hypoglycemia in newborn
Post on 22-Jan-2017
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Dr. Abhishek Goyal
NEONATAL HYPOGLYCEMIA
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.
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.
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.
5+EFFECT OF HYPOGLYCEMIA
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
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.
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.
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."
10+CLINICAL FEATURE1. 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
11+MANAGEMENTInfants 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
12+Infants With Symptomatic Hypoglycemia
Symptomatic hypoglycemia Bolus 2 ml/kg
10% dextroseIV glucose infusion @ 6 mg/kg/minMonitor 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 every6 hrs;
↑ oral feeds;Monitoring to continue 6 hrly
Stop IV fluids whenthe rate is 4 mg/kg/minand the infant is stable
Stop monitoring when 2values are more than 50 on
full oral feeds
Blood sugar <50 mg/dL
Increase glucose @ 2mg/kg/min tilleuglycemia
Increase till the glucoseinfusion rate is >12
mg/kg/min
Resistant hypoglycemia
HydrocortisoneDiazoxide (not in SGA)Glucagon (not in SGA)
Octreotide
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
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
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
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Investigation for resistant hypoglycemiaCritical 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
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
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
19+ADDITIONAL TESTS:
Endocrine Evaluation Insulin GH Cortisol/ACTH T4,TSH GlucagonMetabolic work up ABG/Blood NH3/ lactate Plasma or urine amino acids Urine organic acids Urine ketones/Urine reducing substance
20+
Na /K-adrenal insufficiency MRI brain-hypothalamic/pituitary pathology CT abdomen-islet cell adenoma
Genetic testing – to look for mutations
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)
22+
Hypoglycemia
Urine non glucose red substance
Present absent
Galactosemia ketones
23+
ketones
high low(nonketotic HG)
gluconeogenic FA oxidation defect
defect or or
Organic acidemia Ketogenic defect
Hyperinsulinism
24+DIFFERENTIAL DIAGNOSIS:
SepsisCNS diseaseMetabolic
abnormalities(hypocalcemia,hyponatremia,hypernatremia,hypomagnesemia,pyridoxine deficiency)
Adrenal insufficiencyRenal failureLiver failureHeart failure
25+
THANK YOU!
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
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