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Anesthesia & Analgesia:
doi: 10.1213/ANE.0b013e3181c98131
Editorial: Editorials

Water Water Everywhere: Standardizing Postoperative Fluid Therapy with 0.9% Normal Saline

Moritz, Michael L. MD*; Ayus, Juan Carlos MD, FACP, FASN†

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From the *Division of Nephrology, Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, The University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; and †Renal Consultants of Houston, Houston, Texas.

Accepted for publication November 4, 2009.

Address correspondence and reprint requests to Michael L. Moritz, MD, Division of Nephrology, Children's Hospital of Pittsburgh of UPMC, One Children's Hospital Dr., 4401 Penn Ave., Pittsburgh, PA 15224. Address e-mail to moritzml@upmc.edu.

In this issue of the journal, Bailey et al.1 review the pediatric perspectives on crystalloids and colloids. Although the merits of each solution have been continually debated over the years, the choice of the proper postoperative crystalloid solution has become clear.

Patient safety is one of the nation's most pressing health care challenges. There have recently been increased efforts to standardize perioperative care to prevent postoperative complications and deaths. To this end, the World Health Organization has published a surgical safety checklist,2 which in a prospective study was demonstrated to reduce hospital mortality by almost 50%.3 One aspect that was not addressed was standardizing postoperative fluid therapy. Hyponatremic encephalopathy is a serious but underappreciated complication of surgery. There have been numerous reports of death or permanent neurologic injury from hyponatremic encephalopathy in otherwise healthy children and adults after common surgical procedures.4–7 With >200 million surgical procedures performed annually worldwide,8 we project the morbidity rate for postoperative hyponatremic encephalopathy to be >200,000 cases annually, based on previous projections done in the United States.5 The primary reason for this complication is the routine administration of hypotonic fluids in the postoperative period and the failure to recognize and treat hyponatremic encephalopathy when it develops. There is good reason to believe that the complication of postoperative hyponatremic encephalopathy could be virtually eliminated by a policy of administering 0.9% sodium chloride (NaCl) postoperatively when parenteral fluids are needed. In 2003,9 we proposed that 0.9% NaCl be administered for the prevention of hospital-acquired hyponatremia in high-risk pediatric patients, in particular postoperative patients, and we have since extended these recommendations to include adults.9,10 This generated a significant amount of controversy.11,12 Since that time, data have emerged from prospective studies in children to show that 0.9% NaCl effectively prevents hyponatremia, whereas hypotonic fluids lead to hyponatremia.13–15

Hospital-acquired hyponatremia (Na <135 mEq/L) primarily results from 2 factors in conjunction: (a) an impaired ability to excrete free water because of arginine vasopressin (AVP) excess, and (b) the administration of hypotonic fluids.12,16 Postoperative patients are at high risk for developing hyponatremia because they have multiple stimuli for AVP production including pain, stress, nausea and vomiting, positive pressure ventilation, the administration of narcotics, and intravascular volume depletion. The combination of these factors places virtually all postoperative patients at risk for developing hyponatremia.

Hyponatremia is not an inevitable consequence of AVP excess. For hyponatremia to develop, there must also be a source of free water. The majority of the morbidity and mortality from postoperative hyponatremic encephalopathy has occurred in patients receiving hypotonic IV fluids.6,7 Despite the recognition of this serious complication, recent consensus guidelines in the United Kingdom continue to recommend hypotonic fluids in the postoperative period.17,18 It must be realized that any fluid that has a tonicity, sodium plus potassium, less than that of the aqueous phase of plasma water (154 mEq/L), is a hypotonic fluid and is capable of producing hyponatremia. Even though a normal plasma sodium is 140 mEq/L, plasma is 7% anhydrous, which makes the sodium concentration in the aqueous phase of plasma water approximately 150 mEq/L. Therefore, 0.45% NaCl (Na 77 mEq/L) and lactated Ringer solution (Na 130 mEq/L) are hypotonic in relation to the plasma sodium and can produce hyponatremia. In theory, even 0.9% NaCl can result in hyponatremia, in the presence of AVP excess where the urine osmolality is >500 mOsm/kg. This is of particular concern in patients with central nervous system (CNS) injury, in whom AVP levels and urine osmolality can be extremely elevated, and even a small decrease in serum sodium can contribute to neurologic deterioration and mildly hyponatremic values.10,19 To the best of our knowledge, there is not a single report in the literature of a neurologic complication related to the use of 0.9% NaCl in a patient without underlying CNS disease.

