Neonatal Hypoglycemia

Definition

The S.T.A.B.L.E. Program defines hypoglycemia as:

“Glucose delivery or availability is inadequate to meet glucose demand” (Karlsen, 2006)

What is Normal?

Defining a normal glucose level <2.6mmol/l in term or preterm

McGowan, 1999 as cited by Verklan & Walden

High risk of Hypoglycemia

Normal newborns – if feeding is delayed for 3-6 hours after birth

At-Risk Infants Macrosomic infant >4kg

Preterm – 15%

SGA – 15%

IDM – 20%

Sick baby (perintal asphyxia, rhesus disease, sepsis, hypothermia, polycythemia)

Infants at Highest Risk

< 37 weeks gestationInfant of a diabetic motherSmall for gestational ageLarge for gestational ageStressed/ill infantsExposure to certain medications

Treatment of preterm laborTreatment of hypertensionTreatment of type 2 diabetesBenzothiazide diureticsTricyclic antidepressants in the 3rd trimester

Why is hypoglycemia a problem?

Glucose is the primary fuel for the brain.

The brain needs a steady supply of glucose to function normally.

Glucose is the fetus’s only source of carbohydrate.

Why is hypoglycemia a problem?

“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 neonate’s 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.

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!

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.

Factors that negatively affect glucose availability after birth

Inadequate Glycogen

Increased Utilization of Glucose

Excessive Insulin

Inadequate Glycogen

Glycogen stores increase rapidly in the last month of the 3rd trimester

Preterm infants are born before this occurs. What little glycogen is available is used up rapidly and their supply is depleted.

Inadequate Glycogen

SGA – birth weight < 10 percentile. Chronically stressed infants have higher metabolic demands and use up available glucose for growth and survival.

Markedly post-mature infants are at increased risk due to increased metabolic demand.

Increased Utilization of Glucose

Sick/Stressed infantsCauses increase in metabolic demand

Uses up glucose quickly.

These include all sick, premature and SGA infants.

Excessive Insulin - IDM

Infants of Diabetic MothersMany consequences for the neonate

Single most important factor in determining the outcome for the infant is maternal glucose control

IDM – Effects on Fetus

Glucose crosses the placentaInsulin does not cross the placentaResults – fetus produces own insulin in the presence of elevated glucose from the mother

IDM – Risks > general population

Birth injury is doubled

C/S is tripled

NICU admission is quadrupled

Stillbirth is x 5 greater

Congenital anomalies are x 2 – 5 greater

Nursing Management

Identify infant at risk

On admission, 1, 2, 4 hours later, then once hypocount stable 6 hourly for 24-48 hours

If well baby at risk immediate feeding

Unwell baby- start iv dextrose 10%

Signs & Symptoms of Hypoglycemia

Jitteriness

Irritability

Hypotonia

Lethargy

High-pitched cry

Hypothermia

Poor suck

Tachypnea

Cyanosis

Apnea

Seizures

Cardiac arrest

Treatment

HPC< 1.5/ baby symptomatic

IV D10% 2ml/kg, followed by D10% 60-90ml/kg/day (day 1 of life)

HPC 1.5-2.5 feeding

Prevention

Increase awareness of conditions that predispose an infant to hypoglycemia

Early screening of at-risk infants

Early and frequent feedings

Maintain temperature

Persistent hypoglycemiaRe-evaluate infant

Sent RBS

Increase D10% by 30ml/kg/day or use dextrose 12.5% or 15%(through central line)

If still hypoglycemic despite of >10mg/kg/min, conseder glucagon IV30-100mcg/kg/hr max 0.5mg/dose

Don’t use glucagon in SGA/adrenal insufficiency baby

Otherwise can use hydrocortisone 2.5-5mg/kg/dose bd

Clinical approachRule out liver failure, septicemia, severe systemic illness, SGA, maternal DM etc.

When is hypoglycemia relation to feeding?

Any hepatomegaly?

Clues for endocrine cause.

hypothyroidism?

Small genitalia?

hyperpigmentation

SGA?

Transient neonatal hypoglycemia

Prematurity, intrauterine growth retardation, perinatal asphyxia

Maternal hyperglycemia due to diabetes or iatrogenic glucose administration

Sepsis

Prolonged fasting (e.g., due to inadequate breast milk or condition interfering with feeding)

Congenital hypopituitarism

Congenital hyperinsulinism, several types, both transient and persistent

Inborn errors of carbohydrate metabolism such as glycogen storage disease

Blood to be taken

Ketones serum, urine

Blood lactate

Blood ammonia

Free fatty acid

Serum cortisol, insulin, growth hormone

Young childrenProlonged fasting

Diarrheal illness in young children, especially rotavirus gastroenteritis

Idiopathic ketotic hypoglycemia

Isolated growth hormone deficiency, hypopituitarism

Insulin excess

Hyperinsulinism due to several congenital disorders of insulin secretion

Insulin injected for type 1 diabetes

Hyperinsulin Hyperammonia syndrome (HIHA) due to Glutamate dehydrogenase 1 gene. Can cause mental retardation and epilepsy in severe cases.[22]

Gastric dumping syndrome (after gastrointestinal surgery)

Other congenital metabolic diseases; some of the common include

Maple syrup urine disease and other organic acidurias

Type 1 glycogen storage disease

Type III glycogen storage disease. Can cause less severe hypoglycemia than type I

Phosphoenolpyruvate carboxykinase deficiency, causes metabolic acidosis and severe hypoglycemia.

Disorders of fatty acid oxidation

Medium chain acylCoA dehydrogenase deficiency (MCAD)

Familial Leucine sensitive hypoglycemia [23]

Accidental ingestions

Sulfonylureas, propranolol and others

Ethanol (mouthwash, "leftover morning-after-the-party drinks")