Adult Hypertrophic Pyloric Stenosis #

Although cases of hypertrophy of the pyloric musculature in adults (AHPS) had been reported previously, Morton (l930) first concluded that the condition seemed to constitute a definite clinical entity. He described 3 cases, aged 63, 42 and 39 years, in each of in each of whom radiographic examination had shown a constant, tubelike narrowing of the pyloric ring and immediate prepyloric area, 2.5 to 3.0 cm in length in one of the cases. (Measurements were not given in the other two). At operation the lesion was found to be due to hypertrophy of the pyloric muscularis externa in all instances; there were no associated lesions such as gastric or duodenal ulceration.

Kirklin and Harris (l933) described the radiographic signs of AHPS as elongation and narrowing of the pyloric canal together with evidence of gastric outlet obstruction. While these signs were not pathognomonic, a distinctive sign was a concave indentation of the base of the duodenal bulb, produced by partial invagination of the hypertrophied pyloric muscle into the duodenum. (Comment: It has subsequently been shown that various other conditions, ranging from normal contraction of the pyloric sphincteric cylinder to pyloric carcinoma, may produce similar duodenal indentation, as described in Chapters 13 and 33). In 50 cases of pyloric muscular hypertrophy in adults associated lesions of the upper gastrointestinal tract, such as gastric and duodenal ulceration, were present in 35.

North and Johnson (l950) stated that many cases of secondary pyloric hypertrophy, i.e. cases in whom the hypertrophy was associated with either benign or malignant gastric ulceration, had been reported prior to that time. The associated lesion was often situated away from the pyloric region in the more proximal part of the stomach. In primary AHPS, on the other hand, there were no associated gastric lesions. They were able to collect 59 case reports of verified primary AHPS, and described 5 cases of their own. It was stated that the lesion was not always easily recognizable at operation, a firm mass, or at least a thickening, being usually but not invariably palpable. When the condition was suspected, and when the exterior of the stomach appeared normal, a gastrostomy with examination of the lumen and palpation of the wall was necessary. Although the normal variations in the thickness of the pyloric musculature had not been clearly defined at that time, Truesdale (1915) had previously determined that the normal thickness of the "sphincter" (presumably referring to the pyloric ring) was 5.0 mm on an average, while Horwitz et al. (l929) found the range in thickness to vary from 3.8 to 8.5 mm with an average of 5.8 mm; both made their measurements upon fixed specimens in which the "sphincter" had been sectioned. North and Johnson (l950) found that in most of the recorded cases of primary AHPS in which data were available, the pyloric muscle measurements were considerably above this normal range and the same applied in their cases. The outstanding pathological feature of the lesion was hypertrophy and hyperplasia of the circular muscle layer, which was thickest at the pyloric ring, diminishing gradually over the "antrum" for a distance of 3.0 to 4.0 cm. The longitudinal muscle coat might also show a moderate grade of hypertrophy and the submucosa and mucosa might contain foci of cellular infiltration, consisting of plasma cells, lymphocytes and some neutrophils. Macroscopically the condition caused an unyielding tumor occupying the distal 3.0 to 4.0 cm of the stomach. The macroscopic appearances of infantile hypertrophic pyloric stenosis (IHPS) and primary adult hypertrophic pyloric stenosis (AHPS) were almost identical.

McNaught (l957) described 5 cases of AHPS, in 3 of whom there was no associated lesion, while in 2 an associated gastric ulcer was found at operation. It appears from the description that the ulcer was away from (i.e. proximal to) the area of muscular hypertrophy in both cases. This author found the lesion in AHPS to be comparable to simple hypertrophic pyloric stenosis in infants, and to him it was clear that the lesion was limited to the canalis egestorius or pyloric sphincteric cyclinder, as postulated by Torgersen (1942).

Craver (l957) reported 11 cases of AHPS encountered during a 24 year period. In 5 of these there was no concomitant upper gastrointestinal lesion, in 3 there was associated gastric ulceration, in 2 associated duodenal ulceration and in one associated haemorrhagic gastritis. (Comment: It is not stated clearly what the location of the gastric ulcers was, but it appears if they were proximal to the area of muscular hypertrophy). The gross appearance at operation resembled that found in IHPS, with a firm, unyielding, fusiform or circular tumor mass occupying the distal 3.0 to 4.0 cm of the stomach. The consistency varied from that of soft rubber to cartilage and it was thickest at the pyloro- duodenal junction, thinning out gradually over the "antrum"; distally it stopped abruptly at the pyloric ring. In 8 of the cases measurements showed that the muscular thickness ranged from 12 to 20 mm, with an average of 15.4 mm. This was 2 to 3 times the average thickness (7.1 mm) found in a series of normal controls. Microscopically there was both hypertrophy and hyperplasia of the circular layer, the muscular fibres being increased in size as well as in number. There were no inflammatory changes or oedema.

