Neonatal Hypoglycemia

1. Neonatal Hypoglycemia Amy Bloomquist, RNC,MSN

2. Definition • The S.T.A.B.L.E. Program defines hypoglycemia as: • “Glucose delivery or availability is inadequate to meet glucose demand” (Karlsen, 2006)

3. 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)

4. 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

5. 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

6. 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

7. 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

8. 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

9. 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

10. 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

11. Factors that negatively affect glucose availability after birth • Inadequate Glycogen • Increased Utilization of Glucose • Excessive Insulin Karlsen, 2006

12. 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

13. 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.

14. 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

15. 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

16. 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

17. 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

18. 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.

19. 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

20. Effect on CNS • Anencephaly • Spina bifida • Caudal dysplasia • CNS damage as a result of • Birth trauma (macrosomia) • Glucose and electrolyte abnormalities • Perinatal asphyxia

21. Other Effects on the Neonate • RDS • CHD • VSD • Asymmetric septal hypertrophy • Thickened myocardium • Transposition of the greater vessels • Polycythemia and vascular sludging

22. 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

23. 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 Monitoring Kenner, 1998

24. Jitteriness Irritability Hypotonia Lethargy High-pitched cry Hypothermia Poor suck Tachypnea Cyanosis Apnea Seizures Cardiac arrest Signs & Symptoms of Hypoglycemia Verklan & Walden, 2004

25. 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

26. Prevention • Increase awareness of conditions that predispose an infant to hypoglycemia • Early screening of at-risk infants • Early and frequent feedings • Maintain temperature

27. 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.