The key words used when researching this review: Neonatal hypoglycaemia/hypoglycemia, New-born hypoglycaemia, Low plasma glucose level, New-born/Infant low blood sugar, Hypoglycaemia in preterm/high risk neonates, Hypoglycaemia/breastfeeding, gluconeogenesis/ketone bodies. The databases and search engines used: Google scholar, CINHAL and Medline. Hypoglycaemia is common among neonates, therefore Healthcare professionals must be aware of the risk factors that predispose infants, allowing for early screening so that asymptomatic hypoglycaemia can be detected and treated early preventing more severe or symptomatic hypoglycaemia.
This essay will examine the physiology behind neonatal hypoglycaemia and the neonates at risk, addressing the symptoms and management of neonates which historically has been complicated by a lack of consensus on a clinical definition of a normoglycaemic range. This topic is valuable to the student midwife as you often come across babies that are reluctant to feed or sleepy when assisting breastfeeding within the early postnatal period.
How as a health professional can one determine which neonates slow to feed should we be more concerned about, considering hypoglycaemia and the dangers of a repeatedly low blood glucose level, whilst also bearing in mind the mother’s history, the birth, gestation, weight and health of the neonate? To bring Neonatal hypoglycaemia into context this essay will outline a recent case scenario I came across on a Post-natal ward in London. A Late Preterm Male Infant was born weighing 2440g at 35 weeks + 2 days gestation to a Primiparous mother of 40 years.
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Gravida 1, Para 0. (O Positive, Rubella Immune).
She had previously been admitted to the Maternal and Fetal Assessment Unit after suffering from Pre-term premature rupture of membranes (PPROM) at 32 weeks + 4 days, due to a fall, her pregnancy was low risk before this with no complications. She was given Dexamethasone a steroid to promote the maturation of the fetus’ lungs and Erythromycin an antibiotic used for the management of PPROM and sent home a week later. The labour was induced at 35 weeks using 2mg of Prostin.
After 12 hours she was given IV Benzilpennicillin and Syntocinon with an Epidural. Labour progressed for another 18 hours to fully and the baby was born by assisted forceps delivery and episiotomy, with cord around the neck at 14:45. Apgar was 9 at one minute and 10 at five minutes, baby weighed 2440g. On initial examination the he was in good condition. By 15:00 The Neonate was put on PROM OBS for 24hours with a plan for the first Pre-feed True Blood Glucose test (TBG), before the 2nd feed and to aim for two consecutive TBG’s of >2.
5mmol/l and to commence skin to skin and to breastfeed as soon as possible. At 16:00 skin to skin and breast feeding was attempted with a successful feed for 10 minutes with good attachment and sucking seen. By 17:20 mother and baby were taken to the post-natal ward, and baby was observed to be alert and active with good tone. At 18:00 The 1st Pre feed TBG was taken with consent at approximately 4 hours of age, using a heel prick test, collected in a yellow top paediatric tube and analysed by a YSI True Blood Glucose and Lactate Machine in NNU. The TBG result was 1.
33mmol/l below the threshold of 2. 5mmol/l, the on call paediatrician was informed immediately. By 19:00 the baby was seen by the on call SHO, who noted that the baby was asymptomatic but unable to latch on to the breast successfully, as mum was very tired a plan was put into place to Top Up 40mls/kg/day of formula via cup feed, equal to 12mls per feed every 2- 3 hours and to document feeds on a feed chart. By 19:30 the baby had taken 12mls of formula by cup. At 22:00 the 2nd TBG result was 1. 72mmol/l Lactate 1. 1mmol/l, with the baby’s temperature being 36. 2C.
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With possible hypothermia compounding the problem of depleting neonatal energy stores, he was placed in a hot cot at 37C to maintain his temperature for the night. The SHO was informed and a plan put in place to increase feeds to 60mls/kg/day, equal to 18mls per feed via cup every 2-3 hours. The baby’s 3rd TBG was repeated at 01:45 with a result of 1. 60mmol/l and Lactate 1. 83mmol/l. The SHO was informed, with a plan to do a septic screen, begin IV Benzylpenicillin and Amikasin and increase feeds to 90/mls/kg/day, 27mls per cup feed and transfer to Transitional Care.
Temperature was 36. 7 whilst out of hot cot for more than half an hour and he was taking 27mls by cup every 2-3hours. The next TBG was 2. 33mmol/l at 03:33, 40 minutes post feed. According to trust guidelines the blood glucose levels must remain between 2. 0-2. 50mmol/l on 2 consecutive occasions, with an assessment by an experienced DR before discontinuing blood glucose monitoring. The next two were 2. 7mmol/l and 3. 2mmol/l and the baby had passed meconium by 11:00 and was alert and rooting.
No more TBG’s were now needed until weaning commenced from cup feeding formula to fully breastfeeding. With close observation, blood glucose tests and regular feeding this baby managed to pull through an episode of asymptomatic hypoglycaemia, possibly brought on by the risks associated with being born slightly premature and having low substrate stores. The long labour and an assisted delivery with a nuchal cord could have led to more of his endogenous glucose stores being used, as could the possibility of neonatal sepsis.
The slight delay in skin to skin and feeding of more than an hour, possibly due to suturing of the episiotomy, could have led to the neonate using up more of the already depleted substrate stores. In neonates hypoglycaemia is a relatively common occurrence which can become a potentially serious problem if left undiagnosed or untreated in neonates within a high risk category for the condition. The incidence in the entire population of “high-risk” infants may be as high as 30%.
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(McGowan 1999) For the majority of healthy term infants a drop in glucose levels after birth is expected and a normal reflection of metabolic adaption to extrauterine life as they have built up alternative fuels in the liver and adipose tissue to compensate. “Healthy term babies who do not have any risk factors for hypoglycaemia should not have routine blood glucose measurements taken unless they show clinical signs”(Hawdon, 2012) During pregnancy Glucose Homeostasis is maintained in utero through a steady supply of glucose from the mother via the placenta.
Following birth and cord clamping, there is an abrupt removal of glucose supply and blood glucose concentration then naturally decreases reaching a low point around 1-3 hours post birth, a normal physiological adaption. This decrease in glucose concentration is in fact an essential process that activates the neonates own glucose production, initiating gluconeogenesis. Endocrine changes bring a rise in plasma glucagon and a decrease in plasma insulin, starting glycogenolysis, which mobilises glucose from glycogen stores in the liver, (gluconeogenesis).
Ketone bodies are also produced through ketogenisis and lipolysis the release of fatty acids from triglyceride stores (Wardle, 2009).
The neonate’s brain depends on a steady supply of glucose as its main source of fuel. If blood glucose levels are repeatedly low in at risk neonates this could potentially cause long-term neurological damage resulting in intellectual disability, developmental delay, epilepsy or cerebral palsy.
The symptoms of hypoglycaemia are not often obvious as similar symptoms are often seen in sick neonates. Some symptoms include jitteriness, irritability, lethargy, hypotonia poor feeding and temperature instability. The more major symptoms like apnoea, seizures or coma are more likely to lead to brain damage and must be acted on with treatment immediately by admission to NNU and given a 10% glucose IV infusion as this will prevent hypoglycaemia in the majority (Hawdon 2012).
As many cases of hypoglycaemia are asymptomatic routine screening for this condition in high risk neonates is recommended. The majority of cases of hypoglycaemia can be predicted by early identification of the neonates who have one or more risk factors. Infants at a higher risk due to limited storage of glycogen in the liver and lower brown fat stores are; growth restricted and small for gestational infants due to placental insufficiency, preterm infants of
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