The Pyloric Sphincteric Cylinder in Health and Disease

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Chapter 38 (page 194)

Associated Gastroduodenal Lesions

Most cases of prolapse of gastric mucosa into the duodenum occurred de novo, in the absence of other lesions of the upper gastrointestinal tract. However, in a considerable number of cases other lesions were also encountered during the radiological, surgical or post mortem examinations. The most frequent associated conditions were the following:

Duodenal Ulceration. Not infrequently active duodenal ulceration was encountered (Pendergrass 1930; Scott 1946; Manning and Gunter 1950; Zimmer 1950; Keet 1952). Cases associated with healed duodenal ulceration were also described (Eliason et al. 1926; Archer and Cooper 1939; Fermin 1950).

Gastric Ulceration. Melamed and Hiller (1943) described a case in which a large gastric ulcer was situated on the prolapsed mucosa. In other cases active gastric ulceration was located elsewhere in the stomach, i.e. away from the prolapsing mucosa (Hawley et al. 1949; Keet 1952).

Changes in the Pyloric Musculature. Changes of a hypertrophic or fibrotic nature in the pyloric musculature with consequent narrowing of the pyloric aperture were reported by various authors. Meyer and Singer (1931), Archer and Cooper (1939) and Zacho (1948) noted a perceptible thickening in the pyloric musculature in some of their cases. In a verified case of Ferguson (1948) the pyloric muscle was greatly hypertrophied. In his 3 cases Rees (1937) found the pyloric muscle to be constricted, having the appearance of a white fibrous ring in one case. Manning and Gunter (1950) noted thickening of the pyloric muscular ring in 4 of their 6 cases. Zimmer (1950) described a case with a duodenal ulcer and acute inflammatory changes in the pyloric mucosa and musculature. From these descriptions no clear picture emerged as to the nature and extent of the pyloric hypertrophy.

Cases with an abnormally wide pyloric aperture have also been described. Eliason et al. (1926) noted this feature in one case which came to operation. In the cases described by Nygaard and Lewitan (1968) and by Köhler (1950), the radiographs showed the pyloric aperture to be widely dilated.

Gastritis. Differences of opinion regarding the histology, pathogenesis and classification of gastritis have been referred to previously (Chap. 28). In the present context it is to be expected that different authors may have used different criteria in diagnosing gastritis. A number of cases of transpyloric prolapse of gastric mucosa have been described in which "gastritis" was mentioned as an associated lesion.

Bohrer and Copleman (1938) described one case in which there was associated acute and subacute gastritis. In two verified cases of Norgore and Shuler (1945) the pyloric region showed evidence of chronic gastritis. Histological examination of the resected mucosa in 5 operated patients described by Scott (1946), showed a slight increase in lymphocytes, plasma cells and eosinophils throughout the mucosa and submucosa; however, this was not considered sufficient to warrant a diagnosis of gastritis. Judd and Moe (1947) described a case in which erosive gastritis and infiltration by plasma cells were present. A verified case described by Nygaard and Lewitan (1948) had chronic gastritis and healed erosions. One of the 3 verified cases of Hawley et al (1949) showed a moderate infiltration of the gastric mucosa with plasma cells and lymphocytes. The second case showed no gross evidence of gastritis, and the third, in which 2 gastric ulcers were also present, had acute on chronic inflammatory reaction in the pyloric area. Two cases of verified circular prolapse studied by Manning and Gunter (1950) both showed chronic gastritis with heavy infiltration of lymphocytes and plasma cells in the prolapsed mucosa, submucosa and muscularis mucosae. In his verified case Teng (1962) found the submucosa to be thickened and oedematous; there was mild inflammatory reaction without ulceration. White et al. (1966) found the prepyloric mucosal folds to be hyperaemic and oedematous with a granular, inflammatory appearance.

Possible True Complications

Ulceration and Haemorrhage. Cases with superficial ulceration of the prolapsed mucosa and consequent slow oozing of blood from the ulcerated surfaces were described by a number of authors (Pendergrass and Andrews 1935; Bohrer and Copleman 1938; Archer and Cooper 1939; MacKenzie et al 1946; Scott 1946; White et al. 1966). In some cases massive gastro-intestinal haemorrhage occurred (Ferguson 1948; Moon and Speed 1949; Fredel 1960). The above authors usually regarded ulceration and haemorrhage as a true complication of the condition.

Obstruction of the Pyloric Aperture by Redundant Gastric Mucosal Folds. Gastric mucosa prolapsing into the duodenum may, at times, pile up in the form of large, redundant prepyloric folds causing obstruction at the gastric outlet (Schmiedin 1911; Eliason et al 1926; Scott 1946; Judd and Moe 1947; Zacho 1948; Fredell 1960). (In the 2 cases of Zacho there was associated pyloric muscular hypertrophy). It seems that redundant prepyloric mucosal folds, causing obstruction, may also be regarded as a true complication.

Malignancy and Prolapse of Gastric Mucosa

Malignancy does not appear to be a complication of gastric mucosal prolapse. The presence of benign papillomata on prolapsed mucosa was reported by Pendergrass and Andrews (1935). In one of the polyps a small plaque of malignant tissue was encountered; it was considered to be an incidental finding not directly related to the prolapse. One other case associated with malignancy was described, namely that of Rubin (1942), in which the malignant polypoid process involved the entire gastric mucosa. This appeared to be a case of general gastric polyposis with malignant degeneration, not confined to the prolapsed mucosa. According to Nygaard and Lewitan (1948) no instance of malignant change in a true case of transpyloric mucosal prolapse had been reported up to that time. This statement still appears to be valid at the present time. However, a primary gastric carcinoma may prolapse into the duodenum, causing a rounded, intraluminal filling defect in the bulb, as described by Joffe et al. (1977).

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