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PEDIATRICS Vol. 113 No. 5 May 2004, pp. 1395-1396


COMMENTARY

Hospital-Acquired Hyponatremia: Why Are There Still Deaths?

Michael L. Moritz, MD and Juan Carlos Ayus, MD

Division of Nephrology, Department of Pediatrics, Children’s Hospital of Pittsburgh, University of Pittsburgh School Medicine, Pittsburgh, PA 15213-2538
Department of Medicine, University of Texas Health Science Center, San Antonio, TX 78229-3900

Intravenous fluids are probably the most frequently prescribed medication for hospitalized children. The current practice of administering hypotonic fluids to children is based largely on recommendations of Holliday and Segar,1 made almost 50 years ago and on their assumption that the electrolyte composition of intravenous fluids should approximate the composition of human and cow milk. The safety of these recommendations has never been established. There have been >50 cases of death or permanent neurologic injury in children over the past decade from hospital-acquired hyponatremia resulting from the administration of hypotonic fluid.25 In a recent contribution to Pediatrics, we introduced the concept of administering isotonic saline (0.9% sodium chloride) in maintenance fluids to prevent hospital-acquired hyponatremia.6 In an accompanying editorial, Holliday et al7 argued that the administration of isotonic saline is unsafe and that hyponatremia results from egregious fluid management.

In this issue of Pediatrics, a study by Hoorn et al8 supports our hypothesis that the routine administration of hypotonic fluids is dangerous and can result in unnecessary deaths. In this article, Hoorn et al assess the relationship of intravenous fluid administration and the development of hospital-acquired hyponatremia. They found that 10% of children with normal serum sodium at presentation to the emergency department go on to develop hyponatremia. Of the 40 patients with hospital-acquired hyponatremia, 2 had neurologic sequelae and 1 child died from cerebral edema due to an acute fall in serum sodium from 142 to 128 mmol/L. The main contributing factor for developing hospital-acquired hyponatremia was the administration of hypotonic fluids. Since their article was submitted for publication, there have been additional reports of death and hyponatremic encephalopathy resulting from hypotonic fluid administration.911

The data in this article, in conjunction with numerous previous reports of hospital-acquired hyponatremic encephalopathy in children, indicate that the current practice of administering hypotonic maintenance intravenous fluids in children is unsafe and should be abandoned. We disagree with the authors’ recommendations that hypotonic fluids should be avoided only in postoperative patients and those with low normal serum sodiums (PNa < 138 mmol/L). Their data do not support these recommendations, because the majority of patients who developed hyponatremia in their study had a serum sodium >137 mmol/L, and the 1 death occurred in a patient with a serum sodium of 142 mmol/L. The administration of intravenous fluids should be considered an invasive procedure, and all hospitalized patients should be considered at risk for developing hyponatremia. The current practice of routinely administering hypotonic fluids is unphysiologic, given the numerous stimuli for antidiuretic hormone production in hospitalized children. How many more children will die unnecessarily? One is too many. Many tragic deaths could be avoided by the administration of isotonic saline. Although no one parenteral fluid can be administered safely to all children, isotonic saline would seem to be the safest fluid for most children. The administration of hypotonic fluid is unnecessary unless there is a free-water deficit or ongoing free-water losses.12 Until proof exists that the administration of isotonic saline could be harmful, the routine practice of administering hypotonic fluids should be abandoned.


    FOOTNOTES
 
Received for publication Nov 25, 2003; Accepted Nov 25, 2003.

Address correspondence to Michael L. Moritz, MD, Division of Nephrology, Children’s Hospital of Pittsburgh, 3705 Fifth Ave, Pittsburgh, PA 15213-2538. E-mail: michael.moritz{at}chp.edu


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  1. Holliday MA, Segar WE. The maintenance need for water in parenteral fluid therapy. Pediatrics. 1957;19 :823 –832[Abstract/Free Full Text]
  2. Arieff AI, Ayus JC, Fraser CL. Hyponatraemia and death or permanent brain damage in healthy children. BMJ. 1992;304 :1218 –1222
  3. Halberthal M, Halperin ML, Bohn D. Lesson of the week: Acute hyponatraemia in children admitted to hospital: retrospective analysis of factors contributing to its development and resolution. BMJ. 2001;322 :780 –782[Free Full Text]
  4. Moritz ML, Ayus JC. La Crosse encephalitis in children. N Engl J Med. 2001;345 :148 –149[Free Full Text]
  5. McJunkin JE, de los Reyes EC, Irazuzta JE, et al. La Crosse encephalitis in children. N Engl J Med. 2001;344 :801 –807[Abstract/Free Full Text]
  6. Moritz ML, Ayus JC. Prevention of hospital-acquired hyponatremia: a case for using isotonic saline. Pediatrics. 2003;111 :227 –230[Abstract/Free Full Text]
  7. Holliday MA, Segar WE, Friedman A. Reducing errors in fluid therapy. Pediatrics. 2003;111 :424 –425[Free Full Text]
  8. Hoorn EJ, Geary D, Robb M, Halperin ML, Bohn D. Acute hyponatremia related to intravenous fluid administration in hospitalized children: an observational study. Pediatrics. 2004;113 : 1279–1284
  9. Hanna S, Tibby SM, Durward A, Murdoch IA. Incidence of hyponatraemia and hyponatraemic seizures in severe respiratory syncytial virus bronchiolitis. Acta Paediatr. 2003;92 :430 –434[Web of Science][Medline]
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  12. Moritz ML, Ayus JC. The pathophysiology and treatment of hyponatraemic encephalopathy: an update. Nephrol Dial Transplant. 2003;18 :2486 –2491[Free Full Text]

PEDIATRICS (ISSN 1098-4275). ©2004 by the American Academy of Pediatrics

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