neonatal hypoglycemia

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NEONATAL HYPOGLYCEMIA

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Neonatal Hypoglycemia. Definition. The numerical definition varies from institution to institution: Numbers based on population studies of plasma glucose concentrations during first 48-72 hours of life with hypoglycemia defined as a plasma glucose level more than 2 SD below the population mean - PowerPoint PPT Presentation

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Page 1: Neonatal Hypoglycemia

NEONATAL HYPOGLYCEMIA

Page 2: Neonatal Hypoglycemia

Definition

• The numerical definition varies from institution to institution:– Numbers based on population studies of plasma

glucose concentrations during first 48-72 hours of life with hypoglycemia defined as a plasma glucose level more than 2 SD below the population mean

• Most institutions use plasma glucose <40mg/dl on the 1st day of life and less than 40-50mg/dl after 24 hours of life

• Physiologic definition: when glucose supply for cells is inadequate to meet glucose demands

Page 3: Neonatal Hypoglycemia

Incidence

• Estimated to be 10% of live births if first feeding is delayed for more than 3-6 hours after birth

• Percentage is even higher for at-risk populations:– Preterm infants– SGA infants– LGA infants– Infants of diabetic mothers

Page 4: Neonatal Hypoglycemia

Pathophysiology

• Newborns have high brain-to-body weight ratio -> higher glucose demand

• Impaired establishment of normal glucose homeostasis during transition from intrauterine to extrauterine life -> hypoglycemia

• Normal glucose homeostasis requires supply to meet demands

• Supply is dependent on adequate stores of glycogen, gluconeogenesis precursors, functioning hepatic enzymes, and a functioning endocrine system

• Demands depend on the metabolic rate of the infant, which can be increased in times of stress (i.e. sepsis, asphyxia)

Page 5: Neonatal Hypoglycemia

Clinical Manifestations

• Asymptomatic• Tachypnea• Apnea• Respiratory distress• Tachycardia• Bradycardia• Jitteriness• Lethargy

• Hypotonia• Weak suck• Temperature

instability• Seizures

Page 6: Neonatal Hypoglycemia

Etiology

Diminished glucose production Increased glucose utilization from

hyperinsulinemia Increased glucose utilization without

hyperinsulinemia Metabolic Disorders Endocrine Disorders Other

Page 7: Neonatal Hypoglycemia

Diminished Glucose Production Premature infants have diminished

reserves because glycogen is deposited during the 3rd trimester of pregnancy

Infants with intrauterine growth restriction (IUGR) and who are SGA have reduced glycogen stores because of: Low intrauterine insulin levels Chronic intrauterine hypoxia

Page 8: Neonatal Hypoglycemia

Increased Glucose Utilization Due to Hyperinsulinemia

Infant of a diabetic mother Maternal intrapartum treatment with

glucose Beckwith-Wiedemann syndrome Insulinoma

Page 9: Neonatal Hypoglycemia

Infant of a Diabetic Mother

Intermittent maternal hyperglycemia -> fetal hyperglycemia and hyperinsulinemia -> hypoglycemia once intrauterine glucose supply from mother is interrupted

Hypoglycemia occurs in 27% of infants of diabetic mothers (IDMs)

Happens in the first few hours of life Most common in macrosomic IDMs Premature &/or SGA IDMs are also at

higher risk

Page 10: Neonatal Hypoglycemia

Beckwith-Wiedemann Syndrome

Fetal overgrowth syndrome with characteristic features: Macroglossia Growth >90% Abdominal wall

defects Ear creases/pits Renal abnormalities Hemi-hyperthrophy Hyperplasia of

organs (such as the pancreas)

Page 11: Neonatal Hypoglycemia

Beckwith-Wiedemann Syndrome Incidence: 1 in 15,000 births Etiology: Sporadic mutation (85%), AD (15%) 50% have transient hypoglycemia caused by

hyperinsulinemia from hyperplasia of the pancreas

Increased risk for malignancy: Wilms tumor, hepatoblastoma, neuroblastoma,

gonadoblastoma Monitored with abdominal US and alpha-

fetoprotein q6months until 6 y/o

Page 12: Neonatal Hypoglycemia

Insulinoma

Tumor of the pancreas that produces too much insulin

Very rare in children Most are benign

tumors, only about 5-10% are malignant

Treatment is surgical If unable to surgically

remove, treat with diazoxide or octreotide to reduce insulin secretion

Page 13: Neonatal Hypoglycemia

Increased Glucose Utilization Without Hyperinsulinemia

States of stress such as hypothermia, perinatal asphyxia, sepsis, and heart failure increase usage and depletion of glycogen stores

Polycythemia - increased utilization of glucose by the increased mass of RBCs

Page 14: Neonatal Hypoglycemia

Metabolic Disorders

Inborn errors of metabolism: Defects in carbohydrate metabolism

Glycogen Storage Disease Glycogen Synthase Deficiency Galactosemia Fructose Intolerance

Defects in amino acid metabolism Maple Syrup Urine Disease Propionic Acidemia Methylmalonic Acidemia

