Editorial

Bronchopulmonary dysplasia (BPD) is a common adverse outcome of premature birth, affecting approximately 40% of those born prior to 29 weeks of gestation. It has long term adverse consequences including recurrent respiratory symptoms requiring treatment and lung function abnormalities at school age and adolescence. In this issue, Drs. Davis and Sweet highlight that BPD is caused by a combination of insults on the developing lung precipitated by preterm birth and its subsequent respiratory management. In particular, they note the common pathway linking the various causative factors is inflammation which, in the developing lung, induces airway remodelling with an adverse effect on lung function. They emphasize that management should be directed towards prevention with strategies aimed at minimising early lung injury and oxidative stress, including delivery room stabilisation and mechanical ventilation techniques that aim to avoid volutrauma and atelecto-trauma. Meta-analysis of randomised trials of “invasive” ventilation has demonstrated that only prophylactic high frequency oscillation is associated with a reduction in BPD, but the effect is modest and inconsistent across the fifteen trials included in the Cochrane review. Over the first year after birth, studies have demonstrated lung function deterioration in prematurely born infants. Results of a non-randomised study suggest this may be avoided by use of prophylactic HFO. Yet certain trials have demonstrated use of HFO may increase short term neurological complications. It is therefore essential that there is long term follow up of infants entered into such trials and hence the real risk benefit ratio of this ventilation mode can be determined. Sudden infant death syndrome (SIDS) remains the leading cause of postnatal deaths in the United States. Prematurely born infants have an increased risk of SIDS, particularly if slept prone (odds radio of over 40) and also if their mothers smoked during pregnancy. In this issue Drs. Omojokun and Moon have reviewed the evidence for the pathophysiology of SIDS and maternal risk factors. They highlight that recent data have demonstrated associations between SIDS and specific polymorphisms, including genes involved in the autonomic system development, cardiac ion channels and infection, inflammation and metabolism. They suggest that the interaction between environmental and genetic factors contributes to SIDS susceptibility.