The main theories of<unk>  passage into amniotic fluid are caused by fetal maturity or from foetal stress as a result of hypoxia or infection. Other factors that promote the passage of<unk>  in utero include placental insufficiency, maternal hypertension, pre-eclampsia and maternal drug use of tobacco and cocaine. However, the exact mechanism for<unk>  passage into the amniotic fluid is not completely understood and it may be a combination of several factors.<unk>  passage as a result of foetal distress There may be an important association between foetal distress and hypoxia with MSAF. It is believed that foetal distress develops into foetal hypoxia causing the foetus to defecate<unk>  resulting in MSAF and then perhaps<unk> . Other stressors which causes foetal distress, and therefore<unk>  passage, includes when umbilical vein oxygen saturation is below 30%. Foetal hypoxic stress during parturition can stimulate colonic activity, by enhancing intestinal peristalsis and relaxing the anal sphincter, which results in the passage of<unk> . Then, because of intrauterine gasping or from the first few breaths after delivery,<unk>  may develop. Furthermore,<unk>  of thick<unk>  leads to obstruction of airways resulting in a more severe hypoxia. It is important to note that the association between foetal distress and<unk>  passage is not a definite cause-effect relationship as over ¾ of infants with MSAF are vigorous at birth and do not have any distress or hypoxia. Additionally, foetal distress occurs frequently without the passage of<unk>  as well.<unk>  passage as a result of foetal maturity Although<unk>  is present in the gastrointestinal tract early in development, MSAF rarely occurs before 34 weeks gestation. 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. 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<unk>  in post-term pregnancies may reflect the maturation and development of the peristalsis within the gastrointestinal tract in the newborn.
Meconium aspiration syndrome
Infantile apnea
Tracheoesophageal fistula
Tracheomalacia
Laryngotracheal stenosis
Upper airway resistance syndrome
Transient tachypnea of the newborn
Laryngomalacia