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Parturition, Lactation & Postpartum Physiology

Name: Parturition, Lactation & Postpartum Physiology
Creator: Veli Bakalov, MD

How the uterus decides to deliver and the breast decides to feed

Reproductive·Pregnancy·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Placental CRH rises exponentially near term, is stimulated (not suppressed) by cortisol, and drives fetal ACTH, adrenal cortisol and DHEA-S for placental estrogen.
Labor follows a functional progesterone withdrawal and rising estrogen effect, even though serum progesterone stays high until the placenta delivers.
Estrogen induces oxytocin receptors, connexin-43 gap junctions and prostaglandin synthesis; PGE2 ripens the cervix and PGF2α contracts the myometrium.
Ferguson reflex: cervical stretch → hypothalamic signal → posterior-pituitary oxytocin → stronger contractions (positive feedback); oxytocin receptors are Gq-coupled.
Fetal cortisol induces type II pneumocyte surfactant; an L:S ratio >2 indicates mature lungs, and antenatal betamethasone at ~24–34 weeks reduces RDS, IVH and NEC.
High progesterone blocks milk synthesis during pregnancy; its fall after placental delivery lets milk come in at 2–3 days.
Prolactin (anterior pituitary, released as dopamine falls) makes milk and suppresses GnRH; oxytocin (posterior pituitary) ejects milk and contracts the uterus.
Colostrum is rich in secretory IgA; breast milk is low in vitamins D and K, so infants get daily vitamin D and a single IM vitamin K dose at birth.
Uterine involution takes ~6 weeks, lochia runs rubra → serosa → alba, and VTE risk peaks in the first 6 weeks postpartum.

Initiation of labor

The placental clock. The placenta secretes corticotropin-releasing hormone (CRH) in amounts that rise exponentially through the third trimester, while the CRH-binding protein in maternal plasma falls near term, so free CRH climbs steeply. Unlike hypothalamic CRH, which cortisol suppresses, placental CRH is stimulated by cortisol, creating a feed-forward loop. A faster-than-normal rise is associated with preterm delivery. CRH drives fetal ACTH, and the fetal adrenal responds with cortisol, which matures the lungs, and DHEA-S, which the placenta converts to estrogens.

Functional progesterone withdrawal. Progesterone keeps the uterus quiet, yet human serum progesterone stays high until the placenta delivers. Labor instead follows a functional withdrawal: the myometrium shifts toward the repressive PR-A receptor isoform and metabolizes progesterone locally, while the estrogen effect rises. The progesterone-receptor antagonist mifepristone ripens the cervix and provokes contractions, showing how central progesterone action is.

Placental CRH risesFree CRH climbs as its binding protein falls; cortisol amplifies it
Fetal HPA activationACTH → adrenal cortisol and DHEA-S → placental estrogen
Hormone balance shiftsFunctional progesterone withdrawal with a rising estrogen effect
Contraction-associated proteinsOxytocin receptors, connexin-43 gap junctions, COX-2 and prostaglandin receptors
LaborCoordinated contractions and cervical ripening

Contraction-associated proteins. Estrogen upregulates myometrial oxytocin receptors, connexin-43 gap junctions that electrically couple myocytes so contractions spread as a synchronized wave, and prostaglandin synthesis and receptors.

Cervical ripening, contractions and the Ferguson reflex

Prostaglandins. Decidua and fetal membranes produce prostaglandins with two roles. PGE2 ripens the cervix by activating collagen breakdown and increasing hyaluronan and water, so the cervix softens, thins and dilates. PGF2α, with PGE2, stimulates myometrial contraction. Dinoprostone (PGE2) and misoprostol (PGE1) are used to ripen the cervix before induction. COX inhibitors such as indomethacin can delay preterm labor for the same reason, at the cost of premature constriction of the ductus arteriosus and oligohydramnios.

Oxytocin. Made in the paraventricular and supraoptic nuclei and released from the posterior pituitary, oxytocin binds Gq-coupled myometrial receptors: phospholipase C generates IP3, Ca2+ is released and myosin light-chain kinase drives contraction. Oxytocin also stimulates decidual prostaglandin release.

Ferguson reflex. As the fetal head presses on the cervix and upper vagina, afferent signals reach the hypothalamus and trigger oxytocin pulses. Stronger contractions push the head lower and stretch the cervix further, a positive-feedback loop that continues until delivery.

