Meconium aspiration syndrome (MAS) is defined as respiratory distress in a newborn infant born through meconium-stained fluid whose symptoms cannot otherwise be explained. MAS occurs in approximately 2-10% of infants born through meconium-stained fluid. The incidence as a function of gestational age takes on a U-shaped curve, with a nadir at 31 weeks and greater incidence before and after that time. Other risk factors include being black, South Asian, post-mature, and small-for-gestational-age.
Meconium is a thick, black-green substance consisting of desquamated intestinal and skin cells, gastrointestinal mucin, lanugo hair, fatty material from the vernix caseosa, amniotic fluid, and intestinal secretions. It is first passed into amniotic fluid during the first trimester, but its release into amniotic fluid normally decreases after 16 weeks gestation. Increased vagal tone from umbilical cord compression or increased sympathetic tone from hypoxia can stimulate peristalsis and relaxation of anal sphincter tone, increasing the amount in amniotic fluid. If it reaches the hypopharynx, especially in a hypoxic neonate, meconium can be aspirated into the trachea and lung with subsequent gasping after birth, leading to MAS.
The pathophysiology of MAS is multifactorial. Aspirated meconium can cause:
(1) Airway Obstruction: either complete or partial. Complete obstruction produces atalectasis. Partial obstruction can cause air trapping as gas enters dilated airways stretched open during inspiration but is unable to leave smaller airways that are collapsed during expiration. This ball-valve phenomenon leads to alveolar overdistension, a barrel-shaped chest, and air leak phenomenon (pneumothorax, pneumomediastinum, pneumopericardium, pulmonary interstitial emphysema).
(2) Chemical Inflammation: direct injury and inflammation occurring after 1-2 days following aspiration can cause an exudative and inflammatory pneumonitis characterized by release of cytokines, epithelial disruption, proteinaceous exudation, alveolar collapse, loss of surfactant, and cellular necrosis.
(3) Infection: even though meconium itself is sterile, it reduces the antibacterial activity of amniotic fluid. In addition, the mucopolysaccharide component of meconium is a growth medium for subsequent nosocomial infection.
(4) Hypoxia and Persistent Pulmonary Hypertension: hypoxia resulting from alveolar hypoventilation, lung injury, and V/Q mismatching increase pulmonary vascular resistance, leading to persistent pulmonary hypertension of the newborn.
According to the most recent guidelines for Neonatal Advanced Life Support (Circulation 2010;112:S516-38), even though depressed infants born through meconium stained amniotic fluid are at increased risk for MAC, tracheal suctioning has not been associated with a reduction in MAC or associated mortality. Nevertheless, in resuscitating a depressed neonate, I still choose to perform endotracheal suctioning because it may, theoretically, make ventilation easier. Endotracheal suctioning of meconium is not necessary for a vigorous neonate.
The mortality of MAC is as low as 1.2%, however, with severe parenchymal involvement and pulmonary hypertension, the mortality is a high as 20%. With severe involvement, the chance of developing reactive airway disease in the first 6 months of life is as high as 50%.