NEONATAL HYPOGLYCAEMIA

DEFINITION
Glucose delivery or availability is inadequate to meet glucose demand.
KarlsenK.TheSTABLEProgram.STABLEProgram, Utah. 2001.

< 2.6mmol/L in term and preterm infants

Peads protocol

50 110 mg/dl (2.75 6.05 mmol/L) (Karlsen, 2006) > 40 mg/dl (2.2 mmol/L)(Verklan & Walden, 2004) > 30 term (1.65mmol/L) > 20 preterm (1.10 mmol/L)(Kenner & Lott, 2004) > 45 mg/dl (2.47mmol/L) (Cowett, R. as cited by Barnes-Powell,
2007)

 Hypoglycemia is the most common metabolic problem in neonates. 1.3-3 per 1000 live births
emed

Clinical features

Asymptomatic

Poor feeding

Convulsions

Apnoea and cyanosis

Hypotonia Jittery and irritability

Why is it a problem
Glucose is the primary fuel for the brain. The brain needs a steady supply of glucose to function normally. Glucose is the fetuss only source of carbohydrate.

Fig. 1 Bilateral occipital lesions typical of neonatal hypoglycemic brain injury

 Compared with adults, infants have a higher brain to body weight ratio, resulting in higher glucose demand in relation to glucose production capacity. Cerebral glucose utilization accounts for 90% of the neonates glucose consumption

Preparation for Birth

Fetal plasma glucose is 60 80% of the maternal glucose level. The fetus stores glucose in the form of glycogen (liver, heart, lung, and skeletal muscle). Most of the glycogen is made and stored in the last month of the 3rd trimester.

Karlsen, 2006

Preparation for Birth

The fetus has limited ability to convert glycogen to glucose and must rely upon placental transfer of glucose to meet energy needs. When the infant is born, the cord is cut and so is the major supply of glucose!

Haney, 2005

Preparation for Birth

The transition from fetus to newborn creates a significant energy drain on the newborn. The newborn is now required to meet increased metabolic demands while changing the energy source from a placenta-supplied source to an external food source.

Haney, 2005

Whos at Risk? What could be the cause?

3 basic mechanisms
Limited glycogen stores Hyperinsulinism Diminished glucose production

Limited Glycogen store/supply

Prematurity Perinatal stress/distress SGA Disorders of Glycogen metabolism
Glucose 6-phosphatase def Amylo-1,6 glucosidase def Phosphorylase def
limit either glycogen metabolism or glucose release resulting in excess glycogen stores,hepatomegaly and hypoglycemiainherited primarily as autosomal recessive

Hyperinsulinism
Infant of Diabetic mother Beckwith Wiedemann Syndrome Maternal Drug Effects on neonatal glucose metabolism
Chlorpromazine & benzothiazides Propanolol Terbutaline Inappropriate intrapartum maternal glucose administration

Diminished Glucose Production

SGA
Decreased glycogen stores and impaired gluconeogenesis

Inborn error of metabolism

Aminoacidopathies (amino acids involved in gluconeogenesis)

Others
Hypothermia, Sepsis, Perinatal asphyxia
Normal glycogen stores but inadequate to meet increase energy demand

Cortisol and Growth hormone deficiencies

Secondary to effects on hepatic glycogenolysis and gluconeogenesis

Polycythemia
Direct result of increased glucose consumption by the red cell massas well as secondary to effects on the intestinal absorption of substrates.

High Risk Infants

Infants of diabetic mothers Small for gestational age Preterm infants Macrosomic infants wt > 4.0 kg Sick babies including
Perinatal asphysia Sepsis Hypothermia Polycythaemia

Management
Prevention and early detection
Identification of babies as risk Immediate feeding Supplement feeding until breastfeeding astablished Regular glucometer monitoring

 If blood sugar levels < 2.6 mmol/l or symptomatic

Iv bolus D10% at 2-3 ml / kg D10% drip at 60-90ml/kg/day

 Glucose monitoring should be done hourly until reflo stable >2.6mmol/l for 2 readings Then 2 hourly x 2 Then 4 6 hourly

Glucose requirement
Glucose requirement (mg/kg/min) for IV Drip
% dextrose x rate (ml/hour) weight (kg) x 6

Glucose requirement (mg/kg/min) for formula feeds

(g of glucose per day) x 1000
Wt x 24 x 60
formula feeding = 7.5 gm in 100 ml glucose in (g) per day = total feeding (ml) x 7.5 100

Total glucose requirements target

6 to 8 mg/kg/min

Importance of glucose load

Numerical measurement of a current regime Maintain a similar glucose load if hypoglycaemia is controlled with a particular IV dextrose regime
Allow calculations of a mix formula feeding and IV dextrose.

Step up glucose delivery if persistent hypoglyceamic

 IV glucagon 30 100 mcg/ kg over 20 mins or IM glucagon 100 mcg/kg (maximum 3 doses Should not be used in SGA patients where liver stores are reduced

Investigations
RBS FBC Urine ketone Se cortisol Growth hormone Insulin level VBG Review cord tsh

 Failure to find large ketones with hypoglycemia suggests that fat is not being metabolized from adipose tissue (hyperinsulinism) or that fat cannot be used for ketone body formation (enzymatic defects in fatty acid oxidation)

 Neonates with symptomatic hyperinsulinemic hypoglycemia generate inappropriately low serum cortisol counterregulatory hormonal responses

 B/O N
Delivered at EMLSCS in view of macrosomia Apgar score 9/10 Suctions clear BW 4.55 kg

Mother
BG A +ve HIV/VDRL NR Antenatally
Type 2 diabetes HbA1c 7.0% Total insulin usage 40 units per day

 No risk of sepsis
No prematurity No pprom No chorioamionitis No maternal pyrexia

 Admitted at 4 hours of life in view of infant of diabetic mother for observation Reflo at 4 hours of life 2.9mmol/L Was started on feeding 80cc/kg/day Repeated reflo post feeding was 2.7mmol/L

 On exmination
Hypotonia Jittery on provocation No cyanosis No seizure No apnoea No rapid breathing No hepatospleenomegaly No macroglosia

Plan
1. IV D10% 10 cc slow bolus 2. IV D 10% 9.5 ml / hour total fluid 50 ml/kg/day 3. Total feeding 30ml / 3 hourly total fluid 50 ml/kg/day 4. IM glucagon 0.2 mg stat

5. If persistant hypoglycaemia <3 mmol/l again to take all blood and urine investigation and to increase total fluids to 120ml/kg/day IV D10% 11.5ml/hour feeding 35ml/3 hourly total glucose load = 4.2 = 3.2 = 7.4

6. If still hypoglycaemic, to increase concentration to 12.5% IV D12.5% 11.5 ml/hour = 5.3 feeding 35ml/3 hourly = 3.2 total glucose load = 8.5 mg/kg/min 7. If still persistent, to increase concentration to 15% and start glucagon infusion 10mcg/kg/hour IV D15% 11.5 ml/hour = 6.3 feeding 35ml/3 hourly = 3.2 total glucose load = 9.5 mg/kg/min