27 - Duodenogastric Reflux

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. Ehrlein (l98l) pointed out that the function of the pyloric sphincter in preventing duodenogastric reflux had not been clarified. (It was explained that the term "pyloric sphincter" in this context referred to the pyloric ring). It was difficult to record contractions over a long period of time in humans. In animals it was possible to measure the external diameter of the pylorus with induction coils, and to determine pressure changes simultaneously by means of implanted strain gauge transducers (Ehrlein l980). The method was used in canines to investigate possible co-ordination of gastric and duodenal motility, gastroduodenal reflux at the same time being observed fluoroscopically. In the digestive state the pylorus opened when a peristaltic wave involved the commencement of the "antrum", closing when the wave reached the pyloric sphincter. Contraction maxima of the duodenal bulb most often occurred a fraction of a second before, or after, contraction maxima of the pyloric sphincter. Consequently there was incomplete closure of the pylorus during duodenal contraction, allowing duodenogastric reflux to occur; it was produced by atypical segmental contractions of the bulb. In the interdigestive state different phases were encountered. In the first phase, in the absence of contractile activity in the stomach and duodenum, no reflux occurred. In the second and third phases imperfect timing of pyloric and duodenal contractions, as in the digestive state, sometimes resulted in duodenogastric reflux.

Various derivatives of 99mTc-IDA have now been used extensively in the study of duodenogastric reflux, notably 99mTc-BIDA (butyl iminodiacetic acid) and 99mTc-HIDA. These tests have certain minor limitations in common (Thomas et al, l984). For instance, anatomical definition of the stomach was often complicated by overlap of the left lobe of the liver and the duodeno-jejunal flexure; delineation of the gastric "antrum" was poor, and as it was close to the duodenal bulb, minor degrees of reflux might not be detectable; and computer analysis of small volumes of reflux might be difficult to interpret.

Two further limitations of the cholescintigraphic tests, in our view, are the following:

  1. As only bile constituents are labelled, the tests apply to reflux of bile into the stomach; they are not a measure of reflux of the other constituents of duodenal juice, of which pancreatic exocrine secretion is the most important. It may be useful to have a test able to demonstrate reflux of duodenal contents (as opposed to bile only), into the stomach.

  2. At present the tests do not visualize the pylorus clearly, i.e. it is not possible to determine the extent of contraction or relaxation of the pyloric region in relation to reflux.

A Double-Contrast Radiographic Test for Duodenogastric Reflux #

As a modification of the double-contrast upper gastrointestinal radiographic examination, we have described the following radiographic test for duodenogastric reflux (Keet l982). In this test the pylorus is clearly visualized and its diameter can be determined during reflux; in addition, the relationship of reflux to pyloric and duodenal contractions may be studied. The test is non-invasive and does not entail the use of catheters, intubation or the administration of pharmacological agents (which may alter motility).

The patient, standing behind the radiological TV monitor after a 12-hour overnight fast, is instructed to swallow 4 to 5 mouthfuls of a micropulverized barium suspension, e.g. Micropaque (Adcock-Ingram, Johannesburg) ordinarily used for upper gastrointestinal radiographic examinations. Immediately afterwards a gas-producing agent is swallowed, e.g. 2 x 50 Gastrast tablets (Toho Kagaku Kenyusho, Tokyo), followed by 2 mouthfuls of water containing a few drops of Telament liquid (Adcock Ingram, Johannesburg). The barium accumulates in the lower part of the stomach while the gas distends the fornix. While the patient is instructed not to eructate, the table is immediately tilted into the horizontal position. With the arms abducted throughout the examination, the supine subject is now rotated into the left anterior oblique position (right side down) till barium enters the duodenal bulb. As soon as duodenal filling is achieved, the subject is rotated rapidly through 90 degrees into the right anterior oblique position. This causes the remaining barium in the stomach to descend into the fornix, while the gas is displaced and ascends into the pyloric region, which now constitutes the uppermost part of the stomach. Consequently the first part of the duodenum is filled with barium, while the pyloric region up to the ring is filled with gas (Fig. 27.1). The competence of the pylorus can now be studied, radiographs being taken at appropriate times. Duodenogastric reflux through the pylorus into the gas-containing part of the gastric lumen is clearly visible (Fig. 27.2). (This should not be confused with the normal orad movement of barium often seen during contraction of the pyloric sphincteric cylinder as described in Chap. 13). Should no reflux be observed, or should the duodenum empty its contents prematurely, positioning of the patient is repeated. Generally speaking, the manoeuvre is repeated 4 to 5 times during each test. The effects of compression of the second or third parts of the duodenum may also be studied.

