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WakeMed's 24-48 hour Blood

Glucose monitoring protocol


Laura Parrish PNP
Objectives
● Review hypoglycemia experience with risk
factors
◦ Apgar <6
◦ Maternal beta blocker

● Discuss
Wakemed’s hypoglycemia
protocol for infants >24 hrs of life.
How maternal beta blockers induce infant
hypoglycemia
● Intrauterineexposure to maternal beta
blockers cause a sympathetic blockade in
the infant
● Beta-blockers can cross the placenta,
causing a decrease in glycogenolysis
● Beta blockers mask symptoms of
hypoglycemic including tremors

● Bateman BT, Patorno E, Desai RJ, et al. Late Pregnancy β Blocker Exposure and Risks of Neonatal Hypoglycemia and
Bradycardia. Pediatrics. 2016;138(3):e20160731. doi:10.1542/peds.2016-0731
How does perinatal stress cause
hypoglycemia
● Perinatalstress can cause a transient
hyperinsulinism that may persist for
days to months
● Hyperinsulinism diagnosis
◦ Elevated insulin
◦ Suppressed BHOB
◦ 30 point rise in glucose after glucagon
injection
Rationelle for 24-48 protocol
● Normal neonatal glucose adaptation may
take 48 hrs to normalise
● WakeMed culture included monitoring
infants in the second 24 hrs of life
Case study
● 39 wk AGA infant born via vaginal delivery
● Risk factors: 1 min Apgar 5 (nuchal cord)
● Initial BG 47mg/dL
● Second BG was 28 mg/dL - gel given
● Subsequent BG were 41, 43, and 47 mg/dL
● BG at 27 hrs was 44 mg/dL
● Gel, feeding, and skin to skin were
implemented
● Remaining prefeed BG’s were 56, 60 and 58
Practice highlights post 24 hrs
● Obtain prefeed BG after 24 hrs of life in
conjunction with newborn screen
● BG <50 at 24hrs is due to:
◦ Lack of substrate therefore supplementation is
required
◦ Continued dysregulated insulin secretion
● Physiologic
● Pathologic
● Unresponsive to one dose of gel in Newborn
Nursery requires NICU admission
NICU admissions before and after
implementation of glucose gel

Average 13.2%

Average 17%
History
● Thank you
Postnatal glucose adaption
● Fetal plasma glucose concentration approximately 70% to 80% of that of the
maternal venous plasma glucose concentration.
● Insulin does not cross the placenta; therefore, the fetus must secrete insulin
independently.
● With the clamping of the umbilical cord, the neonate’s supply of glucose ceases
while insulin secretion continues.
● The residual fetal insulin leads to a rapid decline in plasma glucose within the
first hours of life.
● To overcome decreasing glucose concentrations, the release of
counterregulatory hormones such as glucagon and cortisol in combination with
the production of endogenous glucose through gluconeogenesis and
glycogenolysis occurs.
● In healthy neonates, feeding is also initiated within approximately 12 hours of
birth
● If NPO other metabolic substrates such as ketones will likely increase to offset
the effects of lower glucose concentrations.
● Transient hypoglycemia can occur during the first hours of life because of a
slow or immature fasting adaptation process.
Srinivasan G, Pildes RS, Cattamachi G. Plasma glucose values in normal neonates
a new look. J Pediatr. 1986;109(1):114–117. et al.
Glucose hemostasis
● Insulin and glucagon are released from pancreatic islet cells during the fed and fasting states. β-cells within islet
cells contain ATP-sensitive potassium channels (KATP channels) and voltage- gated calcium channels (VGCC)
that coordinate the secretion of insulin; while glucagon is secreted from α-cells.

● Increasing glucose concentrations activate glucokinase, and β-cell glycolysis begins. This glycolytic pathway along
with free fatty acids increases adenosine triphosphate (ATP) production within the β-cell. KATP channels consist
of two subunits, the sulfonylurea (SUR) and the inward rectifier potassium channel (Kir6.2) subunits. The
increase of ATP activates the SUR subunit, which closes the KATP channel. With the closing, depolarization of
the cell occurs, leading to an influx of Ca2+ through the VCGG, stimulating the release of insulin.11 In contrast,
decreasing glucose concentrations during the fasting state stimulate the release of glucagon. The exact
mechanism is not completely understood; however, the mechanism may also be related to KATP channels within
the α-cells.12 Glucagon helps regulate gluconeogenesis and glycogenolysis within the liver as a counterregulatory
agent to insulin.

● Exaggerated insulin secretion from β-cells can occur during the first few hours to days of life, resulting in
hyperinsulinemia, which is the leading cause of hypoglycemia in neonates.5 Many mechanisms have been
associated with this hypersecretion of insulin. The most prevalent cause of persistent hyperinsulinemia is the loss
of function mutation of the KATP channel, which may lead to profound hypoglycemia. Other less common
mechanisms include mutations of mitochondrial enzyme (GDH), activating mutation in glucokinase, and mutations
of short-chain 3-hydroxyacyl-coenzyme A dehydrogenase.5 Hyperinsulinemia may be of a transient, prolonged,
or persistent nature, leading to various degrees of severity of hypoglycemia.

● Sweet CB, Grayson S, Polak M. Management strategies for neonatal hypoglycemia. J Pediatr Pharmacol Ther.
2013;18(3):199–208. doi:10.5863/1551-6776-18.3.199