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Neonatal Hypoglycemia Pathogenesis

Neonatal Hypoglycemia: Pathogenesis Normal physiology Placenta supplies fetal circulation with glucose Clamping of the umbilical cord stops the source of glucose Blood glucose level declines rapidly in the first 2-3 hours of life Low glucose causes an ↓ in insulin and an ↑ in epinephrine, cortisol and glucagon Glucagon and epinephrine act on receptors in the liver and skeletal muscle to promote gluconeogenesis (glucose production from non- carbohydrate sources), glycogenolysis (breakdown of glycogen into glucose), and fatty acid oxidation (conversation of fatty acids to ATP) Low glucose levels stimulate the neonate’s appetite, allowing them to adapt to intermittent feeds Infant feeding regularly on a diet with sufficient carbohydrates creates a consistent plasma glucose concentration Pregnant Parent Causes Impaired Glucose Production Inadequate Glucose Supply Pregnant parent using β-blockers β-blockers prevent epinephrine from binding to adrenergic receptors in skeletal muscle and liver Blocked sympathetic signaling in these organs prevents glycogenolysis ↓ Breakdown of glycogen into glucose Infant of a parent with diabetes Parent has a high level of glucose in their blood The fetus receives a glucose-rich blood supply Fetal pancreatic β cells ↑ insulin production Post-birth, glucose levels in the infant’s circulation ↓ but insulin levels remain high Excessive glucose uptake into cells Fetus born with a metabolism disorder (e.g. organic amino acid disorder, disorder of glycogen metabolism, disorder of gluconeogenesis) Genes that make proteins or hormones responsible for production, breakdown and regulation of glycogen are mutated Fetus born with an endocrine disorder (e.g. congenital adrenal hyperplasia, hypopituitarism, Turner Syndrome) Pituitary and/or adrenal gland dysfunction ↓ release of hormones that regulate glucose balance Fetal growth is restricted, fetus is small for gestational age, or is premature (<37 weeks gestation) Glycogen is deposited during the 3rd trimester of pregnancy. Infants born early have fewer stores; smaller infants born at term have ↓ stores, ↑ insulin sensitivity, & poorly coordinated counter- regulatory hormones ↑ Glucose demand for the transition to life out of the womb Glycogen stores used up quickly Perinatal stress (e.g. sepsis, asphyxia) Stress stimulates fetal adrenal glands to ↑ epinephrine secretion Fetal pancreatic ⍺- cells ↑ glucagon secretion ↑ Breakdown of muscles and fat for glucose- building blocks Glycogen stores used up quickly ↑ Glucose usage as fetal metabolic demands ↑ to manage stress Fetal β-cells secrete inappropriately high levels of insulin despite hypoglycemic state; this hyperinsulinism state can last for months & resolve spontaneously ↓ Serum glucose Neonatal hypoglycemia Authors: Dasha Mori Reviewers: Michelle J. Chen *Dr. Danielle Nelson *MD at time of publication Blood glucose < 2.6 mmol/L in term & preterm infants within 72 hours of birth or < 3.3 mmol/L after 72 hours of birth Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published July 19, 2024 on www.thecalgaryguide.com