Fig. 27.1. Duodenal bulb filled with barium. Pyloric sphincteric cylinder filled with gas and distended

Fig. 27.2. Reflux of barium (arrow) from the duodenum into the pyloric sphincteric cylinder, which is relaxed

Advantages #

The main advantages of this method appear to be the following:

  1. Because of the clear images produced by radiography, the diameter and competence of the pylorus may be studied in relation to both duodenal contraction waves and the motility of the pyloric part of the stomach, i.e. the pyloric sphincteric cylinder. Little attention has been paid to duodenogastric reflux in relation to pyloric motility in previous investigations.

  2. If it is assumed that the barium suspension in the duodenal lumen represents duodenal contents, the procedure will determine the presence or absence of reflux of duodenal contents, i.e. of duodenal juice (in contrast to bile only).

  3. No medication (e.g. anticholinergics or cholecystokinin) is administered, thus allowing the study of pyloric competence in the absence of pharmacological modification.

  4. There is no gastric intubation (thus eliminating nausea) and the pylorus is not traversed by a tube (or has been traversed immediately before observation, as in the test of Keighley et al. l975).

  5. The test is quick and simple to perform, and may be followed by a "conventional" upper gastrointestinal radiographic examination.

Disadvantages #

  1. Radiation to the patient should be considered, but measurements showed that this was minimal and could be discounted since a small (11.0 x 8.0 cm), localized aperture was used, not more than two 11.0 x 8.0 cm film exposures were needed for record purposes, and screening time generally did not exceed 90 to 120 seconds.

  2. In a minority of patients, depending on the direction of the pyloroduodenal axis, it may not be possible to obtain a side view of the duodenum and pylorus, the barium-filled bulb being projected over the pyloric aperture.

  3. The examination is performed in the interdigestive phase and in the supine position only.

  4. While there is no doubt about the ability of the procedure to illustrate the presence or absence of reflux, quantification cannot be accurate as only a rough impression of the quantity of reflux is gained.

Results in Normal Subjects #

Having received approval of the Ethical Committee, the test was performed in 14 informed, volunteer, asymptomatic male medical students between the ages of 23 and 27 years. In 9 of the subjects no duodenogastric reflux occurred. In 2 subjects there was minimal reflux on one occasion only (three further "rotating manoeuvres" failed to produce reflux). In 3 subjects moderate reflux occurred. In each it was seen two or three times during four "rotating manoeuvres". One of these subjects was re-tested a week later, with similar results.

Duodenal Motility

In all 14 normal subjects duodenal peristalsis appeared normal on the TV monitor and the duodenum emptied normally. In all there also occurred retrograde movement of barium in the duodenal lumen, which appeared to result from "segmental" contraction waves in the third part of the duodenum. While these contractions did not proceed along the duodenal walls, but remained localized to the third part, they forced barium in an orad direction, at times as far as the bulb; barium in the lumen distal to these contractions was forced in an aborad direction.

In all normal subjects the second part of the duodenum was also compressed as far as possible by means of the gloved hand on the anterior abdominal surface. This did not occlude the lumen completely, did not prevent aborad movement, and did not initiate retrograde movement. The results were the same with and without partial compression of the second part of the duodenum.

