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Meconium aspiration syndrome and extracorporeal membrane oxygenation
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Introduction |
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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
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