Preterm Birth

Known and suspected risk factors for preterm birth include: obesity, maternal short stature, uterine “overdistention” (a large uterus), placental abruption (decidual hemorrhage), hypoxic stress-induced activation of the fetal hypothalamic-pituitary-adrenal axis, sterile myometrial inflammation, vaginal microbiome changes, infectious chorioamnionitis, and ethnicity. Maternal short stature and obesity predispose to obstruction of uterine venous return, which may increase the risk of preterm birth by exacerbating fetal, placental, myometrial, and vaginal hypoxia and by increasing abdominal venous pressures. In a woman with a tense pregnant abdomen, this physiology might resemble an incipient abdominal compartment syndrome. Uterine “overdistention” (a large uterus) may predispose to preterm birth because of Laplace’s law, which describes how myometrial wall tension and tissue pressure will be greater in a large uterus than in a small one. Increased wall tension and tissue pressure will tend to reduce perfusion of both myometrium and placenta. Recurrent episodes of myometrial ischemia and reperfusion due to intermittent obstruction of uterine venous return might create sterile myometrial inflammation which converts the quiescent myometrial phenotype to the contractile phenotype, thus provoking preterm labor. Increased decidual venous pressure caused by obstruction of uterine venous return may promote decidual hemorrhage, thrombin formation, and myometrial contraction. Vaginal edema and hypoxia caused by obstruction of uterine venous return might promote a change in the vaginal microbiome, which might promote ascending infectious chorioamnionitis and preterm labor and birth.