Paediatrics chapters
Neonatal hypoglycaemia, hypocalcaemia and infant of diabetic mother
Low blood glucose and low calcium in the newborn: definitions, who is at risk, the vague signs, how to treat them with feeds, IV dextrose and calcium gluconate, and the many problems of the infant of a diabetic mother.
- Akbar defines neonatal hypoglycaemia as blood glucose below 40 mg/dL in term (below 30 mg/dL in preterm) babies; at-risk babies are IDM, SGA, preterm, LGA, sick or cold babies, and signs are jitteriness, poor feeding, lethargy, apnoea and seizures.
- Treat with early feeds; if low despite feeding or symptomatic, give 10% dextrose 2 mL/kg then an infusion of about 6 mg/kg/min; persistent cases suggest hyperinsulinism.
- The infant of a diabetic mother is large and plethoric with hypoglycaemia (within 1-2 hours), hypocalcaemia, RDS, polycythaemia, jaundice, septal hypertrophy and congenital anomalies from fetal hyperinsulinism.
On this page
Overview
Glucose and calcium both fall after the cord is cut, when the supply from the mother stops. Healthy term babies adjust quickly, but small, preterm, sick and diabetic-mother babies cannot. Untreated hypoglycaemia can cause permanent brain damage, and hypocalcaemia can cause seizures.
Both problems are common, both have vague signs, and both are cheap to detect and treat, which makes them favourite exam topics.
Glucose at birth
- In the womb glucose crosses the placenta by facilitated diffusion; fetal levels are about two thirds of the mother's.
- After the cord is clamped, glucose falls to its lowest at 1-2 hours, then rises and settles (mean about 65-71 mg/dL by 3-4 hours).
- The newborn needs about 6 mg/kg/min of glucose (Nelson: 6-8 mg/kg/min; babies with hyperinsulinism may need two to three times this); early feeding prevents hypoglycaemia.
Neonatal hypoglycaemia
Definition
Akbar defines it as blood glucose below 40 mg/dL in a term baby or below 30 mg/dL in a preterm baby; many units now treat below about 45 mg/dL. It is:
- Transient if it lasts less than 7 days (most cases).
- Persistent if it lasts more than 7 days: think of hyperinsulinism or endocrine causes.
Causes and risk groups
| Mechanism | Causes |
|---|---|
| Low stores or intake | Prematurity, SGA/IUGR, post-maturity, delayed or poor feeding |
| Hyperinsulinism (high use) | Infant of diabetic mother, Rh haemolytic disease (erythroblastosis), Beckwith-Wiedemann syndrome, insulin-secreting tumours or nesidioblastosis, maternal beta-blockers |
| High demand or stress | Sepsis, birth asphyxia, hypothermia, polycythaemia, RDS, after exchange transfusion |
| Endocrine and metabolic | Hypopituitarism, adrenal insufficiency, glycogen storage disease, galactosaemia |
Akbar gives an incidence of about 8.1% in term LGA and 14.7% in SGA babies, and 25-50% in infants of diabetic mothers.
SGA babies become hypoglycaemic because of low glycogen stores; IDMs become hypoglycaemic because of too much insulin.
Clinical features
Many at-risk babies have no symptoms, so screen them.
- Jitteriness or tremors (the commonest sign)
- Poor feeding, lethargy, limpness, apathy
- Weak or high-pitched cry
- Apnoea, cyanotic spells, tachypnoea
- Seizures, eye rolling, coma
- Sweating, sudden pallor, hypothermia, heart failure
Because these signs are non-specific, a quick improvement after glucose supports the diagnosis.
Bedside strips measure whole blood glucose, which reads about 15% lower than plasma, and are inaccurate at low levels. Confirm a low strip result with a laboratory sample, but do not delay treatment.
Monitoring at-risk babies
Akbar suggests checks at about 1, 2, 4, 6, 12 and 24 hours of age (more often in IDMs), stopping when pre-feed levels are stable above about 50 mg/dL on oral feeds.
Management
| Situation | Action |
|---|---|
| Low glucose, baby well and able to feed | Feed (breast milk or formula) and recheck soon |
| Still low after feeding or unable to feed | Start IV 10% dextrose at about 6 mg/kg/min (3.6 mL/kg/hour) |
| Symptomatic (seizures, apnoea, lethargy) | Bolus 10% dextrose 2 mL/kg IV, then infusion at 6-8 mg/kg/min, increasing as needed |
| No IV access | Umbilical venous line; glucagon IM/IV if glycogen stores are adequate (for example IDM) |
| Needs high concentrations | Up to 12.5% dextrose peripherally; higher (for example 25%) only through a central line |
| Persistent hyperinsulinism | Diazoxide (Akbar: 5-8 mg/kg/day orally), octreotide; surgery for tumours |
- Recheck glucose 30-60 minutes after any change.
