Abstract
Pulmonary hypoplasia secondary to congenital diaphragmatic hernia, oligohydramnios, etc., is an important cause of neonatal morbidity and mortality. In fact, pulmonary hypoplasia is the most common finding (up to 26%) in neonatal autopsies (1). Moreover, more than 20,000 babies are born every year in the United States before 27 weeks of gestation (canalicular stage of lung development). These disorders have in common an incomplete development of the lungs. In addition to the risk of death, these conditions can also cause severe respiratory distress at birth and serious long-term morbidities (2). Currently, the management is primarily supportive and there are not specific treatments designed to accelerate the development of the lungs.
Highlights
Pulmonary hypoplasia secondary to congenital diaphragmatic hernia, oligohydramnios, etc., is an important cause of neonatal morbidity and mortality
As a mechanism to increase the pressure inside the lung to accelerate development, has been used in animal models [19] and in humans fetuses affected by congenital diaphragmatic hernia [20]
Past investigations in fetal lambs have shown that lung fluid composition after tracheal ligation was critical to promote lung development, since acceleration of growth and differentiation was not observed when lung fluids were replaced with normal saline [22, 23]
Summary
Pulmonary hypoplasia secondary to congenital diaphragmatic hernia, oligohydramnios, etc., is an important cause of neonatal morbidity and mortality. The management is primarily supportive and there are not specific treatments designed to accelerate the development of the lungs. The lungs are unique in that their growth and development depends primarily on extrinsic factors and on mechanical forces [3,4,5,6,7].
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