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Neonatal Hypoglycemia
Amy Bloomquist, RNC,MSN
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Definition
The S.T.A.B.L.E. Program defines hypoglycemia as:
“Glucose delivery or availability is inadequate to meet glucose demand” (Karlsen, 2006)
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What is Normal?
Defining a normal glucose level remains controversial
50 – 110 mg/dl (Karlsen, 2006)
> 40 mg/dl (Verklan & Walden, 2004)
> 30 term, > 20 preterm (Kenner & Lott, 2004)
> 45 mg/dl (Cowett, R. as cited by Barnes-Powell, 2007)
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McGowan, 1999 as cited by Verklan & Walden
Incidence of Hypoglycemia
Overall Incidence = 1- 5/1000 live births
Normal newborns – 10% if feeding is delayed for 3-6 hours after birth
At-Risk Infants – 30%LGA – 8%
Preterm – 15%
SGA – 15%
IDM – 20%
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Karlsen, 2006
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.
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Verklan & Walden, 2004
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”.
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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
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!
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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.
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Karlsen, 2006
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
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Karlsen, 2006
Factors that negatively affect glucose availability after birth
Inadequate Glycogen
Increased Utilization of Glucose
Excessive Insulin
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Karlsen, 2006
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.
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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.
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Karlsen, 2006
Increased Utilization of Glucose
Sick/Stressed infantsCauses increase in metabolic demand
Uses up glucose quickly.
These include all sick, premature and SGA infants.
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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
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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
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IDM - Incidence
106,000 in 1999Rate of Type II Diabetes has increased by 33% in past 20 yearsWomen at highest risk
African-AmericanHispanicAmerican IndianAsianObese
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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 motherExcessive formation of oxygen radicals that damage the mitochondriaThis increase in oxidative stress results disrupts vascularization of the developing tissues.
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IDM – fetal anomalies
Hyperglycemia alters the expression of regulating genes leading to altered cellular mitosis and the normal timing of cell death. Excessive cell death results in fetal anomalies.Caudal regression syndromeHydronephrosisRenal agenesisMicropenisCystic kidneysIntestinal atresias
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Effect on CNS
Anencephaly
Spina bifida
Caudal dysplasia
CNS damage as a result of Birth trauma (macrosomia)
Glucose and electrolyte abnormalities
Perinatal asphyxia
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Other Effects on the Neonate
RDS
CHD VSD
Asymmetric septal hypertrophy
Thickened myocardium
Transposition of the greater vessels
Polycythemia and vascular sludging
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Nursing Management
Complete evaluation and review of systems
Early breast or bottle feeding within 30 minutes
Glucose monitoring within 1 hour
Monitor pre-feeding levels thereafter
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Kenner, 1998
Monitoring
Serum glucose level is the gold standard
Bedside glucose levels are for screening
Monitor at least hourly until glucose level has stabilized
Know your hospital policy for monitoring infants at risk for hypoglycemia
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Verklan & Walden, 2004
Signs & Symptoms of Hypoglycemia
Jitteriness
Irritability
Hypotonia
Lethargy
High-pitched cry
Hypothermia
Poor suck
Tachypnea
Cyanosis
Apnea
Seizures
Cardiac arrest
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Karlsen, 2006
Treatment
Oral feedings as tolerated
If glucose is very low or the infant is not able to feed orally:
2ml/kg of D10W IV bolus
Follow up screenings within 30 minutes
Repeat bolus if glucose is < 50 mg/dl
If unable to stabilize glucose consider increasing IV rate or glucose concentration
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Prevention
Increase awareness of conditions that predispose an infant to hypoglycemia
Early screening of at-risk infants
Early and frequent feedings
Maintain temperature
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References
Barnes-Powell, L. (2007). Infants of Diabetic Mothers: The effects of hyperglycemia on the fetus and neonate. Neonatal Network, 26(5) p. 283-289.
Karlsen, K. (2006) The S.T.A.B.L.E. Program. Pre-transport/Post-resuscitation Stabilization Care of /sick Infants, Guidelines for Neonatal Healthcare Providers. 5th Edition.
Kenner, C., Lott, J. (2004). Neonatal Nursing Handbook. Elsevier.
Verklan, M., & Walden, M. (2004). Core Curriculum for Neonatal Intensive Care Nurses. Elsevier.