Three recent prospective randomized studies in almost 300 postoperative children have confirmed that 0.9% NaCl effectively prevents the development of postoperative hyponatremia and that hypotonic fluids consistently produce a decrease in serum sodium.13–15 Two of these studies found that the development of hyponatremia was unrelated to the rate of fluid administration but was primarily related to the sodium concentration of the IV fluid.14,15 Hypotonic fluids produced a decrease in serum sodium even when administered at between 50% and 66% of standard maintenance therapy. The development of hypernatremia was not a significant complication, even in patients receiving normal saline who were restricted to 50% of standard maintenance therapy.14

There is no rationale for administering hypotonic fluids in the postoperative setting. Concerns about development of excessive intravascular volume, hypernatremia, hyponatremia from desalinization, or acidosis from administration of 0.9% NaCl, are unfounded. In general, the administration of 0.9% NaCl will produce neither excessive intravascular volume nor hypernatremia, nor will it worsen hyponatremia. When normal saline is administered in the presence of AVP excess, as is seen in the syndrome of inappropriate antidiuretic hormone secretion, the body will preserve extracellular volume at the expense of serum osmolality by excreting a hypertonic urine.20,21 This physiologic natriuresis will drive the urine output to prevent excessive intravascular volume and will also result in the renal generation of free water, which will prevent the development of hypernatremia.22,23 It is a misconception that 0.9% NaCl in and of itself will contribute to the development of hyponatremia by inducing a desalinization process, as is often quoted.24 The renal generation of free water and excretion of a hypertonic urine is a well-known physiologic phenomenon that occurs when IV fluids are administered in the presence of euvolemic states of AVP excess.25 In the absence of AVP excess, a so-called desalinization will not occur. 0.9% NaCl is also no more likely to produce acidosis than any other commercially available NaCl solution. All commercially available NaCl-containing solutions, including 0.9%, 0.45%, and 0.2% NaCl, are acidic with a pH of approximately 5. This is not attributable to the chloride content in the solution, because the pH of 0.9% NaCl in a glass bottle is 7, but is rather attributable to a chemical reaction between the solution and the IV fluid bag. The majority of IV fluids bags are made from a derivative of polyvinyl chloride and are permeable to carbon dioxide; therefore, no commercially available IV fluid contains sodium bicarbonate because the bicarbonate would dissipate out in the form of carbon dioxide. If large volumes of 0.9% NaCl are administered rapidly, as can occur intraoperatively, a mild dilutional acidosis can occur, but this should not develop at standard maintenance rates postoperatively. Lactated Ringer solution does have an advantage over 0.9% NaCl, because it contains lactate, which can be converted to bicarbonate by the body, but unfortunately it is slightly hypotonic in relation to the plasma and can produce a decrease in serum sodium.7 Lactated Ringer solution would be more suitable for the perioperative setting if the manufacturers would increase the sodium concentration to 150 mEq/L.

No single IV fluid can be used safely in all situations. Extracellular volume overload could develop if excessive amounts of 0.9% NaCl were administered in the presence of significant renal impairment or congestive heart failure. Similarly, 0.9% NaCl could result in hypernatremia if administered to a patient with renal or extrarenal free water losses as is seen with nephrogenic diabetes insipidus or high nasogastric output. Thus, we have recommended that hypotonic fluids be restricted in their use to patients with either hypernatremia (Na >145 mEq/L) or ongoing urinary or extrarenal free water losses and that patients at risk for extracellular volume overload have their volume of fluid restricted.

