Long-Term Sequelae of Neonatal Lung Disease

In neonatal lung disease, chemical and physical noxious stimuli, microbial aggression, host defence, and an ill-timed exposure to the extrauterine environment all act together in compromising the integrity of the maturing lungs. Pulmonary sequelae, therefore, are determined by the severity of congenital lung disease, but also reflect the multitude of secondary injuries to the newborn child.Various studies have shown that pulmonary function abnormalities in survivors of neonatal lung disease remain highly prevalent despite often favourable clinical outcomes. Mildly impaired compliance, a tendency towards hyperinflation, airway obstruction, and a high prevalence of airway hyperresponsiveness may describe a general pattern of functional remnants in these children. In addition, the possibility of persistently elevated pulmonary artery pressures even in asymptomatic individuals must be kept in mind. Physicians concerned with the follow-up of these patients must be aware of the many extra-pulmonary health issues that need to be regarded. Informed guidance of patients and parents is of importance both in order to prevent stigmatization of these children as overly vulnerable as well as for an early recognition of treatable respiratory problems which might otherwise not be fully apprehended due to a long-standing history of pulmonary disease.With the exception of chronic lung disease of prematurity, long-term follow-up of pulmonary sequelae of neonatal lung diseases so far has referred to children born before the introduction of lung protective ventilation strategies. It thus remains to be seen whether with improved neonatal management and survival of severely sick neonates the profile of long-term pulmonary sequelae will drift towards greater morbidity. The uniqueness of neonatal lung disease is its temporary coincidence with a vulnerable period of lung maturation. As a consequence, outcome is not only determined by the circulatory and gas exchange capacity of the lungs at birth, but also by the extent of secondary adaptations of the pulmonary architecture to the mostly precocious exposure to extrauterine environment and medical intervention. Before the recognition of oxygen toxicity and barotrauma as important mediators of secondary lung injury [1, 2], long-term outcome of neonatal lung disease was substantially influenced by the aggressiveness of mechanical ventilation and hence the severity of neonatal respiratory distress [3]. The resulting pulmonary sequelae were represented by the histopathological features of classic bronchopulmonary dysplasia (BPD). With the introduction of surfactant therapy and the implementation of lung-protective ventilation strategies, long-term respiratory outcome has become increasingly determined by the size and maturity of the newborn child and by the multitude of comorbidities with pulmonary involvement encountered during infancy and childhood [4-6]. With better survival of more vulnerable very low birth weight (VLBW) infants the prevalence of pulmonary sequelae has not declined as could have been expected from improved management of the more mature neonates [7, 8]. Chorioamnionitis, postnatal infection, and patent ductus arteriosus further augment the risk of secondary lung damage in the prematurely born children [9-12]. If the consequent structural changes are severe enough to cause ongoing compromise of pulmonary function, chronic lung disease (CLD) of infancy results, as defined by prolonged need for oxygen supplementation with or without ventilatory support [13].

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