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HYPOGLYCEMIA AND HYPERGLYCEMIA Izaskun C. Ganao
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Hypoglycemia Almost all fetal glucose is derived from the maternal circulation The severing of the umbilical cord abruptly interrupts the source of glucose To maintain adequate glucose levels Glycogenolysis of hepatic stores inducing gluconeogenesis Feeding During this transition, glucose levels fall in the first 1 to 2 hours and then increase and stabilize at 65 to 70 mg/dl by the age of 3 to 4 hours
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Incidence 16% of LGA 15% of SGA
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Definition of hypoglycemia: Operational Threshold Indication for action; not diagnosis Lower than therapeutic goal Dependent on clinical state and age Do not define normal or abnormal Provide margin of safety
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Cornblath’s description of operational thersholds Healthy term infant <24 hours of age – 30 to 35 mg/dl is acceptable; should be raised to 45 mg/dl after feeding >24 hours – 45-50mg/dl Infant with abnormal signs of symptoms – 45 mg/dl Asymptomatic infants with risk factors for low blood sugar – 36 mg/dl For any baby, if glucose levels are 45mg/dl
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There is no single value by which brain injury definitely occurs Normal asymptomatic babies may have a transient glucose level in the 30s that will increase spontaneously or with feeding Goal 45 mg/dl in the 1 st day >50 mg/dl after the 1 st day
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Etiology 1. Hyperinsulinemic hypoglycemia Infants of diabetic mothers Congenital genetic hyperinsulnism Secondary to other conditions: Birth asphyxia Developmental syndromes such as Beckwith-Wiedemann syndrome) Congenital disorders of glycosylation Erythroblastosis Maternal tocolytic therapy with beta-sympathomimetic agents (terbutaline) Malposition umbilical artery catheter used to infuse glucose in high concentration into the celiac and superior mesenteric arteries – stimulating insulin release from the pancreas Abrupt cessation of high glucose infusion After exchange transfusion with blood containing high glucose concentration Insulin-producing tumors
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Etiology 2. LGA 3. Decreased production/stores Prematurity IUGR Inadequate caloric intake Delayed onset of feeding
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Etiology 4. Increased utilization / decreased production a. Perinatal stress Sepsis Shock Asphyxia Hypthermia Respiratory disetress Postresuscitation
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b. Defects in carbohydrate metabolism Glycogen storage disease Fructose intolerace Galactosemia c. Endocrine deficiency Adrenal insufficiency Hypothalamic deficiency Congenital hypopituitarism Glucagon deficiency Epinephrine deficiency
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d. Defects in amino acid metabolism Maple syrup urine disease Propionic acidemia Methylmalonic acidemia Tyrosinemia Glutaric acidemia type II Ethylmalonic adipic aciduria e. Polycythemia - higher glucose utilization f. maternal therapy with beta-blockers
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Diagnosis Symptoms Tremors, jitteriness, irritability Seizures, coma Lethargy, apathy, limpness Poor feeding, vomiting Apnea Weak or high-pitched cry Cyanosis asymptomatic
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Diagnosis Screening Done in infants with risk factors and with symptoms 30 to 60 minutes of life IGDM SGA Erythroblastosis fetalis (hyperinsulinism)
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Differential Diagnosis Sepsis CNS disease Toxic exposure Metabolic abnormalities (hypocalcemia, hypo or hypernatremia, hypomagnesemia, pyridoxine deficiency) Adrenal insufficiency Heart, renal, and liver failure
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Management Well infants at risk (IGDM) Measure blood glucose levels and treat accordingly Other asymptomatic infants at risk HGT on the 1 st 1 to 2 HOL Breastfeed or give formula ASAP then every 2 to 3 hours 20 to 25 mg/dl – IV glucose. Goal is to maintain the glucose >45 mg/dl in the 1 st 24 hours and >50 thereafter
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Management Feeding Asymptomatic with hgt 30mg/dl Breastfeeding or formula Repeat hgt 1 hour after onset of feeding Glucose water not recommended
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IV therapy Indications Inability to tolerate oral feeding Symptoms Oral feedings do not maintain normal glucose levels Glucose levels less than 25mg/dl Urgent treatment 200mg/dl of glucose over 1 minute, to be followed by continuing therapy Equivalent to 2ml/kg of dextrose 10% in water (D10W) IV
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IV therapy Continuing therapy Glucose infusion at 6 to 8 mg of glucose/kg/minute D10W at a rate of 86.4ml/kg/day or 3.6 ml/kg/hr gives 6 mg/kg/minute of glucose Glucose infusion rate (GIR) (GIR) in mg/kg/min= dextrose % concentration x ml/kg/day 144 e.g.: an infant receiving D10W at 80ml/kg/day GIR= 10 x 80 = 5.6 mg/kg/min. 144
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IV therapy Continuing therapy Repeat hgt after 20 to 30 minutes then hourly until stable to determine if IV therapy still needed Additional bolus infusions of 2mg/kg of D10W may be needed If glucose is stable and in acceptable range, continue feedings and taper infusions as permitted by glucose levels prior to feeding May give D10W at maintenance rate Infants with hyperinsulinism or IUGR – 12 to 15 mg of dextrose per kg per minute (often as 15% or 20% dextrose water)
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IV therapy May give hydrocortisone at 5mg/kg/day to reduce peripheral glucose utilization Diazoxide – for persistently hyperinsulinemic infants Octreotide – if diazoxide not effective Glucagon – for mobilization of glucose (if the infant has good glycogen stores) Imaging studies for pancreatic function
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Hyperglycemia Whole blood glucose level of >125mg/dl or plasma glucose level of >145mg/dl Common in infants with LBW receiving parenteral glucose Clinical problems Hyperosmolarity Osmotic diuresis if osmolarity >300 mOsm/L Possible diabetes mellitus
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Etiology Exogenous parenteral glucose Drugs Steroids Caffeine Theophylline Phenytoin Diazoxide ELBW infants Lipid infusion
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Etiology Sepsis – due to depressed insulin release, cytokines, endotoxin resulting in decreased glucose utilization “stressed” premature infants Hypoxia Surgical procedures Neonatal DM – usually SGA term infants, no gender predilection, with family hx of DM Diabetes due to pancreatic lesions
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Etiology Transient hyperglycemia associated with ingestion of hyperosmolar formula Hepatic glucose production Immature development of glucose transport proteins (GLUT-4)
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Treatment Hgt monitoring in premature infants and infants with abnormal symptoms ELBW infants should start with a GIR of at least 4 to 6 mg/kg/min Parenteral nutrition ASAP in LBW infants. Some amino acids promote insulin secretion Feeding Exogenous insulin therapy of glucose levels >250mg/dl Oral sulfonylureas (long term therapy)
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