Neonatal Hypoglycemia

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  • 1. HYPOGLYCEMIA IN NEWBORN Dr.David Mendez Miami Childrens Hospital Kidz Medical Services
  • 2. INTRODUCTION • Common metabolic problem • Blood glucose in newborns are generally lower than older children & adult • Fetal glucose level maintained at 2/3 of maternal B.glucose by transplacental route • Glucose level fall in Ist 1-2 hrs,lowest value at age of 3 hrs, increase and stabilise by 4 hrs. • New born – glycogenolysis, gluconeogenesis and exogenous nutrients.
  • 3. DEFINITION Defined as a blood glucose level of <40mg % regardless of gestational age and whether or not symptoms are present Whipple’s triad: • low glucose level documented by accurate lab method • Signs and symptoms of hypoglycemia • Resolution of signs and symptoms on restoration of blood glucose levels.
  • 4. ETIOLOGY • Fetal or Neonatal Hyperinsulinism – ↑utilization of glucose.  Decreased production or store  Increased utilization and/or decreased production
  • 5. Hypoglycemia of the newborn  Fetal or Neonatal Hyperinsulinism – ↑utilization of glucose.  Babies born to Diabetic mothers(15-25 % GDM,2550% DM)  LGA infants-16%  Erythroblastosis  Islet cell hyperplasia  Beckwith-Weidemann(macrosomia,microcephaly,omphalocoele,macroglos sia,visceromegaly).
  • 6. Hypoglycemia of the newborn Insulin producing tumors(islet cell adenoma).  Maternal therapy with tocolytics like terbutaline,ritodrine, OHA and diuretics (chlorothiazide)  Glucose infusion through UAC –high glucose into celiac,SMA—stimulate insulin from pancreas
  • 7. Hypoglycemia of the newborn  Decreased production or store:  Prematurity  IUGR (15% in SGA)  Inadequate calorie intake  Delayed onset of feeding
  • 8. Hypoglycemia of the newborn  Increased utilisation or decreased production: Perinatal stress Sepsis/shock/asphyxia/respiratory distress/hypothermia/post resuscitation. Exchange transfusion Heparinised blood with low glucose level CPD blood (relatively hyperglycemic---reactive hypoglcemia Defects in carbohydrate metabolism Glycogen storage disease Fructose intolerance Galactosemia
  • 9. Hypoglycemia of the newborn  Endocrine deficiency Adrenal insufficiency Hypothalamic deficiency Hypopituitarism (neonatal emergencies such as apnea, cyanosis, or severe hypoglycemia with or without seizures, hyperbilirubinemia, and micropenis. ) Glucagon def Epn deficiency  Defects in amino acid metabolism MSUD,propionic acidemia,MMA,tyrosinemia
  • 10. Hypoglycemia of the newborn • Polycythemia -higher glucose utilization by increased mass of RBC  Maternal therapy with beta blockers -Prevention of symp stimulation of glycogenolysis &epinephrine induced increase in FFA
  • 11. DIAGNOSIS • SYMPTOMS Tremors,jitteriness,irritability,seizures,lethargy, poor feeding,vomiting ,limpness,weak or high pitched cry ,cyanosis ASYMPTOMATIC. • MEASURMENT OF BLOOD GLUCOSE glucometer- 15% lower than plasma levels Lab diagnosis-sample obtained and analyzed promptly (18mg/dl/hr)
  • 12. MANAGEMENT • The major long-term sequelae of severe, prolonged hypoglycemia are mental retardation, recurrent seizure activity, or both. • Permanent neurologic sequelae are present in 25–50% ofbabies with severe recurrent symptomatic hypoglycemia • These sequelae are more likely when alternative fuel sources are limited, as occurs with hyperinsulinemia • Anticipation and prevention –key to management of infants with risk factors for HG
  • 13. Routine screening in babies with risk factors • SGA/Smaller of the discordant twin • IDM/LGA • Preterm <35 weeks • On IVF/TPN • Prolonged hypoxia /hypothermia/polycythemia/septicemia/ suspected IEM
