with MAS requiring mechanical ventilation. Surfactant decreases the need for ECMO in
MAS.
Pneumonia/Sepsis:
Bacterial endotoxin causes release of vasoconstrictors. They also cause loss of
surfactant function and decreased aeration of lungs and induce pulmonary edema by
increasing vascular permeability.
Respiratory Distress syndrome:
Increased reactivity of pulmonary arteries after 34 weeks of gestation predisposes late
preterm infants with RDS to pulmonary hypertension when gas exchange is impaired
because of surfactant deficiency. With the increase in late preterm deliveries since mid-
90s, RDS has become an important risk factor for PPHN
Idiopathic PPHN:
Structurally abnormal pulmonary vasculature may occur in idiopathic PPHN. These
changes consist of abnormal thickening of media and adventitia of pulmonary arteries
and hypoxemia in the absence of recognizable parenchymal lung disease. As pointed
out above, prenatal ductal constriction from maternal intake of NSAIDs can lead to this
altered adaptation. However, these structural changes can also occur in severe
meconium aspiration syndrome, lung hypoplasia and ACD.