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Lisa A. Lubbers, RN MSN CNP October 16, 2014 South Dakota Perinatal Association No financial interest 1. • Identify 3 risk factors for hypoglycemia in neonates 2. • Identify 3 main factors impacting blood glucose after birth 3. • Identify 3 symptoms of hypoglycemia in neonates Primary fuel for the body-brain has higher demand for glucose Brain can’t store adequate amounts in the form of glycogen like liver, skeletal/cardiac muscle can Needs a steady supply Irreversible neuronal injury can result from hypoglycemia Hypoglycemic brain more vulnerable to damaging effects of ischemia -sick infants have increased requirements Glycogenesis-process by which unneeded glucose is converted to glycogen for storage Glycogenolysis-process which causes the breakdown of glycogen back into glucose Gluconeogenesis-production of glucose in the liver by means of nonglucose precursors like lactate, pyruvate, glycerol, and amino acids Insulin-secreted by pancreatic BETA cells in response to increase in plasma glucose Decreases blood glucose by promoting glycogen formation, suppressing hepatic glucose release, driving peripheral uptake of glucose. Doesn’t control entry of glucose in the brain or liver Glucagon-secreted by pancreatic ALPHA cells Promotes glycogenolysis and gluconeogenesis Opposes effect of insulin by raising blood glucose Other counter regulatory hormones-cortisol, growth hormone, catecholamines Fetus stores glucose as glycogen and develops enzymatic process for mobilization of stored energy prior to birth Limited ability to convert glycogen to glucose as a fetus so relies on placental transfer (facilitated diffusion) of glucose to meet energy demands Fetus is capable of gluconeogenic activity using lactate if needed to meet metabolic demands in utero When the cord is cut enzymes activate the breakdown of glycogen back into glucose molecules in the infants body After Delivery In Utero High insulin : glucagon ratio -Suppresses lipolysis {subcutaneous fat} -Glycogen deposition { last 30% fetal life} High glucagon : insulin ratio { catecholamine release} -Release of glucose from glycogen -Term infants have enough hepatic glucose for 10 hours -Induces enzymes for gluconeogenesis •Occurs about4-6 h of age •Enzymes reach Adult levels by 1-2 wk-slower in preterm Immediate postnatal drop is physiologic Balance between hepatic glucose output and substrate uptake Hepatic output dependent on adequate glycogen stores, endogenous gluconeogenic precursors, normal functioning gluconeogenic and glycogenolytic systems and normal endocrine system At birth, glycogen stores greater than adults, but 2x greater basal glucose utilization equals rapid depletion Hormonal and enzymatic activities in FETUS promote anabolism and substrate accretion Hormonal and enzymatic activities in NEWBORN provide for glucose homeostasis after abrupt interruption of maternal glucose supply-this needs to occur in the course of seconds! Metabolized Production of energy-via glycolysis several different ways in BODY: Aerobic Metabolism-1 molecule of glucose yields 36 molecules of ATP for energy Anaerobic Metabolism-1 molecule of glucose yields 2 molecules Storage as glycogen Conversion to gluconeogenic precursors Brain :glucose is completely oxidized to provide 99% of cerebral energy production Brain is another story-dependent on enzymes and reactions GLUT proteins transport glucose across blood brain barrier into brain cells During hypoglycemia ketone bodies, lactate, glycerol, and AA can also be converted to pyruvate and citric acid cycle—so another source but not efficient http://davisdialogues.blogspot.com/2011_08_01_archive.html Glucose requirement for a healthy near term/term infant is 5-8 mg/kg/min (D10W at 80 ml/kg/day gives a GIR of 5.5mg/kg/min) Many other factors can contribute to requirements-may need much more App: glucose infusion rate calculator GIR (mg/kg/min)= IV rate X %dextroseX.167 wt