Comparison of plasma electrolytes of perinatally asphyxiated and normal term babies

1 Introduction

Disorders of fluid and electrolyte balance are among the commonest derangements encountered in perinatal asphyxia [1]. Perinatal asphyxia or neonatal hypoxia-ischemia is a temporary interruption of oxygen availability that implies a risky metabolic challenge, even when the insult does not lead to a fatal outcome [2]. In Nigeria, perinatal asphyxia contributes a higher percentage to neonatal deaths with a larger proportion of these deaths occurring in the first 48 hours of life [3 –8]. The incidence of perinatal asphyxia in Nigeria varies from centre to centre ranging from 26.5 per 1000 in Jos [9] to 83.8 per 1000 in Benin City [7]. These electrolyte aberrations can stem from acute kidney injuries triggered by the asphyxia [8]. Acute kidney injury (AKI) is the leading cause for nephrology consults with attendant high mortality rate [8]. An underlying clinical correlate is a rapid decline in GFR usually associated with decreases in renal blood flow with sequel ischemia and hypoperfusion [9]. There is also an inflammatory aspect which causes extensive injury normally associated with insensitivity to vasodilator therapy. Sublethal injury represents an important component in AKI, as it may profoundly influence GFR and renal blood flow [9].

Electrolytes abnormalities such as hyponatremia and hypocalcemia in neonates with various degree of perinatal asphyxia have been documented in previous studies [10 –13]. Hyponatremia in birth asphyxia is traceable to excessive sodium loss, or most often, to the inability of the neonatal kidney to reabsorb sodium especially from hypoxic injury to the kidneys [13, 14]. Hypocalcemia seen in newborn babies with perinatal asphyxia may be attributed to impaired parathyroid function characterized by low serum parathyroid hormones in the neonate, which is exaggerated with sickness [15, 16]. Furthermore, in neonates with asphyxia, hypomagnesemia could be due to increased magnesium consumption during the ischemic insult or ongoing losses caused by ischemic damage to renal glomeruli and tubules [17]. Again diuresis and loss of electrolytes may occur during therapeutic hypothermia because of decreased solute absorption in the loop of Henle with attendant overstimulation of the receptor which opens the calcium channels in the cell membrane of the postsynaptic neurons, resulting in an influx of calcium ions [13, 18, 19].

Considering high mortality and morbidity associated with perinatal asphyxia in newborn and with the paucity of data on electrolyte abnormality in new-born with perinatal asphyxia in our locality, this study was therefore carried out to document and compare plasma electrolytes of perinatally asphyxiated and normal term babies within 48 hours of life when babies require no exogenous electrolytes.

2 Materials and methods

3 Methods

The study was a comparative cross-sectional hospital-based study whereby subjects and matched controls were enrolled in consecutive sampling method applying inclusion and exclusion criteria. Thus a total of 84 newborn babies comprising 42 subjects and 42 controls were consecutively recruited for the study.

Both subjects and controls were babies born at term (gestational age of 37 completed weeks through 41 weeks) of age within 48 hours and weighing 2.5 kg or more admitted to the neonatal special care unit and postnatal ward respectively. Subjects had Apgar score of less than seven at first minute and controls were with Apgar score of seven or greater at first minutes of birth. Babies that had obvious congenital malformations such as cyanotic congenital heart disease, meningomyelocele etc, history of diuretic use in the mother intrapartum, suspected metabolic disease, history of receiving general anesthesia, pethidine, phenobarbital, and other drugs that may cause depression in babies and history of peripartum fever in the mother were excluded. The plasma Sodium, Potassium, bicarbonate and ionized Calcium levels were estimated in auto-analyzer (i-STAT analyzer MN: 300 Abbott point of care Inc.) by the ion selective electrode method, which is based on the principles of potentiometry. The results of the subject and control groups were compared in order to determine whether there was any difference in plasma sodium, potassium, bicarbonate and ionized calcium levels between these groups.

4 Results

Out of the 42 subjects recruited, 19 (45.2%) were males and 23 (54.8%) were females while there were 20 (47.6%) males and 22 (52.4%) females controls (p = 0.83) with male to female ratio of 1:1.2 in subjects and 1:1.1 in controls. The mean age of the subject and control were 19.36±10.28 hours and 19.31±9.83 hours respectively as shown in Table 1.

