Endocrine Abstracts

A 40 year old lady known to have type 1 diabetes on insulin pump therapy presented with hypertension at 33 weeks gestation. Treatment with labetalol 100 mg bd was initiated but she was admitted at 34 weeks due to lack of BP control. Sodium levels were 136 mmol/l (135–145 mmol/l) on admission. Labetalol was increased to 300 mg tds and she was discharged after 4 days with a sodium level of 129 mmol/l. She was readmitted at 35 weeks with pre-eclampsia as evidenced by severe headaches, persistent hypertension (186/92 mmHg), a high uric acid (400 umol/l), low platelet count (91×10⁹/l) and proteinuria (1557.1 mg/24 hrs). Her sodium rapidly dropped to 125 mmol/l. Urine sodium was 38 mmol/l, urine osmolality: 267 mOsm/kg, serum osmolality: 269 mOsm/kg. The patient was euvolemic with normal thyroid and adrenal function. These results were consistent with SIADH. Labour was induced but an emergency caesarean section was performed in view of signs of foetal distress. The baby’s sodium level was 127 mmol/l. The mother’s fluid intake was restricted to 1.25 litres/day initially and then to 2 litres/ day. Within 48 hours of delivery, her sodium improved from 125 to 133 mmol/l. Proteinuria decreased to 759.9 mg/24 hrs and platelet count and uric acid normalised. Pre eclampsia is associated with reduced intravascular volume which may stimulate ADH release resulting in SIADH. Foetal sodium rapidly equilibrates with maternal sodium and this can cause foetal jaundice, tachypnoea and seizures if serum sodium is <130 mmol/l. Acute hyponatremia further increases the likelihood of seizures in pre eclampsia. Management includes fluid restriction and delivery in a timely manner.