- Wean the infusion slowly once glucose stays normal (Akbar: above 45 mg/dL) for 24-48 hours on full feeds.
Do not push concentrated dextrose into a newborn's peripheral vein; it damages the vein and triggers more insulin release. The bolus is 10% dextrose, 2 mL/kg.
Glucose infusion rate (GIR)
GIR (mg/kg/min) = dextrose concentration (%) × infusion rate (mL/kg/day) ÷ 144
A 3 kg baby on 10% dextrose at 3.6 mL/kg/hour
Glucose given = 3.6 × 0.1 g = 0.36 g/kg/hour = 360 mg/kg/hour
GIR = 360 ÷ 60 = 6 mg/kg/min
Same result by formula: 3.6 × 24 = 86.4 mL/kg/day; 10 × 86.4 ÷ 144 = 6 mg/kg/min
Prognosis
Good when treated quickly. Brain damage, developmental delay and epilepsy follow prolonged or recurrent symptomatic hypoglycaemia, especially with seizures and in persistent hyperinsulinism.
Neonatal hypocalcaemia
Definition
- Total serum calcium below 7 mg/dL (Akbar and Nelson), or ionised calcium below 3-3.5 mg/dL (Nelson). Levels normally fall to their lowest at 24-48 hours.
- Early: in the first 3 days.
- Late: after 3 days (usually in the first or second week).
Causes
| Early (first 3 days) | Late (after day 3) |
|---|---|
| Prematurity (poor response to PTH) | High phosphate load: feeding with cow's milk or unmodified formula |
| Infant of diabetic mother (functional hypoparathyroidism, hypercalcitoninaemia) | Hypomagnesaemia |
| Birth asphyxia | Hypoparathyroidism: transient, DiGeorge syndrome, maternal hyperparathyroidism (suppresses the baby's glands) |
| IUGR, sepsis, shock | Vitamin D deficiency (maternal deficiency, maternal anticonvulsants) |
| Exchange transfusion with citrated blood, bicarbonate, alkalosis | Renal disease, diuretics |
Late hypocalcaemia with seizures in a baby fed cow's milk is caused by its high phosphate load; switch to breast milk.
Clinical features
- Often no symptoms in early preterm hypocalcaemia.
- Jitteriness, irritability, twitching, increased tone, clonus and brisk reflexes.
- Seizures (typical of late hypocalcaemia), apnoea, poor feeding.
- Laryngospasm and stridor; tetany and carpopedal spasm are rare in newborns.
- ECG: prolonged QTc (above 0.4 seconds).
Investigations
Serum total and ionised calcium, magnesium, phosphate, alkaline phosphatase; PTH and vitamin D in persistent cases; ECG.
Management
- Symptomatic: 10% calcium gluconate IV, given slowly and diluted (Akbar: 1-2 mL/kg over about 5 minutes; Nelson: 2-4 mL/kg over 10-15 minutes), with ECG/heart rate monitoring (risk of bradycardia and arrhythmia) and a careful watch on the drip site (extravasation causes skin necrosis).
- Then maintenance calcium IV or orally.
- Asymptomatic preterm babies: maintenance calcium in IV fluids only.
- Not responding: give magnesium sulphate (50% solution IM; Akbar 0.1-0.2 mL per kg, Nelson 0.1 mL/kg repeated every 8-12 hours), because low magnesium blocks PTH secretion and action.
- Treat the cause: breast milk instead of cow's milk, vitamin D for deficiency, long-term treatment for hypoparathyroidism.
Do not mix calcium with bicarbonate (it precipitates), and never give calcium as a rapid push.
Infant of a diabetic mother (IDM)
Pathophysiology
- Maternal hyperglycaemia crosses the placenta and causes fetal hyperglycaemia.
- The fetal pancreas responds with beta-cell hyperplasia and fetal hyperinsulinism (insulin does not cross the placenta).
- Insulin is a growth hormone in the fetus: it drives fat, glycogen and protein deposition, causing macrosomia and organomegaly (heart, liver), but not the brain.
- At birth the glucose supply stops while insulin stays high, causing hypoglycaemia in the first hours.
- Insulin antagonises cortisol in the lungs and delays surfactant, causing RDS even near term.
- Poor control at conception causes congenital malformations (high glucose is teratogenic).
Maternal sugar → fetal sugar → fetal insulin → big baby, low sugar, stiff lungs.
Clinical features
- Large, plump, plethoric baby with a puffy face (some are normal size or SGA if the mother has vascular disease).
