Pathogenesis of oxytocin-induced neonatal hyperbilirubinaemia.
100 term (gestation at least 37 weeks), vertex presenting, vaginally delivered, and fetomaternal blood-group-compatible neonates were studied to evaluate the pathogenesis of neonatal hyperbilirubinaemia induced by oxytocin. 50 infants were born after oxytocin infusion for augmentation of labour and the other 50 were delivered spontaneously. The babies born after oxytocin induction of labour attained significantly higher serum bilirubin levels at age 72 +/- 12 hours than the controls. Infants born after oxytocin showed significant hyponatraemia, hypo-osmolality, and enhanced osmotic fragility of erythrocytes at birth. These biochemical and physiological alterations can be explained by the antidiuretic effects of oxytocin and concomitant administration of large quantities of electrolyte-free dextrose solutions used to administer it. Our observations suggest that cord serum sodium and/or osmolality should be estimated and infants with serum sodium less than 125 mmol/l and/or osmolality less than 260 mmol/kg should be considered for prophylactic administration of phenobarbitone.
D004912:Erythrocytes; D006801:Humans; D007010:Hyponatremia / Q000139:chemically induced; D007231:Infant, Newborn; D007567:Jaundice, Neonatal / Q000097:blood / Q000139:chemically induced*; D009994:Osmolar Concentration; D009996:Osmotic Fragility / Q000187:drug effects; D010121:Oxytocin / Q000009:adverse effects*
D010121:Oxytocin