EP676 - ECE_1786 - Ketamine induced Hyponatremia

Abstract

Abstract Ketamine is a dissociative anaesthesia which also has analgesic properties and is also used in pain management and depression1. As it produces an out-of-body and rewarding experience, there is a potential danger for abuse of this medication2.Cystitis and cholangiopathy are recognized side effects of ketamine use3,however, published data on ketamine-induced hyponatremia is scarce.The exact pathophysiology is not clear though it has been postulated that ketamine stimulates the release of antidiuretic hormone from the hypothalamus. Here, we describe an unusual case of acute hyponatremia likely induced by ketamine recreational use. A 25-year-old malnourished gentleman presented with 1-week history of progressive lethargy and global weakness, having used ketamine recreationally for several years. He did not have recent GI losses (vomiting or diarrhoea) and did not ingest excessive amount of water or alcohol. The initial biochemistry revealed profound hyponatremia (Na 100 mmol/l). The paired serum (205 mosm/kg) and urine osmolality (313 mosm/kg) and urine sodium 93, suggested SIADH, however clinically patient appeared dehydrated and malnourished. The cortisol level was sufficient (561 nmol/l). It was unclear if hyponatremia was acute or subacute-on-chronic with last normal sodium level noted five years earlier. Given the neurological symptoms of acute confusion and unsteadiness, the patient was treated with half the usual volume hypertonic saline (75 ml of 2.7% NaCl ) over 20 minutes. A cautious approach was implemented due to the potential risk of over-correction given his apparent malnourishment. He was admitted to ICU and treated with slow intravenous fluid (0.9% NaCL 80 ml/hr). His Na level overcorrected by 11 mmol/l in 24-hours with polyruia, and was halted by stat 1 mcg dose of desmopressin. The patient went on to develop acute kidney injury with polyuria needing repeat administration of desmopressin which had minimal effect, suggesting ADH resistance and possible tubular injury. It was deemed that hyponatremia was multifactorial, secondary to ketamine-induced renal salt-wasting (likely tubular damage) and an element of inappropriate ADH secretion in the context of critical illness. The sodium level steadily improved with slow IVF and by day-8 of admission, the patient had full recovery. This case uniquely highlights ketamine as a rare cause of hyponatremia which was severe enough to warrant use of hypertonic saline and ITU admission.