Available online 26 March 2024, 151888

Optimal respiratory support can only be achieved if the ventilator strategy utilized for each individual patient at any given point in the evolution of their disease process is tailored to the underlying pathophysiology. The critically ill newborn infant requires individualized patient care when it comes to mechanical ventilation. This can only occur if the clinician has a good understanding of the different pathophysiologies of a variety of conditions that can lead to respiratory failure. In this chapter we describe the key pathophysiological features of bronchopulmonary dysplasia, meconium aspiration syndrome and lung hypoplasia syndromes with emphasis on congenital diaphragmatic hernia. We review available evidence to guide management an provide specific recommendations for pathophysiologically-based mechanical ventilation support.

During the weeks to months of newborn intensive care unit (NICU) stay, the lung pathology and pulmonary mechanics of the premature infant changes over time. Many NICU providers are familiar and comfortable with providing ventilatory support for an extremely preterm infant with respiratory distress syndrome (RDS). However, with insufficient support from high-quality evidence, ventilating an infant with established severe bronchopulmonary dysplasia (BPD) is more difficult and significant

Meconium staining of amniotic fluid is relatively common, especially in infants born beyond 40 weeks gestation but significant aspiration of meconium, i.e. meconium aspiration syndrome (MAS), is much less frequent and is becoming more uncommon as obstetricians now seldom allow pregnancies to continue much beyond 40 weeks.2425 The exact incidence of MAS may be difficult to determine accurately, because of the challenges of distinguishing the clinical and radiographic features of MAS from other

Pulmonary hypoplasia remains one of the most challenging neonatal lung disorders to manage. Lung hypoplasia typically occurs as a consequence of severe oligohydramnios (such as with prolonged premature rupture of the membranes or lack of fetal urine),48 or extrinsic compression (e.g. congenital diaphragmatic hernia (CDH) or other space-occupying intrathoracic masses) during key phases of fetal lung development, the pseudoglandular to early saccular phases.49,50 Impaired lung growth is the

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