Discussion:
While the causes of hyponatremia may be multifactorial, the primary treatment strategy remains consistent for both thiazide and non-thiazide associated euvolemic hyponatremia which is the removal or correction of the underlying etiology along with free water restriction. For patients with severe symptomatic hyponatremia, hypertonic saline and vasopressin receptor antagonist (VRAs) have been found to be effective.10,11,14,15 However, the role of VRAs for TAH has yet to be established.10,14
Additionally, urea oral powder has been used to treat both thiazide and non-thiazide associated hyponatremia.1,15 Greater than 90% of oral urea is readily absorbed from the upper gastrointestinal tract and is freely filtered by the glomerulus.1,15Approximately 50% of urea is passively reabsorbed within the nephron and the remaining filtered urea is excreted in the urine. Urea promotes sodium homeostasis by increasing free water elimination through osmotic diuresis and by reducing sodium loss from natriuresis.15 Urea is generally safe and well tolerated. The most commonly reported adverse effects are dysgeusia, nausea and hypokalemia.15 When compared to hypertonic saline and VRAs, urea has not been associated with the development of osmotic demyelinating syndrome even in the setting of rapid correction of sodium. Urea does not induce hepatotoxicity and it can be administered in high doses without precipitating acute renal failure.15
Furthermore, potassium repletion in patients with hyponatremia must be carried out cautiously as increased potassium results in the shift of sodium from the cell into the extracellular fluid. Thus, treatment strategies must be altered to account for the potassium supplementation asĀ osmotic demyelination following potassium repletion has occurred.16
In summary, perioperative clinicians must maintain vigilance for severe hyponatremia as the cause of postoperative neurological decline and be familiar with the clinical management of hyponatremia to prevent devastating neurological injury.