Hypoglycaemia Final

8/2/2019 Hypoglycaemia Final

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NEONATAL HYPOGLYCAEMIA


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DEFINITION

Glucose delivery or availability is inadequate tomeet 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)


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Hypoglycemia is the most common metabolic

problem in neonates.

1.3-3 per 1000 live births emed


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Clinical features

Jittery and irritabilityApnoea and cyanosis

Hypotonia

Poor feedingConvulsions

Asymptomatic


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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


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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 for90% of the neonates

glucose consumption


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Karlsen, 2006

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.


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Haney, 2005


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!


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Haney, 2005


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.


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Whos at Risk? What could be the

cause?

3 basic mechanisms

Limited glycogen stores

Hyperinsulinism

Diminished glucose production


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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 hypoglycemia-inherited primarily as autosomal recessive


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Hyperinsulinism

Infant of Diabetic mother

Beckwith Wiedemann Syndrome

Maternal Drug Effects on neonatal glucose

metabolism Chlorpromazine & benzothiazides

Propanolol

Terbutaline

Inappropriate intrapartum maternal glucoseadministration


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Diminished Glucose Production

SGA

Decreased glycogen stores and impaired

gluconeogenesis

Inborn error of metabolism

Aminoacidopathies (amino acids involved in

gluconeogenesis)


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Others

Hypothermia, Sepsis, Perinatal asphyxia

Normal glycogen stores but inadequate to meetincrease energy demand

Cortisol and Growth hormone deficiencies Secondary to effects on hepatic glycogenolysis and

gluconeogenesis

Polycythemia

Direct result of increased glucose consumption by thered cell massas well as secondary to effects on theintestinal absorption of substrates.


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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


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Management

Prevention and early detection

Identification of babies as risk

Immediate feeding

Supplement feeding until breastfeeding

astablished

Regular glucometer monitoring


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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


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Glucose monitoring should be done hourly

until reflo stable >2.6mmol/l for 2 readings

Then 2 hourly x 2

Then 4 6 hourly


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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 formulafeeds

(g of glucose per day) x 1000Wt x 24 x 60

Total glucose requirements target 6 to 8 mg/kg/min

formula feeding = 7.5 gm in 100 ml

glucose in (g) per day

= total feeding (ml) x 7.5

100


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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 persistenthypoglyceamic


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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


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Investigations

RBS

FBC

Urine ketone

Se cortisol

Growth hormone

Insulin level

VBG

Review cord tsh


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Failure to find large ketones with

hypoglycemia suggests that fat is not being

metabolized from adipose tissue

(hyperinsulinism) or that fat cannot be usedfor ketone body formation (enzymatic defects

in fatty acid oxidation)


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Neonates with symptomatic

hyperinsulinemic hypoglycemia generate

inappropriately low serum cortisol

counterregulatory hormonal responses


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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


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No risk of sepsis

No prematurity

No pprom

No chorioamionitis

No maternal pyrexia


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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


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On exmination

Hypotonia

Jittery on provocation

No cyanosis No seizure

No apnoea

No rapid breathing No hepatospleenomegaly

No macroglosia


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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


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5. If persistant hypoglycaemia


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6. If still hypoglycaemic, to increase concentration to12.5%IV D12.5% 11.5 ml/hour = 5.3feeding 35ml/3 hourly = 3.2

total glucose load = 8.5 mg/kg/min7. If still persistent, to increase concentration to 15%and start glucagon infusion 10mcg/kg/hourIV D15% 11.5 ml/hour = 6.3feeding 35ml/3 hourly = 3.2

total glucose load = 9.5 mg/kg/min

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Hypoglycaemia Final