Neonatal Hypoglycaemia
Summary
Neonatal Hypoglycaemia is the most common metabolic disturbance in the newborn period. Glucose is the primary substrate for cerebral metabolism. Prolonged or severe hypoglycaemia can cause neuronal necrosis and permanent neurodevelopmental impairment (Occupital lobe injury, Cerebral Palsy). The operational threshold for intervention (BAPM 2017) is generally less than 2.6 mmol/L, though lower levels are physiologically normal in the first few hours ("Transitional Hypoglycaemia"). [1,2]
Clinical Pearls
The "Jittery" Baby: Jitteriness (tremor) is the classic sign. To distinguish it from a seizure:
- Jitteriness: Stops when you hold the limb.
- Seizure: Continues despite holding (clonic movement).
Asymptomatic is Common: Most babies with low blood sugars look completely normal. This is why we screen "At Risk" groups (Preterm, SGA, IDM) routinely, regardless of symptoms.
Hyperinsulinism Trap: Babies who require very high glucose infusion rates (>10-12 mg/kg/min) almost certainly have Hyperinsulinism (e.g., Congenital Hyperinsulinism or Beckwith-Wiedemann). They need Diazoxide, not just more sugar.
Risk Factor Groups ("The Big Three")
- Increased Demand (Hyperinsulinism):
- IDM (Infant of Diabetic Mother): High maternal glucose crosses placenta -> Fetal Pancreatic Hyperplasia -> Post-natal high insulin.
- LGA (Large for Gestational Age): >90th centile.
- Beckwith-Wiedemann Syndrome.
- Decreased Stores (Glycogen Depletion):
- IUGR (Small for Gestational Age): less than 2nd centile. Malnutrition in utero.
- Preterm: less than 37 weeks. Brown fat/liver stores not laid down until T3.
- Increased Consumption (Metabolic Stress):
- Sepsis.
- Hypothermia (Babies burn sugar to stay warm).
- Hypoxia/HIE.
Transitional Hypoglycaemia
- In utero, fetus relies on maternal glucose (via placenta).
- At birth, supply is cut (clamping cord).
- Glucose naturally falls to a nadir (can be 1.0-1.5 mmol/L) at 1-2 hours.
- A surge of Glucagon and Catecholamines triggers Glycogenolysis and Ketogenesis (using Brown Fat) to provide fuel.
- In "At Risk" babies, this adaptation fails.
Symptoms (Neuroglycopenia)
Timing
- General: Macrosomia (IDM) vs Wasting (IUGR).
- Dysmorphism: Macroglossia + Omphalocele + Ear creases = Beckwith-Wiedemann. Midline defects = Hypopituitarism.
- Neurology: Alertness, Tone, Suck.
Screening
- Heel Prick: Pre-feed monitoring for at-risk babies (at 2h, then every 3h).
- Confirmation: If heel prick is low, ALWAYS confirm with a formal Gas/Lab sample (heel prick meters are inaccurate at low levels). Do NOT delay treatment while waiting.
The "Hypo Screen" (Critical Sample)
Take during the hypoglycaemia (before correcting) if cause unclear or persistent:
- Insulin / C-Peptide: Should be suppressed. If detectable = Hyperinsulinism.
- Ketones: Should be present. If absent = Hyperinsulinism or Fatty Acid Oxidation Defect.
- Cortisol / Growth Hormone: Exclude pituitary failure.
- Free Fatty Acids.
Management Algorithm (BAPM 2017)
NEONATAL HYPOGLYCAEMIA
↓
SYMPTOMATIC?
(Seizures, Apnoea, Jittery)
┌─────────┴─────────┐
YES NO
↓ ↓
ADMIT NICU RISK FACTOR?
IV DEXTROSE (IDM, SGA, Low)
BOLUS 2ml/kg ↓
FEED & WARM
Recheck 30m
↓
STILL < 2.6?
┌───┴───┐
YES NO
↓ ↓
BUCCAL GEL ROUTINE
(Dextrose) CARE
+ FEED
↓
STILL < 2.6?
↓
ADMIT NICU
IV FLUIDS
Steps
- Keep Warm: Hypothermia worsens hypo.
- Oral Feed: Breast/Formula.
- Buccal Dextrose Gel (40%): (200mg/kg). Massaged into cheek. Effective, cheap, avoids NICU admission. (SugarBABIES Trial).
- IV Dextrose:
- Bolus: 10% Dextrose 2ml/kg (Only if symptomatic/seizing).
- Infusion: 60-90 ml/kg/day of 10% Dextrose.
- Refractory: Increase concentration (12.5%, 15% via Central Line).
- Drugs:
- Glucagon IM: (mobilises glycogen - useless in IUGR who have no glycogen).
- Diazoxide: K-channel opener. Inhibits insulin release.
- Octreotide: Somatostatin analogue.
- Neurodevelopmental: Cerebral Palsy (spastic diplegia).
- Cognitive: Learning difficulties.
- Visual: Cortical blindness (Occipital lobe necrosis).
- Transient: Excessive/prolonged hypo correlates with poor school performance at age 10.
- Congenital Hyperinsulinism: High risk of brain injury without aggressive management.
Key Guidelines
| Guideline | Organisation | Key Recommendations |
|---|---|---|
| BAPM Framework | BAPM (2017) | Operational threshold less than 2.6 mmol/L. Emphasis on "Keep Warm and Feed". |
| AAP Guidelines | AAP (US) | Similar thresholds. |
Landmark Evidence
1. SugarBABIES Trial (Lancet 2013)
- RCT showing 40% Dextrose Gel rubbing into buccal mucosa reversed hypoglycaemia effectively and reduced NICU admissions. Now standard of care.
2. CHYLD Study
- Showed that even moderate asymptomatic hypoglycaemia is associated with reduced executive function in childhood.
Why is the sugar low?
Babies are used to getting a constant stream of sugar from mum via the umbilical cord. When they are born, that supply is cut, and they have to start "running on their own batteries" (burning fat/milk) until feeding is established.
- Small babies: Have smaller batteries (fat stores).
- Babies of Diabetic Mums: Have too much Insulin (the hormone that lowers sugar), so their sugar drops fast.
Is it dangerous?
Severe, untreated low sugar can starve the brain of energy. We screen frequently to catch it early so this rarely happens.
What is the gel?
It's a sugary gel we rub inside the cheek. It absorbs straight into the blood, giving a quick boost without needing needles.
Primary Sources
- BAPM. Identification and Management of Neonatal Hypoglycaemia in the Full Term Infant. 2017.
- Harris DL, et al. Dextrose gel for neonatal hypoglycaemia (SugarBABIES Study). Lancet. 2013.
- McKinlay CJ, et al. Neonatal Glycemia and Neurodevelopmental Outcomes at 2 Years (CHYLD Study). N Engl J Med. 2015.
Common Exam Questions
- Management: "Symptomatic hypo (seizing), first step?"
- Answer: IV 10% Dextrose Bolus (2ml/kg).
- Diagnosis: "Hypo with NO Ketones + High Insulin?"
- Answer: Hyperinsulinism (Congenital or IDM).
- Prevention: "Key nursing measure for SGA baby?"
- Answer: "Keep Warm" (prevent hypothermia) + Early Feeding.
- Syndrome: "Macroglossia + Hypoglycaemia?"
- Answer: Beckwith-Wiedemann Syndrome.
Viva Points
- Why 2.6? It is an operational threshold based on statistical norms, not a precise biological switch for brain damage.
- D10 vs D50: NEVER use 50% Dextrose in a neonate (causes hyperosmolar skin necrosis). Only use 10%.
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.