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. 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 with MSAF. It is believed that foetal distress develops into foetal hypoxia causing the foetus to defecate meconium resulting in MSAF and then perhaps MAS. Other stressors which causes foetal distress, and therefore meconium 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 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.The association between foetal distress and meconium passage is not a definite cause-effect relationship as over 3⁄4 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 meconium as well. 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.Peristalsis of the foetal intestines is present as early as 8 weeks gestation and the anal sphincter develops at about 20–22 weeks.
The diagnosis is made upon the history of absence seizures during early childhood without other seizure types and the observation of 3 Hz generalized spike waves paroxysmal discharges on the EEG. In children with CAE without atypical features electroclinical features, no neuroimaging is needed. Management
There are three antiepileptic drugs that have been used for the first-line treatment for CAE; these are ethosuximide (ETX), valproic acid (VPA), and lamotrigine (LTG). ETX is an effective first-line treatment for seizures only by blocking the low-threshold calcium currents produced by T-type calcium channels in the thalamus. The peak level occurs after 3–5 hours of intake; steady levels of the drug in the blood are achieved after 7–10 days of the same daily dose. The usual dosage is 20–30 mg/kg/day divided into two doses. Common side effects include gastrointestinal disturbances such as hiccups, vomiting, abdominal discomfort, and diarrheic and exceptionally. The other symptoms, like fatigue, insomnia, dizziness and ataxia. Valproate (VPA) has also been proven effective monotherapy in CAE although ETX is usually preferred as it has a lower impact on attention according to the Childhood Epilepsy study. There are several mechanisms related to VPA’s antiepileptic action, including raising the level of gamma-aminobutyric acid (GABA), calcium-dependent potassium activating, and blocking of voltage-sensitive sodium channels, but there is no specific evidence for the mechanism by which VPA controls absence seizures.