria for symptomatic diffuse esophageal spasm [1-15]. One of the problems in the past was that many studies have used suboptimal

manometric instrumentation and dry swallows, both of which underestimate the peristaltic performance of the esophagus. If one accepts relatively strict criteria, symptomatic diffuse esophageal spasm appears to be a rare condition.

A systematic study with 24-hour pH measurements has not been performed thus far in this patient group. Some patients with apparently functional dysphagia have on conventional manometry only non-specific esophageal motor disorders (NEMD) and, in this patient group, 24-hour pH metry has not been performed systematically. Although it is well known that patients with gastroesophageal reflux may have ah increased incidence of manometrically recorded esophageal motility disturbances, the manometric performance of the esophageal body in reflux patients has not been studied extensively. Older studies that did not yet use perfused catheters demonstrated an increase in repetitive simultaneous contractions in up to 75 p. cent of patients with esophagitis, and suggested that the severity of the esophagitis paralleled the degree of abnormal motility [16, 17]. Subsequent studies, however, using a perfused catheter system, demonstrated that only some 20 p. cent of esophagitis patients exhibited abnormal esophageal body contractility; they were unable to confirm the relation between the severity of the esophagitis and the degree of motor abnormalities [18, 20].

In a recent study of Knuff and co-workers, the main finding in reflux patients, especially in those with Barrett's esophagus, was a decrease in amplitude of the contractions in the distal esophagus as compared to controls [21]. Animal studies have shown that only severe acute esophagitis with transmural inflammation is accompanied by important esophageal motor abnormalities, and that these abnormalities disappear upon healing of the lesions [22, 23]. It remains unknown whether the abnormal motility in patients with severe reflux and esophagitis is the cause or the consequence of the reflux problems.

Whatever the mechanism involved, some patients with severe reflux have on conventional manometric examination in their distal esophagus a motility pattern of non-specific esophageal motor disorders (NEMD), or even diffuse spasm; in these instances, the resting pressure in the lower esophageal sphincter is usually normal or decreased, whereas it is normal or increased in typical primary diffuse spasm. Conversely, when conventional manometry shows a tracing of NEMD or diffuse spasm in the esophageal body and a low resting pressure in the sphincter, reflux must be suspected.

Interesting data on the relation between esophageal motor abnormalities and pH proven reflux have come from studies in patients with angina-like chest pain of noncardiac origin who were examined by 24-hour intraesophageal pH and pressure recordings : in the study by Janssens et al. [24], 18 of 60 patients with non-cardiac chest pain had a manometric picture of multiple non-peristaltic contractions; four of them had proven reflux. Prolonged 24-hour pH and pressure recordings showed a definite esophageal origin of the chest pain in 21 of the 60 patients: reflux was involved in the pain production in 13 patients, 10 of whom had also evidence of abnormal motility.

References

1. Vantrappen G, Janssens J, Hellemans J, Coremans G (1979) Achalasia, diffuse esophageal spasm, and related motility disorders. Gastroenterology 76 : 450-457.

2. Creamer B, Donoghue FE, Code CF (1958) Pattern of esophageal motility in diffuse spasm. Gastroenterology 34 : 782-796.

3. Roth HP, Fleshier B (1964) Diffuse esophageal spasm. Ann Intern Med 61 : 914-923.

4. Nagler R, Spiro HM (1961) Serial esophageal motility studies in asymptomatic young subjects. Gastroenterology 41 : 371-379.

5. Craddock DR, Logan A, Walbaum PR (1966) Diffuse esophageal spasm. Thorax 21 : 511-617.

6. Gillies M, Nicks R, Skyring A (1967) Clinical, manometric, and pathological studies in diffuse esophageal spasm. Br Med J 2 : 527-530.

7. Bennett JR, Hendrix TR (1970) Diffuse esophageal spasm : a disorder with more than one cause. Gastroenterology 59 : 273-279.

8. Orlando RC, Bozymski EM (1973) Clinical and manometric effects of nitroglycerin in diffuse esophageal spasm. N Engl J Med 289 : 23-25.

9. Di Marino AJ, Cohen S (1974) Characteristics of lower esophageal sphincter function in symptomatic diffuse esophageal spasm. Gastroenterology 66 : 1-6.

10. Mellow MH (1977) Symptomatic diffuse esophageal spasm : manometric follow-up and response to cholinergic stimulation and cholinesterase inhibition. Gastroenterology 73 : 237-240.

11. Swamy N (1977) Esophageal spasm : clinical and manometric response to nitroglycerine and long activity nitrates. Gastroenterology 72 : 23-27.

12. Davies HA, Kaye MD, Rhodes J, Dart AM, Henderson AH (1982) Diagnosis of esophageal spasm by ergometrine provocation. Gut 23 : 89-97.

13. Patterson DR (1982) Diffuse esophageal spasm in patients with undiagnosed chest pain. J Clin Gastroenterol 4: 415-417.

14. Kaye MD (1981) Anomalies of peristalsis in idiopathic diffuse esophageal spasm. Gut 22: 217-222.

15. Richter JE, Castell DO (1984) Diagnosis and treatment. Diffuse esophageal spasm : A reappraisal. Ann Intern Med 100 : 242-245.

16. Olsen AM, Schlegel JF (1965) Motility disturbances caused by esophagitis. J Thoracic Cardiovasc Surg 50: 607-612.

17. Affolter H (1966) Pressure characteristics of reflux esophagitis. Helv Med Acta 33 : 395-402.

18. Dodds WJ, Hogan WJ, Miller WN (1979) Reflux esophagitis. Dig Dis Sci 21 : 49-67.

19. Russel COH, Pope CE, Gannon RM, Allen FD, Velasco N, Hill LD (1981) Does surgery correct esophageal motor dysfunction in gastroesophageal reflux? Ann Surg 194 : 290-296.

20. Heddle R, Dent J, Toouli J, Lewis I (1984) Esophageal peristaltic dysfunction in peptic esophagitis (abstract). Gastroenterology 86 : 1109.

21. Knuff TE, Benjamin SB, Worsham F, Hancock JE, Castell DO (1984) Histologic evaluation of chronic gastroesophageal reflux : An evaluation of biopsy methods and diagnostic criteria. Dig Dis Sci 29: 194-201.

22. Henderson RD, Mugashe FL, Jeejeebhoy KN, Szczpanski MM, Cullen J, Marryatt G, Boszko A

(1973) Synergism of acid and bile salts in the production of experimental esophagitis. Can J Surg 16: 12-17.

23. Henderson RD, Mugashe FL, Jeejeebhoy KN, Cullen J, Boszko A, Szczpanski MM, Marryatt G

(1974) The motor defect of esophagitis. Can J Surg 17 : 112-116.

24. Janssens J, Vantrappen G, Ghillebert G (1986) 24-hour recording of esophageal pressure and pH in patients with noncardiac chest pain. Gastroenterology 90: 1978-1984.


Publication date: May 1991 OESO©2015