Meconium Aspiration Syndrome

Physiologic stress at the time of labor and delivery (eg, due to hypoxia and/or acidosis caused by umbilical cord compression or placental insufficiency or caused by infection) may cause the fetus to pass meconium into the amniotic fluid before delivery. Meconium passage may be normal before birth, particularly in term or postterm infants; meconium passage is noted in 4 to 22% of births (and in a higher percentage of postterm births) (1, 2). However, it is never normal for meconium to be noted at the delivery of a preterm infant.

During delivery, approximately 3 to 12% of neonates with meconium passage aspirate the meconium, triggering lung injury and respiratory distress, termed meconium aspiration syndrome.

The mechanisms by which aspiration induces the clinical syndrome probably include:

• Nonspecific cytokine release

• Airway obstruction

• Decreased surfactant production and surfactant inactivation

• Chemical pneumonitis

Underlying physiologic stressors also may contribute. If complete bronchial obstruction occurs, atelectasis results; partial blockage leads to air trapping on expiration, resulting in hyperexpansion of the lungs and possibly pulmonary air leak with pneumomediastinum or pneumothorax. The risk of air leak is further increased because of the decreased lung compliance caused by decreased surfactant production and inactivated surfactant.

Although the pneumonitis caused by the meconium contributes to respiratory compromise in these infants after delivery, the persistent pulmonary hypertension (PPH), caused by both direct lung injury and vasoconstriction as well as perinatal acidosis and hypoxia, can ultimately be the more life-threatening disease.

Neonates also may aspirate vernix caseosa, amniotic fluid, or blood of maternal or fetal origin during delivery, all of which can cause respiratory distress and signs of aspiration pneumonia on chest radiograph.

Signs of meconium aspiration syndrome include tachypnea, nasal flaring, retractions, cyanosis or desaturation, rales, and rhonchi. Infants may become cyanotic.

Greenish yellow staining of the umbilical cord, nail beds, or skin indicates prolonged (several hours) exposure to meconium in utero. Such staining may indicate prolonged fetal distress and possibly the physiologic changes leading to meconium aspiration syndrome. Meconium staining may be visible in the oropharynx and (on intubation) in the larynx and trachea.

Neonates with air trapping may have a barrel-shaped chest and also symptoms and signs of pneumothorax, pulmonary interstitial emphysema, and pneumomediastinum.

• Meconium passage

• Respiratory distress

• Characteristic radiographic findings

Diagnosis of meconium aspiration syndrome is suspected when a neonate shows respiratory distress in the setting of meconium-containing amniotic fluid. Staining is not diagnostic.

Diagnosis is confirmed by chest radiograph showing hyperinflation with variable areas of atelectasis, heterogeneous patchy or streaky opacities, and flattening of the diaphragm. Initial radiograph findings can be confused with the findings of transient tachypnea of the newborn (TTN); however, what often separates infants with meconium aspiration syndrome from those with TTN is the significant hypoxemia present and, sometimes, concomitant PPH. Fluid may be seen in the lung fissures or pleural spaces, and air may be seen in the soft tissues or mediastinum.

Because meconium may enhance bacterial growth and meconium aspiration syndrome is difficult to distinguish from bacterial pneumonia, blood cultures should be drawn.

• Supplemental oxygen for hypoxemia or as a pulmonary vasodilator in infants with PPH

• Continuous positive airway pressure (CPAP), or endotracheal intubation and mechanical ventilation as needed

• Sometimes surfactant

• Sometimes IV antibiotics

• Inhaled nitric oxide in severe cases of PPHInhaled nitric oxide in severe cases of PPH

• Extracorporeal membrane oxygenation (ECMO) if unresponsive to above therapies

Routine deep suctioning (ie, intubating to suction below the vocal folds/cords) of neonates delivered with meconium-stained fluid has not been shown to improve outcome, and intubation for suctioning of a compromised neonate with meconium in the amniotic fluid is not recommended (1–3). However, if the neonate's breathing appears obstructed, suctioning is performed with an endotracheal tube attached to a meconium aspirator. Intubation or nasal CPAP is indicated for respiratory distress, followed by mechanical ventilation and admission to the neonatal intensive care unit. Because positive pressure ventilation enhances risk of a pulmonary air-leak syndrome, regular evaluation (including physical examination and chest radiograph) is important to detect this complication, which should be sought immediately in any intubated neonate whose blood pressure, perfusion, or oxygen saturation suddenly worsens. For treatment, see Pulmonary Air-Leak Syndromes.

Surfactant should be considered for mechanically ventilated neonates with high oxygen requirements; it can decrease the need for ECMO (4, 5) but does not decrease mortality.

Antibiotics (usually ampicillin and an aminoglycoside—such as that used for standard treatment of serious bacterial illness in an ill neonate) are sometimes given. However, studies have shown that use of antibiotics in infants with meconium aspiration does not significantly reduce mortality, incidence of sepsis, length of hospital stay, or duration of need for respiratory support (Antibiotics (usually ampicillin and an aminoglycoside—such as that used for standard treatment of serious bacterial illness in an ill neonate) are sometimes given. However, studies have shown that use of antibiotics in infants with meconium aspiration does not significantly reduce mortality, incidence of sepsis, length of hospital stay, or duration of need for respiratory support (5).

Inhaled nitric oxide up to 20 ppm and high-frequency ventilation (see Inhaled nitric oxide up to 20 ppm and high-frequency ventilation (seeMechanical ventilation) are other therapies that are used if refractory hypoxemia develops; they also may decrease need for ECMO.

Although mortality is approximately 1%, rates of complications such as asthma, developmental delay, and cerebral palsy are increased in survivors of meconium aspiration syndrome (1).

Meconium aspiration with severe persistent pulmonary hypertension can be fatal.