Journal of Medical Sciences

: 2021  |  Volume : 41  |  Issue : 1  |  Page : 17--21

Electrolyte status and plasma glucose levels in birth asphyxia: A case–control study

Kaustubh Bahatkar, CD Aundhakar 
 Department of Paediatrics, Krishna Institute of Medical Sciences (Deemed to be University), Karad, Maharashtra, India

Correspondence Address:
Dr. C D Aundhakar
Department of Paediatrics, Krishna Institute of Medical Sciences (Deemed to be University), Karad, Maharashtra


Background: Birth asphyxia is characterized by hypoxia, hypercarbia, and acidosis during perinatal period and tends to cause hypoxic-ischemic tissue damage and electrolyte imbalance which may lead to perinatal morbidity and mortality. The aim of this study was to assess the electrolyte status and plasma glucose levels in asphyxiated neonates and determine the correlation with different stages of birth asphyxia. Methods: A total of 100 neonates were allocated into two groups (cases and controls; 50 neonates in each) based on the severity of fetal distress by assessing the Apgar score, fetal heart rates, and meconium-stained liquor after baby delivery. The serum levels of sodium, potassium, calcium, and glucose in cord blood were estimated and compared in both the groups by independent t-test and Mann–Whitney U test using R software version 3.6.0. The estimated electrolyte levels were correlated with different stages of asphyxia using Spearman correlation. Results: Among 100 neonates, meconium-stained liquor was observed in 10% of cases and 4% of controls. A statistically significant difference was found between the groups with respect to serum sodium, calcium, and glucose levels (P < 0.05) in contrast to potassium levels (P = 0.162). A significant negative linear correlation was found between serum sodium, calcium, and glucose levels and different stages of hypoxic-ischemic encephalopathy (−0.591r, −0.484r, and −0.221r, respectively). Conclusions: Hyponatremia, hypocalcemia, and hypoglycemia were observed in asphyxiated neonates and were proportionate to the severity level of asphyxia. Hence, immediate cord blood sampling for serum electrolytes and glucose evaluation at high-risk neonates would be the best measure for early diagnosis and severity assessment of perinatal asphyxia.

How to cite this article:
Bahatkar K, Aundhakar C D. Electrolyte status and plasma glucose levels in birth asphyxia: A case–control study.J Med Sci 2021;41:17-21

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Bahatkar K, Aundhakar C D. Electrolyte status and plasma glucose levels in birth asphyxia: A case–control study. J Med Sci [serial online] 2021 [cited 2021 Mar 1 ];41:17-21
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Birth asphyxia (also known as perinatal asphyxia) is the global health concern and the most common cause of early neonatal mortality. According to the World Health Organization, perinatal asphyxia is the “failure to initiate and sustain breathing at birth.” Globally, four to nine million neonates are diagnosed with birth asphyxia each year. In India, the incidence of perinatal asphyxia is 5% and constitutes for 24.3% of neonatal deaths.[1] The factors, such as time taken to first breath, heart rate at 90 s, duration of resuscitation, and Apgar score at 5 min of life, define the outcome of birth asphyxia.[2] The early outcome of birth asphyxia is either neonatal death or presence of hypoxic-ischemic encephalopathy (HIE). The degree of HIE reflects the severity of birth asphyxia and its HIE staging (by Sarnat and Sarnat) aids in the severity assessment of asphyxia.[3]

At cellular level, adequate oxygen supply is prerequisite for metabolism. Transient hypoxia may impair cerebral oxidative metabolism, resulting in acid-base disturbances, especially metabolic acidosis[4],[5],[6] and anaerobic glycolysis. Prolonged hypoxia leads to decreased cardiac output, compromised cerebral blood flow, and a combined hypoxic-ischemic insult. Most of these insults happened during the periods of antepartum and intrapartum in term babies. In asphyxiated neonates, dilutional hyponatremia may occur due to hypersecretion of antidiuretic hormone which may lead to increased water retention.[7] The other possible hypothesis for hyponatremia in neonates with HIE is that the limited capacity of sodium reabsorption (if the concentration of sodium reaching the renal collecting tubules increases, reabsorption does not occur proportionately)[8] and partial resistance to aldosterone.[9] The shift of potassium from the intracellular to extracellular space in early neonatal period may lead to hyperkalemia and depends on the degree of immaturity; more premature babies are more likely to have hyperkalemia. Acute renal failure secondary to asphyxia may lead to hyperkalemia by decreasing the excretion of potassium.[10]

