Intrapartum meconium aspiration can cause inflammatory pneumonitis and mechanical bronchial obstruction, causing a syndrome of respiratory distress. Findings include tachypnea, rales and rhonchi, and cyanosis or desaturation. Diagnosis is suspected when there is respiratory distress after delivery through meconium-tinged amniotic fluid and is confirmed by chest x-ray. Treatment is vigorous suction immediately on delivery before neonates take their first breath, followed by respiratory support as needed. Prognosis depends on the underlying physiologic stressors.
Physiologic stress at the time of labor and delivery (eg, due to hypoxia 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 is noted in about 10 to 15% of births. During delivery, perhaps 5% of neonates with meconium passage aspirate the meconium, triggering lung injury and respiratory distress, termed meconium aspiration syndrome. Postterm infants delivered through reduced amniotic fluid volume are at risk of more severe disease because the less dilute meconium is more likely to cause airway obstruction.
The mechanisms by which aspiration induces the clinical syndrome probably include
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 (see Pulmonary Air-Leak Syndromes) with pneumomediastinum or pneumothorax. Persistent pulmonary hypertension can be associated with meconium aspiration as a comorbid condition or because of continuing hypoxia (see Persistent Pulmonary Hypertension of the Newborn).
Neonates also may aspirate vernix caseosa, amniotic fluid, or blood of maternal or fetal origin during delivery, which can cause respiratory distress and signs of aspiration pneumonia on chest x-ray.
Symptoms and Signs
Signs include tachypnea, nasal flaring, retractions, cyanosis or desaturation, rales, rhonchi, and greenish yellow staining of the umbilical cord, nail beds, or skin. 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 (see Pneumomediastinum).
Diagnosis is suspected when a neonate shows respiratory distress in the setting of meconium-tinged amniotic fluid. Diagnosis is confirmed by chest x-ray showing hyperinflation with variable areas of atelectasis and flattening of the diaphragm. Initial x-ray findings can be confused with the findings of transient tachypnea of the newborn (see see Transient Tachypnea of the Newborn). 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, cultures of blood and tracheal aspirate also should be taken.
Prognosis is generally good, although it varies with the underlying physiologic stressors; overall mortality is slightly increased. Infants with meconium aspiration syndrome may be at greater risk of asthma in later life.
Immediate treatment, indicated for all neonates delivered through meconium, is vigorous suctioning of the mouth and nasopharynx using a DeLee suction apparatus as soon as the head is delivered and before the neonate breathes and cries. If suction returns no meconium and the neonate appears vigorous, observation without further intervention is appropriate. If the neonate has labored or depressed respirations, poor muscle tone, or is bradycardic (< 100 beats/min), the trachea should be intubated with a 3.5- or 4.0-mm endotracheal tube. A meconium aspirator connected to a suction apparatus is attached directly to the endotracheal tube, which then serves as the suction catheter. Suction is maintained while the endotracheal tube is removed. Reintubation and continuous positive airway pressure are indicated for continued respiratory distress, followed by mechanical ventilation and admission to the neonatal ICU as needed. Because positive pressure ventilation enhances risk of pulmonary air-leak syndrome, regular evaluation (including physical examination and chest x-ray) is important to detect this complication, which should be sought immediately in any intubated neonate whose BP, perfusion, or O2 saturation suddenly worsens. See Pulmonary Air-Leak Syndromes for treatment of air-leak syndromes.
Additional treatments may include surfactant for mechanically ventilated neonates with high O2 requirements, which can decrease the need for extracorporeal membrane oxygenation, and antibiotics (usually ampicillin and an aminoglycoside). Inhaled nitric oxide in the range of 5 to 20 ppm and high-frequency ventilation are other therapies that are used if refractory hypoxemia develops; they also may decrease need for extracorporeal membrane oxygenation.
Last full review/revision March 2009 by Anand D. Kantak, MD; John T. McBride, MD
Content last modified February 2012