Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2019) 62 P61 | DOI: 10.1530/endoabs.62.P61

EU2019 Society for Endocrinology: Endocrine Update 2019 Poster Presentations (73 abstracts)

A challenging case of cerebral salt wasting syndrome superimposed on central diabetes insipidus following pituitary tumour apoplexy

Kirsten Mitchell , Carly Lamb & Yared Demssie

University Hospital Ayr, Ayr, UK.

Case history: An 84-year old man with known non-functioning pituitary macroadenoma was admitted with productive cough and headache. Clinical assessment revealed evidence of pneumonia and antibiotic treatment was initiated. However subsequently the patient’s GCS dropped to 12. Left-sided 6th nerve palsy was present, but patient drowsiness precluded visual-field examination. CT brain showed pituitary tumour apoplexy due to haemorrhage, confirmed on MRI. His condition initially improved with intravenous hydrocortisone.

Investigations: Pituitary hormonal profile revealed panhypopituitarism (random cortisol 125 nmol/L, free T4 4.0 pmol/L, TSH 2.9 mU/L, testosterone <1.0 nmol/L, undetectable prolactin and LH/FSH). By day 3 the patient developed polydipsia and polyuria. Overnight water deprivation test confirmed central diabetes insipidus (DI). He was commenced on oral hydrocortisone, levothyroxine, desmopressin and topical testosterone. On day 7, serum sodium dropped to 128 mmol/L. He was initially clinically euvolaemic. Paired serum and urine osmolality were 237 and 752 mmol/L respectively. Urine sodium was elevated (129 mmol/L). Hyponatraemia was initially ascribed to over-replaced DI. Desmopressin dose was reduced and his fluid intake was restricted to 1–1.5 litres/day. Urine output remained high (3–3.5 litres/day), he became progressively dehydrated and serum sodium dropped to 107mmol/L. A diagnosis of cerebral salt wasting (CSW) was made based on clinical hypovolaemia; high urine sodium; and failure of hyponatraemia to improve despite fluid restriction and desmopressin dose reduction.

Results and treatment: The patient received boluses of hypertonic saline (2.7%) for four days in medical high dependency, and serum sodium rose to 120 mmol/L. Thereafter he was maintained on isotonic saline with Slow Sodium tablets to replace urinary sodium loss. Fludrocortisone was added to curtail natriuresis. Serum sodium gradually normalised, and saline infusion, Slow Sodium and fludrocortisone were weaned. He was transferred for rehabilitation six weeks after admission with sodium stable at 135–140 mmol/L.

Conclusion and points for discussion: CSW is a rare cause of hyponatraemia in patients with acute brain injury. The biochemical features of CSW are indistinguishable from syndrome of inappropriate anti-diuretic hormone secretion (SIADH) or over-replacement of desmopressin in DI. Coexistence of CSW with central DI has been described in case reports. In this scenario the diagnosis of CSW may be delayed, as hyponatraemia could be ascribed to desmopressin over-replacement. A useful diagnostic distinction is the patient’s clinical volume status; however assessment can be unreliable if volume deficit in CSW is subtle. Management of CSW involves saline infusion guided by serum sodium and fluid balance monitoring. Fludrocortisone can be a useful adjunct treatment.

Volume 62

Society for Endocrinology Endocrine Update 2019

Society for Endocrinology 

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