- Jittery, tremulous and irritable in the first days; or floppy and poor at sucking.
- Respiratory distress; signs of heart failure.
Complications
| Problem | Points |
|---|---|
| Hypoglycaemia | Commonest (up to 40% in Akbar); within 1-2 hours of birth; worst in macrosomic babies |
| Hypocalcaemia | Up to 50%; lowest at 24-72 hours; related to the severity of maternal diabetes |
| Hypomagnesaemia | With hypocalcaemia |
| Macrosomia and birth trauma | Shoulder dystocia, Erb palsy, Klumpke palsy, fractured clavicle, cephalhaematoma, asphyxia |
| RDS | Delayed surfactant; also TTN after caesarean section |
| Hypertrophic cardiomyopathy | Asymmetrical septal hypertrophy; usually settles over months; may cause heart failure or outflow obstruction |
| Polycythaemia and hyperviscosity | Plethora; can cause renal vein thrombosis |
| Jaundice | From polycythaemia and immature liver |
| Congenital malformations | Heart (transposition of the great arteries, VSD, ASD), neural tube defects, holoprosencephaly, renal agenesis, small left colon syndrome, caudal regression (sacral agenesis) |
The commonest problem in an IDM is hypoglycaemia; the heart lesion most linked to maternal diabetes is transposition of the great arteries, while the cardiomyopathy is septal hypertrophy.
In an IDM with seizures, the timing helps: early (first hours) points to hypoglycaemia; later (day 2-3) points to hypocalcaemia.
Management
- Good control of maternal diabetes before conception and during pregnancy prevents most problems.
- Delivery where neonatal care is available; a paediatrician should attend.
- Feed early (within the first hour) and often; encourage breastfeeding.
- Glucose checks from birth and frequently in the first 24-48 hours; treat hypoglycaemia as above.
- Check calcium, haematocrit (polycythaemia), bilirubin; look for birth injuries and anomalies.
- Echocardiography for a murmur or heart failure.
- Long-term: higher risk of childhood obesity and later diabetes (Akbar: at least 10 times the general population).
Expect: Akbar's definition of hypoglycaemia (below 40 mg/dL term, below 30 mg/dL preterm); risk groups (IDM, SGA, preterm, LGA, sepsis, asphyxia, hypothermia); jitteriness as the commonest sign; 10% dextrose 2 mL/kg bolus then 6 mg/kg/min; maximum 12.5% peripherally; diazoxide for hyperinsulinism; hypocalcaemia below 7 mg/dL with early causes (prematurity, IDM, asphyxia) and late causes (cow's milk phosphate, hypoparathyroidism, low magnesium); slow IV calcium gluconate with ECG monitoring; magnesium for refractory cases; IDM pathophysiology through fetal hyperinsulinism; hypoglycaemia as the commonest IDM problem; macrosomia, RDS, septal hypertrophy, polycythaemia, renal vein thrombosis, TGA, small left colon and caudal regression.
Quick revision
- Hypoglycaemia (Akbar): below 40 mg/dL term, below 30 mg/dL preterm; lowest glucose at 1-2 h.
- Risk: IDM, SGA, preterm, LGA, Rh disease, Beckwith-Wiedemann, sepsis, asphyxia, cold.
- Signs: jitteriness, poor feeding, lethargy, apnoea, seizures.
- Treat: feed; IV 10% dextrose at 6 mg/kg/min; symptomatic bolus 2 mL/kg; max 12.5% peripherally.
- GIR = % dextrose × mL/kg/day ÷ 144.
- Persistent (over 7 days): hyperinsulinism; diazoxide, octreotide.
- Hypocalcaemia below 7 mg/dL; early (first 3 days) vs late (cow's milk, low Mg, hypoparathyroidism).
- Calcium gluconate 10% 1-2 mL/kg slow IV with heart monitoring; magnesium if no response.
- IDM: macrosomia, hypoglycaemia (commonest), hypocalcaemia, RDS, HCM, polycythaemia, TGA, caudal regression.
Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).
FAQ
Why does the infant of a diabetic mother become hypoglycaemic?
Fetal hyperinsulinism continues after birth when the mother's glucose supply stops, so glucose falls within the first hours.
What is the first treatment for symptomatic neonatal hypoglycaemia?
A 2 mL/kg bolus of 10% dextrose IV followed by a continuous dextrose infusion of about 6 mg/kg/min.
Why does feeding with cow's milk cause neonatal seizures?
Its high phosphate load lowers serum calcium, causing late hypocalcaemia and seizures.
Why should magnesium be checked in hypocalcaemia?
Low magnesium stops the parathyroid glands from secreting and acting, so calcium does not correct until magnesium is replaced.