Editing Meconium aspiration syndrome (section)

==Causes==
The main theories of meconium passage into amniotic fluid are caused by fetal maturity or from foetal stress as a result of [[hypoxia (medical)|hypoxia]] or infection.<ref name=":2" /> Other factors that promote the passage of meconium ''in utero'' include placental insufficiency, maternal hypertension, [[pre-eclampsia]] and maternal drug use of [[tobacco]] and [[cocaine]].<ref name=":5" /> However, the exact mechanism for meconium passage into the amniotic fluid is not completely understood and it may be a combination of several factors.

=== Meconium passage as a result of foetal distress ===
There may be an important association between foetal distress and [[hypoxia (medical)|hypoxia]] with MSAF.<ref name=":1" /> It is believed that foetal distress develops into foetal hypoxia causing the foetus to defecate meconium resulting in MSAF and then perhaps MAS.<ref name=":5" /> Other stressors which causes foetal distress, and therefore meconium passage, includes when umbilical vein oxygen saturation is below 30%.<ref name=":2" />

Foetal hypoxic stress during parturition can stimulate colonic activity, by enhancing intestinal [[peristalsis]] and relaxing the anal sphincter, which results in the passage of meconium. Then, because of intrauterine gasping or from the first few breaths after delivery, MAS may develop. Furthermore, aspiration of thick meconium leads to obstruction of airways resulting in a more severe [[hypoxia (medical)|hypoxia]].<ref name=":5" /><ref name=":6">{{Cite journal|last=Fanaroff|first=AA|date=2008|title=Meconium Aspiration Syndrome: Historical Aspects|journal=Journal of Perinatology|volume=28|pages=S3–S7|doi=10.1038/jp.2008.162|pmid=19057607 |doi-access=free}}</ref>

The association between foetal distress and meconium passage is not a definite cause-effect relationship as over {{frac|3|4}} of infants with MSAF are vigorous at birth and do not have any distress or hypoxia.<ref name=":1" /> Additionally, foetal distress occurs frequently without the passage of meconium as well.<ref name=":2" />

=== Meconium passage as a result of foetal maturity ===
Although meconium is present in the [[gastrointestinal tract]] early in development, MSAF rarely occurs before 34 weeks [[gestation]].<ref name=":2" />

[[Peristalsis]] of the foetal intestines is present as early as 8 weeks gestation and the anal sphincter develops at about 20–22 weeks. The early control mechanisms of the anal sphincter are not well understood, however there is evidence that the foetus does defecate routinely into the [[amniotic cavity]] even in the absence of distress. The presence of fetal intestinal enzymes have been found in the amniotic fluid of women who are as early as 14–22 weeks pregnant. Thus, suggesting there is free passage of the intestinal contents into the amniotic fluid.<ref>{{Cite journal|last1=Poggi|first1=SH|last2=Ghidini|first2=A|date=2009|title=Pathophysiology of Meconium Passage into the Amniotic Fluid|journal=Early Human Development|volume=85|issue=10 |pages=607–610|doi=10.1016/j.earlhumdev.2009.09.011|pmid=19836908 }}</ref>

[[Motilin]] is found in higher concentrations in post-term than pre-term foetal gastrointestinal tracts. Similarly, intestinal parasympathetic innervation and [[myelination]] also increases in later gestations. Therefore, the increased incidence of MAS in post-term pregnancies may reflect the maturation and development of the peristalsis within the gastrointestinal tract in the newborn.<ref name=":2" />