hypoglycemia in new born
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HYPOGLYCEMIA IN
NEWBORNDr. Abhijeet Deshmukh
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.
INTRODUCTION
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.
DEFINITION
Fetal or Neonatal Hyperinsulinism – ↑utilisation of glucose.
Decreased production or store
Increased utilisation and/or decreased production
ETIOLOGY
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).
Insulin producing tumours(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
Decreased production or store:
Prematurity IUGR (15% in SGA) Inadequate calorie intake Delayed onset of feeding
Increased utilisation or decreased production:
Perinatal stressSepsis/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
Endocrine deficiencyAdrenal insufficiencyHypothalamic deficiencyHypopituitarism (neonatal emergencies such as apnea, cyanosis, or severe
hypoglycemia with or without seizures, hyperbilirubinemia, and micropenis. )
Glucagon defEpn deficiency
Defects in amino acid metabolism MSUD,propionic
acidemia,MMA,tyrosinemia
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
SYMPTOMSTremors,jitteriness,irritability,seizures,letharg
y, poor feeding,vomiting ,limpness,weak or high pitched cry ,cyanosis
ASYMPTOMATIC.
MEASURMENT OF BLOOD GLUCOSEglucometer- 15% lower than plasma levelsLab diagnosis-sample obtained and analyzed
promptly (18mg/dl/hr)
CLINICALCONFIRMATION-whipples triad
DIAGNOSIS
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
MANAGEMENT
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/ suspected IEM
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
Asymptomatic
25-40mg% <25mg%
Trial of feeds Parenteral
>40 <40
Continue oral feeds and monitor for 48 hrs
Early feeding with glucose water raises BG only transiently and asso with rebound hypoglycemia
Early introduction of breast feedso maintain stable BG levels without rebound HGo keep ketone levels high---alternate fuel during 1st
few days while baby adapts to DBFo enhances gluconeogenesis
IV therapyIndications – intolerance to oral feeds Symptomatic oral feeds not maintaining glucose levels BG level < 25mg/dl
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
Continuing therapy – based on Glucose Infusion Rate
GIR(mg/kg/min) = % dextrose x ml/kg/day 144For eg.86 ml/kg/day of 10% D--GIR 6-8[GIR of 8.33 = 80ml/kg/day of 15%D]
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 hrMonitoring stopped when 2 values on oral feeds >50mg
%
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/diazoxideFurther investigations
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
<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
IDM
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
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
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
Na /K-adrenal insufficiency MRI brain-hypothalamic/pituitary pathology CT abdomen-islet cell adenoma Genetic testing – to look for mutations
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)
Hypoglycemia
Urine non glucose red substance
Present absent
Galactosemia ketones
ketones high low(nonketotic HG) gluconeogenic FA oxidation defect defect or or Organic acidemia Ketogenic defect Hyperinsulinism
DIFFERENTIAL DIAGNOSIS:
Sepsis CNS disease Metabolic
abnormalities(hypocalcemia,hyponatremia,hypernatremia,hypomagnesemia,pyridoxine deficiency)
Adrenal insufficiency Renal failure Liver failure Heart failure
THANK YOU!
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