AIMS: To document, and explain, the pulmonary paradox whereby despite relative lung immaturity, preterm infants exposed to amniotic infection (AI) have better postnatal pulmonary function than those exposed to preeclampsia (PE). METHODS: Lung maturation was characterized in 65 preterm perinatal deaths [AI (n=40) and PE (n=25)] and postnatal respiratory function in 100 preterm survivors [AI (n=50) and PE (n=50)]. RESULTS: At autopsy, lung architecture was in advance of gestational age in 5% of AI infants versus 40% of PE infants (P<0.001). In survivors, the groups were similar in age and Apgar scores. At birth, 40% of the AI group required continuous positive airway pressure or mechanical ventilation versus 24% of the PE group (NS). However, 24 hours later, only 1 AI infant had deteriorated compared to 40% of PE infants (P<0.05). CONCLUSIONS: Accelerated morphologic lung maturation in preterm PE infants does not translate into improved postnatal respiratory function. Most likely, this is due to a relative lack of surfactant, ascribable to low stimulant cytokine and high TNF-alpha levels. An intrauterine history supplemented by an antenatal cytokine profile could identify an increased exogeneous surfactant need in preterm infants exposed to PE.
AIMS: To document, and explain, the pulmonary paradox whereby despite relative lung immaturity, preterm infants exposed to amniotic infection (AI) have better postnatal pulmonary function than those exposed to preeclampsia (PE). METHODS: Lung maturation was characterized in 65 preterm perinatal deaths [AI (n=40) and PE (n=25)] and postnatal respiratory function in 100 preterm survivors [AI (n=50) and PE (n=50)]. RESULTS: At autopsy, lung architecture was in advance of gestational age in 5% of AIinfants versus 40% of PE infants (P<0.001). In survivors, the groups were similar in age and Apgar scores. At birth, 40% of the AI group required continuous positive airway pressure or mechanical ventilation versus 24% of the PE group (NS). However, 24 hours later, only 1 AIinfant had deteriorated compared to 40% of PE infants (P<0.05). CONCLUSIONS: Accelerated morphologic lung maturation in preterm PE infants does not translate into improved postnatal respiratory function. Most likely, this is due to a relative lack of surfactant, ascribable to low stimulant cytokine and high TNF-alpha levels. An intrauterine history supplemented by an antenatal cytokine profile could identify an increased exogeneous surfactant need in preterm infants exposed to PE.