Endocrine Abstracts (2017) 50 EP048 | DOI: 10.1530/endoabs.50.EP048

Pre-eclampsia as a rare cause of severe hyponatraemia

Khyatisha Seejore1, Amal Mighell2 & Alison J. Dawson1


1Department of Diabetes and Endocrinology, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK; 2Maternity Services, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK.


Background: Hyponatraemia is the commonest electrolyte abnormality. It carries a mortality rate of above 50% when plasma sodium concentration falls below 115 mmol/L. We present a case of severe hyponatraemia complicating pre-eclampsia in a primiparous woman.

Case Report: A 23-year old healthy primigravida was admitted at 34 weeks’ gestation following an episode of reduced foetal movements. She was hypertensive (BP 171/98 mmHg) and had 2+ proteinuria. Her sodium level was 133 mmol/L (Normal Range, NR: 135-145 mmol/L) and urine protein-creatinine ratio was 229 mg/mmol (NR: 0-15). Cardiotocography was unremarkable. She was diagnosed with pre-eclampsia (PET) and started on labetalol.

Serum sodium level dropped to 126 mmol/L and two days later, reached a nadir of 114 mmol/L – she developed marked oedema. Further investigations: serum osmolality 255 mOsm/kg (NR: 275-290 mmol/L); urine osmolality 445 mOsm/kg; urine sodium <10 mmol/L; normal thyroid function. Isotonic sodium chloride was carefully administered. She was delivered by caesarean section at 36+1 weeks because of persistent hyponatraemia and worsening symptoms of pre-eclampsia, including suspected acute fatty liver (ALT 1348 iu/L; NR <40 iu/L). A male infant was born (Apgar score 9 at 10 minutes) – he had mild hyponatraemia – corrected by the paediatricians. Within 24 hours of delivery, maternal hyponatraemia had improved to 133 mmol/L. Recovery was complicated by intrapartum sepsis. She was discharged eight days later with normal BP.

Discussion: Pregnancy involves physiological changes affecting water and sodium homeostasis. However, most women with PET do not develop hyponatraemia. We postulate that this was a case of hyponatraemia with hypervolaemia (excess extracellular sodium and total body water) as a result of impaired free water clearance secondary to pre-eclampsia. SIADH was discounted because of low urinary sodium and oedema.

We draw attention to severe hyponatraemia as a rare indication for urgent delivery in pre-eclampsia. This requires multidisciplinary management and continuing postpartum care to ensure favourable maternal/ neonatal outcomes.

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