This document discusses neonatal hyperglycemia, defining it as serum glucose greater than 150 mg/dl or whole blood glucose greater than 125 mg/dl. It notes potential causes like excessive glucose infusion, stress, or insulin-dependent diabetes. Complications are also outlined, such as dehydration, weight loss, and metabolic acidosis. Treatment involves identifying the underlying cause, administering insulin if needed to maintain euglycemia, and monitoring for complications.

2.  Neonatal hyperglycemia is usually
defined as serum glucose greater than
150 mg/dl (8.3 mmol/L) or whole blood
glucose greater than 125 mg/dl (6.9
mmol/L) irrespective of gestational or
postmenstrual age.

3. Neonatal hyperglycaemia is usually defined as
serum glucose greater than 150 mg/dl
(8.3mmol/l) or whole blood glucose greater
than 125mg/dl (6.9mmol/l) irrespective of
gestational or postmenstrual age.
* usually safe target for neonate’s blood glucose
level is 70-150 mg/dl.

4.  Dehydration osmotic diuretics
 Weight loss
 Failure to thrive
 Fever
 Glycosuria (glucose in urine)
 Ketosis
 Metabolic acidosis
 Mostly asymptomatic

5.  Glucose infusion
 Lipid
 stress
 Insulin dependent DM
 Other drugs

6.  High rates of exogenous glucose given to
preterm neonates in infusion and TPN
exceeding rate of glucose production (4-
8mg/kg/min.)
 Formula of calculating glucose infusion rate
:- Mg/kg/min = %dextrose * rate
/wtx6

7.  Increase plasma free fatty acid concentration
 Decrease peripheral glucose utilization
 Inhibit the effect of insulin to supress hepatic
glucose production .

8.  Stress due to
 Disease process
 Medical intervention
 Surgical intervention
 During stress there is release of epinephrine,
glucocorticoids and glucagon.
 Epinephrine decreases insulin secretion from
the pancreatic beta cell & interferes with
peripheral insulin action .

9.  Glucagon promotes glycogenolysis and
release of hepatic glucose.
 Glucocorticoids also enhance hepatic
enzyme activity in the gluconeogenic
pathway, which releases glucose into
the circulation.

10.  Transient neonatal diabetes mellitus(TNDM)
presents early in postnatal life-C-peptide and
plasma insulin are low
 A rebound in C-peptide concentration
typically marks the resolution.
 If it doesn’t resolve it indicates permanent
neonatal DM.
 endogenous insulin deficiency due to failure
of pancreatic beta cells.

11.  Theopylline
 Dexamathasone
 Prostaglandin E

12.  Dehydration-osmotic diuresis
 Intraventricular hemorrhage
 Increase serum osmolarity
 rapid shifting of water
 Ischemic events-brain
 Hyperosmolarity
 lactic acidosis
 decrease regional cerebral blood flow

13.  Steatosis-impairment of hepatic
secretions of triglycerides
 Due to aggressive glucose
administrations
 Prolonged ventilation
 lipogenesis causes increase co2
 increase need for ventilation-
LBW/ELBW
 Electrolyte imbalance
 Infants with glycosuria-increase in
sodium excretion
 due to increase filtered sodium load

14.  Identify underlying etiology
 Prevent complications
 Administer continous insulin infusion safely
to maintain euglycemia and adequate calorie
intake

15.  RBS-confirmation
 Monitor urine for glycosuria and urine
volume (mL/kg/hr) to ensure adequate fluid
balance
 If baby needs additional fluids to counter
renal and extra renal losses
(phototherapy)consider using 5% dextrose or
0.45% saline

16.  Seek and treat serious
underlying disorders especially infection
(septic screen and antibiotics).
 Achieve adequate sedation and pain relief
 Calculate glucose delivery rate
 More than 10mg/kg/min-reduce to 6-
10mg/kg/min
 If hyperglycemia still persist-consider
insulin sliding scale-0.02unit/kg to
0.05unit/kg per hour
 Enteral feeding-promotes pancreatic
function and secretion of insulin
 Hypocount monitored 2-4 hourly-prevent