Pyloric Motility

As indicated previously (Chap. 3), the muscular part of the pyloric ring is considered to be the terminal annular thickening of the pyloric sphincteric cylinder, as described by Cunningham (1906), Forssell (l913) and Torgersen (l942). The cylinder, which is 3.0 to 4.0 cm in length, normally contracts in a segmental (as opposed to "peristaltic") way (Chap. 13). As the ring forms an inherent part of the cylinder, it closes and opens with contraction and relaxation of the cylinder respectively. In all subjects these contractions were normal. Reflux in the 5 subjects occurred either during maximal relaxation of the sphincteric cylinder, (Fig. 27.2), or when it was in a state of partial contraction (Fig. 27.3). It never occurred during maximal contraction of the cylinder.

Fig. 27.3. Barium filling to show partial contraction of sphincteric cylinder. At this stage the pyloric aperture (arrow) is widely patent

Results in Patients #

Having received approval of the Ethical Committee, the test was performed in 100 patients between the ages of l8 and 79 years who, during the ordinary course of events, had been referred for radiographic examinations because of upper gastro-intestinal symptoms, e.g. dyspepsia and epigastric pain.

No Lesion Detected

In 48 patients no macroscopic organic lesion could be demonstrated in the upper gastro- intestinal tract; these were considered to be patients with non-ulcer dyspepsia. Eighteen (± 37 percent) had minimal to moderate duodenogastric reflux. In all cases reflux occurred during those stages of the pyloric cycle in which the pyloric sphincteric cylinder was relaxed (Fig. 27.2), or partially contracted (Fig. 27.3). Reflux never occurred during maximal contraction of the cylinder.

Duodenal Ulceration

In our series there were 25 cases of active duodenal ulceration or duodenal deformity typical of ulceration, l8 (approximately 72 percent) showing moderate duodenogastric reflux.

Gastric Ulceration

We encountered 9 cases of chronic benign ulcer on the lesser curvature of the stomach at varying distances proximal to the pyloric sphincteric cylinder, i.e. not within the cylinder itself. Seven of these showed moderate reflux. In the present series no cases of benign gastric ulceration within the pyloric sphincteric cylinder were seen.

Malignant Gastric Ulceration

In our series 2 cases of malignant gastric ulceration (proved by biopsy) were diagnosed. In one case, with the ulcer on the lesser curvature close to the pylorus (i.e. within the sphincteric cylinder), there was moderate to marked reflux. In the second case, with the ulcer at the incisura angularis, no reflux was seen.

Sliding Hiatus Hernia with Free Gastro-Oesophageal Reflux

There were 9 cases in the present series, 4 showing reflux of duodenal contents into the stomach.

Combined Lesions

In the present series 7 cases had combined lesions, e.g. duodenal ulceration and hiatus hernia. Most of these showed reflux. One of these cases had constant spasticity of the pyloric sphincteric cylinder with irregular and transverse mucosal folds (Fig. 27.4). It was diagnosed radiologically and endoscopically as spasm and chronic gastritis affecting the cylinder. In addition the duodenal bulb was deformed due to ulceration. In this case moderate to marked duodenogastric reflux occurred. Owing to the tube-like spasm of the cylinder, the pyloric aperture was neither fully open nor fully closed, but fixed in a state of partial patency.

Fig. 27.4. Barium filling of spastic pyloric sphincteric cylinder in a case of chronic gastritis. Duodenal bulb deformed

Duodenal Motility

In the last 40 patients of the series, special attention was paid to duodenal motility. In 32 of these the aborad and orad movements of intraluminal barium were identical to those in normal controls. In 8 no orad movement of contrast was seen in the second and third parts of the duodenum, yet in half of these cases duodenogastric reflux occurred. One's impression was that physiological duodenal movements were probably of little consequence in the mechanism of reflux. (By experimentally reversing the pacesetter potential in the duodenum in canines by electrical stimulation, Kelly and Code l977 did produce reflux.)

Pyloric Motility

As in normal control subjects, reflux in patients only occurred while the pyloric sphincteric cylinder was relaxed or in a state of partial contraction; it never occurred during maximal contraction of the cylinder.

