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 Usual rate of glucose utilization is 4-8 mg per
kg/min.
 Glucose regulatory mechanism is sluggish at birth
 When glucose demand is increase / when
exogenous/ endogenous glucose supply is limited .
 Prolonged hypoglycemia may result in long term
neurologic damage.
 Hypoglycemia in the first few days after
birth is defined as “blood glucose levels
below 40 mg/dl.”
 In preterm infants, repeated blood glucose
level below 50 mg / dl maybe associated
with neurodevelopment delay.
 Insulin and glucagon hormones control the blood
glucose level.
 Blood glucose level increases → rate of insulin
secretion increases → stimulates liver to store
glucose as glycogen → when liver and muscle cells
are saturated with glycogen additional glucose is
stored as fat.
 Blood glucose level falls → glucagon level
increases → it promotes conversion of
glycogen in liver back into glucose
(glycogenolysis) → this glucose released in
blood.
 During starvation liver maintain glucose level
by gluconeogenesis i.e formation of glucose
from amino acids and fat.
 Hypothalamus stimulate epinephrine secretion from
adrenal, causing further glucose release from liver.
 After prolong hypoglycemia growth hormone and
cortisol secreted that the decrease the rate of glucose
utilization by body cells.
Hypoglycemia
Insulin
↑
Glucagon ↑ Epinephri
ne ↑
Growth
Hormo
ne ↑
Cortisol ↑
Protein
breakdow
n ↑
Insulin
sensitivi
ty ↓
Fat break
down ↑
Hepatic
glucose
output ↑
Gluconeoge
nesis ↑
Glucose
utilizatio
n ↓
Ketones ↑
Glucose ↑
Decreased substrate availability
•Intrauterine growth retardation
•Inborn errors (fructose intolerance)
•Prolonged fasting without iv glucose
•Glycogen storage disease
•Prematurity
 Infant of diabetic mother
 Erythroblast sis fetalis
 High umbilical arterial catheter
 Islet cell hyperplasia
 Exchange transfusion
 Maternal beta mimetic tocolytic agents
 Abrupt cessation of iv glucose
 Beckwith-wiedemann syndrome
 Cold stress
 Sepsis
 Increase work of breathing
 Prenatal asphyxia
 Pan-hypopituitarism
 Adrenal insufficiency
 Hypo thyroidism
 Polycythemia
 CNS abnormalities
 Congenital heart diseases
 Cyanosis
 Breathing problems
 Hypotonia
 Grunting
 Listlessness
 Irritability or lethargy
 Restlessness
 Altered sensorium
 Twitching and trenmors
 seizures
 Specimen for measurement of glucose should be
obtained from heel stick, venipuncture , or from and
indwelling catheter that does not have glucose
infusing in it
 Infants at risk for hypoglycemia should be screened
by measuring blood sugar by glucometer at ages 1,
2, 4, 6, 9 and 12th. Less frequent measurement are
appropriate if blood glucose is stable.
 Continue surveillance and more frequent
measurement may be needed until blood glucose is
stable > 14mg/ dl or > 50 mg/ dl in very preterm
infants
 Glucometer reading > 40 mg/dl and infant is feeding
normally:
Follow usual nursery protocol
 Glucometer reading 20-40 mg/dl, infant is term and
is able to feed:
 Draw blood for stat blood glucose measurement
 Feed 5 ml/kg of 5%/ dextrose
 Repeat blood glucose 20 min after feeding
 Glucometer reading :
a) < 20 mg/dl
b) < 40 mg/dl and NPO or preterm
c) < 40 mg/dl after feeding
d) < 40 mg/dl and symptomatic
 Draw blood for stat glucose measurement
 Give iv bolus of 2-3 ml/kg of D10W
 Begin continuous infusion of D10W at 4-6 mg/kg per
min
 If infant of diabetic mother begin D10W at 8-10
mg/kg/min
 Repeat blood glucose in 20 min and pursue
treatment until blood sugar < 40 mg/dl
 Increase rate of glucose infusion stepwise in
2mg/kg/min increments upto 12-15
mg/kg/min glucose.
 If hypoglycemia is not controlled with
dextrose infusion then further management
include glucocorticoid,dizoxide,somatostatin
or pancreactectomy.
 When blood glucose is stable for 12-24 hrs,
begin decreasing iv infusion by 1-2 ml/hr if
blood glucose remain >60 mg/dl
 Occipital lobe damage
 Developmental delay
 Heart failure

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Neonatal hypoglycemia

  • 1.
