neonatal hypoglycemia apnec
TRANSCRIPT
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")