64 MALL. [VoL. XIX. 
two millimeters in diameter or larger. The two structures 
become beautifully adjusted, but in the case of most tubal 
pregnancies the small ova and villi float largely in a mass of 
blood, are not adjusted to the decidua, and, apparently, on 
account of impaired nutrition, degenerate. The syncytium 
becomes atrophic, the villi become fibrous, and often leucocytes 
as well as syncytial cells invade the mesoderm of the chorion. 
It naturally follows that when the nutrition of the ovum is 
impaired the most advanced growing point, the embryo, for 
which all is adjusted, should suffer most. Thus it happens 
that in many instances the chorion is not markedly changed, 
but the embryo is almost entirely destroyed or is wanting 
altogether. In a short time the ovum collapses, becomes an 
irregular mass, and its “rootlets,” the villi, are still found 
scattered throughout the blood-clot, or a small heap of them 
are found poorly adjusted in a fold of the tube covered with 
changed and distorted syncytium and decidua. These 
conditions, found so well marked in tubal pregnancies, are also 
found in uterine pregnancies, but in them it is difficult to 
determine whether the degeneration of the chorion follows 
because the embryo has died suddenly or has inherited the 
power to become abnormal. The study of the ova from tubai 
pregnancies demonstrates conclusively, it seems to me, that 
the changes in the chorion are primary, and those in the 
embryo secondary, due to faulty implantation of the chorion. 
Another argument in favor of the view I have advanced 
regarding the production of pathological embryos is obtained 
by studying those embryos in tubal pregnancies which were 
not destroyed at once, but which became well attached and 
grew on towards full term. I mean the fate of the 4 per cent 
of normal embryos found in early unruptured tubal preg- 
nancies. 
