NEONATAL CONDITIONS
Neonatal Hypoglycaemia
A practical guide for SCN clinical staff · Low blood glucose in the newborn - common and transient, but a preventable cause of brain injury
AND FIND
THE CAUSE
Fetal supply & stores
In utero, glucose crosses the placenta continuously by facilitated diffusion, and the fetus lays down glycogen and fat mostly in the third trimester. Fetal insulin is the main driver of this storage.
The birth transition
Cord clamping abruptly cuts off the maternal glucose supply. Blood glucose falls to a physiological nadir at 1-2h, which triggers a counter-regulatory surge - glucagon and catecholamines rise, insulin falls.
Glycogenolysis
Glucagon and adrenaline mobilise hepatic glycogen for a rapid supply of glucose. Stores are small, though, and are used up within hours - sooner in preterm and growth-restricted babies.
Gluconeogenesis & ketones
The liver then makes new glucose from lactate, glycerol and amino acids, and fatty-acid oxidation generates ketones the brain can burn as an alternative fuel. Both pathways are immature in the first days.
Stabilisation with feeding
Enteral feeding supplies substrate and stimulates gut hormones, and over hours to days glucose stabilises as counter-regulation matures. This is why early, frequent feeding is protective.
Where it goes wrong
Hyperinsulinism (infant of a diabetic mother, perinatal stress, some syndromes) both lowers glucose and switches off ketones - removing the brain's back-up fuel. Other routes: low stores (IUGR/preterm), high demand (sepsis, hypothermia, asphyxia), or endocrine deficiency (cortisol, GH).
Brain injury
The newborn brain runs almost entirely on glucose and ketones. Severe or prolonged hypoglycaemia - especially when ketones are suppressed - injures the occipital and parietal cortex, risking later visual impairment, epilepsy and developmental delay.
CLINICAL FINDINGS
- Frequently asymptomatic - screen at-risk babies
- Jitteriness, irritability, exaggerated Moro
- Poor feeding, lethargy, hypotonia
- Apnoea, cyanosis, temperature instability
- Seizures (a late and serious sign)
INVESTIGATIONS
- Confirm a low point-of-care reading with a true (lab) glucose - but do not delay treatment for it
- Screen at-risk infants pre-feed per local protocol
- If persistent/severe, take a "critical sample" at the time of hypoglycaemia: insulin, cortisol, GH, ketones, lactate, free fatty acids, +/- ammonia and acylcarnitines
- Consider a sepsis screen if unwell
- Document the glucose infusion rate (GIR) needed to maintain glucose
COMPLICATIONS & RED FLAGS
- Symptomatic or very low glucose is an emergency - give IV dextrose
- Hypoglycaemia persisting beyond 48-72h needs an endocrine/metabolic work-up
- A high glucose requirement (GIR >8 mg/kg/min) suggests hyperinsulinism
- Severe hypoglycaemia can cause occipital injury - later visual impairment and epilepsy
- Never discharge an at-risk baby without documented stable pre-feed glucoses
MANAGEMENT
Always follow your local hypoglycaemia guideline. Screen at-risk babies, confirm a low without delaying treatment, feed first for mild cases, and use IV dextrose for symptomatic or severe hypoglycaemia.
Asymptomatic / mild
- Consider buccal 40% dextrose gel (0.5 mL/kg) with a feed for at-risk infants
- Feed (breast or formula) and recheck before the next feed
- Keep the baby warm and support feeding
- Escalate if not responding to feeds
Symptomatic / severe
- IV 10% dextrose 2 mL/kg bolus, then a maintenance infusion
- Recheck glucose within 30 minutes and titrate
- Calculate and document the glucose infusion rate (GIR)
- Escalate to central access if high glucose concentrations are needed
Persistent / refractory
- Take a critical sample before correcting if feasible
- GIR >8 mg/kg/min suggests hyperinsulinism - consider diazoxide, discuss with endocrine
- Treat contributing causes (sepsis, hypothermia); involve NICU/NETS
- Hydrocortisone only after a critical sample and endocrine advice
- Screen at-risk babies pre-feed per protocol; confirm low point-of-care readings with a lab glucose but treat first.
- Support early and frequent feeding and keep the baby warm - cold stress worsens hypoglycaemia.
- Watch for jitteriness, poor feeding, lethargy, apnoea or seizures and escalate.
- For IV dextrose: monitor the site, recheck glucose on schedule, and do not stop the infusion abruptly.
Why is there no single numeric definition of neonatal hypoglycaemia?
Which babies do you screen, when, and for how long?
When and how do you take a "critical sample," and what does it tell you?
How do you recognise and manage suspected hyperinsulinism?
Take-home message: Neonatal hypoglycaemia is common and often transient, but symptomatic or persistent low glucose can injure the brain. Screen at-risk babies, confirm with a lab glucose without delaying treatment, feed plus dextrose gel for mild cases, and use IV dextrose for symptomatic or severe hypoglycaemia. Persistent hypoglycaemia needs a critical sample and a search for hyperinsulinism or metabolic disease.
For educational purposes only. Always align management to current ANZCOR/NRP guidelines and your local SCN/NICU or NETS protocols.