Neonatal Hypoglycemia

Amy Bloomquist, RNC,MSN

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 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)

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%

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.

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”.

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.

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!

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.

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

Karlsen, 2006

Factors that negatively affect glucose availability after birth

Inadequate Glycogen

Increased Utilization of Glucose

Excessive Insulin

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.

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.

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.

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 – 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

IDM - Incidence

106,000 in 1999Rate of Type II Diabetes has increased by 33% in past 20 yearsWomen at highest risk

African-AmericanHispanicAmerican IndianAsianObese

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.

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

Effect on CNS

Anencephaly

Spina bifida

Caudal dysplasia

CNS damage as a result of Birth trauma (macrosomia)

Glucose and electrolyte abnormalities

Perinatal asphyxia

Other Effects on the Neonate

RDS

CHD VSD

Asymmetric septal hypertrophy

Thickened myocardium

Transposition of the greater vessels

Polycythemia and vascular sludging

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

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

Verklan & Walden, 2004

Signs & Symptoms of Hypoglycemia

Jitteriness

Irritability

Hypotonia

Lethargy

High-pitched cry

Hypothermia

Poor suck

Tachypnea

Cyanosis

Apnea

Seizures

Cardiac arrest

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

Prevention

Increase awareness of conditions that predispose an infant to hypoglycemia

Early screening of at-risk infants

Early and frequent feedings

Maintain temperature

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.