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In this issue, Dr. D’Oyley reports a rather provocative approach to the perioperative management of hyponatremia, using data from two patients who underwent orthotopic liver transplantation. The author suggests that the routine administration of intravenous furosemide to induce a supranormal diuresis provides a better intraoperative control of serum sodium levels, which can potentially improve the long-term outcome. Hyponatremia is common in patients with chronic liver disease because of low sodium diets, impaired renal handling of free water, and elevated levels of antidiuretic hormone. It may be exacerbated by aggressive diuretic use and is commonly treated with discontinuation of diuretics combined with free water restriction. Despite the evidence that a major tubular effect of furosemide is to inhibit sodium reabsorption in loops of Henle, it has been shown that the administration of the diuretic may result in a net increase in free water excretion in selected patients [1]. The suggested mechanism for an improved water excretion is through an incomplete osmotic equilibration that is achieved during high rates of flow through collecting ducts. Moreover, furosemide may interfere with proximal tubular reabsorption, resulting in an increased delivery of tubular fluid to diluting sites that are unaffected by the drug, and a net increase in the volume of dilute tubular fluid. Therefore, the proposed approach to administer furosemide during liver transplantation may in selected patients result in better perioperative control of hyponatremia. However, cirrhotic patients who require liver transplantation are severely compromised, and have variable degree of renal impairment, [2] making the response to furesmide very unpredictable. Consequently, routine use of furosemide is currently not advised in these patients because it can lead to a worsening of the hyponatremia or too rapid a correction of

Perioperative Control of Serum Sodium for Liver Transplantation: Time for a More Aggressive Approach?