scholarly journals Association of Maternal Preeclampsia with Neonatal Respiratory Distress Syndrome in Very-Low-Birth-Weight Infants

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yu-Hua Wen ◽  
◽  
Hwai-I. Yang ◽  
Hung-Chieh Chou ◽  
Chien-Yi Chen ◽  
...  

Abstract Preeclampsia is a common cause of preterm birth and neonatal morbidity, but its relationship with neonatal respiratory distress syndrome (RDS) remains controversial. We conducted a retrospective cohort study with data from very-low-birth-weight (VLBW) infants born in 1997–2014 from the database of the Premature Baby Foundation of Taiwan to evaluate the relationship between maternal preeclampsia and neonatal RDS. In total, 13,490 VLBW infants were enrolled, including 2200 (16.3%) infants born to preeclamptic mothers. The mean (standard deviation) gestational ages were 30.7 (2.5) weeks in the preeclamptic group and 28.6 (2.9) weeks in the control (non-preeclamptic) group. Severe RDS was defined according to the surfactant therapy requirement. The incidence of severe RDS was lower in infants exposed to maternal preeclampsia than in controls [28.9% vs. 44%; odds ratio (OR), 0.52; 95% confidence interval (CI), 0.47–0.57]. However, after adjustment for confounders, the OR for severe RDS development in the preeclampsia group was 1.16 (95% CI, 1.02–1.31). Other factors, such as gestational age, birth weight, female sex, and antenatal receipt of two or more steroid doses were significantly protective against RDS in multivariate regression analysis. This study revealed that maternal preeclampsia slightly increases the risk of severe RDS in VLBW infants.

PEDIATRICS ◽  
1987 ◽  
Vol 79 (6) ◽  
pp. 1005-1007
Author(s):  
Meenakshi K. Jhaveri ◽  
Savitri P. Kumar

Times of first stool passage were studied in 171 infants who weighed less than 1,500 g at birth. Delayed passage (greater than 48 hours) was noted in 20.4% of this group. Significant differences were noted between the delayed and nondelayed groups for gestational age, presence of severe respiratory distress syndrome, and the time of the first enteral feeding. In very low birth weight infants, delay in the passage of the first stool is a common occurrence. This delay is probably due to physiologic immaturity of the motor mechanisms of the gut, lack of triggering effect of enteral feeds on gut hormones, and the presence of severe respiratory distress syndrome, which may singly or in concert adversely affect gastrointestinal motility.


PEDIATRICS ◽  
1996 ◽  
Vol 98 (2) ◽  
pp. 204-210 ◽  
Author(s):  
Alok Rastogi ◽  
Subuola M. Akintorin ◽  
Michelle L. Bez ◽  
Pablo Morales ◽  
Rosita S. Pildes

Background. Surfactant therapy now has a well-established role in the treatment of neonates with respiratory distress syndrome but has failed to reduce the incidence of bronchopulmonary dysplasia (BPD). We conducted a double-blind, placebo-controlled trial to test the hypothesis that dexamethasone therapy given during the first 12 days of life to very low birth weight infants would be synergistic to surfactant in preventing BPD. Methods. Seventy surfactant-pretreated infants (700-1500 g) who had severe respiratory distress syndrome (a/A ratio, 0.18 ± 0.10; mean airway pressure, 11.1 ± 1.9 cm H2O; fraction of inspired oxygen, 0.81 ± 0.22) were enrolled to receive a 12-day course of dexamethasone (n = 36) or saline placebo (n = 34) starting within the first 12 hours after birth. The starting dose of dexamethasone was 0.5 mg/kg per day, and it was tapered progressively. Results. Ventilator variables at 5 to 14 days were significantly improved in those infants who received dexamethasone compared with those who received the placebo. The effect seem to be more marked in infants weighing less than 1250 g at birth. Significantly more infants could be extubated by 14 days of age in the dexamethasone group (26 of 32 vs 14 of 32). Dexamethasone therapy reduced the incidence of BPD at 28 days (odds ratio, 0.1; 95% confidence interval, 0.03 to 0.3) and eliminated BPD at 36 weeks' postconceptional age. Dexamethasone-treated infants had greater weight loss at 14 days (12.9 ± 6.4% vs 3.7 ± 8.6%, respectively) and higher blood pressures from days 3 to 10. However, no differences were seen in time to regain birth weight, hypertension (1 infant in each group), or incidence of intraventricular hemorrhage. Conclusions. We found an additive effect between dexamethasone and surfactant in improving pulmonary status and reducing the incidence of BPD. Compared with the placebo, dexamethasone therapy was more effective in reducing the incidence of BPD in surfactantpretreated very low birth weight infants.


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