The newborn brain could be described as finicky at best. One of the most difficult things to treat are those things that we can’t see. When a baby is delivered and goes on to develop neurological manifestations, it remains a difficult puzzle to sort out as to what the cause is. Of course, we use all manner of technology to sort this out. The use of EEG, amplitude integrated EEG are helpful in this regard to give us a window into brain excitability but we use all manner of technology to sort this out. When it comes down to it, though we often rely on clinical signs to give us a best guess into whether or not hypoxic injury is at the root of the problem. This, of course, is not always easy as although we have criteria such as those written out by the Canadian paediatric Society to rely on, not all babies fit nicely into the box that provides an easy diagnosis.
For reference, these are the criteria that are recommended by the Canadian paediatric Society for determining who should receive therapeutic hypothermia.
In spite of these criteria, sometimes when babies have Apgar scores or cord blood gases that don’t meet criteria for therapeutic hypothermia, they may still go on to have a seizure. In some of these babies, it is likely that they still experienced a hypoxic injury at some point in time that they have recovered from. In these cases, having a super imposed, metabolic, derangement can tip the scales and cause an already excitable brain to manifest neurological manifestations.
The Brain Does Not Like Low Sodiums
One such abnormality that can tip the scales is a low serum sodium. Babies can develop such derangements from a hypoxic insult that leads to an acute kidney injury. The resultant damage leads to water retention from a poorly functioning, kidney and a dilutional effect on the bloodstream. This usually occurs over time and is not commonly present in the first few hours after birth. When this is seen though with sodium levels below 125 in the first few hours after birth, the likely cause is not renal injury. What is interesting about this phenomenon is that the etiology is most likely related to factors that occurred during labour.
Pregnancy its self has a tendency towards, maternal impairment of water excretion. There is a higher volume status in the pregnant woman and some degree of impairment of excretion of a water load. Maternal hyponatraemia has been described in situations of maternal water, intoxication or provision of excessive dilute fluids to the labouring mother. Add to this, that there is cross-reactivity between oxytocin and ADH receptors in the kidney, and you create a potential problem that a mother can become hyponatraemic simply from frequent administration of oxytocin or Syntocinon. It is possible therefore to have a mother in labour who receives an excessive amount of fluid whether by oral intake or IV and with oxytocin administration develop hyponatremia herself. What follows in terms of the fetus who is an innocent bystander is the eventual development of hyponatremia in utero. As the maternal sodium concentration declines this leads to a difference in maternal and fetal sodium levels. Water flows by osmosis to the fetus and begins to dilute out their blood and bring the sodium levels in line with maternal levels. What comes next can be troublesome to the fetus.
Resultant Seizures
Blake O et al published the paper Therapeutic hypothermia and outcome in hyponatraemic encephalopathy secondary to maternal water intoxication which describes this exact scenario in the setting of maternal water intoxication. The K-series describes three babies all whom developed seizures and had mild The case series describes three babies all whom developed seizures and had mild perinatal asphyxia yet went on to develop seizures. The laboratory results are shown below.
What is most remarkable from the table is the level of serum sodium in the newborns at 1 hour of age. Generally levels of sodium below 125 and certainly 120 can lead to neurological manifestations including seizures and these infants were certainly affected. Much like I explained at the outset of this piece children could be afflicted with a mild form of encephalopathy from hypoxia, and in these cases, each infant by 10 minutes of age had excellent Apgar scores. What I propose, though is that the brain after even a more mild degree of Perinatal asphyxia is more prone to neonatal seizures. I have to say over the years. I have often checked electrolytes after a baby presents with seizures and rarely are they sufficiently abnormal to explain the finding. What I am presenting to you. Here is a special circumstance, in which babies who might not otherwise have seizures, such as those with mild asphyxia go on to have significant convulsions due to the superimposed insult.
The goal of this post was to increase awareness of this phenomenon. Next time you are looking into the events leading up to seizures in a newborn, don’t forget to ask about what fluids a mother received during labour and specifically what her oral intake was like. Don’t forget to have a careful look as well at the amount of oxytocin she received during labour as the combination may be just enough to tip the scales and lied to Neonatal seizures in a baby, who otherwise would not have developed any of those manifestations! While you are at it, take the time to check a maternal sodium and if mother and baby match or at least are both hyponatremic to a similar level you likely have your answer as to what the ethology is.
A bigger question and one that we don’t have the answer to is whether in the presence of hyponatremia and mild asphyxia therapeutic hypothermia offers much benefit. Unfortunately this answer is going to be a tough one to come by as you can’t create an RCT since the numbers are so small but I suspect that most when in doubt will choose to get that temperature down!