Chorioamnionitis, surfactant, and lung disease in very low birth weight infants

Recently, Been et al (J Pediatr 2010; 156: 10-5) have shown an important correlation between chorioamnionitis and response to surfactant therapy. In their study, very preterm infants exposed to chorioamnionitis with a fetal inflammatory response had an inferior response to surfactant treatment than those without fetal inflammatory response or no exposure to chorioamnionitis. Moreover, infants exposed to chorioamnionitis and presenting inflammatory response progressed more frequently to bronchopulmonary dysplasia (BPD). This observation further refines previous reports suggesting that chorioamnionitis can increase the risk of BPD (Pediatrics 1996;97:210-5; J Pediatr 2002;140:171-6).
The finding by Been et al. is supported by previous data, obtained on animal models, demonstrating that inflammation has a large effect on the efficacy of surfactant treatment. Indeed, synthesis of pulmonary surfactant lipids and proteins was proved to be affected by TNF-α and interleukins as well as by intraamniotic exposure to the gram-negative bacterial cell wall components.
In their study, Been et al have stratified the chorioamnionitis exposure group according to the presence of a fetal inflammatory response. This categorization may contribute to the explanations of different patterns of progression from lung injury to BPD (Pediatrics 1999; 103 (Pt 1):759-65) and may provide a different perspective for the analysis of previous data that were not able to find a good correlation between chorioamnionitis and BPD progression (laughton et al.).
The results by Been et al. suggest that chorioamnionitis with fetal involvement can be strongly predictive of the risk for severe respiratory distress syndrome (RDS) that is less responsive to surfactant treatment. This decreased surfactant response with the fetal inflammatory response may reflect more lung inflammation at birth. The progression to BPD may therefore result from suppression or activation of inflammatory responses in the newborn. Antenatal corticosteroid therapy can also modulate the acute inflammation in the fetal lung and subsequent inflammatory responses to interventions such as oxygen exposure and ventilation.
On this basis, "RDS" associated with preterm birth resulting from different causes (e.g., preterm labor of unknown origin, abruption, elective deliveries for preeclampsia, or chorioamnionitis) may not be the same. These infants with quite distinct fetal exposure histories may have varying degrees of "maturation" of lung structure, of the surfactant system, and of lung inflammatory responses. Maybe it is time to refine the diagnosis of RDS. Preterm infants are likely to have more than one lung disease, although RDS is the only diagnosis assigned to most of them.

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