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The pathophysiology of BPD is based on an impairment of lung maturation with prenatal and postnatal multi\u2010hit insults and genetic susceptibility. This multifactorial pathophysiology of BPD suggests that no single \u201cmagic bullet\u201d will prevent it. Thus, to avoid BPD we need to implement a complex and comprehensive strategy.<\/jats:p><jats:p>This strategy is based on ventilatory and non\u2010ventilatory measures. The ventilatory route allows an individualized endotracheal intubation approach. Early lung recruitment with nasal respiratory support (nasal continuous positive airway pressure [NCPAP] or nasal intermittent positive pressure ventilation [NIPPV] \/ synchronized NIPPV [SNIPPV]) and the INSURE (intubation, surfactant and early extubation) approach are discussed. Initial treatment with NCPAP did not reduce the rate of BPD compared to endotracheal ventilation and surfactant administration. While NIPPV\/SNIPPV may have short\u2010term advantages over NCPAP, the effect on BPD needs to be further studied. During hospitalization the respiratory goals should aim for adequate oxygenation, permissive hypercapnia, and gentle ventilation. However, these goals were found to have short\u2010term benefits but did not reduce significantly the rate of BPD. Selective use of a short course of low dose corticosteroids can be considered after the first or second week of life in infants who are unable to be weaned from the ventilator and are at high risk for BPD. Non\u2010ventilatory measures include early nutritional support with fluid restriction, caffeine and consideration of vitamin A. Hemodynamic significant patent ductus arteriosus (PDA) may be associated with BPD, but medical or surgical treatment of PDA were not shown to decrease BPD. Each component and the strategy as a whole needs to be further studied in large randomized prospective studies or by meta\u2010analyses, especially in the target population of extremely premature infants who are the most prone to BPD. 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