Does BPD contribute to the occurrence of cerebral palsy among infants born before 28 weeks of gestation?

Some studies suggest that preterm infants with bronchopulmonary dysplasia (BPD) are at increased risk for subsequent cerebral palsy (CP). The analysis of a potential BPD-CP association is complex for several reasons. First, BPD often follows exposures thought to influence CP risk, which include extremely preterm birth, cerebral white matter damage, necrotizing enterocolitis, pneumothorax and prolonged mechanical ventilation (MV). In addition, a number of important changes in neonatal intensive care practices have been introduced over the past 15 years that might modify both BPD and CP risk. Among these, it is possible to include a more widespread use of some treatments, such as surfactant, antenatal corticosteroids and indomethacin, as well as an increased intrapartum antibiotic prophylaxis accompanied by reduction in rates of early neonatal sepsis. Last, the use of high dose postnatal steroids, which increased in the 1990s and has decreased since, is associated both with reduced severity of BPD and increased risk of CP.
An American group has recently explored the relationship between BPD and CP phenotypes (i.e., quadriparesis, diparesis, and hemiparesis), while considering both potential shared antecedents as well as possible intermediaries in the causal pathway to CP.
In particular, 1047 infants born before the 28th week of gestation were included. Two levels of BPD were defined based on the receipt of supplemental oxygen at 36 weeks postmenstrual age (PMA), with or without the need for mechanical ventilation. Children underwent neurologic examinations at 24 months and CP diagnoses were made using an algorithm based on topographic localisation.
Overall, the results showed that the 536 infants with BPD were at increased risk of all three CP phenotypes. In a multivariable analyses that adjusted for potential confounders, receipt of supplemental oxygen without MV at 36 weeks PMA (BPD) was not associated with increased risk of any CP phenotype. In contrast, BPD accompanied by MV at 36 weeks PMA (BPD/MV) was associated with a nearly six-fold increased risk of quadriparesis and a four-fold increased risk of diparesis.
In conclusions, this study indicates that the associations between BPD and CP are attenuated when variables associated with prematurity and correlates of illness severity are considered. The residual association between BPD and CP varies by BPD severity and CP phenotype, and BPD/MV appeared strongly associated with an increased risk of quadriparesis and diparesis. No association was found with hemiparesis, but the analysis might have been limited by the small size of this subgroup in the present study. Although the observational nature of this study does not allow detecting any causal inferences, future investigations of preventive therapies or pathophysiological mechanisms underlying the BPD-CP relationship should take into account the likelihood of variability in antecedent relationships among CP phenotypes.

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