Neonatal Hypoglycemia PI Project
Karen Lynne BSN RNC-MNN RNC-LLN - SH Intermediate Level Nursery
Neonatal Hypoglycemia (NH) is one most common and life threatening issues
neonates face during transition to extrauterine life. (2,3,4,6) The fetus
relies entirely on maternal supply and placental transfer of glucose,
amino acids, fatty acids ketones and glycerol for its energy needs. There
is no fetal production of glucose and does not normally occur until after
birth. Also, insulin does not cross the placenta; therefore, the fetus
must secrete its own. After birth, and clamping of the umbilical cord,
the abrupt cessation of maternal nutrition, with continued neonatal secretion
of insulin causes a drop in newborn blood glucose. To counteract the dropping
glucose levels, the infant begins the process of gluconeogenesis (the
conversion of glucose from non- carbohydrates such as glycerol, fatty
acids, lactate and amino acids) and glycogenolysis (the breakdown of glycogen).
(2,4,5,6) If feeding is not initiated (enteral intake of glucose), ketone
metabolism will be stimulated.
This process causes a normal transitional hypoglycemia in the newborn with
glucose levels falling during the first two hours after delivery, then
stabilizes by four to six hours of age. Concentrations then rise more
slowly in the next few days to concentrations similar to those seen in
older children and adults.
Clinically significant NH reflects the imbalance of glucose utilization
and supply. The authors of several literature reviews have concluded that
there is no consensus regarding who is at risk, the specific plasma glucose
value for hypoglycemia, what level and duration might cause neurologic
injury, or optimal management of neonatal hypoglycemia. Cornblath et al
summarized this lack of consensus:
"Unfortunately, untoward long-term outcomes in infants with one or
two low blood glucose levels have become the grounds for litigation and
for alleged malpractice, even though the causative relationship between
the two is tenuous at best... The definition of clinically significant
hypoglycemia remains one of the most confused and contentious issues in
contemporary neonatology." (2)
In response to the confusion, Cornblath et al developed a concept of an
“operational threshold” for practitioners to use as a guide
in treatment, based on the most current evidence. The threshold is not
a diagnosis or indicator of future sequelae, but an indicator of action.
Its focus is on the individual and does not clarify for how long or how
far below the threshold a value can be before treatment is started. (2)
In March 2011, the American Academy of Pediatrics presented a report to
“provide a practical guide and algorithm for the screening and subsequent
management of neonatal hypoglycemia.” (1) According to the guidelines,
infants at highest risk for significant hypoglycemia are SGA and LGA infants,
those born to mothers with diabetes, or are late-preterm. Routine monitoring
of blood glucose level is recommend on at risk infants and those who have
clinical manifestations of NH.
On the SH LDRP inpatient unity, hospital policy follows AAP guidelines
for the care and management of infants in regards to Neonatal Hypoglycemia.
In early 2015, it came to my attention from our physicians that infants
at risk are not being captured, and there are others who have not had
monitoring completed by the guidelines. This Quality Improvement (QI)
Project was meant to improve patient care determining the reasons at risk
infants have not been monitored according to AAP guidelines.
Data collected showed five main reasons that some of the infants were
falling off the AAP guidelines fell into five categories: missed maternal
risk factors, algorithm not started appropriately, missed glucose checks,
glucose checks stopped too early, and extra glucose checks obtained. Through
a series of staff education (bulletin board inservice and peer to peer
inservice) and assistance with understanding the algorithm, we were able
to decreased the percentage of infants missing AAP guidelines by almost
50%, meeting our primary goals to recognize infants at risk of disturbances
in postnatal glucose homeostasis and provide a margin of safety by early
measures to prevent and treat low concentrations of serum glucose.
1. Amercian Academy of Pediatrics Committee on Fetus and Newborns (2011).
Postnatal glucose homeostasis in LatePreterm and Term Infants. Pediatrics,
2. Cornblath M, Hawdon J, et al. Controversies Regarding Definition of
Neonatal Hypoglycemia: Suggested Operational Thresholds. Pediatrics 2000;
3. Sweet C, Grayson S, Polak M. Management Strategies for Neonatal Hypoglycemia.
J Pediatr Pharmacol Ther 2013; 18(3): 199-208
4. Pathogenesis, screening, and diagnosis of neonatal hypoglycemia. Retrieved
5. Wight N, Marinelli K, and The Academy of Breastfeeding Medicine. ABM
Clinical Protocol #1: Guidelines for Blood G;ucose Monitoring and Treatment
of Hypoglycemia in Term and Late-Preterm Neonates, Revised 2014. Breastfeeding
Medicine 2014; 9(4): 173-179
6. Hay W, Tonse R, et al. Knowledge Gaps and Research Needs for Understanding
and Treating Neonatal Hypoglycemia: Workshop Report from Eunice Kennedy
Shriver National Institute of Child Health and Human Development. J Pediatr
2009; 155(5): 612-617