Background
Meconium aspiration syndrome (MAS) is the aspiration of stained amniotic fluid, which can occur before, during, or immediately after birth. Meconium is the first intestinal discharge from newborns, a viscous, dark-green substance composed of intestinal epithelial cells, lanugo, mucus, and intestinal secretions (eg, bile). Water is the major liquid constituent, comprising 85-95% of meconium; the remaining 5-15% of ingredients consists of solid constituents, primarily intestinal secretions, mucosal cells, and solid elements of swallowed amniotic fluid, such as proteins and lipids.
Meconium is sterile and does not contain bacteria, which is the primary factor that differentiates it from stool. Intrauterine distress can cause passage of meconium into the amniotic fluid. Factors that promote the passage in utero include placental insufficiency, maternal hypertension, preeclampsia, oligohydramnios, infection, acidosis, and maternal drug abuse—especially use of tobacco and cocaine.
As noted above, meconium-stained amniotic fluid may be aspirated before or during labor and delivery. Because meconium is rarely found in the amniotic fluid prior to 34 weeks' gestation, meconium aspiration primarily affects infants born at term and postterm.
The incidence of MAS has drastically reduced over last few years owing to changes in obstetric practice. Currently, not many pregnancies continue beyond 40 weeks of gestation, resulting in a reduction of meconium stained amniotic fluid and the risk of MAS.
Pathophysiology
In utero meconium passage results from neural stimulation of a maturing gastrointestinal (GI) tract, usually due to fetal hypoxic stress. As the fetus approaches term, the GI tract matures, and vagal stimulation from head or spinal cord compression may cause peristalsis and relaxation of the rectal sphincter, leading to meconium passage.
The effects of meconium in amniotic fluid are well documented. [1] Meconium directly alters the amniotic fluid, reducing antibacterial activity and subsequently increasing the risk of perinatal bacterial infection. In addition, meconium is irritating to fetal skin, thus increasing the incidence of erythema toxicum. However, the most severe complication of meconium passage in utero is perinatal aspiration of stained amniotic fluid (before, during, or immediately after birth)—ie, meconium aspiration syndrome (MAS). Aspiration of meconium-stained amniotic fluid may occur if the fetus is in distress, leading to a gasping breathing pattern. This aspiration induces hypoxia via four major pulmonary effects: airway obstruction, surfactant dysfunction, chemical pneumonitis, and pulmonary hypertension. [1]
Airway obstruction
Complete obstruction of the airways by meconium results in atelectasis. Partial obstruction causes air trapping and hyperdistention of the alveoli, commonly termed the ball-valve effect. Hyperdistention of the alveoli occurs from airway expansion during inhalation and airway collapse around inspissated meconium in the airway, causing increased resistance during exhalation. The gas that is trapped (hyperinflating the lung) may rupture into the pleura (pneumothorax), mediastinum (pneumomediastinum), or pericardium (pneumopericardium).
Surfactant dysfunction
Meconium damages surfactant and may also inhibit surfactant synthesis. [2] Several constituents of meconium, especially the free fatty acids (eg, palmitic, stearic, oleic), have a higher minimal surface tension than surfactant and strip it from the alveolar surface, resulting in diffuse atelectasis. [3]
Chemical pneumonitis
Enzymes, bile salts, and free fatty acids in meconium irritate the airways and parenchyma, causing a release of cytokines (including tumor necrosis factor (TNF-α, interleukin (IL)-1β, IL-6, IL-8, IL-13), which initiate a diffuse pneumonitis that may begin within a few hours of aspiration.
All of these pulmonary effects can produce a gross ventilation-perfusion (V/Q) mismatch.
Persistent pulmonary hypertension of the newborn
To complicate matters further, many infants with meconium aspiration syndrome (MAS) have primary or secondary persistent pulmonary hypertension of the newborn (PPHN) as a result of chronic in utero stress and thickening of the pulmonary vessels. PPHN further contributes to the hypoxemia caused by meconium aspiration syndrome. [4, 5]
Finally, although meconium is sterile, its presence in the air passages can predispose the infant to pulmonary infection.
Etiology
Factors that promote the passage of meconium in utero include the following:
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Placental insufficiency
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Maternal hypertension
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Preeclampsia
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Oligohydramnios
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Maternal drug abuse, especially of tobacco and cocaine
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Maternal infection/chorioamnionitis
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Fetal hypoxia
Epidemiology
United States data
In the industrialized world, meconium in the amniotic fluid can be detected in 8-25% of all births after 34 weeks' gestation. Historically, approximately 10% of newborns born through meconium-stained amniotic fluid developed meconium aspiration syndrome (MAS). However, changes in obstetric and neonatal practices appear to be decreasing its incidence. [6] MAS was the admission diagnosis for 1.8% of term neonates in one large retrospective study from 1997-2007. [1]
International data
In developing countries with less availability of prenatal care and where home births are common, the incidence of MAS is thought to be higher and is associated with a greater mortality rate.
Age-, sex-, and race-related demographics
MAS is exclusively a disease of newborns, especially those delivered at or beyond the mother's estimated due date. [1] MAS affects both sexes equally.
A study of 499,096 singleton live births in London, England, reported the rates of meconium-stained amniotic fluid varied by ethnicity: It was 22.6% in the black population, 16.8% in south Asian groups, and 15.7% in the white population. [7] The study also demonstrated that meconium-stained amniotic fluid occurred more often in later-gestational-age pregnancies and in babies in the breech presentation.
Prognosis
Most infants with meconium aspiration syndrome (MAS) have complete recovery of pulmonary function; however, MAS infants have a slightly increased incidence of respiratory infections in the first year of life because the lungs are still in recovery. Severely affected infants have an increased risk of developing reactive airway disease (RAD) in the first 6 months of life. [8]
Children with MAS may develop chronic lung disease from intense pulmonary intervention.
Prenatal and intrapartum events that initiate the meconium passage may cause the infant to have long-term neurologic deficits, including central nervous system (CNS) damage, seizures, intellectual disability, and cerebral palsy.
Morbidity/mortality
A large retrospective analysis demonstrated the overall mortality rate for MAS to be 1.2% in the United States. [1] The mortality for MAS resulting from severe parenchymal pulmonary disease and pulmonary hypertension is as high as 20%. Other complications include air-leak syndromes (eg, pneumothorax, pneumomediastinum, pneumopericardium) and pulmonary interstitial emphysema, which occur in 10-30% of infants who have MAS. The neurologic disabilities of survivors are not due primarily to the aspiration of meconium, but rather owing to in utero pathophysiology, including chronic hypoxia and acidosis. [9]
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Air trapping and hyperexpansion from airway obstruction.
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Acute atelectasis.
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Pneumomediastinum from gas trapping and air leak.
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Left pneumothorax with depressed diaphragm and minimal mediastinal shift because of noncompliant lungs.
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Diffuse chemical pneumonitis from constituents of meconium.
