HYDATIFORM DEGENERATION IN TUBAL AND UTERINE PREGNANCY. 357 



common if it were due to endometritis. Taussig (1911) also stated that leucoeytic 

 infiltration of the decidua is frequently present in hydatiform moles, but insisted 

 that "leucoeytic infiltration in the placenta then should not be interpreted as 

 infection. * * * Inflammation and infection should be kept apart." I presume 

 Taussig really meant infiltration and infection should be kept apart, and the ques- 

 tion then turns upon the structure of the normal decidua and the significance of 

 infiltration for the development of the ovum. 



It may be recalled that Marchand (1904) reported the presence of isolated 

 groups of small cells in the normal decidua which looked like mononuclears under 

 low magnification, and which he believed often have been confused with them. 

 But even granting this, and the further facts that the exact histologic changes in 

 the decidua are not fully known, and that it is rather difficult to ascertain just what 

 decidual changes are regarded as evidence of the existence of an endometritis, any 

 one examining a large series of cases of hydatiform degeneration aborted with the 

 decidua can not doubt the presence of marked decidual changes in a very large 

 percentage of them. These changes are not limited to infiltration with scattered 

 round cells or erythrocytes, or to focal accumulation of the same, but often extend 

 to almost complete fibrosis, as shown in figure 39, so that experienced investigators 

 have mistaken the thin, fibrous decidua for a part of the chorionic membrane. 



It is true that the existence of these changes in the deciduae themselves does 

 not necessarily imply that they were antecedent to the implantation of the ovum, 

 but fortunately the clinical histories and material from curettage often supply 

 crucial evidence. From such cases and from the cumulative weight of evidence 

 from the large series of cases here reported, the great majority of which showed 

 decidual infiltration or other changes suggestive of endometritis, the frequent 

 association of abnormal deciduse with hydatiform degenerations is evident. The 

 fact that the incidence of hydatiform degeneration in the tubal was somewhat higher 

 than that in the uterine series might be regarded as contradicting this relationship, 

 but such is not the case. The mucosa of the tubes at best is an unfavorable nidus 

 for implantation because of the absence of decidual formation alone. Hence, even 

 if salpingitis were somewhat less frequent than endometritis, proper nidification in 

 the tube could easily more than account for the existing differences. Hence the 

 higher incidence of hydatiform degeneration in the tubal series in fact becomes 

 confirmatory of the conclusion that abnormal nidification really may be responsible 

 for the advent of hydatiform degeneration. 



The only fact which might be interpreted as indicating that germinal defects 

 primarily are responsible for the development of hydatiform degeneration is the 

 relatively higher incidence of the condition in older women. Against this, however, 

 stands the other fact that such women also show the cumulative effects upon the 

 endometrium of age, endometritis and pregnancy. Furthermore, since hydatiform 

 degeneration so often follows one or two normal births or abortions, it would be 

 impossible to find an adequate explanation for the release of the defective ova so 

 often after and not before these events. 



I am reminded also in this connection of a case the detailed history of which 

 is fully known. It is that of a robust young woman who successively gave birth 



