Meconium aspiration syndrome and extracorporeal membrane oxygenation

Meconium aspiration syndrome (MAS) is a common cause of lung disease in neonates. Meconium staining of amniotic fluid occurs in around 10% of all deliveries at term. Asphyxia before birth stimulates intestinal peristalsis and relaxation of the anal sphincter, and in more severe cases, gasping in utero, leading to meconium aspiration. Respiration after birth draws meconium firstly into the major airways and subsequently into the smaller airways, where it may cause obstruction, atelectasis, air trapping, and pneumothorax. Meconium can also cause a chemical pneumonitis and inactivation of surfactant, further impairing gas exchange and potentiating barotrauma. Infants with severe MAS rapidly develop pulmonary hypertension with right to left shunting through a patent foramen ovale and at the level of the arterial duct; this shunting further potentiates hypoxia. Severe MAS occurs in around 1 in 500 births,1 and is characterised by profound hypoxaemia, where the coexistence of parenchymal lung damage and severe pulmonary hypertension can result in a vicious cycle of clinical decline, which is often simply exacerbated by the necessary escalation of “conventional” treatment.

As the field of perinatology has advanced, much attention has been focused on the prevention of MAS, with emphasis on timely delivery and skilled neonatal resuscitation. In infants born with meconium staining of the liquor, the oropharynx should be suctioned before they take their first breath, preferably while …