Normal Labor and Delivery

LABOR: DEFINITION AND PHYSIOLOGY Labor is defined as the process by which the fetus is expelled from the uterus. More specifically, labor requires regular, effective contractions that lead to dilation and effacement of the cervix. This chapter describes the physiology and normal characteristics of term labor and delivery. The physiology of labor initiation has not been completely elucidated, but the putative mechanisms have been well reviewed by Liao and colleagues. Labor initiation is species-specific, and the mechanisms in human labor are unique. The four phases of labor from quiescence to involution are outlined in Figure 13-1. The first phase is quiescence and represents that time in utero before labor begins when uterine activity is suppressed by the action of progesterone, prostacyclin, relaxin, nitric oxide, parathyroid hormone–related peptide, and possibly other hormones. During the activation phase, estrogen begins to facilitate expression of myometrial receptors for prostaglandins (PGs) and oxytocin, which results in ion channel activation and increased gap junctions. This increase in the gap junctions between myometrial cells facilitates effective contractions. In essence, the activation phase readies the uterus for the subsequent stimulation phase, when uterotonics, particularly PGs and oxytocin, stimulate regular contractions. In the human, this process at term may be protracted, occurring over days to weeks. The final phase, uterine involution, occurs after delivery and is mediated primarily by oxytocin. The first three phases of labor require endocrine, paracrine, and autocrine interaction between the fetus, membranes, placenta, and mother. The fetus has a central role in the initiation of term labor in nonhuman mammals; in humans, the fetal role is not completely understood (Figure 13-2). In sheep, term labor is initiated through activation of the fetal hypothalamicpituitary-adrenal axis, with a resultant increase in fetal adrenocorticotrophic hormone and cortisol. Fetal cortisol increases production of estradiol and decreases production of progesterone by a shift in placental metabolism of cortisol dependent on placental 17α-hydroxylase. The change in the progesterone/estradiol ratio stimulates placental production of oxytocin and PG, particularly PGF2α. If this increase in fetal adrenocorticotrophic hormone and cortisol is blocked, parturition is delayed. In contrast, humans lack placental 17α-hydroxylase and there is no increase in fetal cortisol near term. Rather, in humans, uterine activation may be potentiated in part by increased fetal adrenal production of dehydroepiandrostenedione, which is converted in the placenta to estradiol and estriol. Placental estriol stimulates an increase in maternal (likely decidual) PGF2α, PG receptors, oxytocin receptors, and gap junctions. In humans, there is no documented decrease in progesterone near term and a fall in progesterone is not necessary for labor initiation. However, some research suggests the possibility of a “functional progesterone withdrawal” in humans: Labor is accompanied by a decrease in the concentration of progesterone receptors, as well as a change in the ratio of progesterone receptor isoforms A and B in both the myometrium and membranes. More research is needed to elucidate the precise mechanism through which the human parturition cascade is activated. Fetal maturation may play an important role, as well as maternal Labor: Definition and Physiology 267 Mechanics of Labor 268 Uterine Activity (Powers) 270 The Fetus (Passenger) 270 The Maternal Pelvis (Passage) 272 Cardinal Movements in Labor 275 Engagement 275 Descent 277 Flexion 277 Internal Rotation 277 Extension 277 External Rotation 277 Expulsion 277 Normal Progress of Labor 277 Interventions Affecting Normal Labor Outcomes 279 Active Management of Labor 279 Second Stage of Labor 280 Spontaneous Vaginal Delivery 280 Delivery of the Placenta and Fetal Membranes 281 Episiotomy, Perineal Injury, and Perineal Repair 281