Subsequent Tests #

Shortly after the above radiographic test for duodenogastric reflux was described (Keet l982), a similar procedure was mentioned by Hughes et al. (l982). Minimal reflux was considered to be a slight trickle through the pylorus, moderate reflux that which extended to the "antral" region of the stomach, and gross reflux that which extended to the body of the stomach. Duodenogastric reflux was found to be present in 6 (27 percent) of 22 normal subjects and in 128 (32 percent) of 396 patients with non-ulcer dyspepsia. Statistically there was no significant difference in incidence between the normal controls and dyspeptic patients.

Using a 99mTc-EHIDA test, Niemela et al (l984) found reflux in 14 of 33 normal controls. With a similar test Wolverson et al (l984) noted duodenogastric reflux in 6 of 13 normal controls. With a nasogastric aspiration technique Wolverson et al (l984) found that 8 of 15 normal controls had reflux. By measuring the intragastric bile acid concentration by means of a nasogastric suction technique, Gotthard et al. (l985) showed that large fluctuations in reflux might occur during a 24 hour measuring period. Of 12 normal control subjects 10 showed reflux, with low daytime values and frequent high peaks in bile acid concentration during the night.

Discussion #

Normal subjects

Du Plessis (l965) stated that slight duodenogastric reflux was a normal occurrence. Capper et al. (l966) found no reflux in 15 normal controls, while it occurred in one out of 12 normal subjects in Flint and Grech's (l970) series. Nevertheless Flint and Grech were of the opinion that the pylorus was normally competent, i.e. it did not allow reflux. Rovelstad (l976) stated that it was debatable whether duodenogastric reflux was a normal phenomenon, while Donovan et al (l977) found no reflux in normal controls. Nicolai et al. (l980) on the other hand, demonstrated a median reflux of 4.3 percent of an intravenously injected dose of radioactive technetium-labelled IDA.

In 5 of 14 normal subjects, and in l8 of 48 non-ulcer dyspeptic patients, Keet (l982) found minimal to moderate duodenogastric reflux. Hughes et al. (l982) found reflux in 6 of 22 normal subjects and in 128 of 396 patients with non-ulcer dyspepsia, the incidence in the two groups being more or less the same. Similar results were obtained by Niemela et al. (l984), who noted reflux in 14 of 33 normal control subjects, and by Wolverson et al. (l984) who found reflux in 6 of 13 controls. The findings of Gotthard et al. (l985) pointed to large fluctuations in reflux, with higher peaks occurring nocturnally.

It is concluded that mild to moderate duodenogastric reflux occurs in approximately one third of normal subjects, and in one third of patients with non-ulcer dyspepsia, as shown (inter alia) by the radiological tests of Keet (l982) and Hughes et al. (l982). In other words, the pylorus is normally not competent in a significant percentage of normal subjects and approximately the same percentage of patients with non-ulcer dyspepsia.

Duodenal Ulceration

Du Plessis (l965) stated that in some cases of duodenal ulceration, reflux was excessive. Capper et al. (l966) found moderate or gross reflux in 33 percent or duodenal ulcer cases, Donovan et al (l977) in 24 percent, while Valenzuela and Defilippi (l976) stated that the incidence of reflux in patients with duodenal ulceration was not significantly different from that in controls. Of 7 cases Nicolai et al. (l980) found increased reflux in 2 only; in both, pyloric deformity was also present.

In our series there were 25 cases of active duodenal ulceration or duodenal deformity typical of ulceration, l8 (approximately 72 percent) showing moderate duodenogastric reflux. Hughes et al. (l982) found reflux in 53 percent of one group of patients with duodenal ulcer, and in 32 percent of patients in another group. Of 60 patients with duodenal ulceration Wolverson et al. (l984) found 32 (53 percent) to be reflux positive.

It is concluded that duodenogastric reflux occurs in a significant percentage of cases with duodenal ulceration; the incidence, as reported by different authors, varies from approximately 24 percent to approximately 72 percent. As cyclical activity of the pyloric sphincteric cylinder is normal in the vast majority of cases of duodenal ulceration (Chap. 30), the reflux is difficult to explain on the basis of pyloric dysfunction.