In a series of 25 cases coming to laparotomy, Desmond and Swynnerton (l957) found associated gastric ulceration in 12, duodenal ulceration in 6, pyloric ulceration in one and mucosal prolapse in 2, while 6 cases had no associated lesion (some cases had more than one associated condition). At operation the lesion presented as a white, regular, glistening muscular mass with a normal serosa and a loose, lax submucosa. (Comment: The finding is similar to the appearance seen during experimental truncal vagal stimulation in canines as described in Chap. 32). It could readily be differentiated from a grey, irregular, infiltrative type of carcinoma. Lumsden and Truelove (l958) described cases which showed that AHPS might be a sequel to IHPS, or it might arise de novo in adults. In the first category 5 patients who had received medical treatment for hypertrophic pyloric stenosis in infancy, showed radiological abnormalities campatible with AHPS in later life. Similar cases were described by other authors (Chap. 23); most of these adult cases were symptom-free.

Skoryna et al. (l959) described 6 cases with the morphology based on Torgersen's anatominal concepts. In 2 cases there was hypertrophy of the circular musculature of the pyloric canal (i.e. presumably the pyloric sphincteric cylinder) without other macroscopic lesions in the stomach and duodenum (one of the cases showed microscopic evidence of chronic gastritis); these were labelled cases of diffuse primary pyloric hypertrophy without associated proximal gastric lesions. In one case hypertrophy of the circular musculature of the "pyloric canal" was associated with a gastric ulcer on the lesser curvature 6.0 cm orally to the pylorus (i.e. approximately 3.0 cm orally to the commencement of the sphincteric cylinder) together with associated chronic gastritis; this was called a case of diffuse primary pyloric hypertrophy associated with a proximal gastric lesion. In another case there was moderate hypertrophy of the musculature of the entire pyloric canal, with a relatively greater degree of hypertrophy of the circular muscle on the lesser curvature at the muscle knot; there was no associated gastric or duodenal lesion, and Skoryna et al. (1959) considered it to be an example of primary pyloric hypertrophy of the focal type. (This case is also quoted in Chap. 25). One case exhibited benign ulceration within the confines of the "pyloric canal" (with muscular hypertrophy of its walls), and another had pyloric muscle hypertrophy with extensive surrounding adhesions and fibrosis, suggesting a previous inflammatory process (probably a duodenal ulcer). These 2 cases were considered to be pyloric muscular hypertrophy secondary to a distal obstructive lesion, e.g. obstructive complications of pyloric or duodenal ulceration.

Knight (l961) described 7 cases of AHPS; four of these were of a focal nature and are considered elsewhere (Chap. 25). Two of the remaining cases had diffuse enlargement of the pyloric musculature similar to IHPS, without evidence of gastric or duodenal ulceration. Gallstones were present in one of these, for which a cholecystectomy was performed. Both cases needed pyloroplasty. In the last case there was diffuse pyloric muscular hypertrophy involving a segment 2.5 cm in length, with a benign gastric ulcer 6.0 cm proximal to the pylorus. According to Knight (1961), hypertrophy in IHPS involves the entire circumference, while in the adult it may involve only a localized segment of the pyloric musculature. In IHPS hypertrophy always seems to occur as a primary condition, without associated upper gastro-intestinal pathology, while in the adult associated peptic ulceration or gastritis is common. This author found the thickness of the "pylorus" in 10 fresh post-mortem adult stomachs to range from 4.0 to 7.0 mm, with an average of 5.1 mm, while the thickness ranged from 10 to 15 mm in AHPS. The gross appearance of the pylorus in AHPS was similar to that of IHPS.

Edwards (1961) recognized two types of AHPS, viz. an idiopathic form, in which no other gastric lesion was present, and a secondary form in which there was some associated lesion such as gastric or duodenal ulceration or gastric carcinoma. It was stated that the etiology remained doubtful and among the possibilities to be considered were persistence of the infantile form, degeneration of the myenteric plexus and long continued pylorospasm. Pathologically the circular musculature was increased in thickness from the usual 3.0 to 8.0 mm to a maximum of 30 mm with an average of 15 mm. Radiologically elongation and narrowing of the pyloric canal was present.