Normally, gestational age is directly proportional to cord plasma total calcium concentration.[11] At the time of delivery, abrupt termination of calcium transport across the placenta decreases the plasma calcium levels, which in turn leads to increased secretion of serum parathyroid hormone (PTH). In birth asphyxia, PTH secretion is slowed down in response to postnatal fall in plasma calcium levels and hence hypocalcemia.[12] Abnormally low glucose levels may cause encephalopathy which in turn leads to long-term neurological illness. In birth asphyxia, there is a severe glycogen depletion secondary to catecholamine release and idiopathic hyperinsulinemia and hence hypoglycemia.[13] The extent of brain damage is profound with hypoxia and hypoglycemia, and the early diagnosis is still a challenging issue in neonatal care. Further, the severity of birth asphyxia defines the degree of electrolyte imbalance.[14]

Although there are several studies reporting the underlying physiological association between electrolyte imbalance and hypoxic tissue damage, but majority of the studies determined electrolyte levels at 24 h of life or later.[13] Very few studies have considered cord blood sampling (immediately after birth) for the analysis of electrolytes and glucose.[15] Case–control studies to develop the correlation of electrolyte disturbances and glucose levels with severity of birth asphyxia are still lacking. In this regard, this case–control study was conducted to find the correlation of electrolyte status and glucose levels in cord blood with the severity of asphyxia.


This prospective, observational study was carried out for 1.6 years ranging from December 2012 to May 2014 in neonatal intensive care unit (NICU) at a tertiary care teaching hospital, Karad, Maharashtra, India. Totally 100 neonates were delivered in the Department of Obstetrics and Gynaecology and were enrolled in the study after obtaining ethical committee clearance from our institution (viz. Krishna Institute of Medical Sciences (Deemed-to-be) University; KIMSDU/IEC-307/008/06/12/2012) and consents from all the parents. Data regarding sex and birth weight of the baby, maternal history, Apgar score, meconium staining of amniotic fluid, and birth events (parity, gestational period, and mode of delivery) were recorded in a predesigned pro forma.

Asphyxiated and nonasphyxiated neonates were considered as case and control groups, respectively, each with 50 neonates based on inclusion and exclusion criteria [Table 1]. The blood samples from umbilical cord were collected in both the groups immediately after birth, and all the neonates were evaluated clinically and neurologically. During the immediate neonatal period at NICU, the asphyxiated neonates were monitored for HIE (as per Sarnat and Sarnat staging).[3] Sarnat and Sarnat staging is a three-stage clinical criterion to assess the severity of neonatal encephalopathy (mild, moderate, and severe) in early neonatal period.[3] The asphyxiated neonates were also evaluated for other systemic effects of asphyxia. The cord blood samples were sent for analysis of serum electrolytes (sodium, potassium, and total calcium), glucose, complete blood count, septic screen total leukocyte count, absolute neutrophil count, band cell ratio, C-reactive protein, and creatinine. The levels of serum glucose and serum electrolytes were analyzed by A25 autoanalyzer and electronic Na-K analyzer (by Abbott Healthcare Pvt. Ltd., Mumbai), respectively.{Table 1}

Statistical analysis

Statistical analysis was done using R version 3.6.0 software (Revolution Analytics, Mountain View, CA, United States). Normality of the data was determined using the Shapiro–Wilk test. The continuous and categorical variables are presented in mean ± standard deviation and frequency tables, respectively. A comparison between cases and controls was done using independent t-test and Mann–Whitney U-test. The correlation between ordinal and continuous data was determined using Spearman correlation. P < 0.05 was considered statistically significant at 95% confidence interval.


Of the 100 neonates, 68 were male neonates; the mean birth weight in the case and control groups was 2.85 ± 0.37 and 2.73 ± 0.13, respectively. Out of 50 cases, the incidence of asphyxia was predominant in males (72%). The gestation period of 37–40 weeks was observed in both the groups [Table 2].{Table 2}

Majority of the cases (38%) were delivered by cesarean section and instrumental delivery. A higher proportion (74%) of cases were born to primigravida mothers [Table 2]. Before getting stable spontaneous respiration, all the cases were subjected to resuscitation accompanying >1 min of positive pressure ventilation. Significantly, all the cases had Apgar score <5 at 1 min of life, and none of the neonates had Apgar score <3 at 5 min of life [Table 3]. The cases (10%) have more tendencies toward meconium-stained liquor than controls (4%) and make a major contribution in the prognosis of respiratory distress associated with asphyxia.{Table 3}

All the cases presented with respiratory distress, followed by poor feeding (64%), hypotonia (22%), lethargy (22%), seizures (16%), and oliguria (12%). On neurological examination, all controls were normal and had no signs of respiratory distress, poor feeding, hypotonia, lethargy, seizure, and oliguria. The majority of cases had mild HIE (30%).

