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)
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%
McGowan, 1999 as cited by Verklan & Walden
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.
Karlsen, 2006
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”.
Verklan & Walden, 2004
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.
Karlsen, 2006
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.
Haney, 2005
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
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.
Karlsen, 2006
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.
Karlsen, 2006
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 – 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 1999
Rate of Type II Diabetes has
increased by 33% in past 20 years
Women at highest risk
African-American
Hispanic
American Indian
Asian
Obese
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
Excessive formation of oxygen radicals
that damage the mitochondria
This 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 syndrome
Hydronephrosis
Renal agenesis
Micropenis
Cystic kidneys
Intestinal 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
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
Kenner, 1998
Signs & Symptoms of
Hypoglycemia
Jitteriness
Irritability
Hypotonia
Lethargy
High-pitched cry
Hypothermia
Poor suck
Tachypnea
Cyanosis
Apnea
Seizures
Cardiac arrest
Verklan & Walden, 2004
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
Karlsen, 2006
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. Pretransport/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.