1. Dr. Abhijeet Deshmukh

2.  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.

3.  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.

4.  Fetal or Neonatal Hyperinsulinism –
↑utilisation of glucose.
 Decreased production or store
 Increased utilisation and/or decreased
production

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,omph
alocoele,macroglossia,visceromegaly).

6.  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

7.  Decreased production or store:
 Prematurity
 IUGR (15% in SGA)
 Inadequate calorie intake
 Delayed onset of feeding

8.  Increased utilisation or decreased production:
 Perinatal stress
Sepsis/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

9.  Endocrine deficiency
Adrenal insufficiency
Hypothalamic deficiency
Hypopituitarism
(neonatal emergencies such as apnea, cyanosis, or severe
hypoglycemia with or without seizures, hyperbilirubinemia, and
micropenis. )
Glucagon def
Epn deficiency
 Defects in amino acid metabolism
MSUD,propionic acidemia,MMA,tyrosinemia

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.  SYMPTOMS
Tremors,jitteriness,irritability,seizures,lethargy,
poor feeding,vomiting ,limpness,weak or
high pitched cry ,cyanosis
ASYMPTOMATIC.
 MEASURMENT OF BLOOD GLUCOSE
glucometer- 15% lower than plasma levels
Lab diagnosis-sample obtained and analyzed
promptly (18mg/dl/hr)
 CLINICALCONFIRMATION-whipples triad

12.  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

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/ suspected
IEM

14.  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

15. Asymptomatic
 25-40mg% <25mg%
 Trial of feeds Parenteral
 >40 <40
 Continue oral feeds
and monitor for 48 hrs

16.  Early feeding with glucose water raises BG only
transiently and asso with rebound hypoglycemia
 Early introduction of breast feeds
o maintain stable BG levels without rebound HG
o keep ketone levels high---alternate fuel during 1st
few days while baby adapts to DBF
o enhances gluconeogenesis

17.  IV therapy
Indications –
 intolerance to oral feeds
 Symptomatic
 oral feeds not maintaining glucose levels
 BG level < 25mg/dl

18. 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

19. Continuing therapy – based on Glucose Infusion Rate
GIR(mg/kg/min) = % dextrose x ml/kg/day
144
For eg.86 ml/kg/day of 10% D--GIR 6-8
[GIR of 8.33 = 80ml/kg/day of 15%D]

20.  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
hr
Monitoring stopped when 2 values on oral feeds
>50mg%

21.  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/diazoxide
Further investigations

22.  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

23.  <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

24. 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

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 persistent
hyperinsulinemia
 Epinephrine
 Subtotal pancreatectomy

26. 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

27.  Na /K-adrenal insufficiency
 MRI brain-hypothalamic/pituitary pathology
 CT abdomen-islet cell adenoma
 Genetic testing – to look for mutations


28.  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)

29.  Hypoglycemia
Urine non glucose red substance
Present absent
Galactosemia ketones

30. ketones
high low(nonketotic HG)
gluconeogenic FA oxidation defect
defect or or
Organic acidemia Ketogenic defect
Hyperinsulinism

31. DIFFERENTIAL DIAGNOSIS:
 Sepsis
 CNS disease
 Metabolic
abnormalities(hypocalcemia,hyponatremia,h
ypernatremia,hypomagnesemia,pyridoxine
deficiency)
 Adrenal insufficiency
 Renal failure
 Liver failure
 Heart failure