The fetal membrane is a flexible structure that encloses the fetus within the uterine cavity, storing amniotic fluid and adapting to the continuous development of the fetus, thus providing a favorable spatial environment for fetal growth. As such, the fetal membrane plays a protective role for the fetus [11].Several factors can contribute to the premature rupture of membranes, including reproductive tract infections, uneven stress on the membranes, external forces, and potentially a combination of these factors [12]. Among these, reproductive tract infections are considered a primary cause of poor pregnancy outcomes, such as premature rupture of membranes, preterm birth, and postpartum infections, and they are closely linked to PROM [13–14].In the later stages of pregnancy, a large number of microorganisms colonize the vaginal tract of pregnant women. These microorganisms maintain a dynamic balance, interacting and constraining each other to preserve the equilibrium of the vaginal microbiota [15].When PROM occurs, the continuous leakage of amniotic fluid can disrupt the normal bacterial community in the vagina, weakening the immune resistance of pregnant women and disturbing the microecological balance of the vaginal environment. This disturbance can increase the survival and proliferation of pathogenic bacteria. Given the close connection between the vagina and the amniotic cavity, these proliferating pathogens can easily lead to uterine infections, potentially resulting in infections in the fetus or newborns[16–17].
Using neonatal infection as the dependent variable in this study, and the duration of PROM, length of the first stage, length of the second stage, nulliparity, placental inflammation, fetal tachycardia, prenatal fever, amniotic fluid contamination, and reproductive tract GBS colonization as independent variables, the analysis indicated that the duration of PROM,length of the first stage, length of the second stage, placental inflammation, fetal tachycardia, prenatal fever, amniotic fluid contamination, and GBS colonization were all independent risk factors for neonatal infection(p < 0.05).The OR values were 0.90, 1.18, 5.91, 20.11, 2.59, 7.03, 8.13, and 5.19, respectively.A possible explanation for this may be that pregnant women with a prolonged rupture of membranes experience a continuous flow of vaginal fluid, which increases the likelihood of pathogenic microorganisms entering the uterine cavity, thereby increasing the risk of neonatal infection [18].Additionally, the length of the first and second stages of labor also correlates with an increased risk of neonatal infections. As labor progresses, the risk of complications such as grade III amniotic fluid contamination and fetal distress increases, which can result in neonatal asphyxia. A weakened neonatal immune response further raises the risk of infection [19].GBS is a common opportunistic pathogen in clinical practice, and some pregnant women may have GBS colonization in the reproductive tract during late pregnancy[20].When PROM occurs, the immune system is compromised, allowing GBS to invade the amniotic cavity through the ruptured membranes, leading to reproductive tract infections and complications such as chorioamnionitis, maternal sepsis, and neonatal pneumonia[21–22].Pregnant women with reproductive tract infections may present with symptoms such as prenatal fever and fetal tachycardia, which are closely linked to subsequent neonatal infections [23].The presence of placental inflammation confirms an infection in the amniotic cavity and is also a risk factor for neonatal infection. This study collected prenatal WBC and CRP levels, finding that inflammatory markers were higher in the infected group compared to the uninfected group. This suggests that pregnant women in the infected group may have been at a higher risk of infection than those in the uninfected group.
This study further analyzed neonatal complications and found that, among the 500 pregnant women with premature rupture of membranes, 77 cases resulted in neonatal infections, yielding an infection rate of 15.4%. Of these 77 cases, 19 (24.6%) had pneumonia, 8 (10.4%) had respiratory distress syndrome, 10 (13.0%) had respiratory failure, 40 (52.0%) experienced early-onset neonatal infections, and 11 (14.3%) had severe infections among the 77 cases of neonatal infections.
In summary, there are multiple risk factors for neonatal infection in pregnant women with premature rupture of membranes, and the risk factors identified in this study warrant clinical attention.When PROM occurs in the present of one or more risk factors, it is important to aiminister antibiotics promptly to prevent infection, to terminate the pregnancy in a timely fashion, and to reduce risks of the newborns as soon as possible to prevent and decrease the occurrence of neonatal infections.The analysis of neonatal complications in this study offers valuable insights for clinical practice. However, this study has limitations, such as being a single-center study with a small sample size, which may introduce certain biases into the fingings. Future research should aim to expand the sample size and involve multiple-centers to improve the reliability of the results.