ESA-SRB-AOTA 2019

Severe hyponatraemia as the presenting manifestation of empty sella syndrome (#588)

Kay Hau Choy 1 , Tegan van Gemert 2
  1. Department of Endocrinology and Metabolism, Concord Repatriation General Hospital, Concord, NSW, Australia
  2. Wollongong Hospital, ISLHD, Wollongong, NSW, Australia

Case: An 85-year-old male—with a history of laryngeal cancer previously treated with radiotherapy—was admitted with lethargy and confusion. He was diagnosed with severe hyponatraemia with a nadir sodium level of 107 mmol/L (range: 135-145mmol/L). Serum and urine chemistries were consistent with syndrome of inappropriate antidiuretic hormone (ADH) secretion (SIADH). Investigation for hyponatraemia revealed a low morning cortisol of 133 nmol/L (range: 167-507nmol/L), with subnormal synacthen stimulation and inappropriately normal adrenocorticotropin hormone. Prolactin and IGF-1 levels were low. Thyroid function tests showed low free T4 and free T3 with a normal TSH on a background of pre-existing hypothyroidism, consistent with inadequate thyroid hormone replacement. His pituitary profile was in keeping with panhypopituitarism. A pituitary MRI demonstrated findings consistent with empty sella syndrome, which was suspected to be a consequence of previous radiotherapy. His hyponatraemia gradually normalised following initiation of hydrocortisone, hypertonic saline and fluid restriction. Thyroxine dose was increased. He was discharged home on low-dose hydrocortisone. His sodium level remained stable two months post-discharge.

Discussion: Hyponatraemia is the most common electrolyte abnormality encountered in clinical practice, with an estimated incidence of 15–30%.1 Appropriate management of hyponatraemia is vital as in its severe form it has a high morbidity and mortality. Rapid correction of hyponatremia risks causing cerebral demyelination which is often fatal.2 Hyponatremia as the presenting manifestation of empty sella syndrome is uncommon. Its clinical presentation is similar to SIADH, but fluid restriction alone is unable to fully correct hyponatraemia. The cause of ADH secretion in hypopituitarism-associated hyponatraemia is due to adrenal insufficiency. The glucocorticoid deficit is not an osmotic, but a physiological stimulus for ADH secretion.3 Glucocorticoid replacement has been shown to reverse the impaired water diuresis of this disorder by increasing the renal excretion of solute free water and is therefore the mainstay of treatment in this context.3-5

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