ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2019) 63 P695 | DOI: 10.1530/endoabs.63.P695

Severe salt wasting syndrome due to spontaneous epidural haematoma

Aoife Garrrahy1,2, Osamah Hakami1, Iona Galloway1, Stephen McNally3, Rory Dwyer4, Christopher J Thompson1,2 & Mark Sherlock1,2

1Academic Department of Endocrinology, Beaumont Hospital, Dublin, Ireland; 2RCSI Medical School, Dublin, Ireland; 3Department of Neurosurgery, Beaumont Hospital, Dublin, Ireland; 4Department of Anaesthesia, Beaumont Hospital, Dublin, Ireland.

Hyponatraemia is commonly encountered in neurosurgical units. Salt wasting syndrome is rare, and thought to occur due to ANP- and BNP-mediated natriuresis, leading to hypovolemic hyponatraemia. A 31 year old male was transferred to the National Neurosurgical Unit with a 12 hour history of back pain, progressive lower limb weakness and sensory loss. MRI demonstrated an epidural haematoma, extending from C7 to T3, and he underwent emergency decompressive laminectomy. Vasopressin, noradrenaline and 0.9% saline were administered for spinal shock; initial plasma sodium concentration (pNa) was normal, 139 mmol/l (RR 133–145 mmol/l). Within 24 hours of admission, he became polyuric (8000 ml/24 h) and pNa dropped to 122 mmol/l, accompanied by slurred speech. 3% saline infusion was commenced, and the rate quickly up-titrated to 100 ml/hr to maintain pNa in the normal range. Further investigations confirmed a large volume natriuresis (urine output (UO) 6 liters/24 h, urine sodium 205 mmol/l, urine osmolality 614 mOsm/kg) and BNP was elevated (2483 pg/ml, RR 0-97), in keeping with a diagnosis of salt wasting syndrome. Echocardiogram was normal. Aldosterone was undetectable (<138 pmol/l), renin 7.2 mIU/l (RR 9-103), and co-peptin 1.7 pmol/l. On day 3 of admission, vasopressin infusion was stopped, resulting in a rapid aquaresis (4500 ml), and rise in pNa of 16 mmol/l in 4 hours. 3% saline was held to allow pNa to drop to prevent over-rapid correction, and vasopressin was restarted. BNP fell to normal limits over seven days, but he remained polyuric (6–14 liters/day) and hyponatraemic (pNa 120–130 mmol/l, despite 3% saline 100–200 ml/hour). This persistent aquaresis, despite normalisation of BNP concentration suggested not only BNP-related natriuresis, but also a loss of baroregulated vasopressin secretion, so that when vasopressin was held, significant hypotonic polyuria and rapid increase in pNa occurred. Oral fludrocortisone was commenced on day 12 and oral dDAVP on day 14. UO fell to 4–6 liters/day. Subsequently, indomethacin was introduced to decrease glomerular filtration rate. Over the next three weeks, UO fell and dDAVP was weaned down to stop, UO fell to 2–3 liters/day and pNa normalised. Aldosterone and renin concentrations remained undetectable, and fludrocortisone 100mcg was continued. He was discharged to his referring hospital 10 weeks from initial presentation. This case illustrates two discrete pathophysiological mechanisms of dysnatremia post-spinal injury (a) BNP-mediated natriuresis leading to hypovolemia, with lack of compensatory action of renin-angiotensin-aldosterone system, and of (b) baroregulated vasopressin release. Targeting these physiological derangements with volume repletion, aldosterone, plus dDAVP, was required to reduce urine volume and normalise pNa.

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