Physiological hyponatraemia in pregnancy reflects adaptive changes in fluid homeostasis, with serum sodium levels typically in the range 130–135 mmol/L. Hypertensive disorders affect 3–8% of pregnancies worldwide, and early-onset preeclampsia (<34 weeks of gestation) occurs in approximately 6.3 per 1000 births and is associated with significant maternal and perinatal morbidity. Hyponatraemia has been reported in approximately 9% of pregnancies complicated by preeclampsia and is increasingly recognised as a marker of severe disease; however, its pathophysiology and optimal management remain incompletely defined. This report describes the case of a 32-year-old woman, with type 1 diabetes mellitus, chronic hypertension, and chronic kidney disease, who presented at 24 + 4 weeks of gestation with severe early-onset preeclampsia and profound hyponatraemia (Na 118 mmol/L). Laboratory evaluation indicated hypervolaemic hyponatraemia. Despite fluid restriction, her serum sodium continued to decline, and antihypertensive therapy was maximised. She received antenatal corticosteroids and underwent emergency caesarean section. Perioperative hypertonic saline was administered, and her sodium normalised by day 4 postpartum. The neonate had moderate hyponatraemia that rapidly normalised as well as prematurity-related complications that required management. Severe hyponatraemia in preeclampsia is rare and requires multidisciplinary management, including careful fluid and electrolyte strategy and timely delivery. Serum sodium monitoring should form part of surveillance for patients with severe preeclampsia. • Profound hyponatraemia can complicate early-onset preeclampsia. • The hypervolaemic dilutional pattern supports placental pathophysiology. • The sFlt-1/PlGF ratio aids diagnosis in superimposed preeclampsia. • Refractory hyponatraemia may signal the need for delivery. • Sodium typically normalises postpartum following removal of the placenta.
Horsburgh et al. (Fri,) studied this question.