Nutrition for extremely low birth weight infants (ELBW) at risk of developing bronchopulmonary dysplasia (BPD) is critical to the prevention, amelioration, and recovery from this severe lung disorder. A “new” form of BPD has emerged owing to increased survival of ELBW immature infants who have benefited from improved ventilatory regimens, use of prenatal and postnatal steroids and postnatal surfactant. The histopathologic picture of alveolar and capillary hypoplasia of the “new” BPD differs from the “old” BPD, such that the new BPD is less fibrotic than its earlier counterpart, and there is a significant component of delayed alveolar development and perhaps permanent alveolar underdevelopment. Unfortunately, targeted treatment strategies to optimize normal lung development and prevent BPD remain elusive.

Bronchopulmonary dysplasia has been referred to as an “oxygen radical disease of prematurity.” A state of oxidative stress is a hallmark of BPD owing to a combination of exposure to high oxygen concentrations starting shortly after birth and increased production of reactive oxygen species as a result of cytokine activation during infections and inflammations. The antioxidant availability to counter such oxidative stress is likely to be inadequate in ELBW infants due to extreme immaturity and meager nutritional stores. Administration of antioxidant nutrients such as vitamin E and N-acetylcysteine have been proposed as a means of prevention or attenuation of the severity of BPD. Vitamin A, which may stimulate re-epithelialization of lung tissues, and inositol, which promotes maturation of surfactant phospholipids, have been investigated as preventive measures against BPD.