Chapter 29 (page 140)

The Pyloric Sphincteric Cylinder in Health and Disease

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Chapter 29 (page 140)

Lawson (l972) studied the antral mucosa by means of gastroscopy and biopsy in 25 patients with gastric ulceration "in the usual position" along the lesser curvature. (Comment: It appears if the ulcers were situated a considerable distance proximally to the pyloric aperture). The biopsies were taken at a point half-way between the ulcer and the pyloric aperture, in an area in which the antral mucosa appeared normal macroscopically. In 10 cases the surface epithelium, pyloric glands and mitotic activity were normal. In the remaining 15 cases marked histological changes were seen, with chronic atrophic gastritis in 7 and increased mitotic activity in 8. The findings supported the view that a diffuse mucosal lesion of the "antrum" was associated with gastric ulceration situated proximally to the antrum. It was not clear whether the gastritis or the gastric ulcer was the primary event.

Fisher and Cohen (l973) studied pyloric sphincter pressures in 10 patients with gastric ulceration, both before and after healing, and in 10 normal control subjects. (Comment: The pyloric ring was equated with the sphincter). The ulcer was situated high on the lesser curvature in 1 case, on the middle of the lesser curvature in 4, in the prepyloric region in 3 and in the "pyloric channel" in 2. Intraluminal pressures were determined by means of an open-tipped, 5-lumen catheter assembly, with all patients in the right lateral decubitus position. It was found that the gastroduodenal junction of patients with an active gastric ulcer was characterized by a zone of high pressure similar to that in normal subjects. The pyloric pressure in patients with gastric ulcer was 4.2 ± 0.9 mm Hg as compared to 6.2 ±: 1.3 mm Hg in normal subjects. Duodenal acidification in normal subjects increased the pyloric pressure to 25 mm Hg, but had no effect in patients with active gastric ulceration. Intravenous administration of secretin and cholecystokinin gave similar results. The studies suggested pyloric sphincter dysfunction in patients with gastric ulceration, probably leading to increased duodenogastric reflux. As similar findings were obtained after healing, it appeared unlikely that gastric ulceration was the cause of the pyloric incompetence. (Comment: The results of manometric studies in normal subjects by Fisher and Cohen are discussed in Chap. 15). Fisher and Boden (l975) subsequently reported that pyloric sphincter dysfunction could be reversed by gastric acidification, but that the mechanism of the dysfunction remained unclear.

Liebermann-Meffert and Allgöwer (l977) pointed out that while the factors leading to gastric ulceration were not fully understood, some abnormality of the pylorus, e.g. antral stasis or duodenogastric reflux, had been implicated. In an attempt to elucidate the problem, detailed studies of anatomical changes in the pyloric region were performed in 77 surgical resection specimens of patients with gastric ulceration. In 10 the ulcer was immediately adjacent to the pylorus ("pyloric ulcers") while in 67 it was situated in other parts of the stomach ("non-pyloric ulcers"); the findings were compared with those of 50 control subjects. While all controls had a soft antropyloric wall, considerable patchy induration of the wall was felt in 41 of 54 gastric ulcer specimens. The pyloric diameter in controls had a range of 15 mm to 22 mm; in the ulcer specimens the range was 10mm to 22 mm. In 22 of 45 ulcer specimens the pyloric ring was smaller than the lower limit of normal, and bouginage was found to be difficult as the ring was more rigid than in controls, although it had not caused obstruction.

According to Liebermann-Meffert and Allgöwer (l977) the pyloric and prepyloric musculature was of uniform thickness in control subjects, while nodular or fusiform muscular thickening, often involving only part of the circumference, was frequently found in ulcer specimens (Chap. 25). In 9 of these cases the muscular hypertrophy was circular, involving the whole pyloric ring uniformly. In all cases considerable fibrosis was seen in the thickened musculature. Diffuse submucosal thickening, probably due to a combination of oedema and connective tissue hypertrophy, was found in the ulcer cases, and the mucosa often appeared coarse and roughened. The number of Auerbach's plexuses and the corresponding number of nerve cells was significantly reduced in cases of gastric ulcer, being only half that seen in controls. All the changes occurred in the antropyloric wall irrespective of the site of the ulcer. It was concluded that the thickness of the gastric wall at the pylorus and in the distal 5.0 cm of the "antrum", was increased in patients with gastric ulcer. Although the mucosa, submucosa and muscular layers were affected, the changes were most marked in the latter. Muscle hypertrophy was not necessarily uniform, was usually associated with fibrosis, and histological abnormalities of the muscle cells were common. The intramural ganglia were markedly reduced in number and those which were present commonly showed abnormal nuclei. Since the muscle and ganglia were involved in normal motility, it was reasoned that the above features were consistent with a disturbance of normal physiological mechanisms at this site. Whether this was a cause or the consequence of duodenogastric reflux, or whether it formed a link in the chain of events leading to gastric ulceration, remained uncertain.

In 8 cases in whom a gastric ulcer was situated on the lesser curvature or anterior gastric wall, Meister et al. (l979) found histologically verified chronic atrophic gastritis and intestinal metaplasia with mild or moderate dysplasia in all. These mucosal changes were especially prominent in the proximal regions of the resection specimens.

Liebermann-Meffert et al. (l98l) found that intraoperative electrical stimulation of the vagal trunks caused a distinct intragastric pressure rise in patients with gastric ulcer, duodenal ulcer, combined gastric and duodenal ulcer, and in non-ulcer controls. However, the amplitude, duration and integrated motor response in the stomach was significantly greater in the patients with gastric ulcer than in the other groups. It was concluded that gastric ulceration did not cuase hypomotility of the gastric reservoir (i.e. the corpus and fundus), but that it was probably associated with a disturbance of the antral pump mechanism. The intrinsic morphological alterations of the antropyloric wall could render antral contractions less effective, leading to impaired gastric drainage and stasis.