Endocrine Abstracts

A 32-year-old primigravida woman, low risk pregnancy, BMI 20, presented at 29 weeks of gestation with headache and mildly raised blood pressure and normal laboratory tests. The patient had no signifcant medical history and the pregnancy to date had been uneventful. Physical examination showed blood pressure (BP) of 145/93 mm Hg. (Baseline, 100/70 mm Hg). Laboratory tests showed a baseline sodium of 134 mmol/l, with the rest of the biochemistry normal. She had been commenced on Labetalol. At 29+4 weeks, the patient was admitted with headache, feeling unwell, leg and hand oedema and raised blood pressure. Physical examination showed BP of 168/105mm Hg with significant pedal oedema and proteinuria +4. Other physical findings were unchanged. Laboratory investigations showed serum sodium level of 122 mmol/l), with normal kidney and liver function test results. A urine osmolality was elevated at 433 mmol/kg while her urine sodium measured at 22 mmol/l and her urine potassium at 33 mmol/l. A short synacthen test was normal including normal thyroid biochemistry. The patient was admitted for observation including blood pressure monitoring. Liver function test results and serum uric acid level were normal. A growth scan of the foetus showed normal growth. Subsequent BP readings were under control while her urine protein creatinine ratio was 100 mg/mmol. During her hospital stay, her serum sodium level continued to decline. Although she was put on fluid restriction, her hyponatremia continued to worsen, with development of generalised oedema and imaging picking up sub pulmonary pleural effusion and mild pericardial effusion. Volume overload signs included engorged neck veins, presacral oedema were evident. Laboratory signs of severe preeclampsia as elevated liver enzymes (ALT 248), thrombocytopenia (platelets at 77) was also seen. In addition, her urine protein creatinine ratio had further increased to 416 mg/mmol. Essentially, she had developed severe hyponatremia in the setting of preeclampsia. Decision for delivery was made at 30 weeks by elective CS and planned admission to intensive care unit after multidisciplinary team discussion including obstetrician, Endocrinologist, neonatologist, cardiologist and anaesthetist. She was delivered by caesarean section, which was uneventful. Magnesium sulphate was given before delivery for neuroprotection and continued 24 hrs post-partum to reduce the risk of seizures. Serum sodium levels improved after 48 hrs post-delivery and returned to normal values on day 5 post-partum as well as the oedema. This presentation highlights the importance of hyponatremia as a prognostic factor guiding management of severe pre-eclampsia.