3 articles
Prolonged premature rupture of membranes predisposes to intrauterine infection and chorioamnionitis, both of which have significant implications for neonatal outcomes. While chorioamnionitis has been linked to accelerated surfactant production and reduced respiratory distress syndrome, it is also associated with long-term pulmonary injury, including bronchopulmonary dysplasia and pulmonary hypertension. The objective of the study is to investigate the association between prolonged premature rupture of membranes, chorioamnionitis, and respiratory outcomes among preterm infants ≤34 weeks of gestation.
A prospective cohort of 108 preterm infants admitted to the Neonatal Intensive Care Unit of the Mother and Child Institute, Chișinău, between October 2023 and July 2024, was divided into two groups: infants born to mothers with clinical/histological chorioamnionitis (n = 54) and controls (n = 54). Maternal risk factors, incidence of prolonged premature rupture of membranes incidence, Apgar scores, type and duration of respiratory support, and pulmonary complications were analyzed. Statistical significance was tested using chi-square and logistic regression.
Prolonged premature rupture of membranes was significantly more frequent in chorioamnionitis group (67% vs. 22%, p<0.001). Infants exposed to chorioamnionitis had lower 1-minute Apgar scores, greater need for invasive ventilation (5.9 ± 10.6 vs. 2.2 ± 4.8 days, p<0.05), and prolonged hospitalization. BPD incidence was higher in the chorioamnionitis group (25.9% vs. 3.7%, p<0.05). Mortality did not differ significantly between groups (27.8% vs. 22.2%).
Prolonged premature rupture of membranes is strongly associated with chorioamnionitis, which in turn significantly increases the risk of long-term pulmonary complications in preterm infants. Early recognition of prolonged premature rupture of membranes, antibiotic prophylaxis, antenatal corticosteroids, and interdisciplinary obstetric–neonatal management are essential to reduce the burden of bronchopulmonary dysplasia.
According to specialized literature, X-rays are also used in the diagnosis and suspicion of chronic broncho-pulmonary disease (bronchopulmonary dysplasia (BPD)), in premature children.
The study included 105 premature babies who were divided into the study group – premature babies with bronchopulmonary dysplasia (BPD) and the control group – premature babies without BPD. Data were statistically analyzed using Microsoft Excel, MedCalc, SPSS and Contingency Table Analysis as a method of evaluating the performance of a diagnostic test.
Radiological changes of discoidal atelectasis type in subjects with BPD were detected in 49.1% in the basic group versus 13.5% in the control group (χ2 = 15.431; p < 0.0001), subsegmental ones 47.2% vs 25.0% (χ2 = 5.586; p = 0.018); pulmonary emphysema areas 62.3% vs 5.8% (χ2 = 37.182; p < 0.0001), opaque fibrosis sectors 50.9% vs 11.5% (χ2 = 18.911; p < 0.0001); signs of pulmonary hypertransparency 47.2% vs 1.9% (χ2 = 28.843; p < 0.0001); microcystic formations 41.5% vs 5.8% (χ2 = 18.482; p < 0.0001). Depending on the severity degrees of BPD, changes such as discoidal atelectasis were noted, in those with mild grade – 50% medium grade – 38.5%, severe grade – 56.3% (χ2 = 16.502; p < 0.001), subsegmental atelectasis 41.7%, vs 38.5% (χ2 = 7.956; p = 0.047), pulmonary emphysema areas 58.3%, vs 38.5%, vs 87.5% (χ2 = 45.138; p < 0.0001); microcystic formations, 33.3%, vs 53.8%, vs 43.8% (χ2 = 20.502; p < 0.0001).
The changes recorded on radiological examination in mild, moderate, and severe cases of BPD in premature babies are of the type discoidal atelectasis, areas of emphysema, opaque sectors of fibrosis, pulmonary hypertransparency, microcystic formations.
Oxidative stress can be defined as the imbalance of the redox state of a certain system including living one (organelle, cell, organ/tissue), which excessively produces reactive oxygen and/or reactive nitrogen species (ROS/RNS) that exceed the capacity of the antioxidant defense system, which have the ability to slow down or even prevent the oxidative damage of macromolecules. Oxidative stress is a pathogenic mechanism of a large variety of diseases, including pulmonary one.
81 preterm born children included in the study were divided into the main group – preterm children with bronchopulmonary dysplasia (BPD), and the control group – preterm children without BPD. The comparison groups were prospectively evaluated clinical, instrumental and laboratory (TPA, prooxidant-antioxidant balance, nitric oxide metabolistes and MDA). Data were statistically analyzed using Microsoft Excel, MedCalc and SPSS and Contingency Table Analysis as a way to evaluate the performance of a diagnostic test.
In preterm children with BPD were found to be decreased by 29% (p < 0.001) the prooxidant-antioxidant balance (PAB) and the nitric oxide metabolistes (NO) level by 12% (p < 0.001) compared to children in the control group. The assessment of tissue oxidative damage markers revealed a significant 62% (p < 0.001) increase in malonic dialdehyde (MDA) content and a 4.86-fold (p < 0.001) increase in total prooxidant activity (TPA) in children with bronchopulmonary dysplasia compared to children in the control group. Our study confirms that TPA, PAB, MDA and NO values are reliable markers of hypoxic tissue damage at children with bronchopulmonary dysplasia and can be recommended for assessing the intensity of oxidative stress.
Pulmonary bronchodysplasia is characterized by the imbalance of prooxidant-antioxidant processes with the exacerbation of prooxidant ones that trigger the oxidative/nitrosative stress and the deterioration of vital chemical compounds.