in kg Preterm Infants Small For Gestational Age (SGA) IDM Large for Gestational Age (LGA) Stressed/Sick Infants Maternal Medications Other causes: Persistent neonatal hyperinsulinism and nesidioblastosis (AR caused by regulatory defects in beta cell function) Beckwith Wiedemann-unknown cause Inborn errors of carbohydrate, protein, or lipid metabolism Endocrine deficiencies (hypopituitarism) Several new genetic mutations have been identified Iatrogenic –umbilical arterial catheter position near pancreas (high T 6-9 low L3-4) The most common causes: Preterm SGA LGA IDM Sick infants Majority of glycogen stored in 3rd trimester Available stores rapidly depleted At TERM 5-8% of liver and muscle weight is glycogen storage Immature counter regulatory response to low glucose concentrations Preterm, SGA lack adipose required for ketone production or unable to mobilize free fatty acids from adipose Preterm-may not have enzymes required for he breakdown of glycogen into glucose (glycogenolysis) Less than 10% for weight Causes Placental insufficiency-chronic stress Chromosome/genetic abnormalities Metabolic disorders Intrauterine viral infection Multiple gestation Nutritional status Maternal chronic illness/stress Ingestion of drugs/toxins Some maternal medications Low glycogen and fat stores Inadequate metabolic control Chronically stressed fetus may use most of the placentally transferred glucose for growth and survival Greater than 90% Insulin is a growth hormone-suppresses glucagon response Causes hyperinsulinemia r/t: Undiagnosed GDM (ethnicity, PCOS, family hx of Type II DM) Inborn errors Endocrine disorders Glucose crosses placenta/insulin does not Fetal glucose level 70-80% of mother’s Infant produces insulin in response to higher blood sugars At cord clamping, glucose supply is gone but insulin production in infant remains elevated The expected nadir is more rapid than non IDM infants (1-6 hours) May take several days to down regulate insulin production Fetal hyperglycemia=increased production Insulin IGF-1 Leptin All lead to stimulation of fetal growth Higher energy needs Hypoxic infants may rely on anaerobic glycolysis (inefficient-large amount of glucose used for low yield) Aerobic metabolism yields 38 ATP per molecule of glucose Anaerobic yields 2 ATP per molecule of glucose Therefore, rapidly deplete stores Current literature does not endorse a particular number (40,45,47,50) Symposium on Pediatric Endocrinology 2014->45 for symptomatic infants and >65 for hyperinsulinism Blood glucose level can only approximate cerebral glucose level All agree treatment for symptomatic infants Goal is to screen infants in high risk groups-and intervene appropriately At risk infants may need to be screened differently depending on their risk factors Consider an evidence based algorithm for your facility Glucose goals may vary depending on disease process, chronological age Consider goal of 50 mg/dl after 24 hours of age-especially if high risk category If requiring high GIR, consider weaning IV for glucose levels >60 mg/dl Potential disruption in bonding/breastfeeding Repeated heel sticks Invasive procedures Uncertainty in what “right” number should be Discrepancy in bedside POC and lab glucose values-POC underestimates Variation in specimen handling and obtainment Infants at risk may have their first low glucose concentrations after 3 normal measurements and even after 24 hours of age 3 normal measures don’t ensure complete transition Consider including 24 hour check into algorithms Need to be certain infant maintains normal glucoses on routine diet for at least 3 feed/fast cycles prior to discharge Screening for and management of postnatal glucose homeostasis in late-preterm (LPT 34–3667 weeks) and term small-for-gestational age (SGA) infants and infants who were born to mothers with diabetes (IDM)/large-for-gestational age (LGA) infants. Committee on Fetus and Newborn Pediatrics 2011;127:575-579 ©2011 by American Academy