A 34-year old pregnant lady had induction of labour with prostaglandins and oxytocin infusion after her due date. She failed to progress in labour and became slightly disoriented. Urgent biochemistry revealed serum sodium of 124 mmol/l. She delivered a healthy baby by forceps but had post-partum haemorrhage of 1.5 l. Oxytocin infusion was continued along with Hartmanns solution. She became drowsy and biochemistry revealed serum sodium of 118 mmol/l, low serum osmolality, high urine osmolality and high urine sodium. Oxytocin infusion was stopped and 0.9% normal saline commenced. She had diuresis of two litres over the next three hours. She clinically improved and serum sodium levels rose to 126 mmol/l. She admitted to drinking plenty of salt free fluids before delivery and had no symptoms and signs of Sheehans syndrome or hypophysitis. Random cortisol was 620 nmol/l and thyroid function tests were normal. Serum levels normalised by the next day and her cognition returned to normal. This lady had dilutional hyponatraemia mainly caused by oral and IV fluids of low sodium content and was exacerbated by oxytocin infusion. Women tend to have asymptomatic low normal sodium due to dilution effect and inability to excrete free water in the later part of pregnancy. Oxytocin has activity on aquaporin receptors usually responsive to anti-diuretic hormone (ADH). Oxytocin administration is not an absolute contraindication and must be used with sodium containing solutions. An acute fall in serum sodium can not only lead to cerebral oedema but can also have serious implications for the baby including neonatal hyponatraemia. Hyponatraemia can be prevented with strict fluid monitoring, aiming to keep fluid balance as neutral as possible, serum sodium checks nearing labour and frequent sodium monitoring during labour. If sodium levels fall, close liaison with endocrinologists to consider oxytocin discontinuation and advice on fluid management is essential.