Christiansen and Grantham (l962) collected 56 case reports published subsequent to the review by North and Johnson (l950), and added 2 of their own. In both their cases the gross and histological appearances were indistinguishable from those of IHPS. Of the 58 cases reviewed, 34 had no associated lesion in the upper gastrointestinal tract, but the remaining 24 had associated pathology, the most common lesions being gastritis (9), cholecysititis (7) and hiatus hernia (4).

Seaman (l963) reported 27 cases of AHPS, of which l8 had an associated gastric ulcer and 2 more had evidence of previous gastric ulceration. It is not clear from the description what the position of the gastric ulcer was in each case. Most of the other cases had microscopic evidence of gastritis, while 2 had duodenal ulceration (one of these also had a gastric ulcer.) There was no evidence of obstruction in the duodenal ulcer cases. While accepting the normal measurements of Horwitz (l929), Craver (l957) and Knight (l961), Seaman (l963) found that the thickness of the pyloric musculature in his cases varied from 9.0 to 15 mm, with an average of 11.2 mm. He found the gross appearance of AHPS to be similar to that of IHPS, the thickest portion of the musculature being at the pyloroduodenal junction, ending abruptly at the duodenum, but decreasing gradually as it faded into the "antrum" on the gastric side. Seaman based the morphology of the lesion in AHPS on the muscular anatomy as determined by Forssell (l913), Cole (l928) and Torgersen (l942).

Wieser et al. (l963) reviewed 44 operatively confirmed cases of AHPS. The condition was defined as any non-carcinomatous wall-thickening in the canalis egestorius, irrespective of its etiology. Two types were recognized, viz. a purely muscular form and a mixed form in which additional evidence of gastritis was present in the mucosa and submucosa. Twenty percent of the cases were associated with hiatus hernia, and gastric ulceration was present in 50 percent; this was probably not coincidental, the ulceration being deemed to be secondary to the pyloric stenosis. Radiologically there was elongation and narrowing of the pyloric canal with a prepyloric outpouching, altered peristalsis and a concave indentation of the base of the duodenal bulb. The condition had to be differentiated from early pyloric carcinoma. Keynes (l965) found that 132 cases of simple, primary or idiopathic hypertrophic pyloric stenosis in adults, i.e. muscular hypertrophy without associated lesions, had been described in the English literature up to that time. These included 64 case reports collected from, or added to the literature by North and Johnson (l950), as well as 56 cases reviewed by Christiansen and Grantham (l962) and 2 new cases added by them. Keynes (l965) described the clinical, radiological and pathological findings in 12 new cases of AHPS, 6 of whom had associated peptic ulceration (3 duodenal, 2 gastric and one pyloric), and were designated "complicated" AHPS. The remaining 6 had no associated upper gastro-intestinal lesion and were of the "simple" variety. The gross appearance of the pylorus in diffuse AHPS, both in the simple and the complicated types, was similar to that in IHPS: a smooth, firm or rubbery hard tumor occupied the region of the pylorus, ending abruptly at the duodenum, where it was at its thickest. From here the muscular thickening gradually decreased towards the proximal end of the pyloric canal. Histologically there was hypertrophy of the circular fibres with occasional moderate longitudinal muscular hypertrophy. Keynes (l965) noted no abnormality in the ganglion cells of the myenteric plexuses. The affected region was limited to the pyloric "canal" (pyloric sphincteric cylinder) as described by Cunningham (1906), Horton (1928) and Torgersen (l942). In infants the hypertrophy was always of the simple variety, since it occurred in the absence of other gastro-intestinal pathology, but in adults it could be complicated. Although simple AHPS was uncommon, Keynes (l965) did not believe it was as rare as the literature seemed to suggest.

