Maternal Group B Streptococcus colonization and neonatal morbidity in premature preterm rupture of membranes
Hirsch DM, Bose D, Baumgardner DJ, Garland JS. Maternal Group B Streptococcus colonization and neonatal morbidity in premature preterm rupture of membranes. J Patient-Centered Res Rev. 2014;1:58.
Presented at 2013 Aurora Scientific Day, Milwaukee, WI
Background/significance: Group B Streptococcus (GBS) colonization is a major cause of infectious morbidity in newborns.
Purpose: Our goal was to determine if markers for neonatal morbidity are affected by perinatal maternal colonization with GBS in women whose pregnancies are complicated by preterm premature rupture of membranes (PPROM) between 24 and 34 weeks gestation.
Methods: We reviewed records of patients admitted to two urban hospitals who underwent PPROM between 24 and 34 weeks gestation between 2000 and 2011 and had a known GBS status. Associated neonatal records were then reviewed for evidence of morbidity. The primary outcome measure was Score for Neonatal Acute Physiology (SNAP). Secondary outcome measures included Apgar score <7 at 5 minutes, umbilical artery pH <7.1, length of latency, and presence of sepsis, bronchopulmonary dysplasia, sepsis or neonatal death. Neonatal outcomes were compared between mothers who were GBS positive versus GBS negative. Multiple gestations and patients with significant obstetrical complications or fetal abnormalities were excluded. Categorical variables were analyzed with Chi-square or Fisher exact tests, ordinal or continuous variables by Mann-Whitney or 2-sample T-tests. Binary logistic regression was used for multivariate modeling.
Results: Of 462 patients meeting inclusion and exclusion criteria, 133 (29%) were GBS positive and 329 GBS negative. Demographic characteristics including maternal age, race, gestational age at delivery, gravity/parity, birthweight, and route of delivery were similar by group. For the primary outcome, neonates born to GBS positive mothers trended toward higher SNAP scores than did those of GBS negative mothers (36.1% vs. 26.1%, p=0.07). On analysis of secondary outcomes, bronchopulmonary dysplasia was present in 20% of neonates born to GBS positive and 12% of GBS negative mothers (p=0.046), and this difference persisted after multivariate analysis, where gestational age was also predictive. Umbilical cord pH <7.1 was present in 2.5% of neonates born to GBS positive and 8.4% of GBS negative mothers (p=0.049). There were no significant differences in Apgar score at 5 minutes <7, latency, presence of sepsis, or neonatal death, although Apgar at 5 minutes <7 approached significance (22.6% vs. 14.9%, p=0.056).
Conclusion: Neonatal morbidity as measured by the SNAP score does not differ by maternal GBS status. However, significant differences in low umbilical artery pH and particularly bronchopulmonary dysplasia provoke further analysis and study.