Neonatal Hypoglycemia. Presented By : Kamlah Olaimat 25\7\2010

Transcription

1 Neonatal Hypoglycemia Presented By : Kamlah Olaimat 25\7\2010

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) Also its defined as a serum glucose value < 40mg\dl in term and preterm infant.

3 What is Normal? Defining a normal glucose level remains controversial 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) There is no evidence to support the hypothesis that preterm infants can tolerate lower glucose level than kamlah term olaimat 25\7\2010 infant

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%

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.

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.

7 Mechanism of hypoglycemia Hyperinsulinism with increased glucose utilization ( infant of DM) Decreased production and storage of glycogen and fat ( preterm infant, IUGR) Increased utilization and decreased production of glucose (prenatal stress )

8 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.

9 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!

10 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.

11 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

12 Factors that negatively affect glucose availability after birth Inadequate Glycogen Increased Utilization of Glucose Excessive Insulin

13 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.

14 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.

15 Increased Utilization of Glucose Sick/Stressed infants Causes increase in metabolic demand Uses up glucose quickly. These include all sick, premature and SGA infants.

16 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

17 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

18 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

19 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.

20 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 Cystic kidneys Intestinal atresias

21 Caudal Regression Syndrome Spectrum of malformation cessation of growth of rostral portion of spinal cord abnormal neural, muscular, skeletal and vascular components Caudal Regression with limbs intact but malformed Sirenomelia Absence of hind limbs, external genitalia, anus and rectum; Potter sequence secondary renal agenesis

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

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

24 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

25 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

26 Signs & Symptoms of Hypoglycemia Jitteriness Irritability Hypotonia Lethargy High-pitched cry Hypothermia Poor suck Tachypnea Cyanosis Apnea Seizures Cardiac arrest

27 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

28

29

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

31 What if hypoglycemia occurs prolonged, recurrent or persistent? Recurrent of Persistent Hypoglycemia: 1) Require infusions of large amounts of glucose (>12 16 mg/kg/min) to maintain normoglycemia

32 What if hypoglycemia occurs prolonged, recurrent or persistent? 1) Persisting or recurring beyond the first 7-14 days of life **Prompt recognition is essential!! These conditions are associated with severe disease at substantial risk of developing severe mental retardation and epilepsy. These include many conditions stated previously including: Hormone deficiencies, Hyperinsulinism syndromes, Defects in carbohydrate, amino acid, fatty acid metabolism

33 What tests should you do? What is your management? Assay for insulin, C-peptide, growth hormone, lactate, free fatty acids, T4, TSH, Urine for reducing substances, ketones, organic acids Management includes: Glucagons (0.3 mg/kg/dose bolus or infusion 1-2 mg/day); Add 1 mg to 24 ml of D10W and run at 1 ml/hour through separate lie Continue to increase the glucose infusion rate to 12-15mg\kg\min Corticosteroid, hydrocortisone 5mg\kg\d Diazoxide 3-5 mg\kg\d. IV, IM, SC Human growth hormone

34 A man with a watch knows what time it is. A man with two watches is never sure Thank you for your attention. I hope it was interesting. Please give your feed back,, you may not write your name.

35 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. Pretransport/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.