Aim The effect of ventilator modes on regional tissue oxygenation in premature neonates with respiratory distress syndrome (RDS) has yet to be delineated. Previous studies have looked at global oxygen delivery and have not assessed the effects on regional tissue oxygenation. Our aim in this study was to assess such tissue oxygenation in premature babies with RDS in relation to differing modes of ventilation using near‐infrared spectroscopy (NIRS). Methods In 24 stable preterm infants with RDS, undergoing elective wean in ventilator mode, cerebral and muscle tissue oxygenation were assessed using NIRS. Infants were weaned from high‐frequency oscillator or jet ventilator to conventional invasive ventilation (CV) or extubated from CV to non‐invasive mechanical ventilation. Data at 30 minutes prior and at one hour after change in ventilator mode were compared (paired t test). Results In babies changed from high‐frequency oscillation to CV, jet to CV and CV to non‐invasive ventilation, the differences in cerebral NIRS (mean ± SD) were 1.7 ± 9.9%, 2.3 ± 5.7% and 2.1 ± 8.4%, respectively. The concomitant changes in muscle NIRS were −2.9 ± 8.5%, 8.1 ± 9.7% and 3.6 ± 22.4%, respectively. No changes were statistically significant. Conclusion Our data suggest that there is no alteration in regional tissue oxygenation related to ventilator mode in stable preterm infants with improving RDS.
Background: The etiopathogenesis of late preterm (LPT) birth is undetermined. Placental histopathology, which reflects an adverse intrauterine environment and is reportedly associated with preterm labor and neonatal morbidities, has not been studied in LPT infants.Purpose: We investigated placental pathological lesion as markers of an adverse intrauterine environment during LPT labor.Methods: This retrospective case-control study compared placental histopathological and clinical variables between LPT and term neonates. Placental variables included chorioamnionitis, funisitis, hemorrhage, abruption, infarction, calcification, and syncytial knots. Maternal variables included age, substance abuse, pregnancyassociated diabetes mellitus and hypertension, duration of rupture of membrane, antibiotic use, and magnesium sulfate, whereas, those of neonates included gestational age, birth weight, race, sex, and Apgar scores. Standard statistical proedures were applied to analyze the data.Results: Chorioamnionitis (50% vs. 17.8%, <i>P</i><0.001) and funisitis (20% vs. 4.4%, <i><i>P</i></i>=0.002) were more common in term infants. Placental infarction rate was insignificantly higher in LPT infants (25.6% vs. 14.3%, <i><i>P</i></i>=0.08). The mothers in the LPT group were older (30.4 years vs. 28.1 years, <i><i>P</i></i>=0.05; odds ratio [OR], 1.06; 95% confidence interval [CI], 0.998–1.12, <i><i>P</i></i>=0.056) and more often suffered from hypertension (28.9 vs. 12.9 %, <i><i>P</i></i>=0.02), and received magnesium sulfate (48.9 vs. 20%, <i>P</i>< 0.001; OR, 2.86; 95% CI, 1.12–7.29, <i>P</i><0.05). Duration of rupture of membrane was higher in term infants (13.6 hours vs. 9.1 hours, <i>P</i><0.001). Chorioamnionitis (OR, 0.33; 95% CI, 0.13–0.79; <i>P</i><0.05) was associated with a lower risk of LPT delivery.Conclusion: Placental infection is not a risk factor for LPT births. There is a nonsignificant predominance of vascular anomalies in LPT placentas. Higher maternal age, magnesium sulfate therapy, and maternal hypertension are clinical risk factors for LPT labor.
mothers living in a lower-risk home environment. 1 This indicates that the differences in heritability estimates cannot be entirely explained by the differences in parental education. In addition, parental educational level is not a feasible modifiable target for public health interventions; rather, the specific environmental exposures captured in the home environment measure (eg, food availability in the home) need to be targeted. Therefore, in our view, parental education cannot be used as a proxy measure for the complex environment that is the family home.We thank Dissanayake for highlighting the validity of BMI as a measure of adiposity. Our research group has previously validated parent-report measures of the heights and weights of twin children by examining the correlations between parent and researcher measures in a sample of 228 families (height: Pearson r = 0.90; weight: Pearson r = 0.83). 3 Body mass index remains the most feasible way to estimate adiposity in adults and children, 4 especially in large numbers, such as the Gemini cohort (the sample used in our study 1 ). It is also the most commonly used measure of adiposity, allowing for comparison with future studies and meta-analyses. In relation to ethnicity, only 5% of those who completed the home environment measure identified as nonwhite. This was too small to allow us to undertake analyses stratified by ethnicity. We thank Dissanayake for suggesting epigenetic factors as a potential mechanism involved in the development of childhood obesity. This area of research is of great interest to many obesity researchers 5 but was not the focus of this study, and epigenetic data are not available in this sample.
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