Placental expulsion

Placental expulsion (also called afterbirth) occurs when the placenta comes out of the birth canal after childbirth. The time between the expulsion of the baby and the expulsion of the placenta is called the third stage of labor.

The third stage of labor can be managed actively with several standard procedures, or it can be managed expectantly, with physiological management or passive management. The latter allows for the placenta to be expelled without medical assistance.

Although uncommon in some countries, the placenta is kept and consumed by the mother over the weeks following the birth. This practice is termed human placentophagy and can be harmful.

As the fetal hypothalamus matures, the activation of the hypothalamic–pituitary–adrenal (HPA) axis initiates labor through two hormonal mechanisms. The end pathway of both mechanisms lead to contractions in the myometrium, a mechanical cause of placental separation, which is due to the sheer force and contractile and involutive changes that occur within the uterus, distorting the placentome.

ACTH increases fetal cortisol which acts by two mechanisms:

PTGS in turn produces prostaglandin E2 which is a catalyst for pregnenolone to C-19 steroids, such as estrogen. Estrogen increases:

As the HPA axis activates, the posterior pituitary of the fetus begins to increase production of oxytocin, which stimulates the maternal myometrium to contract.

In the seventh month of pregnancy, the MHC-I complexes increase in the interplacentomal arcade reduces the bi- and tri-nucleate cells, a source of immune suppression in pregnancy. By the ninth month, the endometrial lining has thinned (due to loss of trophoblast giant cells) which exposes the endometrium directly to the fetal trophoblast epithelium. With this exposure and the increase in maternal MHC-I, T-helper 1 (Th1) cells, and macrophages induce apoptosis of trophoblast cells and endometrial epithelial cells, facilitating placental release. Th1 cells attract an influx of phagocytic leukocytes into the placentome at separation, allowing further degradation of the extracellular matrix.