Another point is that, according to investigations made, there are, after all, certain regular quantitative differences in the linear measurements, the total thickness of the merely contracted pyloric wall being 2 to 3 rum.
and that of the hypertrophic pylorus 31 to 5 mm. Besides, the con sistency of the latter is still greater than that of the former.
2. It is possible to completely relax in a given time the antro systolic stomach by slow and gradual injection of water until an internal overpressure of 30 cm. of water has been reached, such relaxation to be judged by the consistency and not by the folds presented by the mucous membrane. On the other hand, in true hypertrophic stenosis the pylorus will not relax under this pressure, according to the unanimous statements of all investigators, sometimes not even under a three times higher pressure which would cause the stomach to burst.
3. According to Bernheim's statement, which has often been cor roborated, the muscle cells and their nuclei are larger in all dimensions than in the normal or contracted pylorus.
As long as these criteria were not known or applied, the question as to whether there was a pathological condition differing from the physiological systole of the pylorus had, as a matter of precaution, to be left undecided. But the author's assumption, expressed in his first publication on the subject, that there was, as a matter of fact, an ana tomical basis for the pronounced clinical picture, has since been cor roborated.
The anatomical findings in cured cases, which from other reasons led to autopsy, are of importance in this connection. In these cases the pylorus had undergone 110 changes (Ibrahim, Wernstedt), while a considerable (compensating?) hypertrophy of the musculature of the other parts of the stomach wall was noticeable.
Outside of the gastric area, occasional dilatations of the lower part of the msophagus with muscle hypertrophy, and not infrequently with various malformations, may also be met with, aside from the mani festations of extreme atrophy.
Various hypotheses have been advanced on the etiology, patho genesis and nature of IIirschsprung's pyloric hypertrophy and stcnosis.
(A) According to the oldest opinions, universally recognized up to about 1897, and occasionally supported at later periods, there is a con genital organic defect, a primary pathologically increased quantitative development of the pyloric wall which constricted the lumen (Hirsch sprung, IS87).
It was assumed that there was a true tumor (fibromyoma), which, however, is irreconcilable with the histological findings. This tumor was explained by a simple excess of development, a local giant growth, produced by nature "in an over-anxious endeavor to supply a sufficient pylolic closure," which overstepped its limits (Cautley). A basis for this opinion was looked for in the relatively frequent occurrence (4 per cent.) of other deformities in the gastric area and other organs. The assump tion of an atavistic deformity as a phylogenetic involution to conditions existing in certain acts of nature, has but a scanty foundation; more plausible is the assumption of an ontogenetic involution to conditions in early fetal life, inasmuch as here the "canalis pylori" may represent a kind of physiological equivalent. Perhaps, however, it is only the pronounced tendency to post-mortem systole in the earliest stages of development that finds expression in this canal.
;Many recent authors are inclined to regard pyloric hypertrophy merely as a part manifestation of hypertrophy of the gastric musculature, the causation of which is relegated to the period of fetal life.
A summarized objection to all these hypotheses, which presuppose a congenital organic defect, is furnished by the fact that the typical anatomical picture of hypertrophic stenosis has never been met with in its characteristic form either in a fetus or in the newborn.
Similarly, the late occurrence of the first symptom which has fre quently been observed, can only be reconciled with the hypothesis of a congenital obstacle on the further supposition that the relative insuffi ciency did not occur until the impairment of the originally present reserve forces of the stomach, or that the additional factor of a second stenotic cause (spasms, folds, inflammatory infiltration of the mucosa) produced this effect.