MECONIUM ASPIRATION SYNDROME
Meconium represents the early passage of stool in the fetus. It is a material that accumulates in the intestines of a fetus and forms the first stools of an infant in the first few days after birth. Meconium is thick, sticky, odorless, and greenish to black in color (O’Toole, 2009). Water is the major component constituting 85% to 95% of meconium; the remaining 5% to 15% primarily includes secretions of the intestinal glands, amniotic fluid, and intrauterine debris, such as bile pigments, fatty acids, epithelial cells, mucus, lanugo, and blood. Meconium is sterile and free of bacteria, differentiating it from subsequent postnatal stools (Geis, 2017). Meconium is found in the intestinal tract as early as 12 weeks gestation (Meerkov & Weiner, 2016). Because meconium is seldom found in the amniotic fluid before the 34th week of gestation, aspiration into the airways before, during labor, and/or at the time of delivery generally affects term and post-term infants. Intrauterine distress may facilitate the passage of meconium into the amniotic fluid and increase the potential for meconium aspiration syndrome (MAS).
MAS is defined as respiratory distress in an infant, usually term, born through meconium-stained amniotic fluid (MSAF) with symptoms that cannot otherwise be attributed to other causes such as infection or retained lung fluid (Fanaroff, 2008). MSAF occurs in 8% to 10% of term deliveries and approximately 2% to 3% of meconium-stained infants will develop MAS, translating to an incidence of one to two per 1,000 live term births per year (Meerkov & Weiner, 2016). Infants, born depressed, through thick MSAF are more likely to develop MAS (Chettri, Adhisivam, & Bhat, 2015). There is a significant correlation in the incidence of MSAF with gestational age, increasing almost linearly from 37 to 42 weeks of gestation (Fischer, Rybakowski, Ferdynus, Sagot, & Gouyon, 2012). Thus, MAS continues to remain a major clinical concern for obstetricians and neonatologists. The presence of meconium in the amniotic fluid under normal circumstances is thought to be a result of increased peristalsis associated with maturation of fetal intestinal function. However, there is enhanced passage of meconium in utero under certain high-risk conditions. Although the mechanisms affecting meconium passage are not fully explained, animal studies have demonstrated increased parasympathetic activity, resulting in increased peristalsis and relaxation of the anal sphincter following episodes of cord compression and fetal hypoxia (Meerkov & Weiner, 2016).
Factors that increase the passage of meconium in utero, often as a consequence of interruption of placental blood flow, include placental insufficiency, maternal hypertension, preeclampsia, oligohydramnios, infection, acidosis, and 199maternal drug abuse, particularly tobacco and cocaine (Geis, 2017