Endocrine Abstracts

A fit and well 41-year-old lady who was 10-days post-partum was referred to our Endocrine team for hyponatraemia (serum sodium 117 mmol/l). She had a spontaneous vaginal delivery but had 1.5L blood loss due to difficulty with placenta removal. Her baby is well with no medical issues. During pregnancy, she was started on aspirin due to maternal age and had diet-controlled gestational diabetes. She presented to hospital with extreme lethargy. She also reported lightheadedness and occipital headaches. Her headaches have been present since her delivery which did not resolve with simple analgesia. She had no previous headaches during her pregnancy. She was concerned about the lack of breastmilk production. She reported no other endocrine symptoms including visual abnormalities. She did conceive naturally. No examination findings of endocrinopathies were detected and clinically she was euvolaemic. There was no postural drop in her blood pressure and her visual fields were intact to red pin.

Investigation findings: Sodium: 117 mmol/l (sodium immediately post-partum: 129 mmol/l) Potassium: 4.6 mmol/l Urea: 3.0 mmol/l Creatinine: 41umol/l eGFR: >90 ml/minute Our impression at this point was hyponatraemia related to presumed lymphocytic hypophysitis. We commenced her on hydrocortisone replacement(10mg/5mg/5mg) whilst waiting for her pituitary panel, and domperidone 10mg TDS to help with her milk supply. Pituitary blood tests: fT4 : 8.9pmol/l, TSH: 1.20mU/l Cortisol: 44 nmol/l (5pm) Prolactin level: 424mU/l IGF-1: 59microgram/l Following this, we commenced additional levothyroxine 75 mg OD. She was keen go home so we organised a 48-hour review. Unfortunately, she returned the next day feeling more lethargic and this time, with nausea and some tingling sensation in her fingers with persisting headaches. Similarly, her clinical examination revealed euvolaemia. Her repeat serum sodium was 113 mmol/l. Her serum osmolality was 236 mmol/kg, urine osmolality 661 mmol/kg and urine sodium 86 mmol/l. With the working diagnosis of SIADH secondary to lymphocytic hypophysitis, we recommended absolute fluid restriction. We monitored her urine output and serum sodium very closely with an aim to achieve 1L negative balance accompanied by safe level of serum sodium rise. Her serum sodium beautifully rose within the next few days with gradual easing of fluid restriction. The Radiology MDT discussion of her MR pituitary concluded changes in keeping with lymphocytic hypophysitis. Lymphocytic hypophysitis is a very rare cause of hyponatraemia. Our case highlights the importance of having an open clinical suspicion and the need for accurate chronological history to clinch the diagnosis and safely manage these patients.