Leading article 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, 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 still at the perineum. However, absence of meconium from the oropharynx does not necessarily preclude aspiration distal to the vocal cords, and routine intubation with endotracheal toilet does not always prevent the subsequent development of MAS. Therefore despite the best eVorts of those resuscitating a meconium aVected neonate, a number of these babies go on to develop MAS, with acute respiratory failure requiring positive pressure ventilation. MAS carries with it not only significant mortality— estimated in one study to be as high as 1 in 12 cases requiring mechanical ventilation—but also major morbidity. Chronic lung disease can result from both the pulmonary eVects of meconium itself and the ventilator induced lung injury, which is often regarded as an “inevitable consequence” of the levels of mechanical ventilation that these neonates receive. Furthermore, the extrapulmonary eVects of prolonged severe hypoxia, in particular on the brain, and the significant incidence of neurological injury should not be underestimated in this vulnerable group of infants. Various ventilator strategies have been suggested for neonates with MAS, particularly to control pulmonary hypertension and provide protection from pneumothorax. Inhaled nitric oxide, a selective pulmonary vasodilator, is typically administered to these infants when available, although previous studies have suggested that it may be less eVective in the subgroup with MAS. This may in part be due to the physical “barrier” to its diVusion across the alveolar membrane which is produced by the presence of meconium in the distal airways. Thus, despite these measures, a small subgroup of patients with MAS go on to develop intractable pulmonary hypertension with profound hypoxia, co-existent with a variable degree of parenchymal lung injury. In these infants, the evidence would suggest that extracorporeal membrane oxygenation (ECMO) is the most eVective mode of treatment. The natural history of pulmonary hypertension is, in most cases, spontaneous recovery with time. The institution of ECMO therefore provides global tissue oxygenation while allowing pulmonary vasculature and lung parenchyma time to recover from the antecedent insults.