Primary Motility  Disorders of the  Esophagus
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OESO©2015
 
Volume: Primary Motility Disorders of the Esophagus
Chapter: Diffuse esophageal spasms (Corkscrew esophagus)
 

What is the incidence of disorders of relaxation ?

M.D. Kaye (Honolulu)

Creamer et al. (1958) [3], in an early study of manometric patterns, studied 16 patients with radiographic features of DES and an additional 56 patients whose symptoms were suggestive of DES but whose radiographs were normal. Resting pressures in the lower esophageal sphincter (LES) were elevated in « most » of the patients with abnormal radiographs and, in 4 of 16, relaxation was absent. Findings in the other 56 patients were «similar ». In some subsequent studies of DES [10, 2,7, 1] LES function was reported to be normal.

The introduction of perfused catheters and less compliant systems led to much greater accuracy in measurement of pressure events, both in the sphincters and in the body of the esophagus. Most of those who have used such systems [9, 5, 11, 8, 4] have reported abnormal LES function in DES, though the incidence of such dysfunction varies considerably from one study to another. DiMarino and Cohen specifically addressed LES function in a report of 27 patients with symptomatic DES. Their patients had dysphagia and/or chest pain, intermittent peristalsis and simultaneous contractions in response to at least 10 p. cent of « wet» swallows. Mean resting LES pressures (mid-respiratory) were 28.2 mmHg, significantly higher than the mean control value of 19.2 and LES pressures exceeded the highest control value in 9 of the 27 patients with DES. Though some LES relaxation with deglutition was seen in all 27 patients, in 10 it was partial, or incomplete, with the percentage decrease in LES pressure ranging between 80 and 34 p. cent, as opposed to 90 p. cent or more in their healthy control subjects. Mean resting LES pressures in patients with partial relaxation were higher (34.0 mmHg, than in patients with normal LES relaxation (24.9 mmHg). Hence, the actual LES pressures at the nadir of relaxation were often substantial in those patients whose relaxation was incomplete. This underlines the potential physiological and clinical significance of this abnormality in the patient with DES so affected.

The highest incidence of abnormal LES relaxation in DES was reported by Kaye (1981) [8]. The clinical characteristics of his twelve patients were, in most respects, similar to those in DiMarino and Cohen's study, except that in two of the twelve peristalsis was not observed in the distal half of the esophageal body. Eleven patients presented with dysphagia and five of these also had chest pain. One patient had odynophagia only. LES pressures in these patients were high, with a range of 15 to 57 mmHg and a mean of 31.5. It should be emphasized that these were end-expiratory pressures which are lower, often substantially so, than mid-respiratory or end-inspiratory pressures. LES relaxation in response to swallowing, though present to some degree in all patients, was incomplete in eight of the twelve.

Precise conclusions regarding the incidence of LES dysfunction in DES are impossible, since criteria for the definition of this disorder and the manometric methods used to study it have not been standardized. It is likely, however, that at least one-third of patients with DES have a manometrically definable abnormality of LES function. This may be an underestimate of functionally significant abnormal relaxation. It must be remembered that a sphincter, in order to satisfy the investigator that it is relaxing normally, must loose tone only to the point that it is not exerting pressure on the orifices of the small tube which passes through it. This does not necessarily mean that it is opening (relaxing) to a normal degree.

The clinical significance of abnormal LES function in DES is underscored by reports that pneumatic dilatation of the LES may be beneficial. Ebert et al. (1983) [6], for example, reported nine patients with symptomatic DES refractory to drug therapy, and abnormal LES function manifest as incomplete relaxation. All patients improved after the procedure. In eight, the improvement was maintained throughout the follow-up period (average 37.4 months). In one patient, symptoms recurred after several months. Clearly, this rather drastic form of therapy should be employed only in the patient who has well documented abnormality of LES function.

References

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

2. Craddock DR, Logan A, Walbaum PR (1966) Diffuse esophageal spasm. Thorax 21 : 511-517.

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

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

5. DiMarino A, Cohen S (1974) Characteristics of lower esophageal sphincter function in symptomatic diffuse esophageal spasm. Gastroenterology 66 : 1-6.

6. Ebert EC, Ouyang A, Wright SH, Cohen S, Lipshutz WH (1983) Pneumatic dilatation in patients with symptomatic diffuse lower esophageal spasm and lower esophageal sphincter dysfunction. Dig Dis Sci 28: 481-485.

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

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

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

10. Roth HP, Fleshier B (1964) Diffuse esophageal spasm. Clinical, radiological and manometric observations. Ann Intern Med 61 : 914-923.

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


Publication date: May 1991 OESO©2015