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Dr. Abhishek Goyal
NEONATAL
HYPOGLYCEMIA
+
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.
2
+
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.
3
+
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.
4
+ EFFECT OF HYPOGLYCEMIA
5
+
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
6
+
 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.
7
+
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.
8
+ 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."
9
+
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
10
+
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
11
+
Infants With Symptomatic Hypoglycemia
12
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)
+  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
144
13
+
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
14
+
Causes of resistant hypoglycemia
 Congenital hypopitutarism
 Adrenal insufficiency
 Hyperinsulinemic states
 Galactosemia
 Glycogen storage disorders
 Maple syrup urine disease
 Mitochondrial disorders
 Fatty acid oxidation defect
15
+ 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
16
+
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
17
+
 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
18
+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
19
+
 Na /K-adrenal insufficiency
 MRI brain-hypothalamic/pituitary pathology
 CT abdomen-islet cell adenoma
 Genetic testing – to look for mutations

20
+ 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)
21
+
 Hypoglycemia
Urine non glucose red substance
Present absent
Galactosemia ketones
22
+
ketones
high low(nonketotic HG)
gluconeogenic FA oxidation defect
defect or or
Organic acidemia Ketogenic defect
Hyperinsulinism
23
+DIFFERENTIAL DIAGNOSIS:
 Sepsis
 CNS disease
 Metabolic
abnormalities(hypocalcemia,hyponatremia,hypernatr
emia,hypomagnesemia,pyridoxine deficiency)
 Adrenal insufficiency
 Renal failure
 Liver failure
 Heart failure
24
+
THANK YOU!
25
+
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
26

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hypoglycemiaabhishek-160926152851.pdf

  • 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.  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. 2
  • 3. + 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. 3
  • 4. + 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. 4
  • 5. + EFFECT OF HYPOGLYCEMIA 5
  • 6. + 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 6
  • 7. +  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. 7
  • 8. + 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. 8
  • 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." 9
  • 10. + 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 10
  • 11. + 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 11
  • 12. + Infants With Symptomatic Hypoglycemia 12 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 144 13
  • 14. + 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 14
  • 15. + Causes of resistant hypoglycemia  Congenital hypopitutarism  Adrenal insufficiency  Hyperinsulinemic states  Galactosemia  Glycogen storage disorders  Maple syrup urine disease  Mitochondrial disorders  Fatty acid oxidation defect 15
  • 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 16
  • 17. + 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 17
  • 18. +  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 18
  • 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 19
  • 20. +  Na /K-adrenal insufficiency  MRI brain-hypothalamic/pituitary pathology  CT abdomen-islet cell adenoma  Genetic testing – to look for mutations  20
  • 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) 21
  • 22. +  Hypoglycemia Urine non glucose red substance Present absent Galactosemia ketones 22
  • 23. + ketones high low(nonketotic HG) gluconeogenic FA oxidation defect defect or or Organic acidemia Ketogenic defect Hyperinsulinism 23
  • 24. +DIFFERENTIAL DIAGNOSIS:  Sepsis  CNS disease  Metabolic abnormalities(hypocalcemia,hyponatremia,hypernatr emia,hypomagnesemia,pyridoxine deficiency)  Adrenal insufficiency  Renal failure  Liver failure  Heart failure 24
  • 26. + 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 26