Latency after preterm prelabour rupture of membranes vs. gestational age: a maturation-growth trade-off

In preterm prelabour rupture of membranes (PPROM), prolonging pregnancy for fetal maturity is traded against infection risk, yet latency is entangled with gestational age. We examined its determinants and, disentangled from gestational age, its impact on fetomaternal outcome.

In a prospective tertiary-centre cohort, 96 singleton pregnancies with PPROM at 28-34 weeks, undelivered at 48 h, were followed to delivery. Admission and pre-delivery haematological and ultrasound measures were recorded. Analyses included Kaplan-Meier, restricted mean survival time, competing-risks and gestational-age-adjusted models.

Median latency was 5 days (IQR 3-11); 61 % delivered within a week. Gestational age at admission was the only predictor (rho -0.21, p=0.037); earlier-gestation women remained undelivered longer (restricted mean 10.5 vs. 6.4 days, p=0.006); amniotic fluid volume did not predict latency (oligohydramnios p=0.700; 6.6 vs. 9.0 days, p=0.084). Longer latency was associated with neonatal complications (OR 10.9), NICU admission (OR 3.4) and caesarean (OR 5.5). The near-zero crude latency-birth-weight correlation reflected gestational-age suppression: at equal gestational age at admission, longer latency meant greater birth weight (+129 g per 10 days, p=0.004), yet at equal age at delivery a lower weight (p=0.033). The neonatal-morbidity association persisted after adjustment (OR 1.21 per day). The serial total-leucocyte-count rise tracked chorioamnionitis (AUC 0.77), the neutrophil-to-lymphocyte ratio did not.

Gestational age at admission, not amniotic fluid volume, governs latency. Prolonged latency is a genuine, double-edged trade-off, not a confounded marker of prematurity: at equal gestational age it yields maturational weight yet restrains growth-for-age and carries a gestational-age-independent morbidity and infection risk.