Preterm premature rupture of membranes, chorioamnion inflammatory scores and neonatal respiratory outcome
Article first published online: 14 SEP 2009
DOI: 10.1111/j.1471-0528.2009.02358.x
© 2009 The Authors Journal compilation © RCOG 2009 BJOG An International Journal of Obstetrics and Gynaecology
Issue

BJOG: An International Journal of Obstetrics & Gynaecology
Volume 117, Issue 1, pages 94–98, January 2010
Additional Information
How to Cite
Zanardo, V., Vedovato, S., Cosmi, E., Litta, P., Cavallin, F., Trevisanuto, D. and Chiarelli, S. (2010), Preterm premature rupture of membranes, chorioamnion inflammatory scores and neonatal respiratory outcome. BJOG: An International Journal of Obstetrics & Gynaecology, 117: 94–98. doi: 10.1111/j.1471-0528.2009.02358.x
Publication History
- Issue published online: 9 DEC 2009
- Article first published online: 14 SEP 2009
- Accepted 24 July 2009. Published Online 14 September 2009.
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Keywords:
- Chronic lung disease;
- fetal inflammatory response syndrome;
- histological chorioamnionitis;
- preterm premature rupture of membranes;
- respiratory distress syndrome
Objective To evaluate whether histological chorioamnionitis (HCA), in the setting of preterm premature rupture of membranes (PPROM), affects infant respiratory outcome.
Design A prospective histological study on 287 consecutive placentas was performed in preterm infants (≤32+6 weeks gestation), categorised into four groups: according to the presence or absence of HCA, in the setting or in absence of PPROM.
Setting Neonatal intensive care unit, Department of Pediatrics, Padua University, Padua, Italy from January 2001 to December 2006.
Results Among the 287 NICU admitted preterm infants, 68/287 (23.6%) presented with HCA, 16/68 (23.5%) with a coexisting fetal inflammatory response, and 74/287 (25.7%) with PPROM. HCA was associated with a greater frequency of vaginal delivery (P < 0.0001), lower gestational age (P < 0.0001) and lower birth weight (P < 0.01). HCA had no effect on fetal lung maturation, however, it was a significant risk factor for CLD (RR; 95% CI 2.08; 1.30–3.33). HCA and the fetal inflammatory response were also significant risk factors for PPROM (RR; 95% CI 2.07; 1.42–3.03 and 2.64; 1.71–4.09 respectively). Conversely, HCA in the setting of PPROM failed to reveal any RDS protection or subtype CLD risk. Multivariate analysis demonstrated significant independent effects of presence of maternal HCA (P = 0.04), gestational age (P < 0.0001) and interaction HCA-gestational age (P = 0.04) on CLD development, regardless of the presence of fetal HCA or fetal HCA-gestational age interaction, PPROM or PPROM-gestational age interaction.
Conclusions Histological chorioamnionitis is a significant PPROM and CLD risk factor, but it fails to provide any protection from RDS. HCA in the setting of PPROM also failed to reveal any RDS protection or subtype CLD risk.

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