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 MSAF in the trachea can cause airway obstruction. With aspiration below the vocal cords, further obstruction, air trapping, and an inflammatory response can result in severe respiratory distress. 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% to 20% of all deliveries. With improved perinatal care, the incidence has decreased. The incidence of MSAF increases from 1.6% at 34 to 37 weeks to 30% at ≥42 weeks. Of infants born through MSAF, approximately 5% go on to develop meconium aspiration syndrome (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 depends on hormonal and parasympathetic neural maturation. The exact mechanisms for in utero passage of meconium remain unclear, but fetal distress, vagal stimulation, and placental dysfunction are probable factors.
Aspiration of meconium. After intrauterine passage of meconium, deep irregular respiration or gasping, associated with fetal hypoxia, can cause aspiration of the MSAF. 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 can result in a ball-valve phenomenon leading to air trapping and alveolar hyperexpansion with a subsequent 20% to 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, identified in the lungs of infants with MAS, 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 can strip surfactant from the surface of the alveoli. Meconium also impacts surfactant production and clearance by affecting phosphatidylcholine metabolism.
Persistent pulmonary hypertension. A third of infants with meconium aspiration develop persistent pulmonary hypertension of the newborn (PPHN). Meconium aspiration alone may result in a delay of the normal decline in PVR. Additional increases in PVR are multifactorial. PVR increases as a direct result of alveolar hypoxia, acidosis, and lung ...