Preterm Birth and Long-Term Pulmonary Function

Introduction 1.1 Lung developmentTo understand the pathophysiology and the outcome of chronic lung disease of infancy, it is essential to understand normal lung development and the host of cofactors that will interfere with both antenatal and postnatal lung development.Lung growth starts in utero and continues to early adolescence going through different phases (Burri, 2006).The embryonic phase, between the 4 th and 7 th week, begins with the formation of a groove in the ventral lower pharynx and a bud at the lower part of the groove.After further elongation and subdivision of the bud, the two main bronchi are formed.Between the 7 th and 16 th week of gestation, known as the pseudoglandular phase, the air conducting trees continue to subdivide to form the terminal bronchioles.During the canalicular phase from the 17 th to the 26 th week of gestation, airway branching is complete with the formation of the primitive saccules.It is also during this phase that the cuboidal epithelium lining the saccules differentiates into type I and type II pneumocytes with concomitant increases in peripheral mesenchyme vascularization.From 27 weeks onwards, during the saccular phase, the lung will begin to prepare for birth with thinning of the connective tissue, secondary septation subdividing the sacculi into smaller subunits or alveoli and the presence of a single capillary layer characteristic of mature alveoli (Hislop et al., 1986;Langston et al., 1984;Post & Copland, 2002).Alveoli continue to increase in number until and beyond birth.At 29 weeks gestation, there are approximately 30 million alveoli and this will increase to some 150 million alveoli by term, one third to half the adult number (Hislop et al., 1986;Langston et al., 1984). Chronic lung disease of infancyChronic lung disease of infancy (CLDI) is a heterogeneous group of diseases that usually evolves from an acute newborn respiratory disorder.These disorders, such as respiratory distress syndrome secondary to preterm birth, meconium aspiration, sepsis, persistent pulmonary hypertension, congenital heart disease and their subsequent treatments, may predispose the infant to the development of CLDI.Bronchopulmonary dysplasia (BPD), the most significant long-term pulmonary complication of preterm birth (Eber & Zach, 2001) was initially defined as the continued dependence on supplementary oxygen for greater than 28 days postpartum (Northway, 1979).However, BPD has been redefined as we www.intechopen.com

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