Transcript Hypoglycemia

Hypoglycemia
Vandana Nayal, MD
Edited May 2005
Definition
 Plasma glucose less than 40 mg/dl
 Immediate questions
1. Has a plasma blood sugar been sent to the
laboratory?
2. Is the baby symptomatic?
3. Is the mother a diabetic?
4. How much glucose is the infant receiving?
Measurement of glucose
 Bedside glucose strips can give incorrect values
if the test is not done properly, if the strips used
are too old, if the hematocrit is very high, or the
glucose level is very low
 There is a wide variation when compared to
laboratory determined plasma levels
– Glucose concentration in whole blood is 10-15%
lower than in plasma
 ALWAYS confirm your measurement in the lab
Symptoms of hypoglycemia
 Apnea, hypotonia, irritability, irregular
respirations, poor sucking or feeding,
exaggerated Moro reflex, cyanosis, tremors, eye
rolling, pallor, seizures, lethargy, temperature
instability and coma
 Rarely bradycardia, tachycardia, high pitched cry,
tachypnea, and vomiting
 Some have no symptoms despite documented
hypoglycemia
Glucose requirement
How much glucose is the infant receiving
in IV fluids?
Normal glucose requirement is 4-10
mg/kg/min
Check to be sure that calculations were
correct
Causes of transient
hypoglycemia
 Perinatal stress
 Sepsis, esp. Gram-negative
 Asphyxia or HIE
 Hypothermia
 Polycythemia
 Shock
 Infant of diabetic mother
 Decreased glycogen stores
 Insufficient amount of glucose administered
 Maternal meds: terbutaline, propranolol
Infants of diabetic mothers
40% of infants of diabetic mothers have
documented hypoglycemia
Diabetic mothers have fluctuating
hyperglycemia that results in fetal
hyperglycemia
– induces pancreatic B-cell hyperplasia =
hyperinsulism
– after delivery, hyperinsulism persists and
hypoglycemia results
Decreased glycogen stores
 Intrauterine growth retardation or small
for gestational age
 Premature infants
 Post-mature infants
Causes of persistent
hypoglycemia
Hormone excess - hyperinsulism
–
–
–
–
Beckwith-Wiedemann syndrome
Islet cell adenoma
Beta cell hyperplasia, dysplasia
Nesidioblastosis
Beckwith-Wiedemann syndrome
(because it is on the boards)
 Macroglossia,
 Hepatomegaly,
Omphalocele,
macrosomia, ear creases,
mild to mod mental
deficiency
 Large kidneys with renal
medullary dysplasia,
pancreatic hyperplasia
 Neonatal
polycythemia,cryptorchid
ism, hypoglycemia(1/2 to
1/3 of cases) which is
responsive to HC
hemihypertrophy,
(increased malignancy)
hepatoblastoma,
immunodeficiency
 US and serial alpha feto
protein every 6 months
till the patient is 6 years
of age to r/o Wilms’s and
hepatoblastoma
 Duplication of 11p15.5
causes BWS. IGF-2 gene
localization to 11p causes
BWS
Persistent hypoglycemia hormone deficiencies
 Growth hormone deficiency
 ACTH unresponsiveness
 Thyroid deficiency
 Epinephrine deficiency
 Glucagon deficiency
 Cortisol deficiency
 Hypoplastic pituitary
 Hypothalamic hormone deficiencies
 Midline CNS malformation
Defects in carbohydrate
metabolism
Glycogen storage disease type 1
Fructose intolerance
Galactosemia
Glycogen sythase deficiency
Fructose 1,6 diphosphatase deficiency
Defects in amino acid
metabolism
Maple syrup urine disease
Propionic acidemia
Methylmalonic acidemia
Tyrosinosis
3-Hydroxy-3-methylglutaryl-CoA lyase
deficiency
Defects in fatty acid metabolism
Medium and long chain deficiency
Approach to hypoglycemia
History and physical
Evaluate infant for symptoms of
hypoglycemia
Look for signs of shock, sepsis, midline
defects, or Beckwith-Wiedemann
syndrome
Laboratory studies for transient
hypoglycemia
Serum glucose level should be sent to the
lab to confirm the paper strip result
CBC with differential to evaluate for
sepsis and to rule out polycythemia
Persistent Hypoglycemia
 Initial studies – Serum glucose, insulin, cortisol,
growth hormone at the time of hypoglycemic
event; serum ketones
 Ratio of insulin to glucose is obtained
– level of >0.3 indicates a non hyperinsulinemic cause
of hypoglycemia
 Serum ketones are low or absent in the presence
of hyperinsulinemia
Follow-up studies for persistent
hypoglycemia
 GH, Free Fatty acids, T3, T4, TSH
 Glucagon, uric acid, lactate, Alanine
 Ketone levels before and 15 min after
administration of glucagon- 0.3mg/kg/dose
 Urine collection for AA, OA, catecholamines,
specific reducing sugars
 Somatomedins (IGF-1, IGF-2, IGF binding
proteins)
 Ultrasound or CT scan of the pancreas
Management
Overall plan to maintain normoglycemia
(level > 45 mg/dL)
Screen those at risk or those with
symptoms suspicious for hypoglycemia
– glucose check every 1-2 hr before feeds until
glucose levels are stable, then every 4 hours
Determine why the baby is hypoglycemic
– obvious reasons or need further work up?
At risk?
 Premature
 SGA, LGA
 BW < 2500 g
 Smaller of discordant twins (wt. Diff. > 25%)
 Asphyxiated infant (5 min Apgar < 5)
 Infants of massively obese mothers
 Infants of diabetic mothers
 Infants with polycythemia, infection,
microphallus/midline defects, anomalies
associated with low glucose (BWS)
Asymptomatic hypoglycemia
 Treatment is controversial
 Term infants, first 6-12 hrs, not high risk
– give early feeding
 Level < 25mg/dl is a medical emergency
– give parenteral glucose - 2-3 ml/kg D10W IV over 2-3
minutes
 Check glucose q 15-30 minutes until stable
 Always follow your institution guidelines
Symptomatic, persistent, or
severe (< 25) hypoglycemia
 If chemstrip values persist < 40 mg/dL or initial
< 25 mg/dl (confirmed by stat lab level)
– Give bolus and start a glucose infusion of 6mg/kg/min
even if the infant is asymptomatic
 Increase level of infusion until normoglycemia is
achieved (> 45 mg/dL)
– Peripheral IV can take up to D13 otherwise will need
central access
 Check glucose levels q 15-30 minutes until stable
 Document improvement in symptoms
Glucagon
If an intravenous line cannot be started,
glucagon can be given to infants with
adequate glycogen stores
– Infants of diabetic mothers have good stores
– less effective in IUGR or SGA
Dose is 300mcg/kg not to exceed1mg total
dose subcutaneously or IM while vascular
access is attempted
Other treatments
 Trial of corticosteroids
– Hydrocortisone sodium succinate mg/kg/day given
intravenously or orally every 12 hours
– prednisone 2mg/kg/day
 If hypoglycemia persists
– Diazoxide (inhibits pancreatic insulin release)m815mg/kg/day PO in 2-3 divided doses or IV 35mg/kg/dose repeat in 20 min if no effect
 Somatostatin analog
– Octreotide 2-10mcg/kg/day sc divided every 6-8h or
continuous IV
 HGH 0.1unit/day