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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

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)
McGowan, 1999 as cited by Verklan & Walden

Infants at Highest Risk


< 37 weeks gestation Infant of a diabetic mother Small for gestational age Large for gestational age Stressed/ill infants Exposure to certain medications
Treatment of preterm labor Treatment of hypertension Treatment of type 2 diabetes Benzothiazide diuretics Tricyclic 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 fetuss 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 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.

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 infants
Causes increase in metabolic demand Uses up glucose quickly.

These include all sick, premature and SGA infants.

Excessive Insulin - IDM


Infants of Diabetic Mothers
Many 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 placenta Insulin does not cross the placenta Results 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% 6090ml/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 hypoglycemia
Re-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 IV30100mcg/kg/hr max 0.5mg/dose Dont use glucagon in SGA/adrenal insufficiency baby Otherwise can use hydrocortisone 2.55mg/kg/dose bd

Clinical approach

Rule 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 children
Prolonged 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")