Primary Motility  Disorders of the  Esophagus
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OESO©2011
 
Volume: Primary Motility Disorders of the Esophagus
Chapter: Achalasia (hypomotility) is the best known entity
 

What are the gastric factors involved ?

G.G. Jamieson (Adelaide)

Reflux esophagitis is usually regarded as being multi factorial in origin. However the most important factor involved is probably lower esophageal sphincter tone, which is usually very low or absent when reflux occurs [15]. As the aim of myotomy is to render the lower esophageal sphincter incompetent, or at least less competent, it is not surprising that reflux develops subsequently in some patients subjected to myotomy.

Gastric factors may be of importance in the development of esophagitis after myotomy in several ways.

• First, reflux material may be made more noxious to esophageal mucosa, either by increasing the content of its acid or by increasing its duodenal content. The influence of hyperacidity in the stomach has been studied in animal preparations. Herron [4], and Ellis [11] both found that the performance of a myotomy of the lower esophageal sphincter in dogs led to esophagitis only when a hyperacid state was artificially superimposed. However in humans with achalasia gastric acid has been found to be either normal [7, 21] or reduced [9, 6].

The importance of gastroduodenal reflux in relationship to reflux disease has been studied mainly in regard to bile, and there is no agreement as to the role it plays [18, 13]. Such reflux does not appear to have been studied in patients with achalasia.

• Second is the role of gastric emptying in leading to post-myotomy esophagitis. The influence of delayed gastric emptying on the development of esophagitis in primary reflux disease remains a controversial topic. Once again this problem does not appear to have been systematically studied in patients with achalasia. One reason for this, no doubt, is the difficulty of delivering a meal to the stomach of patients

with achalasia for performance of a gastric emptying test. (See chapter on Gastric drainage after esophagomyotomy).

• Third is the importance of pre-operative reflux. As low sphincter tone is regarded as important in the genesis of reflux, the somewhat paradoxical suggestion has been made that some patients with achalasia have pre-operative reflux and that this is an important determinant of post-myotomy esophagitis[21]. Several studies have given some support to this idea. Thus Mansoor[17] reported a pre-operative incidence of reflux of 32 p. cent in 38 patients with achalasia. And others have used ambulatory pH monitoring and reported a 64 % incidence of pre-operative reflux in 14 patients [20], and a 17 p. cent incidence in 18 patients [4, 5].

It is difficult to know whether such falls in pH actually represent pathological reflux for several reasons.

• First, in patients with achalasia a single reflux episode can lead to retention of the acid in the esophagus, for a prolonged period of time.

• Second, retention of food in the esophagus may lead to inflammation so-called stasis esophagitis. Smart [22] addressed this problem in 178 patients, also using ambulatory pH monitoring and similarly found a high incidence of acid exposure in the esophagus. However, esophageal contents were analysed and it was found that the low pH was due to lactic acid. Following pneumatic dilatation, there was an overall decrease in acid exposure, although in some individuals acid exposure increased after the dilatation. Therefore, patients in whom pH monitoring shows increased acid exposure cannot automatically be presumed to be at risk of developing post-operative reflux.

• Third and last, is hiatus hernia, a factor where there is general agreement that it is of importance in the genesis of post-myotomy esophagitis. Thus, most authors state that the addition of a myotomy to a patient with a hiatus hernia is followed by a significant risk of esophagitis [21,8, 10, 3]. In one animal study, the myotomised lower esophagus remained competent unless a hiatus hernia was created deliberately [11]. Destruction of the right crus of the diaphragm in humans similarly was followed by a high incidence of reflux [16].

However, those studies which have looked at the concurrence of hiatus hernia and achalasia indicate that it is a relatively rare event with incidences quoted between 0.005 p. cent and 2.3 p. cent [19, 12, 2].

In summary in the individual patient pre-operative risk factors for the development of postmyotomy esophagitis may occasionally be identified. Thus, if a patient has a known problem with delayed gastric emptying, it seems reasonable to add a drainage procedure to the myotomy, but not otherwise. On the rare occasion that a hiatus hernia coexists with achalasia, it seems logical to repair the hernia at the time of myotomy.

