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Dr. Abhishek Goyal
NEONATAL
HYPOGLYCEMIA

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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.
 preterm and SGA may be at highest risk up to 36 h (range 0.8 to
34.2 h)
 There is no single value below which brain injury definitely occur.
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DEFINITION
 The operational threshold for hypoglycemia is defined as that
concentration of plasma or whole blood glucose at which clinicians
should consider intervention.
 it do not define normal or abnormal
 It is <45 mg % 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.
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MECHANISM
 Clinically significant NH is the result of an imbalance between
glucose supply and other fuels such as ketone bodies, which
are released from fat.
 NH caused by a lower glucose threshold for suppression of
insulin secretion
 Decreased expression of enzymes in pathways of hepatic
glycogenolysis, gluconeogenesis,or ketogenesis.
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5. + EFFECT OF HYPOGLYCEMIA
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ETIOLOGY
 Delay in feeding
 Low birth weight infants specially<2000 grams
 Preterm infants ( 35 weeks)
 Small for gestational age infants (SGA) : birth weight <10th
percentile
 Infant of diabetic mothers (IDM)
 Large for gestational age (LGA) infants: birth weight >90th
percentile
 Infants with Rh-hemolytic disease ,erythroblastosis
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 Infants born to mothers receiving therapy with
terbutaline/propranolol/labetalol/oral hypoglycemic agents
 Infants with morphological IUGR.
 Any sick neonate such as those with perinatal asphyxia,
polycythemia, sepsis, shock ,etc., when they are in active phase of
illness.
 Infant on TPN
 Exchange transfusion
Heparinized blood with low glucose level
CPD blood (relatively hyperglycemic---reactive hypoglycemia
Routine screening is recommended in above mentioned conditions.
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SCHEDULE FOR SCREENING
 At risk neonates : 2, 6, 12, 24, 48, and 72 hrs
 Sick infants : Every 6-8 hrs (individualize as needed)
 TPN : Initial 72 h: every 6 to 8 hrs After 72 hr:
once a day
 After Exchange : 2 hrs after infusing CPD blood

Infants exhibiting signs compatible with hypoglycemia at
any time also need to be investigated.
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9. + PITFALL IN GLUCOSE ESTIMATION
1. glucose reagent strips
2. Laboratory diagnosis
3. continuous monitoring
 capillary sugar value is 10% to 15% lesser than that of plasma
value
 Arterial samples have slightly higher value compared to venous
or capillary
 the BGL can fall by 14 to 18 mg/dL per hour in samples that
await analysis.
This problem can be avoided by transporting the blood in tubes
that contain a glycolytic inhibitor such as fluoride."
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CLINICAL FEATURE
1. ASYMPTOMATIC.
2. SYMPTOMATIC
 Tremors, jitteriness ,irritability,seizures, lethargy, poor feeding,vomiting
,limpness,weak or high pitched cry ,cyanosis
 Episodes of sweating, sudden pallor, hypothermia and cardiac arrest
have also been reported.
CLINICALCONFIRMATION-whipples triad
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MANAGEMENT
Infants With Asymptomatic Hypoglycemia
1. If any time Blood sugar 20-45 mg/dL
Trial of oral feeds (expressed breast milk or formula) and repeat
blood test after 1 hour.
a. Repeat BGL is >45 mg/dL, two hourly feeds is
ensured 6 hourly monitoring of BGL for 48 hrs. the target blood
glucose value is 50 to 120 mg/dL.
b.Repeat BGL is <45 mg/dL IV Dextrose is started at
6 mg/kg/min of glucose
2. If any time Blood sugar levels <20 mg/dL
IV Dextrose is started at 6 mg/kg/min of glucose
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Infants With Symptomatic Hypoglycemia
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Symptomatic
hypoglycemia
Bolus 2 ml/kg 10%
dextrose
IV glucose infusion @ 6 mg/kg/min
Monitor hourly till euglycemic and
then 6 hrly
Blood sugar >50
mg/dL
Stable for 24 hours on IV fluids;
2 values of blood sugar >50
mg/dL
Weaning at 2 mg/kg/min every
6 hrs;
↑ oral feeds;
Monitoring to continue 6 hrly
Stop IV fluids when
the rate is 4 mg/kg/min
and the infant is stable
Stop monitoring when 2
values are more than 50 on
Blood sugar <50
mg/dL
Increase glucose @ 2
mg/kg/min till
euglycemia
Increase till the glucose
infusion rate is >12
mg/kg/min
Resistant hypoglycemia
Hydrocortisone
Diazoxide (not in SGA)
Glucagon (not in SGA)

13. +  glucose infusion preferably using an infusion pump and without
any interruption.
 Do not stop glucose infusion abruptly as severe rebound
hypoglycemia may occur.
 Avoid using more than 12.5% dextrose infusion through a
peripheral vein due to the risk of thrombophlebitis.
 If there is persistent hypoglycemia, check the intravenous line
for functioning. Also recheck the intravenous fluid preparation
and infusion rate.
GIR(mg/kg/min) = % dextrose x ml/kg/day
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Resistant/recurrent Hypoglycemia
 when infant fails to maintain normal BGL
despite a GIR of 12 mg/kg/min
 when stabilization is not achieved by 7 days
of therapy
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Causes of resistant hypoglycemia
 Congenital hypopitutarism
 Adrenal insufficiency
 Hyperinsulinemic states
 Galactosemia
 Glycogen storage disorders
 Maple syrup urine disease
 Mitochondrial disorders
 Fatty acid oxidation defect
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16. + Investigation for resistant hypoglycemia
Critical lab sample
 Serum insulin levels
 Serum cortisol levels
 Free fatty acid levels and
Beta hydroxy butyrate
Other sample(if critical sample are
normal)
 Growth hormone levels
 ACTH
 Thyroid profile
 Blood ammonia
 Blood lactate levels
 Urine ketones and reducing
substances
 Urine and sugar aminoacidogram
 Galactose 1 phosphate uridyl
transferase levels
 Genetic testing
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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
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 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
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19. +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
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 Na /K-adrenal insufficiency
 MRI brain-hypothalamic/pituitary pathology
 CT abdomen-islet cell adenoma
 Genetic testing – to look for mutations

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21. + 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)
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 Hypoglycemia
Urine non glucose red substance
Present absent
Galactosemia ketones
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ketones
high low(nonketotic HG)
gluconeogenic FA oxidation defect
defect or or
Organic acidemia Ketogenic defect
Hyperinsulinism
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24. +DIFFERENTIAL DIAGNOSIS:
 Sepsis
 CNS disease
 Metabolic
abnormalities(hypocalcemia,hyponatremia,hypernatr
emia,hypomagnesemia,pyridoxine deficiency)
 Adrenal insufficiency
 Renal failure
 Liver failure
 Heart failure
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THANK YOU!
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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
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