Du Plessis (l966) described 6 cases of what he termed primary hypertrophic pyloric stenosis commencing in adult life without apparent cause. Gastric resection was performed in 2, both of which showed atrophic gastritis and gastric ulceration. These cases would have been classified secondary AHPS by North and Johnson (1950), and primary AHPS associated with a proximal gastric lesion by Skoryna (l959), Knight (l961) and Christiansen and Grantham (l962). Keynes (l965) would have designated them "complicated" AHPS. Du Plessis (l966) looked upon them as "primary" as he considered the gastric ulceration to be the effect of stasis secondary to the pyloric stenosis. In both resection specimens the circular muscle along the greater curvature showed a marked increase in thickness at the pylorus and for a distance of 2.5 cm proximally. Along the lesser curvature the circular muscle was increased in thickness at the pylorus and up to 1.5 cm proximally. In contrast the longitudinal musculature showed a decrease in thickness over the pylorus and for some distance proximally. The ganglion cells in the myenteric plexuses of the 2 cases appeared normal. In 4 cases there was no associated pathology in the stomach and duodenum. Biopsies taken at the time of operation in all 6 cases showed atrophic gastritis and confirmed the deficiency in the longitudinal musculature.

Interpreting his findings on the anatomical concepts of Torgersen (l942), Du Plessis (l966) suggested that the cause of AHPS was a deficiency of the longitudinal musculature of the pyloric canal (i.e. pyloric sphincteric cylinder), which would result in a failure of the canal to shorten during contraction. This would cause an imbalance of longitudinal and circular muscle contractions resulting in functional obstruction. The circular fibres of the fan-shaped muscle would gradually become hypertrophied as a result of repeated ineffective contractions, adding a mechanical element to the obstruction.

Larson et al. (l967) enumerated the generally accepted radiographic signs as lengthening and narrowing of the pyloric canal with an intact mucosal relief, a contrast filled cleft in the centre of the canal and a crescentic indentation of the duodenal bulb. In 10 cases in whom radiographs showed clear evidence of AHPS, surgical exploration revealed a normal stomach in 5, pyloric carcinoma in 2, AHPS in 1, AHPS and a gastric ulcer in 1, while one case showed evidence of prior surgical treatment for IHPS. It was concluded that there was little direct correlation between the radiographic appearance of pyloric elongation and narrowing on the one hand, and pyloric muscle thickness on the other.

Bodon and Haake (l968) called attention to the frequent association of AHPS with hiatus hernia and reported 11 cases of their own. In these cases the surgical solution was to correct the pyloric hypertrophy by means of pyloroplasty or antrectomy, necessitating an abdominal (as opposed to a transthoracic) approach. At operation the diagnosis of pyloric hypertrophy was not difficult, the hypertrophied muscle presenting as a mass 4.0 to 10 mm thick and 1.0 to 5.0 cm long.

At gastroscopy the hypertrophied muscle resembles the uterine cervix, according to Schuster and Smith (l969). The pyloric opening presents as a hole of fixed diameter in the centre of the mound, thus contrasting with the actively mobile pyloric region of normal subjects. The affected region, unlike the normal "antrum", does not respond to anticholinergics.

Bateson et al. (l969) described l7 cases of AHPS, in 4 of whom there was an associated lesser curvature gastric ulcer, and in one a prepyloric ulcer. None of these cases had associated duodenal ulceration. Macroscopically every case showed hypertrophy of the "pyloric and prepyloric muscle", stopping abruptly at the "pyloric canal" (i.e. pyloric aperture) and thinning out gradually over the adjacent part of the "antrum". Although the hypertrophy was most marked at the pyloroduodenal junction, it also involved the wall of the pyloric "antrum", and a more accurate title according to Bateson et al. (l969) would have been hypertrophic pyloric channel disease, the pyloric channel being defined as the area between the duodenum and a point 2.5 cm proximal to the duodenum. In 5 of the cases it was noted that on touching the pylorus with a gloved finger during operation, the pyloric and adjacent antral muscle contracted, becoming hard and pale. (Comment: a similar appearance was seen during experimental truncal vagal stimulation as described in Chapter 32). This spasm probably accounted as much for the radiological appearances as did the degree and extent of muscle hypertrophy and, in their opinion, made careful measurement of the muscle thickness an academic exercise of doubtful value. Microscopically hypertrophy and hyperplasia of the circular muscle fibres was seen with fibrous tissue between the hypertrophied bundles in every case.

In his review Levin (l97l) came to the conclusion that the radiographic diagnosis of AHPS could not be made with a high degree of confidence. While the signs of hypertrophic pyloric stenosis were diagnostic in infants, this was not always the case in adults. Nevertheless several reports had indicated that AHPS represented persistence of a mild form of IHPS. In his view the poor correlation between the radiographic and pathologic findings led to the conclusion that the elongated, narrowed pylorus was at times due to spasm. In those patients proved to have AHPS, gastric or duodenal ulceration or gastritis had been present in the majority. Indirect evidence suggested that these conditions were the sequelae and not the cause of pyloric muscle hypertrophy. It was important to exclude pyloric carcinoma as a cause of the narrowing in every case.

