Background: Despite the common occurrence of intrauterine meconium passage and resultant meconium aspiration syndrome (MAS), controversies regarding the pathophysiology and use of appropriate preventive strategies abound.
Methods: Databases from MEDLINE, MD Consult, and the Science Citation Index were searched from 1964 to the present to find relevant sources of information.
Results and Conclusions: Meconium passage occurs by three distinct mechanisms: (1) as a physiologic maturational event, (2) as a response to acute hypoxic events, and (3) as a response to chronic intrauterine hypoxia. Meconium passage might merely be a marker of chronic intrauterine hypoxia or can predispose to aspiration of meconium and resultant inflammatory pneumonitis, surfactant inactivation, and mechanical airway obstruction. Aspiration can occur in utero with fetal gasping, or after birth with the first breaths of life. Many cases of MAS can be prevented by the strategies addressed in this article, but some will occur despite appropriate preventive techniques. There is not enough evidence to support the use of amnioinfusion as a standard of care for all pregnancies complicated by meconium. Pharyngeal suctioning before delivery of the shoulders is an effective preventive intervention, as is the combination of pharyngeal suctioning followed by intubation and tracheal suctioning. Suctioning of the trachea may be done on a selective basis depending on fetal vigor and consistency of meconium.
Meconium is the green viscous fluid that consists of fetal gastrointestinal secretions, cellular debris, mucus, blood, lanugo, and vernix. It first appears in the fetal ilium between 10 and 16 weeks' gestation. Passage of meconium in utero with staining of the amniotic fluid occurs in 12% to 16% of all deliveries and often is not associated with fetal distress or neonatal death or disability. Meconium passage is rare before 34 weeks of gestational age. Meconium passage occurs in up to 20% of full-term gestations and can occur in more than 35% of pregnancies continuing beyond 42 weeks' gestation. Meconium passage most commonly occurs in small-for-gestational-age and postmature infants. It occurs in association with cord complications and other factors, such as chronic medical conditions or conditions associated with intrauterine growth retardation, which can compromise the uteroplacental circulation Meconium aspiration is defined as the presence of meconium below the vocal cords. This finding occurs in 20% to 30% of all infants with meconium-stained amniotic fluid. Meconium aspiration syndrome (MAS) classically has been defined as respiratory distress that develops shortly after birth, with radiographic evidence of aspiration pneumonitis and a history of meconium-stained fluid. More recently, because of the wide array of possible radiographic findings, MAS had been defined simply as respiratory distress in an infant born through meconium-stained amniotic fluid whose symptoms cannot otherwise be explained. MAS occurs in about 5% of deliveries with meconium-stained amniotic fluid and is one of the most common causes of neonatal respiratory distress. Infants born through meconium-stained amniotic fluid are about 100 times more likely to develop respiratory distress than those born through clear fluid. Even in women at very low risk for obstetric complications, meconium-stained amniotic fluid is common and is associated with a fivefold increase in perinatal mortality compared with low-risk patients with clear amniotic fluid. Death occurs in about 12% of infants with MAS, and MAS is associated with about 5% of all of perinatal deaths. MAS is also associated with neonatal seizures and chronic seizure disorders. Some generally accepted concepts regarding the pathophysiology of meconium passage and the management of meconium aspiration have been challenged in recent years. One such concept is the belief that there is a strong independent association between meconium passage and fetal distress. A recent controversial review by Katz and Bowes, however, concluded that there exists no independent association between meconium passage and fetal distress. Though this study has been criticized, it has focused attention upon meconium passage being related in large part to maturational events only and not to intrauterine stress or hypoxia. We will address such controversies in this article, discuss a rational approach to the pregnancy complicated by meconium-stained amniotic fluid, and address the following questions:
What is the relative importance of each of the various causes of intrauterine meconium passage?
What are the pathophysiologic mechanisms of meconium aspiration and the development of MAS?
What morbidity and mortality are caused directly by aspirated meconium, and to what degree is meconium merely a marker of prolonged intrauterine gestation or the result of chronic hypoxia?
What is the clinical relevance of the consistency (thickness) of meconium?
What measures are effective in the prevention of MAS? In particular, what is the efficacy of amnioinfusion, pharyngeal suction before delivery of the shoulders, endotracheal intubation and suction, and other preventive measures?