Parturition (labour and birth)

The onset of human labour reflects a shift from uterine quiescence to activation rather than a single trigger. Contributing factors include maturation of the fetal HPA axis with rising placental CRH (which stimulates fetal cortisol and DHEA-S, increasing placental estrogen), a functional progesterone withdrawal (altered progesterone-receptor isoforms rather than a fall in serum progesterone), estrogen-induced contraction-associated proteins (oxytocin receptors, prostaglandin receptors and gap junctions), prostaglandins (PGE2 and PGF2α) from the fetal membranes and decidua that ripen the cervix and stimulate contractions, uterine stretch and inflammatory cytokines. Once labour starts, the descending head stretches the cervix and triggers oxytocin release (Ferguson reflex), creating positive feedback.

First stage — from the onset of regular painful contractions to full cervical dilatation (10 cm): a latent phase of effacement and slow dilatation to ≈4 cm, then an active phase of faster dilatation (typically ≈8 h in a first labour, ≈5 h in later labours, with wide variation). Second stage — from full dilatation to birth of the baby: the mother's expulsive efforts add to uterine contractions; the fetus negotiates the pelvis by the cardinal movements (engagement, descent, flexion, internal rotation, extension, restitution, external rotation, expulsion). Third stage — from birth to delivery of the placenta and membranes: the uterus contracts down, shearing the placenta from the decidua; active management (oxytocin and controlled cord traction) shortens this stage and halves the risk of haemorrhage.

Pain of contractions travels with sympathetic afferents to T10–L1; pain from cervical dilatation and the vagina via pelvic splanchnic nerves to S2–S4; perineal pain via the pudendal nerve — explaining the coverage needed by epidural and pudendal blocks.