Discussion #

Most authors agree that adult hypertrophic pyloric stenosis (AHPS) is a rare condition. In approximately 17,000 upper gastrointestinal barium examinations over a 5 year period we diagnosed the condition not more than 3 or 4 times; these patients were lost to follow-up and the diagnosis could not be verified.

Types of AHPS #

Primary, Idiopathic or Simple #

AHPS may occur in the absence of other pathology in the upper gastrointestinal tract. An analysis of 129 verified cases encountered in the literature, showed that 51 had no associated lesions (Table 24.1). In addition to the above Morton (1930) described 3, North and Johnson (1950) 5, Lumsden and Truelove (1958) 5, Christiansen and Grantham (l962) 2, and Larsen et al. (l967) one case of verified AHPS without concomitant lesions. (These were individual cases, not forming part of larger groups). These cases have been termed primary (North and Johnson l950), idiopathic (Edwards l96l) or simple (Keynes l965) AHPS. In order to differentiate the condition from focal hypertrophic pyloric stenosis Skoryna et al. (l959) designated them cases of diffuse primary pyloric hypertrophy without associated proximal gastric lesions.

Table 24.1. Analysis of 129 verified cases of AHPS encountered in the literature

AHPS: adult hypertrophic pyloric stenosis

Secondary or Complicated #

Associated or concomitant lesions in the upper gastrointestinal tract were present in 78 of 129 verified cases of AHPS. In attempting to determine the nature and incidence of the associated lesions, it would have been useful to analyze the figures in Table I; however, this was not possible as the relevant particulars were not given in all instances. A separate series of case reports (some of which did not include cases of primary AHPS) was analyzed to obtain the particulars; this is shown in Table 24.2, in which 81 of 119 cases of AHPS had associated lesions. (Some cases had more than one associated lesion, e.g. gastric ulcer and gastritis. "Other" includes conditions such as previous gastric ulceration, prolapse of gastric mucosa and pyloric adhesions).

Table 24.2. Associated lesions in AHPS

AHPS: adult hypertrophic pyloric stenosis

Where the condition was associated with other lesions it was termed secondary (North and Johnson l950; Edwards l96l) or complicated AHPS (Keynes l965). In order to differentiate these cases from focal hypertrophic pyloric stenosis Skoryna et al (l959) called them diffuse primary pyloric hypertrophy associated with a proximal gastric lesion. Du Plessis (l966) termed the condition primary hypertrophic pyloric stenosis commencing in adult life without apparent cause.

Associated Lesions #

Gastric Ulceration #

It is seen (Table 24.2) that the most common associated lesion is gastric ulceration, followed by duodenal ulceration, hiatus hernia, chronic atrophic or haemorrhagic gastritis, pyloric ulceration, gall bladder pathology, gastric mucosal prolapse and gastric carcinoma, in decreasing order of frequency. Although this is not stated unquivocally in all cases, it appears that in most the gastric ulcer was situated some distance away from, i.e. proximal to, the pyloric region (North and Johnson l950; Craver l957; McNaught l957; Skoryna et al. l959; Knight l96l; Bateson et al. l969). A number of authors held the view that pyloric stenosis was the primary event, with ulceration developing as a result of stasis and retention of gastric acid and pepsin (Wieser et al. l963; du Plessis l966; Levin l97l). This view is open to doubt. It has been shown that gastric ulceration in the body of the stomach was sometimes associated with motility disturbances or spasm of the pyloric sphincteric cylinder (Chap. 29). An alternative explanation, in our view, is that gastric ulceration may, by some as yet unknown mechanism, cause motility disturbances of the cylinder, eventually leading to muscular hypertrophy.

Hiatus Hernia #

Of 44 cases of AHPS described by Wieser et al. (l963), 20 percent had an associated hiatus hernia. Bodon and Haake (l968) described a group of 11 cases in which hiatus hernia was associated with AHPS. This supports the view that there may be an association between lesions of the gastric fornix and the pyloric sphincteric cylinder (Chap. 32).