Fetal lung maturation

Surfactant. Type II pneumocytes make surfactant, mainly dipalmitoylphosphatidylcholine (a lecithin), which lowers alveolar surface tension. Synthesis begins in mid-gestation but reaches mature levels only around 35 weeks. The late-gestation fetal cortisol surge is the main inducer; thyroid hormone helps, and fetal hyperinsulinemia (as in maternal diabetes) inhibits it. An amniotic fluid lecithin:sphingomyelin ratio above 2 indicates mature lungs, while a ratio below 1.5 predicts respiratory distress syndrome (RDS).

Antenatal corticosteroids. When preterm birth is expected within 7 days at about 24–34 weeks, the mother receives betamethasone (or dexamethasone). These fluorinated steroids escape placental 11β-HSD2, which inactivates cortisol and prednisolone, so they reach the fetus, accelerate surfactant production and lung maturation, and lower neonatal RDS, intraventricular hemorrhage, necrotizing enterocolitis and death.

Lactation

Preparing the breast. In pregnancy estrogen drives ductal growth, progesterone drives lobuloalveolar development, and prolactin with human placental lactogen (hPL), supported by cortisol and insulin, differentiates alveolar cells for milk synthesis. Prolactin rises throughout pregnancy, but high progesterone blocks full milk production, so only small amounts of colostrum appear before delivery.

Milk comes in. Delivery of the placenta removes progesterone while prolactin remains high, triggering secretory activation (lactogenesis II) about 2–3 days postpartum. Retained placental fragments delay it. Failure to lactate after massive postpartum hemorrhage suggests Sheehan syndrome, infarction of the enlarged pituitary.

Prolactin and oxytocin in lactation

Feature	Prolactin	Oxytocin
Source	Anterior pituitary lactotrophs	Hypothalamic neurons, released from posterior pituitary
Trigger	Suckling inhibits hypothalamic dopamine	Suckling; also conditioned cues such as an infant's cry
Breast action	Milk synthesis by alveolar cells	Myoepithelial contraction: milk ejection (let-down)
Other actions	Suppresses GnRH → lactational amenorrhea	Uterine contraction → afterpains, faster involution

Lactational amenorrhea. Frequent suckling and high prolactin suppress pulsatile GnRH, lowering LH and FSH so follicles do not mature and ovulation stops. As contraception it is about 98% effective only with exclusive breastfeeding, continued amenorrhea and an infant younger than 6 months.

Colostrum and mature milk. Colostrum, secreted in the first days, is rich in secretory IgA, protein, leukocytes, lactoferrin and carotenoids (hence its yellow color) but lower in fat and lactose. Mature milk, established by about 2 weeks, is rich in lactose, fat and whey proteins. Secretory IgA is not absorbed; it coats the infant's gut mucosa and provides passive mucosal immunity. Breastfeeding lowers infant otitis media and gastrointestinal infection and, in preterm infants, necrotizing enterocolitis.

Breast milk is low in vitamin D, so exclusively breastfed infants receive 400 IU/day from the first days of life. It is also low in vitamin K and the newborn gut is sterile, so every newborn gets IM vitamin K at birth to prevent vitamin K deficiency bleeding. Iron stores run low after about 4–6 months, so breastfed infants need supplemental iron or iron-rich foods.

The puerperium

Involution. The six weeks after delivery return the reproductive tract to its nonpregnant state. Oxytocin-driven contraction of interlacing myometrial fibers compresses the vessels of the placental bed, the main defense against postpartum bleeding. The uterus shrinks from about 1 kg to its prepregnancy size over about 6 weeks and is no longer palpable abdominally by about 2 weeks; breastfeeding speeds this through oxytocin.

Lochia

Stage	Timing	Appearance
Rubra	Days 1–3	Red: blood and decidua
Serosa	About days 4–10	Pink-brown, thinner
Alba	About day 10 to 6 weeks	Yellow-white: leukocytes and decidual cells

Foul-smelling lochia with fever and uterine tenderness suggests endometritis; persistent heavy red lochia suggests retained tissue.

Hypercoagulability. Pregnancy raises fibrinogen and factors VII, VIII and X, lowers protein S and inhibits fibrinolysis, a change that guards against hemorrhage at delivery. After birth these changes persist while venous stasis and vessel injury, especially with cesarean delivery, complete Virchow's triad, so the daily risk of venous thromboembolism peaks in the first ~6 weeks postpartum, higher than at any point antepartum.