Prevention and treatment of hyponatremia in children: old habits die hard

Sirs, In a letter [1] Dr. Ray takes exception to three points that we make in our recent review entitled “Preventing neurological complications from dysnatremias in children” [2]: (1) that the routine administration of hypotonic fluids as originally proposed by Holliday and Segar can result in fatal hyponatremic encephalopathy; (2) that hyponatremic encephalopathy is common in children with severe hyponatremia <125 mEq/l, and (3) our recommendation for treating children with hyponatremic encephalopathy with 3% sodium chloride. We would like to address each point separately. In 2003 we pointed out the dangers of the routine use of hypotonic maintenance fluids [3], as initially proposed by Holliday and Segar [4], and we introduced the concept of using isotonic saline solution (0.9% sodium chloride) for the prevention of hospital-acquired hyponatremia. Since that report, Holliday et al. have revised their fluid recommendations [5] and acknowledged that it “is now evident, that practice [of administering hypotonic fluids to children] is flawed” [6]. Holliday and colleagues’ new recommendations for avoiding hyponatremia are to bolus initially with isotonic saline solution, followed by maintenance therapy with hypotonic fluids [5]. We have published a Letter to the editor in response to their paper, pointing out the short comings of their approach [6]. It has been demonstrated by Hoorn et al. [7] that 28% of patients with acute hospital-acquired hyponatremia were treated in a fashion similar to that recommended by Holliday et al. The case we present, of a 3-week-old who developed permanent brain injury from hospital-acquired hyponatremia, was managed in the fashion recommended by Holliday [2]. Holliday et al. also continue to recommend hypotonic fluids in the post-operative period. We have shown that 37% of post-operative children who received hypotonic fluids developed hyponatremia (Na<135 mEq/l) [8]. Dr. Ray misinterprets the paper by Arieff and Ayus [9], where they report on 16 otherwise healthy children who suffered death or permanent neurological injury from post-operative hyponatremic encephalopathy. Seven of them received hypotonic fluid below or equal to maintenance volume, and none had “extensive extrarenal losses”, as he states. Moreover, Holliday et al. also recommend in the“rare instance when SIADH is suggested” to reduce fluids to “half average”. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is not a rare occurrence in hospitalized patients [7]. While fluid restriction is indicated in patients with SIADH, it makes no physiological sense to administer hypotonic fluids to a patient with an impaired ability to excrete free water. Dr. Ray takes exception to our claim that over 50% of children with a serum sodium <125 mEq/l will manifest signs of hyponatremic encephalopathy. As we acknowledge in our manuscripts: “the true incidence of hyponatremic encephalopathy in hospitalized children is unknown as large prospective studies have not been done” [2]. It is, however, well accepted that neurologic symptoms are relatively common in acute hyponatremia. Our estimate comes from the best data available in the literature, and Dr. Ray does not put forth any data to refute our claim. M. L. Moritz Division of Nephrology, Department of Pediatrics, Children’s Hospital of Pittsburgh The University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA