Perinatal asphyxia refers to a condition during the first and second stage of labour in which impaired gas exchange leads to fetal hypoxemia and hypercarbia. Asphyxia has been shown to be the third most common cause of neonatal death (11%) after preterm birth (24%) and severe infections (12%). Perinatal asphyxia is an end result of significant degree of global hypoxic ischemia during the time of birth. Lack of oxygen delivery from this episode often leads to multiorgan failure. A variety of markers have been examined to identify perinatal hypoxia but studies for early determination of tissue damages due to birth asphyxia are still lacking. Magnesium, the second most common intracellular cation, may play a role in neuroprotection for neonate with perinatal asphyxia. The initial event resulting in fetal hypoxia leading to decreased cardiac output and subsequent decreased cerebral blood flow sets off a cascade of events resulting in brain injury. This observational cross‐sectional study was undertaken in Department of Pediatrics in GMSH‐16 in Chandigarh from January, 2021 to June, 2021. The term babies (37‐41 weeks of gestation) were included in the study. Newborn with congenital anomaly, diabetic mother, small for date babies (IUGR) and mother receiving magnesium therapy during labour were excluded from the study. Sample size was justified with 46 cases. Analysis of data were conducted using IBM SPSS statistical software (version 22.0). With due consideration of all inclusion and exclusion criteria total 46 cases were included in the study. Out of 46 newborns, mild to moderated asphyxia and severe asphyxia were presenting 32 (69.6%) and 14 (30.4%) cases respectively and HIE I were 20 (43.5%), HIE II were 16 (34.8%) and HIE III were 10 (21.7%). The mean serum magnesium level in neonate with mild to moderate asphyxia was 2.1±0.3 and in neonate with severe asphyxia was 1.5±0.5 respectively (independent, t‐test, p = 0.001). Serum magnesium was significantly low in severe birth asphyxia as compare to mild to moderate birth asphyxia (p = 0.001). There was a significant difference in serum magnesium between the HIE stages (ANOVA, p = 0.001). Serum magnesium level was significantly low in HIE stage 3. On post‐hoc test, the difference in serum magnesium between HIE 1 and HIE 2 was not statistically significant (p = 0.398), The difference in serum magnesium between HIE 1 and 3 and HIE 2 and HIE 3 was however statistically significant (p = 0.003 and p = 0.009, respectively). Hypomagnesaemia was found in 3 (15%) neonates in HIE stage I, 3 (18.8%) neonates in HIE stage II, 8 (80%) neonates in HIE stage III. Hypomagnesaemia was significant in all stages of HIE (ANOVA, p = 0.001). Hypomagnesemia was significantly more in HIE stage III as compared to HIE stage I and II (Chi‐square test, p = 0.001). There was a significant correlation between serum magnesium and Apgar score at 1 minute (Pearson’s correlation coefficient, r = 0.518, p = 0.001). The correlation between serum magnesium and Apgar score at 5 minutes was also statistically significant (Pearson’s correlation coefficient, r = 0.379, p = 0.009). Neonates with severe asphyxia and Hypoxic ischemic encephalopathy (HIE) grade III have significant hypomagnesemia. Asphyxia can lead to hypomagnesemia and it is recommended to evaluate levels of magnesium in neonates with asphyxia as a routine test.
Brijesh Kumar Patel, Mohit Sharma, Amit Kumar Singh and Shreya Shrivastava. Correlation of Serum Magnesium with Severity of Asphyxia.
DOI: https://doi.org/10.36478/10.59218/makrjms.2023.512.520
URL: https://www.makhillpublications.co/view-article/1815-9346/10.59218/makrjms.2023.512.520