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OESO©2015
 
Volume: The Esophagogastric Junction
Chapter: GER and gastric motility factors
 

What is the value of electrogastrography in reflux disease?

R.W. McCallum, I. Soykan (Kansas City)

The possible role of gastric motility factors in the pathophysiology of gastroesophageal reflux disease (GERD) is now being appreciated. The presence of gastric contents is a prerequisite for gastroesophageal reflux and a direct relationship between the degree of gastroesophageal reflux and intragastric volume has been demonstrated [1]. In many patients gastroesophageal reflux is part of a disturbance in upper gastrointestinal motility which extends distal to the esophagus (Figure 1). GERD is associated with abnormal motility in the lower esophageal sphincter (LES), the esophageal body, and the stomach [2, 3]. Some patients with GERD complain of vomiting suggesting the possibility of subclinical or overt gastric retention while most complain of indigestion or dyspepsia characterized by abdominal bloating, fullness, postprandial satiety and epigastric discomfort, much of which is explained by delayed gastric emptying [4].

In GERD, a motor abnormality of the stomach is suggested by the observation that the distention of the stomach causes a smaller increase in intragastric pressure in refluxers than in controls [5]. Delayed gastric emptying of liquids and/or solids could be one of the mechanisms which increases the volume of gastroesophageal contents available for reflux into the esophagus [6]. Further, antral motility and transpyloric motility flow are abnormal in some patients with GERD [7]. Since gastroesophageal reflux is more pronounced in the postprandial phase, prolonged gastric emptying would increase the time at risk for gastroesophageal reflux [8]. It has been shown that 40% of GERD patients have delayed gastric emptying of a mixed-solid meal [6]. This finding indicates that delayed gastric emptying plays a significant role in the pathophysiology of reflux by distending the proximal stomach and inducing a gastrosphincteric reflex, associated with more frequent transient relaxations of the LES, this permitting reflux of gastric contents to occur.

Figure 1. Currently accepted factors involved in the pathogenesis of gastroesophageal reflux disease are indicated in this figure. Abnormalities of the electrogastrogram should now be included as part of the impaired antral motility/ delayed gastric emptying that contribute to the pathophysiology as well as the dyspepsia symptoms that are so common in gastroesophageal reflux disease.
180f1

The electrogastrogram (EGG), the cutaneous recording of gastric myoelectrical activity, can be measured by placing electrodes on the abdominal surface. It is now well known that postprandial EGG parameters are able to predict delayed gastric emptying with a significant accuracy. EGG abnormalities are present in most patients with dyspepsia and/or delayed gastric emptying [9]. The presence of EGG abnormalities in patients with dyspepsia and/or delayed gastric emptying, and the presence of upper gastrointestinal smooth muscle abnormalities in many patients with GERD makes it conceivable to detect EGG abnormalities in GERD patients. In a group of well established GERD patients whom my laboratory investigated, 38% had EGG abnormalities [10]. Moreover, 57% of this subgroup had delayed gastric emptying indicating that ~ 50% of GERD patients overall have gastric motor or myoelectrical abnormalities which contribute to the pathogenesis of this entity. The non-invasive and easy to use nature of EGG makes it attractive for studying the upper gastrointestinal motility disturbances that are present in GERD patients. GERD patients who have upper gastrointestinal symptoms may require a prokinetic agent. EGG may be helpful in selecting patients for prokinetic therapy before or in lieu of performing a radionuclide gastric emptying test. As an algorithm, an EGG study for a GERD patient who has upper gastrointestinal symptoms should be recommended. If the result is found to be normal, then a radionuclide gastric emptying test should be performed.

 

In conclusion, GERD patients have a high prevalence of gastric motility and myoelectrical abnormalities which contribute to the pathogenesis of the entity and explain the clinical association of dyspepsia with GERD. These findings also explain that just treating the heartburn aspect of GERD does not address the other aspects of the clinical presentation. A prokinetic agent can attempt to normalize the diffuse esophageal and upper gastrointestinal motility disorder involved in GERD while also reducing heartburn.

References

1. Ahtaridis G, Snapes WJ, Cohen S. Lower esophageal sphincter pressure as an index of gastroesophageal acid reflux. Dig Dis Sci 1981;26:993-998.

2. Behar J, Ramsby G. Gastric emptying and antral motility in reflux esophagitis. Gastroenterology 1978;74:253-256.

3. Holloway RH, Dent J. Pathophysiology of gastroesophageal reflux disease: lower esophageal dysfunction in gastroesophageal reflux disease. Gastroenterol Clin North Am 1990;19:517-536.

4. McCallum RW. Gastric emptying in gastroesophageal reflux and therapeutic role of prokinetic agents. Gastroenterol Clin North Am 1990;19:551-564.

5. Hartley MN, Walker SJ, Mackie CR. Abnormal gastric adaptive relaxation in patients with reflux esophagitis. Gut 1990;31:500-503.

6. McCallum RW, Berkowitz DM, Lerner GE. Gastric emptying in patients with gastroesophagal reflux. Gastroenterology 1981;80:285-291.

7. King PM, Pryde A, Heading RC. Transpyloric movement and antroduodenal motility in patients with gastroesophageal reflux. Gut 1987;28:545-548.

8. Hölscher AH, Weiser HF. Reflux characteristics in health and disease. In: Roman C, ed. Gastrointestinal motility. Lancaster: MTP Press Limited, 1984:63-69.

9. Chen JDZ, Lin Z, Pan J, McCallum RW. Abnormal gastric myoelectrical activity and delayed gastric emptying in patients with symptoms suggestive of gastroparesis. Dig Dis Sci 1996;41:1538-1545.

10. Soykan I, Lin Z, Jones S, McCallum RW. Gastric myoelectrical activity, gastric emptying and correlations with symptoms in patients with gastroesophageal reflux disease. J Invest Med 1997;45:6A.


Publication date: May 1998 OESO©2015