Definition. Meconium is the first intestinal discharge of the newborn infant and is composed of epithelial cells, fetal hair, mucus, and bile. Intrauterine stress may cause in utero passage of meconium into the amniotic fluid. The meconium-stained amniotic fluid may be aspirated by the fetus when fetal gasping or deep breathing movements are stimulated by hypoxia and hypercapnia. The presence of meconium in the trachea may cause airway obstruction as well as an inflammatory response, resulting in severe respiratory distress. The presence of meconium in amniotic fluid can be a warning sign of fetal distress but is not a sensitive independent marker of fetal distress. Mothers with meconium-stained amniotic fluid should be carefully monitored during labor.
All infants that are meconium stained do not develop meconium aspiration syndrome (MAS). MAS is defined by Faranoff as respiratory distress in an infant born through meconium-stained amniotic fluid (MSAF) whose symptoms cannot be otherwise explained. Hallmarks include early onset of respiratory distress in a meconium-stained infant with poor lung compliance, hypoxemia, and a characteristic radiograph of the lungs.
Incidence. The incidence of meconium-stained amniotic fluid (MSAF) varies from 8–20% of all deliveries. Of infants born through a meconium-stained amniotic fluid. 5% go on to develop meconium aspiration syndrome. Meconium aspiration primarily affects term and postmature infants. The passage of meconium in an asphyxiated infant <34 weeks' gestation is unusual and may represent bilious reflux secondary to intestinal obstruction.
In utero passage of meconium. Control of fetal meconium passage depends on hormonal and parasympathetic neural maturation. After 34 weeks' gestation, the incidence of meconium-stained amniotic fluid increases from 1.6% between 34 and 37 weeks' gestation to 30% at ≥42 weeks. The exact mechanisms for in utero passage of meconium remain unclear, but fetal distress and vagal stimulation are two probable factors.
Aspiration of meconium. After intrauterine passage of meconium, deep irregular respiration or gasping, either in utero or during labor and delivery, can cause aspiration of the meconium-stained amniotic fluid. Before delivery, the progression of the aspirated meconium is, as a rule, 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 meconium-stained amniotic fluid can result in acute upper airway obstruction. As the aspirated meconium progresses distally, total or partial airway obstruction may occur. In areas of total obstruction, atelectasis develops, but in areas of partial obstruction a ball-valve phenomenon occurs, resulting in air trapping and alveolar hyperexpansion. Air trapping increases the risk of air leak to 20–50%.
Chemical pneumonitis. With distal progression of meconium, chemical pneumonitis develops, with resulting bronchiolar edema and narrowing of the small airways. Meconium at the alveolar level may inactivate existing surfactant. Uneven ventilation resulting from areas of partial obstruction, atelectasis, and superimposed pneumonitis causes carbon dioxide retention and hypoxemia.
Pulmonary hypertension. A third of infants with meconium aspiration develop persistent pulmonary hypertension of newborn (PPHN). ...
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