Hypoglycemia in new born

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Hypoglycemia in new born

  1. 1. Dr. Abhijeet Deshmukh
  2. 2.  Common metabolic problem Blood glucose in newborns are generally lowerthan older children & adult Fetal glucose level maintained at 2/3 ofmaternal B.glucose by transplacental route Glucose level fall in Ist 1-2 hrs,lowest value atage of 3 hrs, increase and stabilise by 4 hrs. New born – glycogenolysis, gluconeogenesis andexogenous nutrients.
  3. 3.  Defined as a blood glucose level of <40mg %regardless of gestational age and whether ornot symptoms are presentWhipple’s triad: low glucose level documented by accurate labmethod Signs and symptoms of hypoglycemia Resolution of signs and symptoms onrestoration of blood glucose levels.
  4. 4.  Fetal or Neonatal Hyperinsulinism –↑utilisation of glucose. Decreased production or store Increased utilisation and/or decreasedproduction
  5. 5.  Fetal or Neonatal Hyperinsulinism –↑utilisation of glucose. Babies born to Diabetic mothers(15-25 %GDM,25-50% DM) LGA infants-16% Erythroblastosis Islet cell hyperplasia Beckwith-weidemann(macrosomia,microcephaly,omphalocoele,macroglossia,visceromegaly).
  6. 6.  Insulin producing tumours(islet celladenoma). Maternal therapy with tocolytics liketerbutaline,ritodrine, OHA and diuretics(chlorothiazide) Glucose infusion through UAC –highglucose into celiac,SMA—stimulate insulinfrom pancreas
  7. 7.  Decreased production or store: Prematurity IUGR (15% in SGA) Inadequate calorie intake Delayed onset of feeding
  8. 8.  Increased utilisation or decreased production: Perinatal stressSepsis/shock/asphyxia/respiratorydistress/hypothermia/post resuscitation. Exchange transfusionHeparinised blood with low glucose levelCPD blood (relatively hyperglycemic---reactive hypoglcemia Defects in carbohydrate metabolismGlycogen storage diseaseFructose intoleranceGalactosemia
  9. 9.  Endocrine deficiencyAdrenal insufficiencyHypothalamic deficiencyHypopituitarism(neonatal emergencies such as apnea, cyanosis, or severehypoglycemia with or without seizures, hyperbilirubinemia, andmicropenis. )Glucagon defEpn deficiency Defects in amino acid metabolismMSUD,propionic acidemia,MMA,tyrosinemia
  10. 10.  Polycythemia-higher glucose utilisation by increased mass of RBC Maternal therapy with beta blockers-Prevention of symp stimulation of glycogenolysis&epinephrine induced increase in FFA
  11. 11.  SYMPTOMSTremors,jitteriness,irritability,seizures,lethargy,poor feeding,vomiting ,limpness,weak orhigh pitched cry ,cyanosisASYMPTOMATIC. MEASURMENT OF BLOOD GLUCOSEglucometer- 15% lower than plasma levelsLab diagnosis-sample obtained and analyzedpromptly (18mg/dl/hr) CLINICALCONFIRMATION-whipples triad
  12. 12.  The major long-term sequelae ofsevere, prolonged hypoglycemia are mentalretardation, recurrent seizure activity, or both. Permanent neurologic sequelae are present in 25–50% ofbabies with severe recurrent symptomatichypoglycemia These sequelae are more likely when alternativefuel sources are limited, as occurs withhyperinsulinemia Anticipation and prevention –key tomanagement of infants with risk factors for HG
  13. 13. Routine screening in babies with riskfacors SGA/Smaller of the discordant twin IDM/LGA Preterm <35 weeks On IVF/TPN Prolonged hypoxia/hypothermia/polycythemia/septicemia/ suspectedIEM
  14. 14.  After exchange tranfusion Rh Hemolytic d/s Babies born to mothers on terbutaline/b-blockers/OHA Symptomatic babiesScreening 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. 15. Asymptomatic 25-40mg% <25mg% Trial of feeds Parenteral >40 <40 Continue oral feedsand monitor for 48 hrs
  16. 16.  Early feeding with glucose water raises BG onlytransiently and asso with rebound hypoglycemia Early introduction of breast feedso maintain stable BG levels without rebound HGo keep ketone levels high---alternate fuel during 1stfew days while baby adapts to DBFo enhances gluconeogenesis
  17. 17.  IV therapyIndications – intolerance to oral feeds Symptomatic oral feeds not maintaining glucose levels BG level < 25mg/dl
  18. 18. o IV glucose through a peripheral line or UVCo 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/mtFor eg 2 kg infant-4-8 ml of 25% Dex in 2-4mto In asymptomatic baby with low BG levels initialpush of conc sugar →→hyperinsulinism.Therfore, infusion 5-10 ml of 10% D at 1 ml/mt
  19. 19. Continuing therapy – based on Glucose Infusion RateGIR(mg/kg/min) = % dextrose x ml/kg/day144For eg.86 ml/kg/day of 10% D--GIR 6-8[GIR of 8.33 = 80ml/kg/day of 15%D]
  20. 20.  Monitor BG hourly till euglycemic and thereafter 6thhrly If BG > 40mg%,Continue same and monitor When 2 BG values >50 mg%,wean GIR by 2mg/kg/mt6th hrly and start oral feedsStop infusion when baby is stable @4mg/kg/mt for 12hrMonitoring stopped when 2 values on oral feeds>50mg%
  21. 21.  If BG < 40 mg%Repeat bolus & increase GIR by 2mg/kg/mtevery 6 hr till euglycemicIf GIR >12 orHG not resolving by day 7steroids/glucagon/diazoxideFurther investigations
  22. 22.  Check blood glucose after 30 mts of everychange in infusion rate Monitoring of glucose levels--to ensure adequate correction ofhypoglycemia-To avoid hyperglycemia---diuresis---dehydration
  23. 23.  <2kg –parenteral therapy in the 1st hour oflife >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
  24. 24. Hydrocortisone 10mg/kg/day in 2 div doses MOA-decrease peripheral glucoseutilisation, increase gluconeogenesis,increaseeffects of glucagon Rapidly tapered off in few days Before administration of HC ,obtain bloodsamples for insulin and cortisol levels
  25. 25.  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 persistenthyperinsulinemia Epinephrine Subtotal pancreatectomy
  26. 26. ADDITIONAL TESTS:Endocrine Evaluation Insulin GH Cortisol/ACTH T4,TSH GlucagonMetabolic work up ABG/Blood NH3/ lactate Plasma or urine amino acids Urine organic acids Urine ketones/Urine reducing substance
  27. 27.  Na /K-adrenal insufficiency MRI brain-hypothalamic/pituitary pathology CT abdomen-islet cell adenoma Genetic testing – to look for mutations
  28. 28.  Samples to detect insulin levels should bedrawn at the time of low BG Criteria for Diagnosing HyperinsulinismBased 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 toglucagon, 1 mg IV (rise >40 mg/dL)
  29. 29.  HypoglycemiaUrine non glucose red substancePresent absentGalactosemia ketones
  30. 30. ketoneshigh low(nonketotic HG)gluconeogenic FA oxidation defectdefect or orOrganic acidemia Ketogenic defectHyperinsulinism
  31. 31. DIFFERENTIAL DIAGNOSIS: Sepsis CNS disease Metabolicabnormalities(hypocalcemia,hyponatremia,hypernatremia,hypomagnesemia,pyridoxinedeficiency) Adrenal insufficiency Renal failure Liver failure Heart failure

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