Postoperative hyponatremic encephalopathy can be difficult to diagnose because the presenting features are nonspecific and can be confused with other conditions. Headache, nausea, and vomiting are the most universal features of hyponatremic encephalopathy but are also common symptoms of other postoperative conditions.16 An often overlooked clinical presentation of postoperative hyponatremic encephalopathy is neurogenic pulmonary edema,26 now referred to as Ayus-Arieff syndrome.27 Females,6 children,4 and patients with hypoxemia28 or underlying CNS disease19,29 are at highest risk for developing hyponatremic encephalopathy, and in these groups of patients, it can develop even at mildly hyponatremic values.

It is our opinion that any patient suspected of having hyponatremic encephalopathy, even if only mildly symptomatic, should be treated with a 2 mL/kg bolus of 3% NaCl or with a minimum of 100 mL, before proceeding with radiologic investigations.10,30,31 Each bolus will result in at most a 2 mEq/L increase in serum sodium. The bolus can be repeated 2 to 3 times as necessary. This will result in an acute increase in serum sodium of 4 to 6 mEq/L, which will rapidly decrease brain edema and should result in clinical improvement. A patient who does not respond to this therapy likely does not have hyponatremic encephalopathy. No harm could come from this approach, because this degree of correction falls safely within even the most conservative recommendations for correction.32 It must be emphasized that postoperative patients are at low risk for developing cerebral demyelination because this is an acute form of hyponatremia that is unlikely to overcorrect with therapy due to AVP excess.7

Based on all available data, there can be no justification for administering hypotonic fluids in the perioperative setting. It is clear that hypotonic fluids produce a postoperative decrease in serum sodium, from which fatal hyponatremic encephalopathy can follow. Significantly hypotonic solutions such as 5% dextrose in water or 0.2% and 0.45% NaCl should rarely if ever be used in the first 24 to 48 hours after surgery. Near-isotonic fluids such as lactated Ringer solution would best be avoided, and, if used, serum sodium should be monitored. Standardizing postoperative fluid therapy by using 0.9% NaCl could safely eliminate the complication of hyponatremic encephalopathy.

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REFERENCES

1.Bailey AG, McNaull PP, Jooste E, Tuchman JB. Perioperative crystalloid and colloid fluid management in children: where are we and how did we get here? Anesth Analg 2010;110:375–90

2.World Alliance for patient Safety. WHO guidelines for safe surgery. Geneva: World Health Organization, 2008

3.Haynes AB, Weiser TG, Berry WR, Lipsitz SR, Breizat AH, Dellinger EP, Herbosa T, Joseph S, Kibatala PL, Lapitan MC, Merry AF, Moorthy K, Reznick RK, Taylor B, Gawande AA; Safe Surgery Saves Lives Study Group. A surgical safety checklist to reduce morbidity and mortality in a global population. N Engl J Med 2009;360:491–9

4.Arieff AI, Ayus JC, Fraser CL. Hyponatraemia and death or permanent brain damage in healthy children. BMJ 1992;304: 1218–22

5.Ayus JC, Arieff AI. Brain damage and postoperative hyponatremia: the role of gender. Neurology 1996;46:323–8

6.Ayus JC, Wheeler JM, Arieff AI. Postoperative hyponatremic encephalopathy in menstruant women. Ann Intern Med 1992;117:891–7

7.Moritz ML, Ayus JC. Preventing neurological complications from dysnatremias in children. Pediatr Nephrol 2005;20: 1687–700

8.Weiser TG, Regenbogen SE, Thompson KD, Haynes AB, Lipsitz SR, Berry WR, Gawande AA. An estimation of the global volume of surgery: a modelling strategy based on available data. Lancet 2008;372:139–44

9.Moritz ML, Ayus JC. Prevention of hospital-acquired hyponatremia: a case for using isotonic saline. Pediatrics 2003;111: 227–30

10.Moritz ML, Carlos Ayus J. Hospital-acquired hyponatremia—why are hypotonic parenteral fluids still being used? Nat Clin Pract Nephrol 2007;3:374–82