Gastric Ulceration

Du Plessis (l965) found the concentration of bile acid conjugates in fasting gastric aspirates to be abnormally high in cases of gastric ulceration. Capper et al. (l966) found moderate or gross reflux in 66 percent of gastric ulceration patients, while Rhodes et al (l969) and Delaney et al. (l970) mentioned an increased incidence of bile reflux in patients with gastric ulceration. Flint and Grech (l970) stated that the pylorus was incompetent in gastric ulceration and chronic alcoholic gastritis, while the results of Valenzuela and Defilippi (l976) suggested pyloric "sphincter" incompetence in gastric ulceration. Nicolai et al. (l980) found increased reflux in l8 gastric ulcer cases.

In our series (Keet l982) there were 9 cases of benign ulcer on the lesser curvature of the stomach at varying distances proximal to the sphincteric cylinder, i.e. not within the cylinder. Seven of these showed moderate reflux. In the series of Hughes et al. (l982) reflux was present in 21 of 46 patients with gastric ulcer. Although there appeared to be a higher proportion of gastric ulcer patients with reflux, the results did not reach statistical significance when compared with the other dyspeptic patients examined. The impression was that there was no direct association between the degree of reflux and the presence of peptic ulceration, according to Hughes et al. (l982). Niemela et al. (l984) found that of l9 patients with gastric ulcer in the body of the stomach, l7 had reflux. Two patients had both gastric and duodenal ulceration, both showing reflux. Twelve patients had prepyloric and antral gastric ulcers, 8 showing reflux. Of 30 patients with gastric ulceration Wolverson et al. (l984) found l7 (53 percent) to be reflux positive. Gotthard et al. (l985) examined 11 patients with prepyloric ulcer disease (i.e. with the ulcer situated within 2.0 cm of the pyloric ring); in all the intragastric concentrations of bile acid were measured over a 12 hour period. The mean bile acid concentrations in prepyloric ulcer patients were found to be significantly higher than in both controls and duodenal ulcer patients, diurnally as well as nocturnally.

Gastric ulceration is often associated with spasm of the pyloric sphincteric cylinder (Chap. 29). Spasm of the cylinder resembles a normal, partial contraction; at this stage the pyloric aperture is normally open (Chap. 13). In spasm the aperture is "fixed" in the open position. It is surmized that for this reason a high incidence of duodenogastric reflux is to be expected in gastric ulceration.

Malignant Gastric Ulceration

In our series (Keet l982) 2 malignant gastric ulcers were found. In one case, with the ulcer on the gastric lesser curvature close to the pylorus (i.e. within the sphincteric cylinder), there was moderate to marked reflux. In the second case, with the ulcer at the incisura angularis, no reflux was seen.

Sliding Hiatus Hernia with Gastro-Oesophageal Reflux

Donovan et al. (l977) noted duodenogastric reflux in 3 of 8 patients with hiatus hernia. In 10 cases of hiatus hernia Nicolai et al. (l980) found no evidence of increased reflux. In our series (Keet l982) there were 9 cases of hiatus hernia, 4 showing reflux of duodenal contents. There seems to be an association between hiatus hernia and spasm of the pyloric sphincteric cylinder; this may allow increased duodenogastric reflux and may ultimately lead to biliary oesophagitis (Chap. 32).

Combined Lesions

In the present series 7 cases had combined lesions, e.g. duodenal ulceration and hiatus hernia; most of these showed reflux. One of these cases showed a constant spasm of the pyloric sphincteric cylinder with irregular and transverse mucosal folds (Fig. 27.4). It was diagnosed radiologically and endoscopically as spasm and gastritis affecting the cylinder; in addition the duodenal bulb was deformed due to ulceration. In this case moderate to marked duodenogastric reflux occurred. Owing to the tube-like spasm of the cylinder, the pyloric aperture was neither fully open nor fully closed, but fixed in the patent position.

