Placental expulsion

As the fetal hypothalamus matures, activation of the HPA axis (hypothalamic-pituitary-adrenal axis) initiates labour though two hormonal mechanisms. The end pathway of both mechanisms leads to contractions in the myometrium, a mechanical cause of placental separation, which is due to the shear force and contractile & involution changes that occur within the uterus distorting the placentome.

ACTH increases fetal cortisol, which acts by two mechanisms:

• Increases Prostaglandin F2α, which both abolishes the progesterone block, and lowers the oxytocin receptor threshold; and increases expression of relaxin, stretching the pelvic ligaments
• Increases expression of PTGS in the fetal trophoblast cells

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

• Vaginal lubrication
• Softening of collagen fibre structures in the cervix, vaginal, and associated tissues
• Increases contraction associated proteins (i.e. connexins)
• Placental shedding by physiological inflammation, note pathological inflammation often leads to retention of membranes (i.e. placentitis)

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 degration of the extracellular matrix.

After delivery, loss of fetal blood return to the placenta allows for shrinkage and collapse of the cotyledonary villi with subsequent fetal membrane separation.[1]

Active management routinely involves clamping of the umbilical cord, often within seconds or minutes of birth.

Uterine contraction assists in delivering the placenta. Uterine contraction reduces the placental surface area, often forming a temporary hematoma at their former interface. Myometrial contractions can be induced with medication, usually oxytocin via intramuscular injection. The use of ergometrine, on the other hand, is associated with nausea or vomiting and hypertension.[2]

Breastfeeding soon after birth stimulates oxytocin which increases uterine tone, and through physical mechanisms uterine massage (the fundus) also causes uterine contractions.

Controlled cord traction (CCT) consists of pulling on the umbilical cord while applying counter pressure to help deliver the placenta.[3] It may be uncomfortable for the mother. Its performance requires specific training. Premature cord traction can pull the placenta before it has naturally detached from the uterine wall, resulting in hemorrhage. Controlled cord traction requires the immediate clamping of the umbilical cord.

A Cochrane review came to the results that controlled cord traction does not clearly reduce severe postpartum hemorrhage (defined as blood loss >1000 mL) but overall resulted in a small reduction in postpartum hemorrhage (defined as blood loss >500 mL) and mean blood loss. It did reduce the risk of manual placenta removal. The review concluded that use of controlled cord traction should be recommended if the care provider has the skills to administer it safely.[3]

Manual placenta removal is the evacuation of the placenta from the uterus by hand.[4] It is usually carried out under anesthesia or more rarely, under sedation and analgesia. A hand is inserted through the vagina into the uterine cavity and the placenta is detached from the uterine wall and then removed manually. A placenta that does not separate easily from the uterine surface indicates the presence of placenta accreta.

A Cochrane database study[2] suggests that blood loss and the risk of postpartum bleeding will be reduced in women offered active management of the third stage of labour. A summary[5] of the Cochrane study came to the results that active management of the third stage of labour, consisting of controlled cord traction, early cord clamping plus drainage, and a prophylactic oxytocic agent, reduced postpartum haemorrhage by 500 or 1000 mL or greater, as well as related morbidities including mean blood loss, incidences of postpartum haemoglobin becoming less than 9 g/dL, blood transfusion, need for supplemental iron postpartum, and length of third stage of labour. Although active management increased adverse effects such as nausea, vomiting, and headache, women were less likely to be dissatisfied.[5]