Defects in ketogenesis and fatty acid oxidation

Page 15: Neonatal Hypoglycemia

Endocrine Disorders

Deficiency or malfunctioning of the hormones that regulate glucose homeostasis: Cortisol Growth hormone Glucagon Epinephrine Thyroid

These could be associated with hypothalamic, pituitary, or adrenal insufficiency

Page 16: Neonatal Hypoglycemia

Other Causes

Maternal drugs such as terbutaline, labetalol, propranolol -> inhibit glycogenolysis and gluconeogenesis

Neurohypoglycemia: GLUT1 transport protein facilitates glucose

diffusion across blood vessels into the brain and CSF

Deficiency in GLUT1 results in low CSF glucose, but blood glucose levels are normal

Rare disorder that presents as 2-3 months with seizures, developmental delay, and acquired microcephaly

Page 17: Neonatal Hypoglycemia

Evaluation

Blood glucose should be monitored for infants at risk for hypoglycemia: Premature infants SGA infants LGA infants IDMs Infants whose mothers were treated with beta

adrenergic agents or beta blockers Infants under stress requiring more intensive care

(i.e. sepsis, asphyxia)

Page 18: Neonatal Hypoglycemia

Evaluation

Monitor glucose within first 1-2 hours of life or with signs consistent with hypoglycemia

Surveillance should be continued in infants with glucose <40 until feedings well established and levels have stabilized

Low Chemstrips (glucose oxidase reagent strips for rapid screening) should be confirmed with serum glucose level processed by the lab

Page 19: Neonatal Hypoglycemia

Evaluation

Determining Etiology: Consider prenatal/perinatal history Check growth parameters Perform a careful physical exam Screen for sepsis if suspected

Page 20: Neonatal Hypoglycemia

Evaluation

If hypoglycemia persists for >1 week, endocrine and metabolic disorders should be suspected Consult endocrinology At the time of hypoglycemia, obtain:

ACTH/cortisol levels Growth hormone levels Insulin levels Free fatty acids Ketones Pyruvate Lactate

Page 21: Neonatal Hypoglycemia

Evaluation

The following should also be obtained, but can be obtained at anytime:

TSH/T4 levels Serum amino acids Urine organic acids Acylcarnitine profile

Page 22: Neonatal Hypoglycemia

Management

Anticipation and prevention is key In infants who are premature or too ill to

feed, begin parenteral glucose infusion at a rate of at least 6mg/kg/min

Glucose (mg/kg/min) = (% glucose in solution x 10) x (rate of infusion per hour) / (60 x weight in kg)

Page 23: Neonatal Hypoglycemia

Healthy asymptomatic infants Try feeding orally with either formula,

breastmilk, or D10W Use of formula or breastmilk better than

D10W because they provide carbohydrates as well as protein and fats that are metabolized more slowly to provide a sustained supply of substrate

Recheck glucose in 20-30 mins after the feeding and continue to feed q2-3 hrs

Blood glucose should be followed before each feed for 12-24 hours

Page 24: Neonatal Hypoglycemia

Symptomatic infants or infants with very low glucose concentrations

Start parenteral glucose infusions on: Symptomatic infants Infants with a glucose of <20-25 Infants who do not tolerate enteral feedings Infants whose blood sugar remains <40

after a trial of oral feeding

Page 25: Neonatal Hypoglycemia

Symptomatic infants or infants with very low glucose concentrations:

Start with a bolus of 2-4ml/kg of D10W Then begin a glucose infusion of at least

6mg/kg/min Check blood glucose 20-30 mins after bolus to

determine if another bolus is needed, and adjust rate of dextrose concentration to maintain plasma glucose >45mg/dl

Follow blood glucose every 1-2 hours until stable, then can space out monitoring as needed

When the glucose concentration is stable for 12-24 hrs, the glucose infusion rate can be tapered slowly by 10-20% each time the feeds are advanced and the pre-prandial blood glucose is >50-60 mg/dl

Page 26: Neonatal Hypoglycemia

Persistent Hypoglycemia (> 7 days) Corticosteroids stimulate gluconeogenesis

and reduces peripheral glucose utilization should be considered in infants who remain

hypoglycemic after 2-3 days of glucose infusion of >12mg/kg/min

Glucagon can also be used during severe hypoglycemia as a temporizing measure in infants with adequate glycogen stores (i.e. NOT in SGA or premature infants)

Diazoxide/Somatostatin/Octreotide inhibits insulin release for those with persistent hypoglycemia and hyperinsulinemia

Page 27: Neonatal Hypoglycemia

Persistent Hypoglycemia (> 7 days) Human growth hormone for infants

with growth hormone deficiency Nifedipine – case reports have shown

some success with few side effects Subtotal pancreatectomy for

hyperinsulinemia hypoglycemia recurs in up to 1/3 of

patients 40-60% develop DM later in life

Page 28: Neonatal Hypoglycemia

Prognosis

Symptomatic hypoglycemia can result in brain injury

Most common sequelae are: Disturbances in neurological development and

intellectual function Motor deficits (spasticity and ataxia) Seizures* May be related to the underlying etiology of the

hypoglycemia There is inconclusive evidence on the effect

of asymptomatic hypoglycemia on neurodevelopment