Pyloric Motility

Both in normal controls and in patients, duodenogastric reflux only occurred while the pyloric sphincteric cylinder was relaxed or in a state of partial contraction; it never occurred during maximal contraction of the cylinder. During relaxation of the cylinder there is absence of muscular closure of the aperture; mucosal closure may be present (Chap. 13). During partial contraction of the cylinder, occurring as a phase of cyclical contractile activity, the pyloric aperture is open (Chap. 13). Spasm of the cylinder resembles partial, physiological contraction, and is associated with patency of the aperture; it differs from a physiological contraction in that its contraction is permanent. Consequently increased duodenogastric reflux is to be expected in spasticity of the pyloric sphincteric cylinder.

The above does not imply that the phase of contraction of the sphincteric cylinder is the only factor in the pathogenesis of duodenogastric reflux.

Duodenal Motility

Both in normal subjects and in patients, duodenal peristaltic waves and "segmental" contraction waves in the third part of the duodenum appeared to be of little consequence in duodenogastric reflux (vide supra). However, in experimental studies in canines Ehrlein (l981) found that the timing between contractions of the duodenal bulb and the pyloric "sphincter" (right pyloric loop) was not perfect. Contraction maxima of the duodenal bulb often occurred slightly before or after contraction maxima of the "sphincter". Consequently the pyloric aperture was often inadequately closed during contraction of the duodenal bulb, resulting in reflux.

