Premature Rupture of Membranes: Etiology

ETIOLOGY

The cause of PROM is not clearly understood. Sexually transmitted diseases and other lower genital tract condi-tions, such as bacterial vaginosis, may play a role, as such infections are more commonly found in women with PROM than in those without sexually transmitted disease or bacterial vaginosis. However, intact fetal membranes and normal amniotic fluid do not fully protect the fetus from infection, because it appears that subclinical intra-amniotic infection may contribute to PROM. Metabolites produced by bacteria and inflammatory mediators may either weaken the fetal membranes or initiate uterine con-tractions through stimulating prostaglandin synthesis. Therisk of PROM is at least doubled in women who smoke during pregnancy. Other risk factors for PROM include prior PROM (approximately twofold), short cervical length, prior preterm delivery, hydramnios, multiple gestations, and bleeding in early pregnancy (threatened abortion). There is an inverse relation-ship between gestational age and latency (time from PROM until delivery). It also appears that the more severe theresilient oligohydramnios, the greater the risk of infection and, consequently, the shorter the latency.

Chorioamnionitis, infection of the fetal membranesand amniotic fluid, poses a major threat to the mother and fetus. Fetal sepsis is associated with an increased risk for morbidity, particularly neurologic abnormalities such as periventricular leukomalacia and cerebral palsy. This seems to be associated with inflammatory mediators in the fetal environment. Patients with intra-amniotic infection often experience significant fever (>=100.5°F), tachycardia (mater-nal and fetal), and uterine tenderness. Purulent cervical dis-charge is usually a very late finding. The maternal white blood cell (WBC) count is generally elevated, but this find-ing is nonspecific in pregnancy and may be the result of antenatal corticosteroids administration and may be mis-leading. Patients with chorioamnionitis frequently enter spontaneous and often dysfunctional labor. Once the diag-nosis of chorioamnionitis is made, treatment consists of intravenous antibiotic therapy and prompt delivery, either by induction or augmentation of labor, if needed, or cesarean delivery, either for a primary indication or if vagi-nal delivery is expected to be substantially delayed.