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Chapter 27 (page 125)
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).
Various tests have been devised to determine the ability of the pylorus to prevent
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
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.
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