“…While this normally is well tolerated in healthy adults pregnant women have a reduced intrinsic ability to compensate for fl uid overload as water-sparing systems are activated and labour and nausea additionally stimulate ADH secretion [ 7 ] . In addition, oxytocin, structurally similar to vasopressin (ADH), can contribute to water retention by stimulation of the specifi c V2 vasopressin receptors in the kidney [ 6 ] . Babies born after fetal distress or diffi cult delivery, like our 2 patients, have higher circulating ADH concentrations compared to those born uneventfully [ 5 ] and are therefore at risk of exacerbating their hyponatraemia after birth.…”