Endocrine Abstracts

Background: Hyponatraemia is the most frequent electrolyte disturbance in hospitalised patients and is associated with increased morbidity and mortality as well as increased expenditure. Hyponatraemia is a common reason for referral to Endocrinology in the hospital setting however hyponatraemia has a variety of causes many of which do not come under the remit of ‘Endocrinology’.

Aim: To determine the aetiology of severe hyponatraemia in hospital inpatients.

Methodology: Identification of all adult hospital inpatients with a sodium <120 mmol/l in a 6 month period. Retrospective review of hospital records to determine aetiology of hyponatraemia.

Results: Two thirds of patients had more than one cause identified for their hyponatraemia. Of those with a single cause implicated the most common aetiology was drug-induced, mainly due to diuretics, antidepressants and proton pump inhibitors. Other common causes were malignancy, GI salt loss, dehydration and major organ failure. Adrenal insufficiency was seen only rarely and diagnosis was missed on more than one occasion. Syndrome of inappropriate ADH release (SIADH), seen infrequently, was mainly secondary to intra-cranial disease, malignancy, drugs or post-operatively. Most patients with malignancy associated SIADH had small cell lung cancer. The majority of other patients with hyponatremia and malignancy had alternative causes for hyponatraemia such as GI salt loss or hypovolaemia induced non-osmotic ADH release.

Discussion: Adrenal insufficiency and SIADH are infrequent causes of severe hyponatraemia in hospital inpatients. Hyponatraemia is more frequently seen in hypervolaemic states such as cirrhosis, congestive cardiac failure and end stage renal failure and hypovolaemic states such as dehydration, increased GI losses or over-diuresis. Common to many of these causes is a finding of hypotension and intra-vascular volume depletion which raises the possibility that hyponatraemia for many hospital inpatients is due to physiological and appropriate non-osmotic ADH release and thus is still an ‘Endocrine’ pathophysiology.