Serum sodium, calcium, and glucose levels in cord blood were significantly lower in cases compared to controls [Table 4]. A statistically significant difference was found between cases and controls with respect to sodium, calcium, and glucose levels (P < 0.05), whereas potassium did not differ significantly (P = 0.162). The serum sodium, calcium, and glucose levels have a significant negative linear correlation with staging of HIE (−0.591r, −0.484r, and −0.221r, respectively). However, serum glucose levels did not differ significantly between different stages of HIE (P = 0.475) [Table 5].{Table 4}{Table 5}


Perinatal asphyxia is a hypoxic-ischemic insult, which primarily leads to tissue damage, especially brain tissue, followed by electrolyte imbalance. The extent of tissue damage (and severity of asphyxia) is determined by the serum electrolyte status and glucose levels. In our present study, out of 50 cases admitted to NICU, males were more prone to asphyxia, and these findings correlate well with the study by Yadav et al. (72% vs. 54.4%).[15] Among asphyxiated neonates, the higher incidence of perinatal asphyxia was seen in normal and instrumental delivered neonates (64%) when compared to lower segment cesarean section (36%). Furthermore, similar findings were observed in a study by Onyiriuka[16] (71% vs. 29%). The studies by Onyiriuka[16] and Basu et al.[17] did not differ significantly with our study regarding mean birth weight (P = 0.303). A statistically significant difference was found between cases and controls in case of Apgar score at 1 and 5 min of life (P < 0.001), and these findings were in concordance with study by Meena et al.[18] Accordingly, Apgar score serves as an essential diagnostic tool for birth asphyxia.

In our study, blood samples were drawn from the umbilical cord immediately after birth, whereas many previous studies have considered venous blood at 24 or 48 h of life for biochemical analysis.[13] The analysis of cord blood for electrolytes and glucose may help to identify asphyxiated neonates at risk for permanent tissue damage (especially neurological damage) or death already at birth when most radiological and clinical signs are still absent.[19] The mean sodium and calcium levels were significantly lower in cases compared to controls, but serum potassium levels were found to be within the normal range. Similar findings were reported by Basu et al.[17] (122 ± 6, 5.05 ± 0.63, and 6.85 ± 0.95 vs. 138 ± 2.7, 4.19 ± 0.40, and 9.50 ± 0.51). Vandana et al.[20] reported similar findings with respect to serum sodium and potassium levels. Similarly, studies by Rai et al.,[13] Schedewie et al.,[21] and Jajoo et al.[22] reported significantly lower serum calcium levels in asphyxiated neonates than controls. In our study, the decrease in serum sodium and calcium levels in asphyxiated neonates was in positive correlation with HIE severity staging of asphyxia and well correlates with the study by Pallab et al.[17] The present study showed significantly low plasma glucose levels in cases (43.68 ± 10.81) as compared to controls (55.76 ± 10.10), which is in concordance with the study by Lakra et al.[23] (54.4 ± 10.91 vs. 76 ± 15.5, respectively). In accordance with Surjeet et al.,[23] a significant negative correlation was observed between hypoglycemia and HIE severity staging of asphyxia (−0.2216r) in the present study. The asphyxiated neonates with hyponatremia and hypoglycemia are at high risk to develop respiratory distress, impaired growth, poor feeding, cerebral palsy, and hemorrhage, whereas hypocalcemia may cause neuromuscular irritability (myoclonic jerks and seizures). Yadav et al.[15] reported 100% and 40.8% of cases with respiratory distress and poor feeding, respectively, which well correlates with our study (100% and 64%).

As observed from the literature and the present study, the serum levels of sodium, calcium, and glucose in cord blood would be the best indicators to assess the severity of asphyxia (HIE staging) with the extent of injury that the neonate had suffered in the intrauterine environment.

In the present study, we considered Sarnat staging of HIE classification and failed to look after some parameters with this classification, such as electroencephalogram findings and stretch reflexes. We have limited maternal characteristics and could not be able to correlate our findings with maternal risk factors. The electrolyte findings in this study might be reflected by the usage of oxytocin and IV fluids during labor. By taking all these points into consideration, future studies are required for appropriate findings.


Significant hyponatremia, hypocalcemia, and hypoglycemia were observed in asphyxiated neonates and were in positive correlation with the HIE severity staging of asphyxia (from mild to severe). Hence, monitoring of serum electrolytes immediately after birth would be the best measure for early diagnosis and severity assessment of birth asphyxia.

Declaration of patient consent

We have obtained all appropriate written informed consent forms from all parents. In the form, the parents have given their consent for their children's images and other clinical information to be reported in the journal. The patients understand that their children's names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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