References #

  1. Capper WM, Airth GR, Kilby JO. A test for pyloric regurgitation. Lancet l966, 2, 621-623.
  2. Capper WM. Factors in the pathogenesis of gastric ulcer. Ann Roy Coll Surg l967, 40, 21-35.
  3. Cole GJ. The implications of bile in the stomach. Gut l969, 10, 864- 867.
  4. Connell AM. Direct measurement of pyloric diameter and tone in man and their response to cholecystokinin (discussion). In: Gastrointestinal Motility in Health and Disease. Edit Duthie HL. Baltimore, University Park Press l978, p 357.
  5. Cunnigham DJ. The varying form of the stomach in man and the anthropoid ape. Trans Roy Soc Edin l906, 45, 9-47.
  6. Davenport HW. Effect of lysolecithin, digitonin and phospholipase A upon the dog's gastric mucosal barrier. Gastroenterology l970, 59, 505-509.
  7. Delaney JP, Cheng JWB, Butler BA, et al. Gastric ulcer and regurgitation gastritis. Gut l970, 11, 715-719.
  8. Donovan IA, Harding LK, Keighley MRB, et al. Abnormalities of gastric emptying and pyloric reflux in uncomplicated hiatus hernia. Brit J Surg l977, 64, 847-849.
  9. Du Plessis DJ. Some aspects of the pathogenesis and surgical management of peptic ulcers. South Afr Med J l960, 34, 101-108.
  10. Du Plessis DJ. Gastric mucosal changes after operations on the stomach. South Afr Med J l962, 36, 471-478.
  11. Du Plessis DJ. Pathogenesis of gastric ulceration. Lancet l965, l, 974-978.
  12. Ehrlein HJ. Strain gauge transducer for recording gastrointestinal motility in unanaesthetized animals. Zeitschr Gastroenterol l980, l8, l9l-l97.
  13. Ehrlein HJ. Gastric and duodenal motility in relation to duodenogastric reflux in healthy dogs. Scand J Gastroenterol l98l, 16 (Suppl 67), 23-27.
  14. Flint FJ, Grech P. Pyloric regurgitation and gastric ulcer. Gut l970, 11, 735-737.
  15. Forssell G. Über die Beziehung der Röntgenbilder des menschlichen Magens zu seinem anatomischen Bau. Fortschr Geb Röntgenstr l9l3, Suppl 30, l-265.
  16. Gotthard R, Bodemar G, Tjädermo M, et al. High gastric bile acid concentration in prepyloric ulcer patients. Scand J Gastroenterol l985, 20, 439-446.
  17. Grech P. A technique for assessing pyloric reflux. Gut l970, ll, 794- 795.
  18. Hoare AM, Keighley MRB, Starkey B, et al. Measurement of bile acids in fasting gastric aspirates: an objective test for bile reflux after gastric surgery. Gut l978, l9, 166-169.
  19. Hughes K, Robertson DAR, James WB. Duodeno-gastric reflux in normal and dyspeptic subjects. Clin Rad l982, 33, 461-466.
  20. Kaye MD, Showalter JP. Pyloric incompetence in patients with symptomatic gastro-oesophageal reflux. J Lab Clin Med l974, 83, 198-206.
  21. Keet AD. Diameter of the pyloric aperture in relation to the contraction of the canalis egestorius. Acta Rad l962, 57, 31-44.
  22. Keet AD. A new, tubeless radiological test for duodenogastric reflux. South Afr Med J l982, 61, 78-81.
  23. Keighley MRB, Asquith P, Alexander-Williams J. Duodenogastric reflux: a cause of gastric mucosal hyperaemia and symptoms after operations for peptic ulceration. Gut l975, 16, 28-32.
  24. Kelly KA, Code CF. Duodenal-gastric reflux and slowed gastric emptying by electrical pacing of the canine duodenal pacesetter potential. Gastroenterology l977, 72, 429-433.
  25. Kim SK, Rogers LS, Heitzman RE. Reflux alkaline gastritis. Amer J Roentg Rad Ther Nucl Med l972, 115, 271-274.
  26. Lawson HH. Effect of duodenal contents on the gastric mucosa under experimental conditions. Lancet l964, 1, 469-472.
  27. Marriott C, Kellaway IW, Martin GP. The effect of bile salts on the physical properties of mucus (abstract). In: Mucus in Health and Disease. Edit Elstein M, Parke DV. Plenum Press, London l977, p 509.
  28. Muhammed I, McLoughlin GP, Holt S, et al. Non-invasive estimation of duodenogastric reflux using technetium-99mbutyliminodiacetic acid. Lancet l980, 2, 1162-1165.
  29. Nicolai JJ, Silberbusch J, Van Roon F, et al. A simple method for the quantification of biliary reflux. Scand J Gastroenterol l980, 15, 775- 780.
  30. Niemela S, Heikkila J, Lehtola J. Duodenogastric reflux in patients with gastric ulcer. Scand J Gastroenterol l984, 19, 896-898.
  31. Olch IY. Duodenal regurgitation as a factor in neutralisation of gastric acidity. Arch Surg l928, 16, 125-138.
  32. Orchard R, Reynolds K, Fox B, et al. Effect of lysolecithin on gastric mucosal structure and potential difference. Gut l977, l8, 457-461.
  33. Rees WDW, Go VLW, Malagelada JR. Simultaneous measurement of antroduodenal motility, gastric emptying and duodenogastric reflux in man. Gut l979, 20, 963-970.
  34. Rhodes J, Bernardo DE, Phillips SF, et al. Increased reflux of bile into the stomach in patients with gastric ulcer. Gastroenterology l969, 57, 241-252.
  35. Rovelstad RA. The incompetent pyloric sphincter; bile and mucosal ulceration. Amer J Dig Dis l976, 21, 165-173.
  36. Schrager J, Oates MDG. Relation of human gastro-intestinal mucus to disease states. Brit Med Bull l978, 34, 79-82.
  37. Thomas WEG, Jackson PC, Cooper MJ, et al. The problems associated with scintigraphic assessment of duodenogastric reflux. Scand J Gastroenterol l984, l9 (Suppl 92), 36-40.
  38. Torgersen J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l942, Suppl 45, 1-191.
  39. Valenzuela JE, Defilippi C. Pyloric sphincter studies in peptic ulcer patients. Amer J Dig Dis l976, 21, 229-232.
  40. Wolverson RL, Sorgi M, Mosimann F, et al. The incidence of duodenogastric reflux in peptic ulcer disease. Scand J Gastroenterol l984, l9 (Suppl 92), 149-150.
  41. Wormsley KG. Aspects of duodenogastric reflux in man. Gut l972, 13, 243-250.