Meconium is the first intestinal discharge of the newborn infant. In addition to epithelial cells, fetal hair, mucus, and bile, meconium also contains a number of proinflammatory components. With the passage of meconium in utero, the meconium-stained amniotic fluid (MSAF) may be aspirated. The presence of meconium in the trachea can cause airway obstruction and, with aspiration below the vocal cords, further obstruction, air trapping, and an inflammatory response, all of which can result in severe respiratory distress. All infants with meconium-stained amniotic fluid do not develop meconium aspiration syndrome (MAS). Hallmarks include early onset of respiratory distress in an infant with MSAF who presents with poor lung compliance, hypoxemia, and a characteristic lung radiograph.
The incidence of MSAF varies from 8–20% of all deliveries. With improved perinatal care, the incidence has decreased. The incidence of MSAF increases from 1.6% at 34–37 weeks to 30% at ≥42 weeks. Of infants born through an MSAF, ∼5% go on to develop MAS. MAS primarily affects term and postmature infants. The intrauterine passage of meconium by infants <34 weeks' gestation is very unusual and may represent bilious reflux secondary to intestinal obstruction, not MAS.
In utero passage of meconium. Fetal meconium passage depends on hormonal and parasympathetic neural maturation. The exact mechanisms for in utero passage of meconium remain unclear, but fetal distress and vagal stimulation are 2 probable factors.
Aspiration of meconium. After intrauterine passage of meconium, deep irregular respiration or gasping, associated with fetal hypoxia either in utero or during labor and delivery, can cause aspiration of the MSAF. Otherwise, before delivery, the progression of the aspirated meconium is usually impeded by the presence of the viscous liquid that normally fills the fetal lung and airways. Therefore, the distal progression occurs mostly after birth in conjunction with the reabsorption of lung fluid. Early consequences of meconium aspiration include airway obstruction, decreased lung compliance, and increased expiratory large airway resistance.
Airway obstruction. Thick MSAF can result in acute upper airway obstruction. As the aspirated meconium progresses distally, total and partial airway obstruction may occur. Partial airway obstruction may result in a ball-valve phenomenon leading to air trapping and alveolar hyperexpansion with a subsequent 20–50% risk of air leak. Total obstruction may lead to asymmetric areas of atelectasis, resulting in hypoxia and increased pulmonary vascular resistance (PVR).
Chemical pneumonitis. With distal progression of meconium, chemical pneumonitis develops, which causes bronchiolar edema and narrowing of the small airways, all leading to increased hypercarbia and hypoxemia.
Inflammatory mediators. Intrapulmonary meconium triggers the release of a number of proinflammatory cytokines that lead to further airway edema, apoptosis, hypoxia, and increased PVR. Endogenous production of phospholipase A2 has recently been identified in the lungs of infants with MAS and is associated with upregulation of inflammatory mediators, direct injury to the alveolar cell membrane, airway constriction, and surfactant catabolism.
Surfactant dysfunction. The free fatty acids in meconium, due to their higher surface tension, leads to surfactant ...