of Pediatrics Most neonates are free of symptoms-development of symptoms can be ameliorated by presence of alternative substrates Many symptoms can be linked to other issues General Abnormal cry Poor feeding Hypothermia diaphoresis Neurologic Tremors/jitteriness Irritability Lethargy Hypotonia seizures Cardio respiratory Tachypnea Apnea cyanosis Confirm with STAT lab blood glucose but DON’T delay treatment in symptomatic infant Tend to be 10-20% higher than whole blood (POC) values Follow up checks are imperative Should be feed within 1 hour of age Screen 30 minutes after feed Consider gavage feeding if not nursing/nippling well Glucose less than 25 mg/dL (birth to 4 hours) or less than 35 mg/dL (4-24 hours):feed and recheck 1 hour after feeding If still less than 25 or 35:treat with intravenous glucose infusion and/or 2ml/kg D10W bolus D10W at 80 ml/kg/day give GIR of 5.5 mg/kg/min Merits of bolus are debatable, may stimulate insulin and this may pose risk for rebound hypoglycemia Goal: 40-50 mg/dL If hyperinsulinism is suspected consider insulin level, serum ketone bodies, and free fatty acids to confirm diagnosis-if persistent hypoglycemia beyond 24 hours of age Infants with hyperinsulinemia may require >12 mg/kg/min IV glucose to maintain euglycemia! Central IV access if using >12.5% dextrose Worry about fluid overload Weaning Stable glucose 12-24 h Follow preprandial glucose Decrease infusion rate 10-20% each time glucose >50-60 mg/dl Hydrocortisone Decreased peripheral utilization Stimulates gluconeogenesis ? Consider when needing >15 mg/kg/min Glucagon Rapid rise in glucose Must have adequate glycogen stores (not premies or SGA) Temporizing measure 200 mcg/kg IV, SC, IM Response within 20 min-1 hr Lasts up to 2 hours Watch for rebound hypoglycemia Diazoxide-inhibits secretion of insulin Treatment of persistent (more than a few days) or severe hypoglycemia d/t hyperinsulinism Positive response usually 48-72h Sodium and fluid retention is common Somatostatin (octreotide)-inhibitor of growth hormone, glucagon, and insulin Pancreatectomy Sugar Babies Study-published 9/2013 Randomized, double blind, placebo controlled Stratified by maternal diabetes and birth weight Twins assigned independently Placebo was carboxymethyl cellulose gel Large enrollment group (514)-242 became hypoglycemic and were randomized New Zealand 40% dextrose gel with and without feeding Focus on at risk infants 35 weeks or older 48 hours of age or less IDM SGA LGA Keep mom and baby together Potentially no interruption in breastfeeding Decrease use of formula Easy to administer Low cost BG measurements at 1h, q3-4h ac for 1st 24 h then q 6-8h ac for next 24 h Continuous glucose monitor placed SQ as soon after birth as possible and remained for at least 48h or up to 7days until hypoglycemia resolved Breast fed (or syringe fed expressed BM) Formula fed offered up to 60 ml/kg/day 1st day and 90 ml/kg/day on 2nd day Dry baby’s mouth with gauze Squirt a small amount of dextrose gel into a small cup Using a syringe draw up 0.5 ml/kg (200 mg/kg) of gel Using a gloved finger dispense ½ the dose onto the buccal mucosa of one cheek and massage thoroughly Repeat with the other ½ dose in the other cheek Encourage the infant to feed Blood glucose checked 30 min after administration If continued hypoglycemia repeat If reoccurrence treat again, up to 6 doses of gel in 48 hours Primary outcome-treatment failure Blood glucose less than 47 mg/dL 30 min after the second of 2 doses of gel Secondary outcome Admission to NICU Frequency of breastfeeding Volume of breast milk/formula IV dextrose Dextrose gel Method of feeding at 2 weeks Incidence of rebound or recurrent hypoglycemia(glucose <47mg/dL after successful tx) Time to achieve glucose >47 mg/dL Duration of glucose < 47 mg/dL Infants in the dextrose gel group less likely to be admitted for hypoglycemia Treatment babies less likely to receive additional dextrose Rebound hypoglycemia uncommon and