Three theories regarding fetal passage of meconium may explain, in part, the tenuous connection between its detection and neonatal mortality. First, fetuses may pass meconium in response to hypoxia, and meconium therefore signals fetal compromise (Walker, 1953). Second, in utero passage of meconium may represent normal gastrointestinal tract maturation under neural control (Mathews, 1979). A inal theory posits that meconium passage follows vagal stimulation from common but transient umbilical cord entrapment with resultant increased bowel peristalsis (Hon, 1961).
Ramin and associates (1996) studied almost 8000 pregnancies with meconium-stained amnionic fluid delivered at Parkland Hospital. Meconium aspiration syndrome was signiicantly associated with fetal acidemia at birth. Other signiicant correlates of aspiration included cesarean delivery, forceps to expedite delivery, intrapartum heart rate abnormalities, depressed Apgar scores, and need for assisted ventilation at delivery. Analysis of the type of fetal acidemia based on umbilical blood gases suggested that the fetal compromise associated with meconium aspiration syndrome was an acute event. his is because most acidemic fetuses had abnormally increased PC02 values rather than a pure metabolic acidemia.
Dawes and coworkers (1972) observed that such hypercarbia in fetal lambs induces gasping and resultant increased amnionic fluid inhalation. Jovanovic and Nguyen (1989) observed that meconium gasped into the fetal lungs caused aspiration syndrome only in asphyxiated animals.
Ramin and colleagues (1996) hypothesized that the pathophysiology of meconium aspiration syndrome includes, but is not limited to, fetal hypercarbia, which stimulates fetal respiration leading to aspiration of meconium into the alveoli. Lung parenchymal injury is secondary to acidemia-induced alveolar cell damage. In this pathophysiological scenario, meconium in amnionic fluid is a fetal environmental hazard rather than a marker of preexistent compromise. This proposed pathophysiological sequence is not all-inclusive, because it does not account for approximately half of the cases of meconium aspiration syndrome in which the fetus is not acidemic at birth.
Thus, it was concluded that the high incidence of meconium observed in the amnionic fluid during labor often represents fetal passage of gastrointestinal contents in conjunction with normal physiological processes. lthough normal, such meconium becomes an environmental hazard when fetal acidemia supervenes. Importantly, such acidemia occurs acutely, and therefore meconium aspiration is unpredictable and likely unpreventable. Moreover, Greenwood and colleagues (2003) showed that clear amnionic fluid was also a poor predictor. In a prospective study of 8394 women with clear amnionic fluid, they found that clear fluid was an unreliable sign of fetal wellbeing.
Growing evidence indicates that many newborns with meconium aspiration syndrome have suffered chronic hypoxia before birth (Ghidini, 2001). Blackwell and associates (2001) found that 60 percent of neonates diagnosed with meconium aspiration syndrome had umbilical artery blood pH ::7.20, implying that the syndrome was unrelated to the neonatal condition at delivery. Similarly, markers of chronic hypoxia, such as elevated fetal erythropoietin levels and increased nucleated red blood cell counts in newborns, suggest that chronic hypoxia is involved in many meconium aspiration syndrome cases (Dollberg, 2001; Jazayeri, 2000).