Abstract

During the last three decades, there has been an increase in the survival rate of infants with very low birth weight (VLBW) [1, 2]. However, this improvement in survival has been accompanied by the increased rate of long- and short-term morbidities, with bronchopulmonary dysplasia (BPD) one the most common adverse outcomes [3]. Introduction of surfactant and widespread use of antenatal steroids changed the clinical course of respiratory distress syndrome (RDS) as well as the histological picture and natural history of BPD. The incidence of BPD in the VLBW infants varies between centers, ranging from 3% to 43% even when using standardized definitions [1]. Severe cases originally described by Northway (“old BPD”) are rarely seen now. The “new BPD” remains an important problem. The etiology of so-called new BPD is unclear and probably multifactorial. Available evidence suggests that BPD develops as a result of abnormal growth and repair of the immature lungs exposed to repetitive stress of mechanical ventilation (namely, volutrauma and barotrauma), especially via endotracheal tube, aggravated by recurrent infections and chronic inflammation [4]. It is believed that the mere presence of an endotracheal tube may contribute to the development of BPD by impairing natural airway defenses and increasing the risk of infection and inflammation of the upper and lower airways [5]. Yet, a large proportion of preterm and ill term infants requires respiratory support at some point during their hospital stay.

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