similar in frequency in both groups Recurrent hypoglycemia less common in babies in the dextrose gel group Total duration of low glucose concentrations not significantly reduced with dextrose gel Treatment was well tolerated No serious adverse events Treatment more effective than feeding alone for reversal of hypoglycemia in at risk late preterm and term babies in the first 48 hours Babies who received dextrose gel less likely to be admitted to NICU for management of hypoglycemia, to receive additional dextrose gel or formula feeds, or to be fed formula at 2 weeks of age Dextrose gel didn’t increase the risk of rebound or recurrent hypoglycemia Initial concern for dextrose gel adversely affecting breastfeeding, but this wasn’t demonstrated Dextrose gel should be considered for first line management of late preterm and term hypoglycemic babies in the first 48 hours of life Dextrose gel can be a useful ADJUNCT in the evaluation and management of hypoglycemia Multidisciplinary team-pediatricians, neonatologists, nurse practitioners, dieticians, lactation consultants, nursing, pharmacists Algorithm provides GUIDELINE Asymptomatic Infant With Risk Factors •POCT at one hour >45 continue feeds and check 2 additional prefeed POCT •POCT at one hour <45- apply dextrose gel and feed again (breast or formula supplement) Initiate feed within 1 hour 2 hour serum blood glucose •If <20 apply dextrose gel and feed immediately, plan for other intervention •21-44 apply dextrose gel and feed immediately recheck serum and POCT 30 min after feed •>45 continue feeds and check POCT prefeed x 2 •On all at risk infants •If less than 50 supplement 2040 ml every feed and obtain prefeed POCT. 24 hour check Symptomatic Infant •Apply dextrose gel and feed immediately •If unable to feed apply gel while placing IV <45 IV fluids •D10W at 80 ml/kg/day •Consider 2 ml/kg bolus •Every 30 min-1hr until stable •May need increasing GIR •May need supplement if unable to maintain POCT •Follow at 24 hours no matter what POCT Glucose is an important fuel Several reasons why infants are at risk No uniform consensus on definition All agree to treat symptomatic infants Most important to have a uniform strategy at your facility New adjunct-dextrose gel Kris Karlsen-STABLE program Carmen Henke, RN NNP-BC [email protected] American Academy of Pediatrics (2011). Clinical Report: Postnatal Glucose Homeostasis in Late Preterm and Term Infants. Pediatrics. 127(3)575-579. Arya, V.B., Senniappan, S., Guemes, M., Hussain, K. (2014). Neonatal Hypoglycemia. Indian Journal of Pediatrics. 81(1):58-65. Gardner, S.L. et al.. Merenstein and Gardner’s Handbook of Neonatal Intensive Care. 7th edition. 2011:Mosby Harris, D.L., Weston, P.J., Signal, M., Chase, J.G., and Harding, J.E. (2013). Dextrose gel for neonatal hypoglycaemia (the Sugar Babies Study): a randomised, double-blind, placebo-controlled trial. The Lancet. 1-7. doi.10.1016/s0140-6736(13)61645-1. Hawden, J.M. (2013). Definition of neonatal hypoglycemia: time for a rethink? Archives of Disease in Childhood Fetal and Neonatal Edition. 98:F382-383. Karlson, K.A. (2013). The S.T.A.B.L.E. Program: Pretransport/Postresuscitation Stabilization Care of Sick Infants Guidelines for Neonatal Healthcare Providers. 6th ed. McGowan, J.E. (2006). Neonatal Nutrition and Metabolism (2nd ed). (2006). Cambridge University Press. Rozance, P.J. (2014). Update on neonatal hypoglycemia. Current Opinions in Endocrinology Diabetes and Obesity, 21:45-50. Rozance, P.J. (2012). Editorial: Neonatal Hypoglycemia-Answers, but More Questions. 161(5):775-776. Tin, W. (2014). Defining neonatal hypoglycaemia: A continuing debate. Seminalrs in Fetal and Neonatal Medicine, 19:27-32. doi.org/j.siny.2013.09.003. UpToDate (2014). Neonatal Hypoglycemia. Retrieved January 16, 2014 from http://www.uptodate.com/contents/neonatalhypoglycemia Verklan, M.T. and Walden, M.(4th ed.). Core Curriculum for Neonatal Intensive Care Nursing. Saunders Elsevier (2010).