The Pyloric Sphincteric Cylinder in Health and Disease



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Chapter 20 (page 91)


Pathogenesis

Torgersen (1942) showed an illustration in which the canine canalis egestorius (i.e. pyloric sphincteric cylinder), in its entirety, was spastic. He postulated that the appearance of pylorospasm was identical to that seen in a maximal or near maximal normal contraction of the sphincteric cylinder (Chap. 13) during certain stages of vomiting (Chap. 26) and in cases of infantile hypertrophic pyloric stenosis (IHPS) (Chap. 23). All these conditions had the same anatomical "substratum", namely contraction of the musculature of the entire sphincteric cylinder.

Astley (1952) described 10 well-documented cases of infantile pylorospasm in which the spasm involved the canalis egestorius as defined anatomically by Forssell (1913) (Chap. 3). In all these infants, who presented with vomiting, a prepyloric narrowing simulating infantile hypertrophic pyloric stenosis was seen at the radiological examination. The narrowing persisted for periods ranging from 10 minutes to over an hour; it differed from IHPS in degree but not in the extent or shape of the area affected. Continued observation showed that it was neither constantly narrowed nor completely devoid of peristalsis as in IHPS; after a variable interval the narrowed segment relaxed to a certain extent and in some cases it eventually attained a normal calibre. In a few instances the relaxation occurred suddenly while in others intermittent contraction and relaxation was seen. There can be little doubt that these cases of infantile pylorospasm were due to spasm of the pyloric sphincteric cylinder. Astley (1952) mentioned the fact that the radiological appearance simulated a stage in the normal cycle of contraction of what he called the "prepylorus".

Wood and Astley (1952), during an investigation of the causes of vomiting in young infants, described the clinical findings in a group of 12 cases in which the symptoms closely resembled those of IHPS. Some of the cases previously mentioned by Astley (1952) appear to be included in this group. A palpable pyloric tumor was found in 8 of the cases (the term "tumor" indicated a clinically detectable swelling). It resembled the tumor of IHPS, although it differed in consistency, being softer, and it was less well defined. It was usually palpable immediately before or just after a vomit, relaxed quickly and could not be felt repeatedly; as the clinical findings resembled IHPS the condition was called "pseudo-pyloric stenosis". Radiological examination in 4 of the 12 babies showed infantile pylorospasm, i.e. a cylindrical prepyloric narrowing simulating IHPS. However, it lacked the constancy and aperistalsis of IHPS, and continued observation showed that it widened eventually. In 5 of the 12 babies who were operated upon, neither pyloric hypertrophy nor tumor was found, showing that the features were due to spasm of the sphincteric cylinder. In their investigations into the causes of vomiting in more than 100 infants, Astley (1952) and Wood and Astley (1952) did not describe any cases of pylorospasm in which spasm was limited to the pyloric ring.

Craig (l955) pointed out that a palpable, contractile tumor was present in 98 percent of infants with IHPS over the age of 2 weeks. The same significance could not always be attached to the palpation of a contractile pyloric tumor in babies under 2 weeks of age. Initially 2 cases were encountered, both babies under 2 weeks, in whom recurrent regurgitation was associated with a contractile pyloric tumor. Over a period of weeks the symptoms as well as the pyloric tumor disappeared, the only treatment having been daily gastric lavages. Because of the clinical features IHPS was excluded as a cause of the condition. Craig (l955) instituted a prospective study in which 21 infants less than 2 weeks of age, presenting with repeated vomiting but otherwise normal, were examined. Contractile pyloric tumors were palpated in l7. With repeated gastric lavages symptoms subsided within 7 to 14 days, while the tumors disappeared after a period of time varying from 4 weeks to 3 months. In a control group of 115 healthy newborn infants with uninterrupted progress and no feeding difficulties, a palpable pyloric tumor was felt in 25. Of the 21 who were followed up, the tumor disappeared within 6 weeks to 3 months. The pyloric tumors had a fusiform or spheroidal shape and a firm or distinctly hard consistency. They were felt to contract and relax repeatedly, became firmer as feeding continued, and were palpated at successive examinations. A feature of all cases was the large amount of mucus in the gastric lavages. Some of the cases were examined radiologically but this appeared to be incomplete and yielded little relevant information. One of the symptomatic babies, who had a large pyloric tumor resembling IHPS in all respects, was referred for operation, at which no tumor was found.

According to Craig (1955) these cases indicated that a hard, contractile pyloric tumor could be felt in the absence of organic change of the musculature. It was considered to be due to spasm of the fan-shaped pyloric musculature described by Cole (l928). It was evidence not of muscular hypertrophy but of muscular spasm, and resembled the cases of pseudo-pyloric stenosis previously described by Astley (l952).

Atkinson et al. (l957) stated that the concept of spasm of the pylorus presumably derived from the belief that a physiological sphincter existed at the pylorus. It was widely believed that the pyloric ring acted as a sphincter. However, during manometric studies they were unable to find any evidence of a physiological sphincter at the pylorus, and in no instance could a band of increased pressure be demonstrated anywhere at the pyloroduodenal junction (Chap. 15). Although phasic pressure waves were recorded repeatedly in a 4.0 to 5.0 cm long segment of the prepyloric region, no evidence of independent contraction was found at the gastroduodenal junction, i.e. at the pyloric ring. For most of the time the lumen surrounded by the pyloric ring or "sphincter" was more than 7.0 mm in diameter. The closure of the ring was intermittent and brief, occurring as part of the phasic contraction which periodically involved the whole pyloric region. Atkinson et al. (l957) concluded that the concept of spasm of the pyloric ring had been grossly overworked as an explanation for a variety of symptoms.

According to Levin (l971) pylorospasm could at times mimick the "elongated", narrowed pylorus of adult hypertrophic pyloric stenosis.

Swischuk (l978, l980) considered pylorospasm to be a spasm of the "antropyloric" region, by which was meant a tubelike, segmental area extending orally from the ring. It could be difficult to distinguish pylorospasm from some cases of IHPS; in pylorospasm, however, the narrowing was not as intense and there were slight changes in the configuration. A similar deformity of the antropyloric region could also occur in association with gastric ulceration in neonates.

Franken (l982) found infantile pylorospasm a difficult entity to define; the appearances could be very similar to those of IHPS on radiographic study. However, the narrowing seen in infantile pylorospasm was not as constant as in IHPS, and in infantile pylorospasm some peristaltic movement did occur in the affected area. It could be difficult to convince the surgeon that the patient had infantile pylorospasm and not IHPS.


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