Without defining the nature of the lesion in question, the author des cribes its gross and microscopical appearances.
a. External lesion occurs either in scattered foci or in more or less extended plaques, which may be far separated, near to gether, or confluent. The color varies from yellowish-white to blackish red or black. These colors are due to metamorphoses of the blood.
b. In the diseased parts, the tissue is firmer, yet more friable, particu larly in cases with multiple foci.
c. The extent is variable. Sometimes the foci are scattered and vary in size from a pea to a uut; sometimes there are plaques, which may be a few lines broad or may rarely occupy nearly the whole placenta.
d. The most frequent seat is the border ,or the neighboring parts. The next is the fcetal surface, and then, in order, the whole thickness of the organ, the uterine surface, the centre and one third or one half of the entire organ.
e. The state of the tissnes varies. Now we find the placenta filled with numerous and recent clots; now their number has diminished, they are decolorized and include the agglutinated villi. Again, older clots are soft and their centre looks like broth, varying from reddish-brown to yel low, which may, according to Billroth, be true pus, which is denied by Virchow and Robin.
In other e,ases the coagula are stratified, particularly if on the ftetal surface. The tissue may be so hard that it cannot be broken up, in which case it is of a dirty white or gray. The vessels in the diseased parts are generally diminished in calibre (Jacquemier), bat they are sometimes obliterated and atrophied, either primarily or secondarily.
The microscopical appearances, according to Bustamente, are due to changes more or less advanced in the blood, and to secondary changes in the villi.
A. When the lesion is recent, we find coagulated blood around the villi, and, later, fibrin with blood corpuscles in its meshes. The villi in the clot are intact, but their vessels are filled with clotted blood.
B. At a later stage the fibrinous meshes are closer and the red corpus cles fewer, and so changed as to be recognized with difficulty.
The white corpuscles change to connective tissue corpuscles, and the new tissue is very dense. The villi undergo fatty degeneration. The
blood in the vessels becomes granular, and the connective tissue nuclei begin to proliferate. Compound granulation corpuscles appear in the clot. At the most advanced stage of the change, the white corpuscles present one, two or three nuclei. Yellow elastic fibres appear, cross and increase, while the blood corpuscles disappear. The vessels of the -villi become, finally, obliterated. The walls of some of the villi become fatty.
.The mechanism of the lesion is ag follows: The maternal blood current is retarded in the placental sinuses, the blood clots surround the villi and the above changes oc,cur. According as the coagulation is rapid or slow, the coagula are amorphous or striated. Bustamente proposes the name placental thrombosis for this condition. Cauwenberghe says that the blood undergoes the most diverse changes in different parts of the same or of different placentte, just as in vascular thrombi. 1. The decol orized fibrin may remain stratified without other change; 2. The throm bus is transformed into connective tissue; 3. Retrogressive changes occur in the blood, the red corpuscles disappearing and the white undergoing fatty degeneration and being carried away. The fibrin is changed to a pulpy mass like pus, the fibrinous pseudo-pus of Robin, the true pus of Billroth.
The microscope presents the following appearances in these lesions: 1. Transfornuition of the Blood.—In some cases red corpuscles pre-. dominate, in some the fibrin. The white corpuscles may be few and scat tered, or grouped and in layers. The red corpuscles become deformed and decolorized. The pigment may disappear or remain a long time. At this time the fibrin is still flbrillary and the white corpuscles are un changed. Later, the red corpuscles break up, the fibrin becomes gran ular and the white corpuscles become fatty and are disintegrated. When the foci do not enclose villi, the clot may be changed to pseudo-pus. The fibrin may remain unchanged. But may the clot form organized connec tive tissue ? This is admitted by Billroth, Virchow, Cohnheim and Bustamente, but denied by Robin, Cauwenberghe and Maier. Maier says that new connective tissue, when found, is the result of hyperplasia in the decidua-serotina or interstitial placentitis.