Narrative Review on Therapies That Influence Inflammatory Responses During Extremely Premature Perinatal Respiratory Transition.

AIMS AND

METHODS

Advances in neonatal care have extended borderline survival to 22-24 post-conceptional weeks. Present review discusses approaches for prolonging short pregnancies and prevention of serious morbidities in extremely premature infants born before 28 weeks of pregnancy.

RESULTS

Spontaneous extremely premature delivery and foetal alveolar differentiation are induced by inflammatory signals. They either coexist in chorioamnionitis or first premature birth triggers functional differentiation of immature pulmonary alveoli. Infections, other acquired or genetic factors predispose to extremely premature births. Non-steroidal anti-inflammatory agents are effective in tocolysis. However, they are toxic to very premature newborns. In recent animal studies, inhibitors of inflammatory receptors or augmentation of deficient intrauterine anti-inflammatory defences have prevented inflammation-induced preterm deliveries. Antenatal glucocorticoid advances foetal maturity, but glucocorticoid excess interferes with growth and neurodevelopment. Optimizing indications and dosage of glucocorticoid is needed. Despite increasing survival, acute and chronic pulmonary, somatic and particularly neurosensory diseases have barely decreased. Practices of ventilation and multiple other therapies need to be refined for this extremely high-risk population.

CONCLUSION

Aiming to medical treatments that safely prolong extremely premature pregnancies and promote the management and safety of extremely premature infants would increase the healthy life years. These goals require persistent multidisciplinary research.