11.Holliday MA, Segar WE, Friedman A. Reducing errors in fluid therapy. Pediatrics 2003;111:424–5

12.Holliday MA, Ray PE, Friedman AL. Fluid therapy for children: facts, fashions and questions. Arch Dis Child 2007;92:546–50

13.Montanana PA, Modesto i Alapont V, Ocon AP, Lopez PO, Lopez Prats JL, Toledo Parreno JD. The use of isotonic fluid as maintenance therapy prevents iatrogenic hyponatremia in pediatrics: a randomized, controlled open study. Pediatr Crit Care Med 2008;9:589–97

14.Neville KA, Sandeman DJ, Rubinstein A, Henry GM, McGlynn M, Walker JL. Prevention of hyponatremia during maintenance intravenous fluid administration: a prospective randomized study of fluid type versus fluid rate. J Pediatr epub October 7, 2009

15.Yung M, Keeley S. Randomised controlled trial of intravenous maintenance fluids. J Paediatr Child Health 2009;45:9–14

16.Moritz ML, Ayus JC. The pathophysiology and treatment of hyponatraemic encephalopathy: an update. Nephrol Dial Transplant 2003;18:2486–91

17.National Health Service: National Patient Safety Alert. Reducing the risk of harm when administering intravenous fluids to children. Safety alert 22 M. Available at: www.npsa.nhs.uk/health/alerts; accessed October 14, 2009

18.National Health Service Evidence: British consensus guidelines on intravenous fluid therapy for adult surgical patients, 2008. Available at: www.evidence.nhs.uk

19.Moritz ML, Ayus JC. La Crosse encephalitis in children. N Engl J Med 2001;345:148–9

20.Bartter FC, Schwartz WB. The syndrome of inappropriate secretion of antidiuretic hormone. Am J Med 1967;42:790–806

21.Schwartz WB, Bennet W, Curelop S, Bartter FC. A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. Am J Med 1957;23:529–42

22.Moritz ML. Urine sodium composition in ambulatory healthy children: hypotonic or isotonic? Pediatr Nephrol 2008;23:955–7

23.Musch W, Decaux G. Treating the syndrome of inappropriate ADH secretion with isotonic saline. QJM 1998;91:749–53

24.Steele A, Gowrishankar M, Abrahamson S, Mazer CD, Feldman RD, Halperin ML. Postoperative hyponatremia despite near-isotonic saline infusion: a phenomenon of desalination. Ann Intern Med 1997;126:20–5

25.Leaf A, Bartter FC, Santos RF, Wrong O. Evidence in man that urinary electrolyte loss induced by pitressin is a function of water retention. J Clin Invest 1953;32:868–78

26.Ayus JC, Arieff AI. Pulmonary complications of hyponatremic encephalopathy. Noncardiogenic pulmonary edema and hypercapnic respiratory failure. Chest 1995;107:517–21

27.Campbell GA, Rosner MH. The agony of ecstasy: MDMA (3,4-methylenedioxymethamphetamine) and the kidney. Clin J Am Soc Nephrol 2008;3:1852–60

28.Ayus JC, Armstrong D, Arieff AI. Hyponatremia with hypoxia: effects on brain adaptation, perfusion, and histology in rodents. Kidney Int 2006;69:1319–25

29.McJunkin JE, de los Reyes EC, Irazuzta JE, Caceres MJ, Khan RR, Minnich LL, Fu KD, Lovett GD, Tsai T, Thompson A. La Crosse encephalitis in children. N Engl J Med 2001;344:801–7

30.Ayus JC, Arieff A, Moritz ML. Hyponatremia in marathon runners. N Engl J Med 2005;353:427–8

31.Moritz ML, Ayus JC. Exercise-associated hyponatremia: why are athletes still dying? Clin J Sport Med 2008;18:379–81

32.Sterns RH, Nigwekar SU, Hix JK. The treatment of hyponatremia. Semin Nephrol 2009;29:282–99

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