Uterine contraction frequency in the last hour of labor: how many contractions are too many?

OBJECTIVE: Increased frequency of uterine contractions is a component in the cluster of causal conditions that can lead to fetal hypoxia and acidosis and increase the risk for neonatal neurologic injury. For most international obstetrical societies, 5 contractions per 10 min averaged over 30 min is considered as the upper limit of normal uterine activity. We hypothesize that it might be safer to adopt an upper limit of 4 contractions per 10 min. METHODS: We reviewed our 1970's research database containing 475 patients with closely monitored and well-documented labor and neonatal assessments that included cord blood (CB) pH, base excess (BE), and continuous recording of neonatal heart rate (NHR). Using data segregated by the proportion of the last hour before delivery when uterine contraction frequency (UCF) exceeded 4 and 5 contractions per 10 min respectively, we evaluated outcomes (CB BE, pH, Apgar scores at 1 min, the status of NHR at 16 min after birth, and the proportion of births that did not the result from normal spontaneous vaginal deliveries (NSVDs). ANOVA established relationships between UCF cutoffs and these outcomes. Our sample size is sufficiently large to provide the ability of UCF, per se, to accurately detect an alpha region of .05 88% of the time with an effect size of .15. RESULTS: During the last hour prior to delivery, a UCF cutoff at 4 contractions per 10 min performed better than a UCF cutoff at 5 contractions per 10 min to enable the earlier identification of risks for abnormal outcomes. The longer UCF was increased, the worse were the outcomes that were measured, and the region >4 but ≤5 contractions identifies the beginnings of worsening conditions in a variety of measures of poor outcomes. CONCLUSION: Lowering the recommended threshold for UCF from 5 to 4 contractions per 10-minute period as averaged over 30 min facilitates earlier detection of potentially compromised fetuses and is also an important contributor to a multicomponent contextualized approach to risk assessment.

Bacterially induced preterm labor in the mouse does not require maternal interleukin-1 signaling.

OBJECTIVE: We tested the hypothesis that intrauterine bacterial inoculation induces labor via expression of the inflammatory cytokine interleukin-1 (IL-1) in a murine model. STUDY DESIGN: Pregnant mice on day 14.5 of a 19-20 day gestation were inoculated with killed Escherichia coli or sterile media into either (a) the right uterine horn, (b) the right uterine horn following its surgical isolation from the contralateral horn and cervix, or (c) the kidney. Cytokine levels in gestational tissues and maternal serum were determined by use of enzyme-linked immunosorbent assay (ELISA). In a separate experiment, bacterially induced preterm delivery was compared between mice lacking a functional IL-1 receptor and wild-type control litter mates. RESULTS: Killed E coli induced delivery within 48 hours with similar dose-response curves regardless of inoculation site (intact uterine horn, isolated uterine horn, or kidney). Bacterial inoculation of an isolated right horn caused dramatic increases in local expression of IL-1 and IL-6. However, delivery occurred from the uninjected horn without corresponding upregulation of cytokines, with the exception of a modest rise within fetal membranes. Mice lacking a functional IL-1 receptor were no different from wild-type mice in their susceptibility to bacterially induced delivery. CONCLUSION: Bacterially induced labor in the murine model does not require IL-1 signaling.