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 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 3 rd 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 3 rd 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 infants Causes increase in metabolic demand Uses up glucose quickly. These include all sick, premature and SGA infants.

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

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 D 10 W 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 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. 5 th Edition. Kenner, C., Lott, J. (2004). Neonatal Nursing Handbook. Elsevier. Verklan, M., & Walden, M. (2004). Core Curriculum for Neonatal Intensive Care Nurses. Elsevier.