  • 2.  Usual rate of glucose utilization is 4-8 mg per kg/min.  Glucose regulatory mechanism is sluggish at birth  When glucose demand is increase / when exogenous/ endogenous glucose supply is limited .  Prolonged hypoglycemia may result in long term neurologic damage.
  • 3.  Hypoglycemia in the first few days after birth is defined as “blood glucose levels below 40 mg/dl.”  In preterm infants, repeated blood glucose level below 50 mg / dl maybe associated with neurodevelopment delay.
  • 4.  Insulin and glucagon hormones control the blood glucose level.  Blood glucose level increases → rate of insulin secretion increases → stimulates liver to store glucose as glycogen → when liver and muscle cells are saturated with glycogen additional glucose is stored as fat.
  • 5.  Blood glucose level falls → glucagon level increases → it promotes conversion of glycogen in liver back into glucose (glycogenolysis) → this glucose released in blood.  During starvation liver maintain glucose level by gluconeogenesis i.e formation of glucose from amino acids and fat.
  • 6.  Hypothalamus stimulate epinephrine secretion from adrenal, causing further glucose release from liver.  After prolong hypoglycemia growth hormone and cortisol secreted that the decrease the rate of glucose utilization by body cells.
  • 7. Hypoglycemia Insulin ↑ Glucagon ↑ Epinephri ne ↑ Growth Hormo ne ↑ Cortisol ↑ Protein breakdow n ↑ Insulin sensitivi ty ↓ Fat break down ↑ Hepatic glucose output ↑ Gluconeoge nesis ↑ Glucose utilizatio n ↓ Ketones ↑ Glucose ↑
  • 8. Decreased substrate availability •Intrauterine growth retardation •Inborn errors (fructose intolerance) •Prolonged fasting without iv glucose •Glycogen storage disease •Prematurity
  • 9.  Infant of diabetic mother  Erythroblast sis fetalis  High umbilical arterial catheter  Islet cell hyperplasia  Exchange transfusion  Maternal beta mimetic tocolytic agents  Abrupt cessation of iv glucose  Beckwith-wiedemann syndrome
  • 10.  Cold stress  Sepsis  Increase work of breathing  Prenatal asphyxia
  • 11.  Pan-hypopituitarism  Adrenal insufficiency  Hypo thyroidism
  • 12.  Polycythemia  CNS abnormalities  Congenital heart diseases
  • 13.  Cyanosis  Breathing problems  Hypotonia  Grunting  Listlessness  Irritability or lethargy  Restlessness  Altered sensorium  Twitching and trenmors  seizures
  • 14.  Specimen for measurement of glucose should be obtained from heel stick, venipuncture , or from and indwelling catheter that does not have glucose infusing in it
  • 15.  Infants at risk for hypoglycemia should be screened by measuring blood sugar by glucometer at ages 1, 2, 4, 6, 9 and 12th. Less frequent measurement are appropriate if blood glucose is stable.  Continue surveillance and more frequent measurement may be needed until blood glucose is stable > 14mg/ dl or > 50 mg/ dl in very preterm infants
  • 16.  Glucometer reading > 40 mg/dl and infant is feeding normally: Follow usual nursery protocol  Glucometer reading 20-40 mg/dl, infant is term and is able to feed:  Draw blood for stat blood glucose measurement  Feed 5 ml/kg of 5%/ dextrose  Repeat blood glucose 20 min after feeding
  • 17.  Glucometer reading : a) < 20 mg/dl b) < 40 mg/dl and NPO or preterm c) < 40 mg/dl after feeding d) < 40 mg/dl and symptomatic  Draw blood for stat glucose measurement  Give iv bolus of 2-3 ml/kg of D10W  Begin continuous infusion of D10W at 4-6 mg/kg per min
  • 18.  If infant of diabetic mother begin D10W at 8-10 mg/kg/min  Repeat blood glucose in 20 min and pursue treatment until blood sugar < 40 mg/dl
  • 19.  Increase rate of glucose infusion stepwise in 2mg/kg/min increments upto 12-15 mg/kg/min glucose.
  • 20.  If hypoglycemia is not controlled with dextrose infusion then further management include glucocorticoid,dizoxide,somatostatin or pancreactectomy.
  • 21.  When blood glucose is stable for 12-24 hrs, begin decreasing iv infusion by 1-2 ml/hr if blood glucose remain >60 mg/dl
  • 22.  Occipital lobe damage  Developmental delay  Heart failure