Bronchopulmonary Dysplasia

This paper explores BPD’s Pathophysiology, epidemiology, causes, signs and symptoms, and its prevention among others.
According to D’Angio and Maniscalco (2004), the Pathophysiology of Bronchopulmonary dysplasia is much complex and is yet to be fully understood. The following are some of the factors connected with BPD:
Inflammation: The infiltration of granulocyte into the lungs of newborns developing BPD is well documented (D’Angio &amp. Maniscalco, 2004). Animal samples of infant lung injury provide evidence for the role played by granulocyte in BPD’s pathogenesis. There is a fast development of Neutrophil in the bronchoalveolar lavage fluid of newborns with RDS (D’Angio &amp. Maniscalco, 2004). In infants who are later diagnosed with BPD, the decline in Neutrophil counts is delayed. Proinflammatory mediators like cytokines, which attract inflammatory cells into the lungs have been connected with the development of BPD in infants (Mighten, 2012, p. 135. D’Angio &amp. Maniscalco, 2004).
Architectural Disruption: Cellular injury, as well as the destruction, caused when inflammatory cells discharge reactive oxygen and proteases result from granulocytes infiltration into the lung. “The lung protease/antiprotease balance appears to be tilted toward proteolysis in infants who develop BPD” (D’Angio &amp. Maniscalco, 2004, p.309). Infants with a high probability of developing BPD show higher elastase levels.
Fibroproliferation: Transforming growth factor (TGF) – β has been shown by most studies to have a serious inhibitory impact on lung development besides other fibrogenic effects (D’Angio &amp. Maniscalco, 2004). Higher levels of TGFβ have been identified in infants who are later diagnosed with BPD (D’Angio &amp. Maniscalco, 2004). Delayed development of the lung has also been connected with ‘new’ BPD.