Meconium Aspiration Syndrome: The Core Concept of Pathophysiology during Resuscitation

ABSTRACT

Aspiration of meconium produces a syndrome (Meconium Aspiration Syndrome MAS) characterized by hypoxia, hypercapnia, and acidosis. Perinatal hypoxia, acute airway obstruction, pulmonary inflammation, pulmonary vasoconstriction, pulmonary hypertension, and surfactant inactivation all play a role in the pathogenesis of MAS. Most aspiration of meconium probably occurs before birth. Following aspiration, meconium may migrate to the peripheral airway, usually take about 2 hours as demonstrated in animal experiment, leading to airway obstruction and subsequent lung inflammation and pulmonary hypertension. The presence of meconium in the endotracheal aspirate automatically establishes the diagnosis of MAS. Clinical diagnosis can be made in any infant born with meconium staining of amniotic fluid who develops respiratory distress at or shortly after birth and has positive radiographic findings. Prevention of intrauterine hypoxia, early cleaning (suctioning) of the airway, and prevention and treatment of pulmonary hypertension are essential in the management of MAS. Recent studies suggest that avoidance of post-term delivery may reduce the risk of intrauterine hypoxia and the incidence of MAS. Routine intrapartum naso-and oropharyngeal suction does not appear to affect the incidence and outcome of MAS. Endotracheal suction at birth is considered a controversial procedure and only reserved for infants who have severe retraction at birth suggesting an upper airway obstruction. High frequency oscillatory ventilation with nitric oxide or surfactant may improve mortality. Mortality of MAS has improved; the causes of death are related primarily to hypoxic respiratory failure associated with irreversible pulmonary hypertension. Morbidity is affected mostly by perinatal hypoxia.