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
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
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
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
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)
