Abstract
Background: Culture-proven sepsis is the gold standard in early-onset neonatal sepsis diagnosis. Infants born ≤29 weeks gestation after preterm rupture of membranes in the years 2009–2015 were included in a retrospective cohort study performed at a level III fetal-maternal unit. The study aimed to compare culture-proven sepsis, clinical sepsis and positive laboratory biomarkers ≤72 h as predictors of mortality before discharge and the combined outcome of mortality or severe short-term morbidity (severe cerebral morbidity, bronchopulmonary dysplasia and retinopathy). Results: Of the 354 patients included, culture-proven sepsis, clinical sepsis and laboratory biomarkers were positive in 2.3%, 8.5% and 9.6%, respectively. The mortality rate was 37.5% for patients with culture-proven sepsis (3/8), 33.3% for patients with clinical sepsis (10/30) and 8.8% for patients with positive laboratory biomarkers (3/34), respectively. Mortality or severe morbidity occurred in 75.0% of patients with culture-proven sepsis (6/8), 80.0% of patients with clinical sepsis (24/30) and 44.1% of patients with positive laboratory biomarkers (15/34), respectively. Conclusion: In preterm infants after preterm rupture of membranes, clinical sepsis was almost four times more common and at least equally valuable in predicting mortality and mortality or severe morbidity compared to culture-proven sepsis.
Highlights
Preterm premature rupture of membranes, referring to membrane rupture before 37 weeks of gestation and before the onset of uterine contractions, occurs in 3%of pregnancies and is associated with one-third of all preterm births [1]
Chorioamnionitis increases the likelihood of neonatal sepsis, which remains a major cause of neonatal mortality and morbidity in preterm infants [4]
Our results indicate that clinical sepsis was almost four times more common than culture-proven sepsis in preterm infants ≤29 weeks of gestation born after premature rupture of membranes (pPROM)
Summary
Preterm premature rupture of membranes (pPROM), referring to membrane rupture before 37 weeks of gestation and before the onset of uterine contractions, occurs in 3%of pregnancies and is associated with one-third of all preterm births [1]. The underlying pathological process in pPROM includes intrauterine infection from ascending genital tract colonization These infections may lead to increased cytokine activity with consequent enhancement of membrane apoptosis, production of proteases and dissolution of the membrane’s extracellular matrix [1]. PPROM implicates inflammation and infection and is a loss of barrier to infection ascending from the vagina [2] Chorioamnionitis can be both a cause and a result of pPROM, and its highest observed occurrence is in the first week after pPROM [3]. In a prospective registry of very low birth weight infants in the United States, culture-proven early-onset sepsis rate accounts for 3.5% at gestational age
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