A 29-year-old woman was admitted at 33 weeks gestation with pre-eclampsia (BP 145/107 mmHg, 3+ proteinuria and significant oedema). On admission her Na was 133 mmol/l and urinary Na 49 mmol/day (ref range 130260). Twenty-four hours urine protein was 4.43 g/day. Foetal assessment revealed intra uterine growth retardation. She was started on labetolol and the dose titrated upwards to control her blood pressure.
Her serum sodium level gradually fell reaching 120 mmol/l on the seventh day of admission. At this stage the Obstetricians instituted fluid restriction of 1 l/day. Her sodium continued to fall and reached a nadir of 112 mmol/l on the ninth day. At this point, her urine sodium was 3 mmol/l, urine osmolality 318 mOsm/kg. She still showed signs of fluid overload with marked oedema. The Endocrine team were then involved. Her adrenal and thyroid function was normal.
The decision was made to deliver the baby by emergency caesarean section in view of the rapidly falling sodium levels based on the theory that the hyponatraemia would resolve as the stimulus for pre-eclampsia was removed.
After delivery the patient developed a diuresis, her sodium level gradually improved and had returned to near normal 3 days post delivery. Her baby was also initially hyponatraemic with a serum sodium of 114 mmol/l this was actively corrected by the paediatricians.
We believe that the likely explanation for our patients hyponatremia was dilutional; we postulate that our patient may have experienced a reduction in her diluting capacity along with a reduced rate of free water clearance as a consequence of her pre-eclampsia. Severe hyponatraemia in pregnancy is rare with only a few cases reported. However, in view of the great risks posed to both mother and baby we recommend regular monitoring of serum sodium levels in all patients with pre-eclampsia.