Comparison of prostaglandin and mechanical cervical ripening in the setting of small for gestational age neonates.

Objective: The objective of this study is to determine whether cervical ripening with misoprostol (MP) is associated with higher rates of cesarean delivery (CD) compared with dinoprostone (DP) or Pitocin/Foley balloon (PFB) in infants found to be small for gestational age (SGA). Study design: Single center institution based cohort study of all inductions between 2008 and 2012 where birth weight was found to be as SGA (< 10th percentile). Maternal demographic, obstetric, and labor characteristics were compared between SGA births where cervical ripening with MP, DP, or PFB was used as the primary agent. The primary outcome was CD after attempted induction between the three study groups which included MP, DP, and PFB. Secondary outcomes included inability to achieve active labor (defined as cervical dilation of 6 cm or greater), cervical dilation at the time of CD, the incidence of CD for the indication of non-reassuring fetal status, and neonatal outcomes including Apgar scores and admission to neonatal intensive care unit. Multivariable logistic regression was performed to evaluate the association of these outcomes with MP as the induction agent versus the referent groups, PFB. Results: Of 260 inductions where the infant was found to be SGA by birth weight during the 5-year period, 172 (66.2%) patients were induced using MP, 38 (14.6%) with DP, and 50 (19.2%) with PFB. There were no differences in baseline characteristics between groups (age, race, BMI, parity, induction indication, birth weights, or maternal comorbidities). MP did not increase rate of CD which was 25.6%, 26.3%, and 22.0% in the MP, DP, and PFB groups, respectively (p = .86). There were also no differences in incidence of CD for non-reassuring fetal well-being (NRFWB), failure to attain active labor, or cervical dilation at time of CD between induction groups. NICU admission was 18%, 18%, and 16% (p = .94) between MP, DP, and PFB groups, respectively. MP was not associated with an increased rate of CD when compared with the other two agents combined, aOR 0.93 (0.67-1.30, 95% CI). Conclusion: MP appears to have similar efficacy and safety when compared with other cervical ripening agents in pregnancies complicated by SGA.

Damage-Associated Molecular Pattern and Fetal Membrane Vascular Injury and Collagen Disorganization in Lipopolysaccharide-Induced Intra-amniotic Inflammation in Fetal Sheep.

UNLABELLED: To understand the changes in the structural integrity of fetal membranes during intrauterine inflammation, we evaluated the time course of expression and localization of damage-associated molecular patterns (DAMPs) and injury/remodeling in collagen and vascular smooth muscle. Time-mated ewes received intra-amniotic (IA) saline or IA lipopolysaccharide (LPS) for 5 hours to 15 days prior to a preterm delivery at 125 ± 2 days (n = 5-7 animals/group). The DAMP high mobility group box 1 (HMGB1) protein assessed by Western blot was induced within 24 hours after IA LPS in the fetal membranes, and HMGB1 expression was localized to amnion epithelium, chorion vascular endothelium, and infiltrating inflammatory cells by immunohistology. Markers of vascular injury, intercellular adhesion molecule 1, and tissue plasminogen activator messenger RNA (mRNA) expression increased 5 to 12 hours after IA LPS in the chorioamnion indicating vascular injury. Chorion vascular remodeling with increased chorion arteriolar smooth muscle actin expression by morphometric analyses of immunohistology was noted 15 days after IA LPS. Collagen expression was nonhomogeneous by histochemical staining, and there was a trend toward decreased mRNA expression of collagen subunit COL5A1 after IA LPS. CONCLUSIONS: Intrauterine inflammation induced early increases in HMGB1 in the chorioamnion with a concomitant vascular injury followed by chorion arteriolar hypertrophy. There was nonhomogeneous collagen expression in the chorioamnion. These results have implications for understanding the pathogenesis of IA inflammation-induced preterm rupture of membranes.