  • 14. • After exchange tranfusion • Rh Hemolytic d/s • Babies born to mothers on terbutaline/b-blockers/OHA • Symptomatic babies Screening • within 1 hr of birth • IDM-0,1,3,6 ,12,18.24,48,72 hrs • For 72hrs - risk babies • ET-2 hrs after infusing CPD blood
  • 15. • Early feeding with glucose water raises BG only transiently and asso with rebound hypoglycemia • Early introduction of breast feeds o maintain stable BG levels without rebound HG o keep ketone levels high---alternate fuel during 1st few days while baby adapts to DBF o enhances gluconeogenesis
  • 16. • IV therapy Indications –  intolerance to oral feeds  Symptomatic  oral feeds not maintaining glucose levels  BG level < 25mg/dl
  • 17. o IV glucose through a peripheral line or UVC o Urgent treatment- 2 ml/kg(200mg/kg) of 10% dextrose over 2-3 min. o Severe distress – 2-4 ml/kg 25%D(1g/kg glucose) @ 1ml /kg/mt For eg 2 kg infant-4-8 ml of 25% Dex in 2-4mt o In asymptomatic baby with low BG levels initial push of conc sugar →→hyperinsulinism. Therfore, infusion 5-10 ml of 10% D at 1 ml/mt
  • 18. Continuing therapy – based on Glucose Infusion Rate GIR(mg/kg/min) = % dextrose x ml/kg/day 144 For eg.86 ml/kg/day of 10% D--GIR 6-8 [GIR of 8.33 = 80ml/kg/day of 15%D]
  • 19. • Monitor BG hourly till euglycemic and thereafter 6th hrly • If BG > 40mg%,Continue same and monitor • When 2 BG values >50 mg%,wean GIR by 2mg/kg/mt 6th hrly and start oral feeds Stop infusion when baby is stable @4mg/kg/mt for 12 hr Monitoring stopped when 2 values on oral feeds >50mg%
  • 20. • If BG < 40 mg% Repeat bolus & increase GIR by 2mg/kg/mt every 6 hr till euglycemic If GIR >12 or HG not resolving by day 7 steroids/glucagon/diazoxide Further investigations
  • 21. • Check blood glucose after 30 mts of every change in infusion rate • Monitoring of glucose levels-to ensure adequate correction of hypoglycemia -To avoid hyperglycemia---diuresis---dehydration
  • 22. IDM • <2kg –parenteral therapy in the 1st hour of life • >2 kg- can be fed hourly, for 3 or 4 feeds ,and then 2 hrly • As interval increase ,vol ↑ • If by 2 hrs ,despite feeding GRBS< 40 mg%-parenteral therapy
  • 23. Hydrocortisone • 10mg/kg/day in 2 div doses • MOA-decrease peripheral glucose utilisation, increase gluconeogenesis,increase effects of glucagon • Rapidly tapered off in few days • Before administration of HC ,obtain blood samples for insulin and cortisol levels
  • 24.  Glucagon • Mobilising hepatic glycogen stores • Infants with good glycogen stores • Not in preterms and malnourished • 0.025-0.3 mg/kg IM • Diazoxide (2-5mg/kg q8h PO) – in persistent hyperinsulinemia • Epinephrine • Subtotal pancreatectomy
  • 25. ADDITIONAL TESTS: Endocrine Evaluation • Insulin • GH • Cortisol/ACTH • T4,TSH • Glucagon Metabolic work up • ABG/Blood NH3/ lactate • Plasma or urine amino acids • Urine organic acids • Urine ketones/Urine reducing substance
  • 26. • Na /K-adrenal insufficiency • MRI brain-hypothalamic/pituitary pathology • CT abdomen-islet cell adenoma • Genetic testing – to look for mutations •
  • 27. • Samples to detect insulin levels should be drawn at the time of low BG • Criteria for Diagnosing Hyperinsulinism Based on ―Critical‖ Samples • 1. Hyperinsulinemia (p.insulin >2 μU/mL) • 2. Hypofattyacidemia (p. FFA<1.5 mmol/L) • 3. Hypoketonemia (p. β-hydroxybutyrate: <2.0 mmol/L) • 4. Inappropriate glycemic response to glucagon, 1 mg IV (rise >40 mg/dL)
  • 28. • Hypoglycemia Urine non glucose red substance Present Galactosemia absent ketones
  • 29. ketones high gluconeogenic defect or Organic acidemia low(nonketotic HG) FA oxidation defect or Ketogenic defect Hyperinsulinism
  • 30. DIFFERENTIAL DIAGNOSIS: • Sepsis • CNS disease • Metabolic abnormalities(hypocalcemia,hyponatremia,hypernatr emia,hypomagnesemia,pyridoxine deficiency) • Adrenal insufficiency • Renal failure • Liver failure • Heart failure
  • 31. THANK YOU!
