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-containing amniotic fluid and is confirmed by chest x-ray. Infants with respiratory distress are often intubated and placed on mechanical ventilation. Treatment of severely affected infants with surfactant decreases the need for extracorporeal membrane oxygenation but does not affect mortality (1, 2). Prognosis depends on the underlying physiologic stressors.
(See also Overview of Perinatal Respiratory Disorders.)
Extensive physiologic changes accompany the birth process, sometimes unmasking conditions that posed no problem during intrauterine life. For that reason, a person with neonatal resuscitation skills must attend each birth. Gestational age and growth parameters help identify the risk of neonatal pathology.
Etiology of 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 also may be normal before birth, particularly in term or postterm infants; meconium passage is noted in about 10 to 15% of births. However, it is never normal for meconium to be noted at the delivery of a preterm infant. During delivery, perhaps 5% of neonates with meconium passage aspirate the meconium, triggering lung injury and respiratory distress, termed meconium aspiration syndrome. Although the pneumonitis caused by the meconium contributes to respiratory compromise in these infants after delivery, the persistent pulmonary hypertension (PPH) caused by the prenatal and postnatal acidosis and/or hypoxia is equally or even more compromising.
Pathophysiology of 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. PPH can be associated with meconium aspiration as a comorbid condition or because of continuing hypoxia.
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 x-ray.
Symptoms and Signs of Meconium Aspiration Syndrome
Signs of meconium aspiration syndrome include tachypnea, nasal flaring, retractions, cyanosis or desaturation, rales, and rhonchi.
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.
Diagnosis of Meconium Aspiration Syndrome
Meconium passage
Respiratory distress
Characteristic x-ray 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 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 (TTN); however, what often separates infants with meconium aspiration syndrome from those with TTN is the significant hypoxemia present with the 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, cultures of blood also should be taken.
Treatment of Meconium Aspiration Syndrome
Endotracheal intubation and mechanical ventilation as needed
Supplemental oxygen as needed to keep PaO2 high to relax pulmonary vasculature in cases with PPH
Surfactant
IV antibiotics
Inhaled 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 cords) of neonates delivered with meconium-stained fluid has not been shown to improve outcome, and intubation for suctioning of a compromised newborn with meconium in the amniotic fluid is no longer recommended. However, if the neonate's breathing appears obstructed, suctioning is done with an endotracheal tube attached to a meconium aspirator. Intubation or nasal continuous positive airway pressure (CPAP) are indicated for respiratory distress, followed by mechanical ventilation and admission to the neonatal intensive care unit as needed. Because positive pressure ventilation enhances risk of a 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 blood pressure, perfusion, or oxygen saturation suddenly worsens. See Pulmonary Air-Leak Syndromes for treatment.
Surfactant should be considered for mechanically ventilated neonates with high oxygen requirements; it can decrease the need for ECMO (1, 2) but does not decrease mortality.
2).
Inhaled nitric oxide up to 20 ppm and high-frequency ventilation (see Mechanical ventilation) are other therapies that are used if refractory hypoxemia develops; they also may decrease need for ECMO.
Treatment references
1. El Shahed AI, Dargaville PA, Ohlsson A, Soll R: Surfactant for meconium aspiration syndrome in term and late preterm infants. Cochrane Database Syst Rev 12(CD002054):1–36, 2014. doi: 10.1002/14651858.CD002054.pub3
2. Natarajan CK, Sankar MJ, Jain K, et al: Surfactant therapy and antibiotics in neonates with meconium aspiration syndrome: A systematic review and meta-analysis. J Perinatol 36(Suppl 1):S49–S54, 2016. doi: 10.1038/jp.2016.32
Prognosis for Meconium Aspiration Syndrome
Prognosis is generally good, although it varies with the underlying physiologic stressors; overall mortality is increased.
Infants with meconium aspiration syndrome may be at greater risk of asthma in later life.
Key Points
About 5% of neonates with meconium passage aspirate the meconium, triggering lung injury and respiratory distress or have prenatal and postnatal physiology that predisposes them to persistent pulmonary hypertension, which can complicate meconium aspiration syndrome.
Neonates may have tachypnea, nasal flaring, retractions, cyanosis or desaturation, rales, rhonchi, and visible meconium staining in the oropharynx.
Suspect the diagnosis when respiratory distress occurs in neonates who had meconium-containing amniotic fluid.
Do chest x-ray and cultures of blood to exclude pneumonia and bacterial sepsis.
After delivery, if infants have signs of obstructed breathing, suction them using an endotracheal tube attached to a meconium aspirator.
Severe cases require mechanical ventilation and sometimes antibiotics, inhaled nitric oxide, or extracorporeal membrane oxygenation (ECMO).
