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Neonatal Hypoglycemia Clinical Presentation

Neonatal Hypoglycemia: Clinical Presentation Normal physiology Glucose is produced from endogenous lactate, glycerol, and amino acids until glucose supply is established through feeds Hepatic glycogen is broken down to produce glucose in the first 8-12 hours of life Glucose is absorbed in the small intestine and transported into the bloodstream The pancreas responds to ↑ glucose blood concentration by releasing insulin Insulin acts on glucose transporters that line the cell membrane to bring glucose into the cell Glucose is broken down into ATP, which is used by cells for energy Authors: Dasha Mori Reviewers: Michelle J. Chen Dr. Ian Mitchell* *MD at time of publication Neonates with predisposing factors that Neonates that are unable to feed for > 60-120 Infant is large for gestational age (> 90th percentile) or was born to pregnant person with diabetes Fetus was exposed to high levels of glucose through placental circulation Fetus adapted to high blood glucose by producing high amounts of insulin After birth, placental glucose supply is stopped but insulin remains high ↑ Insulin promotes inappropriately ↑ uptake of glucose into cells put them at high risk for hypoglycemia Cells cannot produce enough ATP from glucose to power physiological functions Immature nervous system, use of fatty acids or proteins as an alternate ATP source, or adaptation to low glucose in utero can mask symptoms of hypoglycemia Asymptomatic hypoglycemia Neonates with low blood glucose often don’t show any symptoms and are detected by screening infants who are at a high risk for hypoglycemia min are at risk for hypoglycemia Infant is small for gestational age or experienced fetal growth restriction Smaller neonates have smaller glycogen stores Preterm infants born < 37 weeks Glycogen is stored during the 3rd trimester; preterm infants did not have opportunity to build up stores Loss of glucose source from placental circulation after birth puts preterm neonate at risk for low blood sugar Body’s sympathetic system detects low glucose and triggers physical symptoms (neurogenic symptoms) Symptomatic hypoglycemia Neurons in brain are unable to produce enough ATP and thus function properly, triggering symptoms related to low sugar in the CNS (neuroglycopenic symptoms) Non-specific symptoms are not exclusive to hypoglycemia and warrant further investigation to exclude other differential diagnosis (sepsis, inborn errors of metabolism, neonatal abstinence syndrome, neonatal encephalopathy, perinatal asphyxiation) Jitteriness or tremors Sweating Irritability Tachypnea Pallor Pathologic poor feeding Weak or a high- pitched cry Change in level of consciousness (lethargy or coma) Seizures Pathologic hypotonia for gestational age Apnea Bradycardia Cyanosis Hypothermia Neonates with perinatal stress (e.g. birth asphyxia, meconium aspiration) Body uses more glucose to produce ATP to manage condition causing physiological stress Glucose stores are used up more quickly Born to pregnant person with beta-blocker use Body in stress releases epinephrine to promote sympathetic responses including glycogen breakdown into glucose Beta blockers from placental circulation prevent epinephrine from binding to its receptor in infant’s body Neonatal Hypoglycemia: Asymptomatic and symptomatic hypoglycemia satisfy the criteria of blood glucose < 2.6 mmol/L in both term and preterm infants within 72 hours of birth, and after 72 hours of age glucose < 3.3 mmol/L Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Oct 4, 2024 on www.thecalgaryguide.com