The Pyloric Sphincteric Cylinder in Health and Disease



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Chapter 24 (page 117)

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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  2. Belding HH, Kernohan JW. A morphologic study of the myenteric plexus and musculature of the pylorus with special reference to the changes in hypertrophic pyloric stenosis. Surg Gynaec Obstet l953, 97, 322-334.
  3. Bodon GR, Haake PW. Hiatus hernia and pyloric hypertrophy in the adult. Surgery l968, 63, 430-433.
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