However, in general terms, there is a lack of scientific data to suggest that gastric factors are of importance in the development of esophagitis after myotomy for achalasia.

References

1. Atkinson M, Ogilvie AL, Robertson CS., Smart LH (1987) Vagal function in achalasia of the cardia. Q J Med 63 : 277-303.

2. Binder HJ, Clemett AR, Thayer WQR et al. (1965) Rarity of hiatus hernia in achalasia. N Eng J Med 272 : 680.

3. Black J, Vorbach AN, Collis JL (1976) Results of Heller's operation for achalasia of the oesophagus. The importance of hiatal repair. Br J Surg 63 : 949-53.

4. Cheadle WG, Vitale GC, Sadek S, Cuschieri A (1988) Evidence for reflux in patients with achalasia. A pre and post-operative study. Dig Surg 5:1-4.

5. Cuschieri A (1989) Partial fundoplication after an abdominal Heller's myotomy. Correspondence Br J Surg 76 : 527.

6. Dooley CP, Taylor JL, Valenzuela JE (1983) Impaired acid secretion and pancreatic polypeptide release in some patients with achalasia. Gastroenterology 84: 809-10.

7. Eckardt VF, Krause J, Bolle D (1989) Gastrointestinal transit and gastric acid secretion in patients with achalasia. Dig Dis Sci 34: 665-71.

8. Effler DB (1962) Reconstruction of the esophageal hiatus. Arch Surg 85 : 599-607.

9. Elder JB Gillespie G (1969) The vagus and achalasia. Gut 10: 1045-69.

10. Ellis FH, Gibb SP (1975) Re-operation after esophago-myotomy for achalasia of the esophagus. Am J Surg 129:407-12.

11. Ellis FH, Kaiser JC, Schlegel JR et al. (1967) Esophago-myotomy for esophageal achalasia. Experimental clinical and manometric aspects. Ann Surg 166 : 640.

12. Feldman M (1957) Clinical roentgenology of the digestive tract. 4th Ed. Williams and Wilkin Baltimore.

13. Gotley DC, Morgan AP, Cooper MJ (1988) Bile acid concentrations in the refluxate of patients with reflux oesophagitis. Br J Surg 75 : 587-90.

14. Herron PW, Thomas GI, Merendino CA (1957) An experimental approach to cardiospasm appraisal of the Finney pyloroplasty in the prevention of esophagitis following the Heller myotomy. J Thorac Cardiovasc Surg 34 : 609.

15. Jamieson GG (1988) Mechanisms of gastro-esophageal reflux. ANZ J Surg 58 : 193-5.

16. Jekler J, Lhotka J (1967) Modified Heller procedure to prevent post-operative reflux esophagitis in patients with achalasia. Am J Surg 113 : 251-4.

17. Mansoor KA, Symbas PN, Jones EL (1976) A combined surgical approach in the management of achalasia of the esophagus. Am J Surg 42 : 192-5.

18. Mittal RK, Reuben A, Whitney JO, McCallum RW (1987) Do bile acids reflux into the esophagus ? A study in normal subjects and patients with gastro-esophageal reflux disease. Gastroenterology 92: 371-5.

19. Olsen AM, Holman CD, Andersen HA (1953) Diagnosis of cardiospasm. Dis Chest 23 : 477.

20. Peyton MD, Greenfield LJ, Elkins RC (1974) Combined myotomy and hiatal herniorghaphy, a new approach to achalasia. Am J Surg 128 : 786-90.

21. Rees JR, Thorbjarnarson B, Barnes WH (1970) Achalasia : results of operation in 84 patients. Ann Surg 171 : 195-201.

22. Smart HL, Foster PN, Evans DF, Slevin D, Atkinson M (1987) 24 hour esophageal acidity in achalasia before and after pneumatic dilatation. Gut 28 : 883-7.


Publication date: May 1991 OESO©2011