Retained Placenta in the Cow 79^ 



The pathology of the retention of the fetal membranes is 

 necessarily somewhat foreshadowed by the causes which have 

 been related above. Inflammation of the cotyledons in the cow, 

 or of the placenta in other animals, naturally follows the general 

 course of inflammation of tissues, resulting from infection. It 

 may abate in the course of a 'few days, and the sweUing of the coty- 

 ledons may decrease and result in the release of the incarcerated 

 placental tufts, so that the chorion may finally come away, ac- 

 companied by contraction of the uterus and prompt recovery from 

 the disease. If, however, the infection" is more extensive and 

 virulent, the cotyledon may undergo total necrosis and slough 

 away, still holding firmly incarcerated the section of chorion to 

 which it is attached. We have observed this result in the cow 

 repeatedly, and sometimes it has involved the necrosis and 

 sloughing away of all or nearly all the cotyledons in the entire 

 uterine cavity. 



The ravages of the disease do not always cease with the necro- 

 sis of the cotyledons, but may extend to the walls of the uterus, 

 involving the mucous, muscular and peritoneal coats more or less 

 in their order, and extending beyond the peritoneal covering of 

 the uterus, to involve the peritoneum in general. 



The fetal membranes undergo more or less rapid decomposi- 

 tion, so that in 48 hours, as a rule, they become quite putrid and 

 give off a very fetid odor. The inflammation of the uterine mu- 

 cosa, endometritis, causes a more or less abundant excretion into 

 the uterine cavity, which is usually very fetid and consists of a 

 dirty, grayish, flocculent, semi-fluid or fluid mass, which may 

 vary greatly in amount. Naturally it is mixed with shreds of 

 afterbirth and placenta, and sometimes contains cotyledons which 

 have sloughed away from their pedicles. In some cases, the uter- 

 ine mucosa is covered over with diphtheritic membranes. 



Depending upon the degree of infection, the uterine mucosa or 

 the entire uterine walls may be more or less thickened and 

 changed in consistency. Sometimes the uterine walls are very 

 firm and hard, as a result of an exudative inflammation, especially 

 if the disease is of somewhat long standing. At other times, the 

 walls are very thick and soft, as a result of gangrene. 



When the inflammation of the uterine walls is virulent, and 

 the pathologic changes serious, the uterus quickly loses all con- 

 tractile power and lies as an inert organ. The pathologic secre- 