Relationship to Infantile Hypertrophic Pyloric Stenosis #

Primary AHPS may arise de novo in adult life, or it may be a sequel to infantile hypertrophic pyloric stenosis (IHPS) (Lumsden and Truelove l958; Levin l97l).

A number of authors found that the lesion in AHPS was almost identical, comparable or similar to that of IHPS (North and Johnson l950; Craver l957; McNaught l957; Seaman l963). Christiansen and Grantham (l962) and Heinisch (l967) stated that the gross and histological appearances of AHPS were indistinguishable from those of IHPS; according to Keynes (l965) the appearance of both the simple and complicated varieties of AHPS was similar to that of IHPS.

Anatomical Localization and Operative Features #

In operative and pathological specimens the muscular hypertrophy was thickest at the pyloric ring, ending abruptly at the duodenum, but decreasing gradually over the "antrum" (North and Johnson l950; Seaman l963; Keynes l965). The muscular hypertrophy, extending in an orad direction from and including the pyloric ring, was said to be 2.5 to 3.0 cm in length by Morton (1930), 3.0 to 4.0 cm by North and Johnson (l950) and Craver (l957), 2.5 cm by Knight (l96l) and from 1.0 to 5.0 cm by Bodon and Haake (l968). Bateson et al (l969) called it a tube-like narrowing of the pyloric ring and immediate prepyloric musculature, 2.5 to 3.0 cm in length; as the "pyloric and prepyloric" musculature was involved, they suggested it should be termed hypertrophic pyloric channel disease.

These findings leave little doubt that the muscular hypertrophy in AHPS encompasses the musculature of the pyloric sphincteric cylinder. A number of authors, viz. McNaught (l957), Skoryna et al. (l959), Seaman (l963), Wieser et al. (l963), Keynes (l965) and du Plessis (l966) based the morphology of AHPS on the anatomy as determined by Torgersen (l942). Many other authors, however, did not relate their findings to the anatomy as described by Cunningham (l906), Forssell (l913), Cole (l928) and Torgersen (l942).

Radiographic Features #

As the radiographic features of IHPS are quite reliable, it would be reasonable to expect that the same would hold true for AHPS. However, this is not usually the case. Kirlin and Harris (l933) mentioned elongation and narrowing of the pyloric canal with partial gastric outlet obstruction as some of the more familiar appearances, with a concave indentation of the base of the duodenal bulb (caused by invagination of the hypertrophied musculature) as a distinctive radiological sign. (Comment: The description "elongation of the pyloric canal" was discussed in Chapter 23. It appears to be as inappropriate in AHPS as it is in IHPS. A concave indentation of the base of the duodenal bulb may also be seen under other circumstances, e.g. maximal normal contraction of the pyloric sphincteric cylinder, as described in Chapter 13). Associated lesions, e.g. gastric ulceration or hiatus hernia, may be demonstrable radiographically.

Larson et al. (l967) pointed out that the carefully executed studies of Seaman (l963) revealed data that should prove disquieting to the radiologist who attempted an unqualified diagnosis of AHPS. There was little correlation between the length and width of the pyloric "canal" as seen on radiographs in these cases, and as measured in surgical resection specimens. Levin (l97l) found that the radiographic diagnosis of AHPS could seldom be made with confidence.

No reports of ultrasound investigations in AHPS have been encountered.

The Pathogenesis and Etiology #

Belding and Kernohan (l953) found that in both IHPS and AHPS the number of myenteric ganglion cells and myenteric nerve fibre tracts per unit area of muscle tissue showed a decrease in the affected pyloric region; the majority of myenteric ganglion cells also showed degenerative changes. The hypertrophied circular muscle had a disorganized pattern, and it appeared if there were primary changes in both the myenteric ganglia and the musculature.

Skoryna et al. (l959) suggested that a congenital neuro-muscular dysfunction of the "pyloric canal mechanism" formed a common basis for both IHPS and AHPS; in the former there was a lack of normal regression of the circular musculature of the pyloric canal during early infancy, while in the latter other factors in adult life were involved.

According to Edwards (l96l) the etiology remained uncertain; persistence of the infantile form, degeneration of myenteric plexuses and long continued pylorospasm had to be considered as possible causes. Keynes (l965) and du Plessis (l966) were unable to confirm the presence of abnormal ganglion cells in the myenteric plexuses.

Heinisch (l967) held that macroscopically and microscopically AHPS could not be differentiated from IHPS, and that the pathogenesis and etiology of both remained obscure.

References #

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