The pulmonary paradox in premature infants: in-utero infected lungs do better than those with accelerated maturation

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Abstract
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). 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)]. 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). 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.