Among the 42 subjects, 17 (40.5%) were delivered vaginally, 25 (59.5%) were delivered by cesarean section especially for obstructed and prolonged labor while among the 42 controls, 32 (76.2%) had vaginal delivery and 10 (23.8%) were delivered by cesarean section. Incidence of cesarean section was significantly higher in subject (59%) compared to controls (23.8%), p < 0.001 as shown in Table 2.

Statistically, measured values between the groups were compared using t-test. It was found that mean plasma sodium, bicarbonate and ionized calcium of the subjects were significantly lower than that of the controls; P < 0.001, p = 0.032 and p < 0.001 respectively while the mean plasma potassium level was significantly higher in the subjects than in the controls; p = 0.012 as represented in Table 3.

Electrolyte derangement has been shown to be one of the contributory factors to mortality and morbidity in newborns with perinatal asphyxia. Normal plasma electrolyte reference range of sodium, potassium, bicarbonate and ionized calcium in a newborn baby within 24 to 48 hours of life are; 134– 146 mmol/l, 3.0– 7.0 mmo/l, 21– 28 mmol/l, and 1.07– 1.27 mmol/l respectively [21]. It was noted in the present study that there was significant decrease in plasma sodium, bicarbonate and ionized calcium levels in asphyxiated babies than in control group. This is in consonant with Basu et al. study that noted a significant decrease in extracellular sodium in the asphyxiated babies [10]. The decrease in ionized calcium also is in agreement with Onyiriuka [15], Basu et al. [10] and Jajoo et al. [22] studies, which found significant decreased in serum calcium. Even though, mean plasma potassium level was within normal limits in asphyxiate as well as in control, the potassium levels among cases were statically significantly higher.

Sodium, potassium and calcium are the major electrolytes in human body, and any deviation from their normal levels in blood might cause convulsions and other metabolic abnormalities [10, 19]. Body should maintain optimum level of these electrolytes in blood. Abnormalities in these electrolyte levels may be a risk factor for the brain injury for an already asphyxiated neonate. In another study, Najaf et al. also observed that asphyxiated babies had lower mean serum sodium levels as compared to the control group [23].

It is also documented that the values of serum potassium among the asphyxiated babies were directly related to the severity of asphyxia and inversely proportional to the Apgar scores [10]. It was also seen that rise in the serum potassium level was of no clinical significance, and its changes in the serum levels were not in tandem with the decrease in the levels of calcium and magnesium [10 , 17].

Jajoo and colleagues in their study noted that serum calcium levels when measured at birth, 6 hours, 24 hours, and on 5th day of life in neonates with birth asphyxia were lower than in neonates without asphyxia. There was no change in serum calcium levels of asphyxiated infants who received bicarbonate treatment in comparison to those who did not receive sodium bicarbonate. He then opined that since bicarbonate has no value in arresting this electrolyte anomaly, early and serial monitoring of serum calcium levels would be expedient at birth [22].

We also noted low bicarbonate levels in our subjects when compared to normal. This lower bicarbonate levels in subjects presumably reflects poorer acid-base status in these subjects. Furthermore, low bicarbonate levels could be due to increase glycolytic flux from hypoxia [24]. Although the mechanisms by which hypo-bicarbonatemia causes harm in babies with perinatal asphyxia are not fully understood, it could be associated with disturbances in renal blood flow, periventricular haemorrhage, leucomalacia, increased peripheral vascular resistance, and decreased renal function [25].

6 Conclusion

We conclude that neonates with perinatal asphyxia have a propensity to have abnormal electrolyte levels when compared with normal newborn babies and that these changes in the sodium, potassium, bicarbonate and calcium levels may require early evaluation for the abnormalities. However, more studies with a larger population should be carried out to ascertain or confirm these abnormalities. Electrolytes and metabolic abnormalities are the commonest derangement in critically ill asphyxiated neonates that increase morbidity and mortality. The in-depth knowledge of electrolytes derangement from further studies will be helpful to the clinician in the management of fluid and electrolytes of neonate with perinatal asphyxia.

Conflict of interest

The authors declare that they have no conflict of interest.