  • 32. Neonatal Hypoglycaemia Dr Varsha Atul Shah Dept of Neonatal and Developmental Medicine Singapore General Hospital
  • 33. Extremes of Birth Weight Neonatal Hypoglycaemia Prematurity
  • 34. Definition • Controversial • Operational threshold • Pragmatic approach • i.e. blood glucose level at which clinical intervention should be considered • Indication for action but not diagnostic of disease • Symptomatic: < 45mg/dl (2.5mmol/L) • Asymptomatic & at-risk: < 36mg/dl (2.0mmol/L)
  • 35. • Significant neonatal hypoglycaemia (Whipple’s triad) • Clinical manifestations • Coincident low plasma glucose level (laboratory) • Clinical signs resolve within mins - hrs of establishing normoglycaemia • Therapeutic objective • Raise plasma glucose level > 45mg/dl (2.5mmol/L)
  • 36. • Term breastfed infants • Can utilise ketones as source of energy in absence of glucose during transient starvation • May tolerate low glucose levels better
  • 37. Clinical Features • Non specific • Apathy, lethargy, irritability • Hypotonia, limpness • Sweating, tremors, jitteriness, abnormal cry (weak / high pitched) • Hypothermia • Poor feeding, vomiting • Apnoea, irregular respiration, respiratory distress, cyanosis • Tachycardia, CCF • Seizures, coma • Asymptomatic
  • 38. Aetiology • utilisation of glucose: hyperinsulinism (Hyperinsulinism: inhibit glycogenolysis & gluconeogenesis) • Infant of diabetic mother (IDM) • Erythroblastosis • Beckwith-Wiedemann syndrome • Islet-cell hyperplasia / hyperfunction • Insulin-producing tumours (nesidioblastosis, islet-cell adenoma) • Maternal drugs (salbutamol, chlorpropamide) • Abrupt cessation of high-glucose infusions
  • 39. Infant of diabetic mum “Cherubic” facies
  • 40. Beckwith-Wiedemann Syndrome Macrosomia, macroglossia, omphalocele, hypoglycaemia, microcephaly
  • 41. • production/stores • Prematurity • Intrauterine growth retardation • Inadequate caloric intake Premature IUGR
  • 42. • utilisation and/or production or others • Stress • • • • Sepsis ( utilisation) Shock Asphyxia ( stores) Hypothermia ( utilisation) • Polycythaemia ( utilisation by • Exchange transfusion • Inborn errors of metabolism red cell mass) • Defect in carbohydrate metabolism • Glycogen storage disease, fructose intolerance, galactosemia • Defect in amino acid metabolism • Maple syrup urine disease, propionic acidemia, etc • Endocrine causes • Adrenal insufficiency, hypothalamic deficiency, congenital hypopituitarism, glucagon deficiency, epinephrine deficiency
  • 43. Management • Prevention • Antenatal & intrapartum care • e.g. control of maternal diabetes, causes of prematurity & IUGR • Avoid environmental stress e.g. cold • Early feeding / IV dextrose infusion
  • 44. • Anticipation • Screening 1. At-risk babies a. Maternal e.g. drugs, intrapartum glucose, diabetes, etc b. Neonatal e.g. asphyxia / perinatal stress, premature, SGA / LGA, low birth weight, sepsis, shock, polycythaemia, etc 2. Those with symptoms Non specific; high index of suspicion
  • 45. • Diagnosis • Screening using glucose reagent strips • Within 2 - 3 hrs after birth & before feeding for 24 - 48 hrs & whenever symptomatic (2 - 4 hrly) • Confirmatory laboratory diagnosis important • Do not delay treatment while waiting for result • Analysed promptly to avoid falsely low value due to glycolysis
  • 46. • Treatment • Aim to maintain plasma glucose > 45mg/dl (2.5mmol/L) • IV dextrose • Mini bolus Dex 10% (2ml/kg) followed by infusion • Central line required for high dextrose concentrations (> Dex 10%) • Continued close plasma glucose monitoring to titrate infusion • Avoid abruptly decreasing dextrose infusion (rebound hypoglycaemia)
  • 47. • Adjunct therapy • Considered if persistent hypoglycaemia despite glucose infusion > 10-12mg/kg/min • Glucagon: stimulates glycogenolysis (adequate glycogen stores) (AGA/LGA) • Hydrocortisone: peripheral glucose utilisation, gluconeogenesis, glucagon effects (prem/SGA) • Rarely: • Diazoxide: inhibits insulin secretion • Somatostatin: inhibits insulin & growth hormone release • Subtotal pancreatectomy: decreases insulin release (insulinsecreting tumours)
  • 48. • Most hypoglycaemia resolve in 2 - 3 dys • Persistent / recurrent hypoglycaemia for > 1 week may require evaluation for other causes • e.g. insulin, cortisol, other endocrine & IEM studies during period of hypoglycaemia • During a period of hypoglycaemia, a normal infant’s blood insulin level should be low or absent. If it is very high suggests hyperinsulinism. It inhibits braeking down of glyconen
  • 49. Significance of Hypoglycaemia • Neuronal cell injury, cerebral damage, long term neurologic sequelae • No single value below which or duration beyond which brain injury definitely occurs • ? Vulnerability of brain of infants of different gestational ages • Prevention, prompt treatment important
  • 50. Symmetric patchy hyperintensities in occipital white matter in brain of infant with transient neonatal hypoglycaemia Kinnala Peds 1999
  • 51. Boy with isolated hypoglycaemia: computed tomography at 6 days of age shows cortical and white matter low density that is most severe in the parietal and occipital lobes T2 weighted axial MRI at 10 months of age shows parenchymal loss posteriorly with high signal in the white matter of the parietal and occipital lobes (arrows). Note thin and atrophic gyri (arrowhead) Traill, Arch Dis Child 1998
  • 52. Boy with a variant of glycogen storage disease type 2b. Computed tomogram at 6 days of age shows low density in the cortex and white matter of the parietal and occipital lobes T2 weighted axial magnetic resonance image at 7 years of age shows marked atrophy in the parietal and occipital cortex and underlying cerebral white matter Traill, Arch Dis Child 1998
  • 53. Outcome • Varied • Some have no long term sequelae • Symptomatic / severe / persistent hypoglycaemia • Abnormal neurointellectual development
  • 54. • • • • • Cerebral palsy Epilepsy Cognitive impairment Visual problems Developmental & behavioural disorders
  • 55. Long Term Management • Neurodevelopmental follow up to identify sequelae of neuroglycopenia • Identify growth deficits