By Donald J. Massaro, Gloria DeCarlo Massaro, Pierre Chambon

This reference compiles the most up-tp-date technical and organic facts to be had to survey the state-of-science within the care and administration of sufferers with bronchopulmonary dysplasia, COPD, and other kinds of lung disease-tracking the initiation and development of approaches that reason airway obstruction, the biologic and physiological abnormalities that represent COPD, and the aptitude reversibility of the inflammatory reaction in COPD for enhanced sufferer analysis and remedy.

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Additional resources for Lung Development and Regeneration (Lung Biology in Health and Disease)

Example text

In: Rosenberg HS, Bolande RP, eds. Perspectives in Pediatric Pathology. Chicago: Year Book Medical Publishers, 1975:15–60. Taghizadeh A, Reynolds E. Pathogenesis of bronchopulmonary dysplasia following hyaline membrane disease. Am J Pathol 1976; 82:241–264. Anderson W, Engel R. Cardiopulmonary sequelae of reparative stages of bronchopulmonary dysplasia. Arch Pathol Lab Med 1983; 107:603–608. Erickson A, de la Monte S, Moore G, Hutchins G. The progression of morphologic changes in bronchopulmonary dysplasia.

As Arrested Alveolar Development 15 Stahlman points out in her superb chapter on BPD prevention, maternal factors are dominant in this issue, and go beyond whether or not intrauterine infection is present (61). She makes a forceful argument that the demographic and socioeconomic circumstances of the women who deliver preterm need attention as well. In Bancalari’s recent review, he presents evidence supporting the major role inflammation is now thought to play in the pathogenesis of BPD (62). Ventilation with resultant volutrauma, oxygen therapy with free oxygen radical production, increased pulmonary blood flow due to a patent ductus arteriosus, and perinatal infections can induce the inflammatory response.

Rationale for this strategy sprang from a survey that compared the incidence of BPD at different institutions. The lowest incidence of the disease occurred in a neonatal unit that emphasized the use of continuous positive airway pressure without endotracheal intubation (70). Subsequent reports indicated that the incidence of BPD was greatest among very premature infants who had low PaCO2 values while receiving mechanical ventilation during the first few days after birth (71,72). These observations, coupled with studies showing that lung BPD in Postsurfactant Era 29 inflation with large tidal volumes soon after birth impaired responses to surfactant replacement and induced significant lung injury in preterm lambs (73,74), led to the notion that overzealous respiratory support and associated hypocapnia may predispose the incompletely developed lung to chronic injury and BPD.

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