Hypoglycemia in the Newborn Flashcards

1
Q

Why are newborn brains so prone to the effects of hypoglycemia?

A

1: They are growing a lot during this time

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2
Q

Fetal glycogen storage

A

Much of fetal glycogen storage occurs during the last 30% of gestation, and is promoted by a high insulin:glucagon ratio as well as high cortisol.

If the infant experiences hypoglycemia or hypoxemia during this period, glycogen phosphorylase will be activated to defend the fetal energy supply, however this means that after birth the infant will have less glycogen stored to maintain its blood sugar.

This also means that premature infants have less stored glycogen and are thus at greater risk for hypoglycemia.

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3
Q

The average healthy infant has a ___ supply of glycogen at birth

A

The average healthy infant has a 10 hour supply of glycogen at birth

Consequentially, babies need to start feeding soon after birth.

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4
Q

Paradoxically, both ___ infants and ___ infants are at risk for hypoglycemia

A

Paradoxically, both IUGR infants and LGA infants are at risk for hypoglycemia

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5
Q

Etiologies of transient neonatal hypoglycemia

A
  • Prematurity
  • IUGR
  • Asphyxia
  • Hypothermia
  • Sepsis
  • Maternal diabetes (CDM or GDM)
  • Erythroblastosis fetalis
  • Exposure to beta-agonist tocolytics
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6
Q

Etiologies of neonatal hypoglycemia with prolonged periods of hypoglycemia

A

Familial hyperinsulinism

Inborn errors of metabolism (glycogen storage diseases)

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7
Q

Most common cause of hyperinsulinism of the newborn

A

Maternal diabetes

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8
Q

Mechanism of hyperinsulinism in erythroblastosis fetalis

A

Infants with erythroblastosis fetalis have an increased number of pancreatic beta cells, which thereby causes hyperinsulinism.

The reason for this is not fully understood.

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9
Q

Familial recessive hyperinsulinism

A
  • Defect in the K+-ATP channel in beta cells
  • Causes congenital, persistent hyperinsulinism
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10
Q

___ should be strongly suspected in the term infant who has hypoglycemia without apparent risk factors.

A

Sepsis should be strongly suspected in the term infant who has hypoglycemia without apparent risk factors.

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11
Q

Confirming a diagnosis of hyperinsulinemia in the newborn

A
  • Two ways:
    1. Demonstrate elevated insulin when the infant is hypoglycemic with symptoms
    2. Demonstrate elevation in IGFBP-1 (insulin-like growth factor binding protein-1)
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12
Q

Management of asymptomatic hypoglycemia

A

In infants with hypoglycemia who display no symptoms, enteral feeding with formula may be attempted first.

Formula is better than dextrose in water as its protein and fat will create a sustained elevation in blood sugar, while dextrose will provide only a temporary boost.

Even if concentrations normalize, continue monitoring preprandial and postprandial glucose levels.

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13
Q

Management of symptomatic hypoglycemia

A

Infants with hypoglycemia who are symptomatic should jump straight to IV dextrose therapy.

This should be given as a mini-bolus followed by a dextrose drip. The mini-bolus is to avoid excessive insulin secretion and rebound hypoglycemia.

While receiving drip therapy, they should also continue breastfeeding.

If refractory, adjunct pharmacologic therapies may be employed.

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14
Q

Adjunct pharmacologic therapies for refractory neonatal hypoglycemia

A
  • Hydrocortisone or Prednisone: Decrease peripheral glucose utilization
  • Glucagon: Stimulates glycogenolysis
  • Diazoxide: Inhibits insulin secretion
  • Octreotide acetate (somatostatin acetate): Inhibits insulin and GH release
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15
Q

If refractory to pharmacologic therapy or thought to be due to primary pancreas pathology, ___ is the most premanent intervention for neonatal hypoglycemia

A

If refractory to pharmacologic therapy or thought to be due to primary pancreas pathology, subtotal pancreatectomy is the most premanent intervention for neonatal hypoglycemia

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16
Q

Hypoglycemia brain injury

A

Even as blood sugar varies, CSF sugar remains fairly constant as it is regulated by glucose transporters at the choroid plexus, not just simple diffusion. Infants with moderate hypoglycemia are therefore more at risk of intraventricular hemorrhage due to changes in bloodflow secondary to hypoglycemia rather than neuroglycopenia.

If blood sugar is very low and does result in neuroglycopenia, glutamate builds up in the synaptic clefts and binds to NDMA-receptors (predominant glutamate receptors in the neonatal brain), resulting in excitotoxicity that manifests as seizure and areas of brain necrosis.