Abstract
ObjectiveTo investigate the effect of pathological staging of chorioamnionitis (CA) on complications in preterm infants;MethodsA single-center, retrospective study was conducted to choose singleton preterm infants (gestational age < 37 weeks) from the Department of Obstetrics and Gynecology in our hospital from December 2016 to December 2017. The basic data and placental pathological results were retrospectively collected. According to the placental pathological results of whether inflammation infiltrating amnion, CA 0/I phase was classified into non-amnionitis group, CA II/III phase was classified into amnionitis group, the incidence of common complications in preterm infants was compared. Further, logistic regression was used to analyze the effects of amnionitis on complications after being adjusted to gestational age, birth weight and thrombocytopenia.ResultsA total of 221 preterm infants were enrolled, including 186 cases in non-amnionitis group and 35 cases in amnionitis group. The gestational age of amnionitis group (32.00 ± 2.71 weeks) was significantly lower than non-amnionitis group (34.14 ± 2.06 weeks), birth weight (1.93 ± 0.64 kg) was significantly lower than that of non-amnionitis group (2.26 ± 0.58 kg), and the hospital stay in amnionitis group was significantly longer (25.71 ± 19.23 days), all of the difference above was statistically significant(P < 0.05). The incidence of intraventricular hemorrhage (IVH) in amnionitis group (37.14%) was significantly higher than that in non-amnionitis group (13.98%) (P = 0.002), and the risk of IVH was significantly increased by amnionitis (OR = 3.636, 95%CI: 1.632–8.102); after correction of gestational age, birth weight and thrombocytopenia, the risk of IVH was still significantly increased (OR = 2.471, P = 0.046, 95% CI: 1.015–6.015). And the late-onset IVH was more common (P = 0.009).ConclusionAmnionitis leads to a significant reduction in gestational age and birth weight in preterm infants, and it is an independent risk factor for IVH.
Highlights
Chorioamnionitis, an inflammatory status of the intrauterine or fetal membrane, were divided into histological chorioamnionitis and clinical chorioamnionitis [1]
The gestational age of amnionitis group (32.00 ± 2.71 weeks) was significantly lower than non-amnionitis group (34.14 ± 2.06 weeks), birth weight (1.93 ± 0.64 kg) was significantly lower than that of non-amnionitis group (2.26 ± 0.58 kg), and the hospital stay in amnionitis group (25.71 ± 19.23 days) was significantly longer than that in non-amnionitis group (18.84 ± 16.80 days), the difference was statistically significant(P < 0.05)
It is indicated that histological amnionitis was an independent risk factor for intraventricular hemorrhage in premature infants, which is not affected by gestational age, birth weight and thrombocytopenia, and it had no significant effects on other common complications related to premature birth (P < 0.05)
Summary
Chorioamnionitis, an inflammatory status of the intrauterine or fetal membrane, were divided into histological chorioamnionitis and clinical chorioamnionitis [1]. Chorioamnionitis can cause fetal inflammatory response syndrome (FIRS), which is a subclinical state caused by the activation of the fetal immune system and the release of a large number of inflammatory factors (IL-6, IL-1, IL-8, TNF-α). These inflammatory factors could interfere with the normal expression of fetal brain cytokines, leading to brain damage in preterm infants [5]. Some preclinical studies showed that fetal lung epithelial damage caused by chorioamnionitis could lead to impaired vascular osmotic pressure and apoptosis [6], which increased the secretion of lung surface proteins, but could make the alveolar cell wall thinner [7, 8]. Gantert. et al confirmed that premature delivery and intrauterine inflammation affected the maturation of the fetal intestinal barrier, the intestinal tight junction protein-1 (TJP-1) damaged by bacterial toxins during gestation, resulting in an easy access of microbial toxins to the mucosa and the inner layers of the gut ante- and postnatally [11]
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