Pharmacotherapy in bronchopulmonary dysplasia

  • Firmino Rubaltelli
  • Franca Benini


Bronchopulmonary dysplasia (BPD) is a chronic respiratory disease characterized by tachypnoea, dyspnoea, hypoxia and hypercapnia with a typical radiological picture [1–3]. It includes all those patients with an oxygen dependence of more than 28 days from the first day of life, after assistance by mechanical ventilation during the first week of life [4,5]. BPD is a consequence of hyaline membrane disease (HMD) treated with mechanical ventilation, but can also follow pneumonia and meconium-stained amniotic fluid aspiration. Of increasing frequency, a clinical picture of medium-severity BPD, called chronic lung disease (CLD), occurs in premature babies of very low gestational age, who need mechanical ventilation for their extreme prematurity. In fact, BPD is most frequent in infants weighing less than 1500 g at birth, and has an incidence of 5–38% among mechanically ventilated newborns. In the first year of life, its mortality toll can reach 49%. About 30% of survivors have severe neurological handicaps [4,6]. The pathogenesis of BPD is still unclear. Of importance seems to be the role played by the cells and chemical mediators of inflammation, lured to and then activated in the lungs, when initiating factors (O2, barotrauma, infections and so on) act in a prolonged and excessive way [4,5]. The prevention of BPD consists of limiting the influence of the responsible and predisposing factors in the first days of neonatal life.


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© Macmillan Publishers Limited 1991

Authors and Affiliations

  • Firmino Rubaltelli
  • Franca Benini

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