الفهرس 
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Abstract
Labour is a stressful event for the fetus but it is well tolerated by most fetuses. However, in some infants stress of labour can lead to Hypoxic Ischemic Encephalopathy (HIE) due to metabolic acidosis. HIE remains a major cause of neonatal mortality and morbidity with lifelong chronic disabilities. Such insults are not limited to high risk pregnancies but can also occur in about 50% of low risk pregnancies (Westermaier et al., 2017).
Neonatal Hypoxic Ischemic Encephalopathy is an acute encephalopathy caused by intrapartum or late antepartum brain hypoxia and ischemia and is characterized by clinical and laboratory evidence of acute or subacute brain injury. Persistent hypoxia implies asphyxia, usually associated with hypercarbia and causing metabolic acidosis. The clinical signs of HIE include low Apgar scores, low cord pH, neonatal seizures, and encephalopathy (Amr et al., 2017).
Ischemia (insufficient blood to supply needs) of the non essential organs occurs in early hypoxia; with prolongation, the essential organs ex: (brain, heart and adrenal glands) also become ischemic. Perinatal asphyxia is a condition characterized by an impairment of exchange of the respiratory gases (oxygen and carbon dioxide) resulting in hypoxemia and hypercapnia, accompanied by metabolic acidosis result in a deprivation of oxygen and glucose in the neural tissue (Amr et al., 2017).
The fetus depends on the mother for placental exchange of oxygen and carbon dioxide. This in turn relies on adequate maternal blood gas concentrations, uterine blood supply, placental transfer and fetal gas transport. Disruption of any of these can cause fetal hypoxia. The causes of acute fetal hypoxia and subsequent acidosis include reduced utero-placental blood flow, placental abruption or fetal cord compression. The consequences of acidosis depend on its severity and duration and also the condition of the fetus before the insult (Amr et al., 2017).
An intrapartum monitoring tool with high accuracy is required to ensure fetal wellbeing and diagnosis fetal hypoxia and metabolic acidosis. Labour admission test is a test of fetal well being that is performed when a woman with a low-risk pregnancy is admitted in labour. Its aim is to assess fetal well being and identify fetuses that may be already hypoxic or may not withstand the stress of uterine contractions. Labour admission test refers to an electronic fetal heart rate (FHR) monitoring tracing performed for 20 to 30 minutes upon admission to the labour and delivery unit (Blix et al., 2016).
Intrapartum CTG patterns such as prolonged bradycardia complicated by variable or late decelerations for a period > 30 minutes and loss of beat to beat variability > 90 minutes, recurrent late deceleration, recurrent variable decelerations and sinusoidal pattern, inspite of doing conservative management, warrant immediate delivery without fetal blood sampling. Apgar score of less than 5 at 5 minutes and 10 minutes increases relative risk of cerebral palsy (Li et al., 2013).
The Apgar score is affected by many factors, including maternal medications, gestational age, congenital malformations, cardiorespiratory and neurologic conditions and resuscitation. If the Apgar score at 5 min is 7 or more, it is unlikely that peripartum hypoxia–ischemia caused neonatal encephalopathy (ACOG, 2015).
Asphyxia leads to two phases of cerebral insults: the primary neuronal injury (energetic failure) that occurs at the time of the hypoxic–ischemic insult, where the oxidative energy metabolism of cells decreases, and the secondary neuronal injury that occurs over hours to even days following the accumulation of excessive intra-neuronal calcium as a result of excitatory amino acid stimulation of the N-methyl–D-aspartate (NMDA) cell receptors (Gathwala et al., 2010).
There has been considerable interest in Magnesium Sulfate (MgSO4) because Magnesium alleviates excitotoxic damage by binding to the Magnesium site on the NMDA glutamate channel. There is evidence that it may also reduce secondary inflammation. Stabilized cell membranes inhibit free radical production and improve cardiovascular stability (Sugimoto et al., 2012).