Aspiration of meconium produces a syndrome 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 meconium aspiration syndrome (MAS). Most aspiration of meconium probably occurs before birth. Following aspiration, meconium can migrate to the peripheral airway, leading to airway obstruction and subsequent lung inflammation and pulmonary hypertension. The presence of meconium in the endotracheal aspirate automatically establishes the diagnosis of meconium aspiration. MAS can be diagnosed 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 postterm 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 now is reserved only for infants who are depressed or have respiratory distress at birth. 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.
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