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.