Chapter 27 (page 125)

The Pyloric Sphincteric Cylinder in Health and Disease

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Chapter 27 (page 125)

Chapter 27

Duodenogastric Reflux

Regurgitation of alkaline duodenal juice into the stomach has long been of interest. Previously it was assumed to be a normal, protective reaction in cases of gastric hyperacidity (Olch l928). The studies by Du Plessis (1960, 1962, 1965) and Lawson (l964) tended to show the converse, namely that it might be damaging to the gastric mucosa. It was found that transpyloric duodenogastric reflux constituted one of the causes of chronic and atrophic gastritis, with an attendant decrease in gastric mucosal resistance to ulceration (Du Plessis l960, l965). Transstomal reflux after gastro- enterostomies caused a severe atrophic gastritis (Du Plessis l962).

Under experimental conditions in canines, duodenogastric reflux caused superficial gastritis, atrophic gastritis and epithelial proliferation with an increase in mitotic acitivity (Lawson l964). Excessive reflux of duodenal contents into the stomach appeared to be a factor in the pathogenesis of gastric ulceration (Capper l967; Delaney et al. l970). The canine gastric mucosal barrier was destroyed by lysolecithin and phospholipase A, and if the human gastric mucosa behaved similarly, regurgitation of duodenal contents could be damaging (Davenport l970). In guinea-pigs, lysolecithin produced gastric mucosal damage with macroscopic erosions, showing that reflux from the duodenum was an important factor in causing gastritis and gastric erosions (Orchard et al. l977). Bile salts caused a degradation of gastric mucus in pigs, thus damaging the protective layer on the luminal surface of the epithelium (Marriott et al. l977; Schrager and Oates l978).

Previous Tests

Various tests have been devised to determine the ability of the pylorus to prevent duodenogastric reflux.

The concentration of bile acid conjugates in fasting gastric aspirates has long been used as a quantitative measure of duodenogastric reflux (Du Plessis l965; Kaye and Showalter l974; Valenzuela and Defilippi l976; Hoare et al. l978). Although it is a useful guide it has obvious limitations and may not always be reliable since duodenogastric regurgitation may result simply from the presence of an indwelling gastric tube itself (Capper et al. l966).

A radiographic test was devised by Capper et al. (l966). By threading a thin-bore soft rubber tube through the pylorus, gastrografin was injected directly into the lumen of the duodenum. (Rigid plastic tubes were found to be unsuitable as their stiffness interfered with the normal sphincteric action and rendered the pylorus incompetent). With the tube in situ, and with no contrast medium in the stomach, reflux could be observed on the radiological TV monitor, being categorized as minimal, moderate or gross. Special attention was paid to the relationship of reflux to duodenal contraction waves.

In his investigations Grech (l970) used Capper's test with minor modifications. Keighley et al. (l975) employed a further modification; after injection of 20 ml dilute barium suspension into the duodenum through the transpyloric tube, the tube was withdrawn, followed by 3 minutes of radiographic screening to observe whether reflux was present.

Using a radioactive test, Rhodes et al (l969) injected a dose of ¹⁴C-tagged bile salts intravenously. The concentration of secreted radio-active bile salts in aspirated gastric juice was measured, the value serving as an index of duodenal regurgitation. In Wormsley's (l972) test an indicator substance (polyethylene glycol) was injected into the duodenum, followed by aspiration of gastric juice; this entailed the use of both an intragastric and an intraduodenal tube.

Kim et al. (l972) and Keighley et al. (l975) pointed out that the diagnosis of reflux alkaline gastritis could be made by a combination of gastric analysis, gastroscopy and biopsy. Reflux was present endoscopically, according to Hoare et al. (l978), if there was a pool of bile in the stomach or if reflux occurred throughout the examination. It was acknowledged that the presence of a duodenal tube or gastroscope might lead to reflux. Previously Flint and Grech (l970) had stated that gastroscopy was not a satisfactory method of assessing pyloric reflux when vagal blocking drugs were used. Connell (l978) stated that endoscopy in itself had marked effects on gastro-intestinal motility, and implied that it was not satisfactory for assessing pyloric reflux.

Sophisticated electrical pacing techniques have been used experimentally. Kelly and Code (l977) examined duodenogastric reflux in canines, in which pacing from a site in the distal duodenum reversed the direction of the pacesetter potential from aborad to orad, reversing the direction of propagation of duodenal contents, and resulting in duodenogastric reflux.

Valenzuela and Defilippi (l976) used manometric techniques for direct measurement of pyloric sphincter pressures; this entailed the presence of polyvinyl catheters through the pylorus. By the combined use of duodenal marker perfusion and miniature intraluminal strain gauge transducers, Rees et al (l979) determined the relationship between antroduodenal motor activity, duodenogastric reflux and gastric emptying. Although these refined techniques have yielded valuable data, there remains the lingering suspicion that the presence of gastric or transpyloric tubes might have influenced the results. Cole (l969) had stated previously that even the nausea felt by most intubated patients might account for bile entering the stomach. Rovelstad (l976) reiterated that tube studies could impair the normal closing mechanism of the pylorus.

A radioactive test, based on the differential excretion of iminodiacetic acid (IDA) by the liver, was described by Muhammad et al. (l980). Following the intravenous administration of ^99mTc-labelled p-butyl-IDA, which is completely secreted into the bile, radioactivity was measured in the stomach (in post-gastrectomy patients) by means of a gamma camera. Reflux was expressed as a percentage of the total excreted radioactivity. Nicolai et al. (l980) injected ^99mTc-labelled diethyl-IDA intravenously, followed by aspiration of the tracer from the stomach through a double- lumen nasogastric tube, allowing quantification of reflux. The test also involved the intravenous injection of cholecystokinin to produce gallbladder contraction, with constriction of the pylorus as a side effect.