A. Cause. Acute or chronic hypoxia and/or infection can result in the passage of meconium in utero. In this setting, gasping by the fetus or newly born infant can cause aspiration of amniotic fluid contaminated by meconium. Meconium aspiration before or during birth can obstruct airways, interfere with gas exchange, and cause severe respiratory distress (Fig. 35.1).

B. Incidence. Meconium-stained amniotic fluid (MSAF) complicates approximately 10% to 15% of deliveries. The incidence of MSAF in preterm infants is very low. Most babies with MSAF are 37 weeks or older, and many meconium-stained infants are postmature and small for gestational age. Approximately 3% to 4% of neonates born through MSAF develop meconium aspiration syndrome (MAS), and approximately 30% to 50% of these infants require continuous positive airway pressure (CPAP) or mechanical ventilation.

II. PATHOPHYSIOLOGY. Meconium is a sterile, thick, black-green odorless material that results from the accumulation of debris in the fetal intestine starting in the third month of gestation. The components of meconium include water (72% to 80%), desquamated cells from the intestine and skin, gastrointestinal mucin, lanugo hair, fatty material from the vernix caseosa, amniotic fluid, intestinal secretions, blood group-specific glycoproteins, bile, and enzymes including phospholipase A₂.

A. Passage of meconium in utero. MSAF occurs more commonly in term or postterm pregnancies and rarely prior to 34 weeks’ gestation. MSAF may result from a postterm fetus with rising motilin levels and normal gastrointestinal function, vagal stimulation produced by cord or head compression, or in utero fetal stress. Amniotic fluid that is thinly stained is described
as watery. Moderately stained fluid is opaque without particles, and fluid with thick meconium with particles is sometimes called pea soup.

B. Aspiration of meconium. In the presence of fetal stress, gasping by the fetus can result in aspiration of meconium before, during, or immediately following delivery. Severe MAS appears to be caused by pathologic intrauterine processes, primarily chronic hypoxia, acidosis, and infection.

C. Effects of meconium aspiration. When aspirated into the lung, meconium may stimulate the release of cytokines and vasoactive substances that result in cardiovascular and inflammatory responses in the fetus and newborn. Meconium itself, or the resultant chemical pneumonitis, mechanically obstructs the small airways, causes atelectasis, and a “ball-valve” effect with resultant air trapping and possible air leak. Aspirated meconium leads to vasospasm, hypertrophy of the pulmonary arterial musculature, and pulmonary hypertension that lead to extrapulmonary right-to-left shunting through the ductus arteriosus or the foramen ovale, resulting in worsened ventilation-perfusion ([V with dot above]/[Q with dot above]) mismatch and severe arterial hypoxemia. Approximately one-third of infants with MAS develop persistent pulmonary hypertension of the newborn (PPHN), which contributes to the mortality associated with this syndrome (see Chapter 36). Aspirated meconium also inhibits surfactant function. Several studies suggest that the enzymatic
and sterol components of meconium disrupt the surfactant phospholipids and limit the ability for surfactant to lower surface tension.

D. Severity. MAS is considered mild in infants requiring <40% oxygen for <48 hours and moderate in infants requiring >40% oxygen for >48 hours without air leak. MAS is considered severe in infants who require assisted ventilation for >48 hours and is often associated with PPHN.

E. Sequelae. In utero passage of meconium in term infants has been associated with an increased risk of perinatal and neonatal mortality, severe acidemia, need for cesarean delivery, need for intensive care and oxygen administration, and adverse neurologic outcome. Preterm infants who pass meconium before delivery have similar adverse effects as well as an increased incidence of severe intraventricular hemorrhage, cystic periventricular leukomalacia, and cerebral palsy.