Q J Med 2003; 96: 549-552
© 2003 Association of Physicians
Editorial |
Salt and water: read the package insert
Salt and water are probably the most common therapeutic agents that we give to patients: used improperly, they can be lethal weapons. Rational management of fluid and electrolyte disorders requires that we think of salt (or saline) and water as drugs that have indications, contraindications, and appropriate doses. Such drug information, typically supplied in what Americans call the ‘package insert’, can be found in Tables 1 and 2.
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Water is available in oral form or in parenteral preparations. Because it cannot be infused directly into a small vein without causing haemolysis, intravenous water is usually mixed with glucose. A 4% or 5% dextrose solution is used because the osmolality approximates that of plasma, and thus prevents haemolysis. However, after metabolism of the infused glucose, a solution containing only dextrose becomes equivalent to water. The concentration of salt (or in the case of 4% or 5% dextrose in water, the absence of any) determines the solution’s tonicity.
It is useful to think of intravenous saline as a substitute for dietary salt. A ’normal’ hospital diet with no added salt provides about 4 g or 172 mmol of sodium. Ingested with water, it provides the equivalent of 1.1 l isotonic saline. A litre of isotonic or ‘normal’ (0.9%) saline contains 154 mmol of NaCI, equivalent to 9 g of salt or 3.6 g of sodium. The sodium concentration of isotonic saline is equivalent to the normal sodium concentration of plasma water. If glucose is added to isotonic saline, the solution becomes hyperosmolar but it is still isotonic; after the glucose is metabolized, isotonic saline remains.
The most popular intravenous fluid preparations are actually fixed combination drugs of saline and water. Thus, 1 l of 0.45% saline (a hypotonic solution) is better thought of as a combination of 500 ml of water and 500 ml of isotonic saline. A litre of 0.18% saline in 4% dextrose (a hypotonic solution) is equivalent to 800 ml of water and 200 ml of isotonic saline. Mindless infusion of a fixed combination drug without consideration of the indications and contraindications for each of its components can lead to therapeutic disaster.1–4
In this month’s QJM, Nyestanak et al.1 provide a learned discussion debunking popular myths regarding the need for water. The authors explain why water losses of hospitalized patients are often very low and they warn that giving patients more water than they need can lead to iatrogenic hyponatraemia, a potentially lethal condition. Their article is highly instructive and hopefully it will prompt a reappraisal of some of the recommendations for maintenance fluids that can be currently found in the paediatric literature.
As Nyestanak and colleagues point out, many of us harbour misconceptions about the fate of metabolic water, the importance of respiratory insensible water losses, and the link between water needs and caloric intake. The authors may be correct in suggesting that such physiological confusion is responsible for therapeutic misadventures related to the use of intravenous saline and water. I believe that our misuse of these agents also stems from our failure to think of salt and water as drugs, and to prescribe them as carefully as we would prescribe a drug such as warfarin, modifying the dose to meet a desired endpoint.
Just as the INR defines the need for warfarin, the serum sodium concentration defines the need for water.1,5,6 Prescribing hypotonic fluid to a patient with a serum sodium concentration that is low and falling is the moral equivalent of giving warfarin to a patient with a high INR. Failure to prescribe water when the serum sodium is high and rising is equally indefensible.
The water prescription should be adjusted in response to changes in the serum sodium concentration, anticipating what is about to happen rather than waiting for a grossly abnormal value. If the serum sodium is increasing by 1 mmol/l/day, a 70 kg young man needs about 280 ml more water each day than he is currently getting to avoid progressive dehydration. A 45 kg elderly woman needs about half that much to compensate for the same 1 mmol/l increase in serum sodium concentration. The serum sodium concentration is a simple, accurate guide for the prescription of water.
Saline therapy should also be guided by goals and endpoints, but these are much more difficult to define. The serum sodium concentration is not a guide to the prescription of saline.5 Saline is indicated to repair an inadequately filled intravascular volume or to replace ongoing or anticipated losses of sodium-containing fluid from the vascular space. Laboratory parameters cannot reliably or unambiguously guide the clinician in prescribing saline; therapy must often be based on trial and error with careful evaluation of history, physical findings, body weight, haematocrit, BUN and creatinine. Before giving intravenous saline solutions, dietary sodium should be liberalized and oral salt encouraged. This is more effective than ‘pushing fluids’, which increases the intake of electrolyte-free water instead of isotonic fluid.
Saline stays in the extracellular space (about 20% of body weight) and it therefore effectively expands intravascular volume. Water, on the other hand, is a less effective volume expander because it distributes in total body water (three times saline’s distribution volume). Using water as a volume expander is only appropriate (and often preferable to saline in patients who are not hypotensive) for patients with severe hypernatraemia. Using water instead of saline to correct hypovolaemia in a patient with a normal serum sodium level causes hyponatraemia and usually fails to adequately repair the volume deficit. Planning of saline therapy should be based on the desired amount of volume expansion—a percentage of the normal ECF volume, monitored by measuring body weight—and saline prescriptions should include the total amount of fluid to give, not just the rate of infusion. ‘Open-ended’ fluid orders should be avoided.
Hyponatraemia is not necessarily an indication for therapy with isotonic saline. Hyponatraemia should be corrected by 8 mmol/l day or less.7 Faster rates of correction offer no benefit, and increase the risk of osmotic demyelination.7–9 Excessive correction is usually caused by unanticipated urinary water losses. Water output affects the serum sodium concentration in a quantifiably identical, but opposite manner to that of water administration. Isotonic saline increases the serum sodium concentration if it increases urinary water excretion; if it does not, a litre of retained saline increases the serum sodium concentration by only 1 mmol/l. In hyponatraemic patients with CHF or cirrhosis, isotonic saline does not usually increase water excretion or improve the serum sodium concentration; all it does is worsen oedema. In patients with SIADH, isotonic saline can actually lower the serum sodium concentration, because the infused sodium is excreted in a hypertonic urine.1 In patients with hyponatraemia caused by hypovolaemia, isotonic saline is effective therapy, but too much saline may initiate a large water diuresis, causing the serum sodium concentration to increase by much more than intended.9
In many cases, a small amount of hypertonic saline is a better treatment for hyponatraemia than the indiscriminant infusion of large volumes of isotonic saline. Hypertonic saline must be respected, but it should not be feared. Infusion of 1 ml of 3% saline per kg body weight per hour can be expected to increase the serum sodium by 1 mmol/l/h—an appropriate initial rate of correction for the rare patient with serious symptoms caused by hyponatraemia. In less urgent cases (or after 2–3 h of a high-dose emergency infusion) a carefully monitored infusion of 3% saline at approximately 0.2 ml per kg body weight per hour can be used to carefully increase the serum sodium concentration by no more than 8 mmol/l per day. Co-administration of a loop diuretic such as furosemide, which blocks the ability to concentrate the urine, can be helpful in patients with SIADH.
Compared to many drugs in our therapeutic armamentarium, salt and water are relatively easy to use. Sadly, iatrogenic injury from improper use of these agents is disturbingly common. To avoid some of the more common errors in fluid management, clinicians should remember the package insert when intravenous fluids are prescribed.
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Department of Medicine
Rochester General Hospital
University of Rochester School of Medicine and
Dentistry
Rochester
New York
USA
e-mail: Richard.Sterns{at}viahealth.org
References
1. Shafiee MAS, Bohn D, Hoorn EJ, Halperin ML. How to select optimal maintenance intravenous fluid therapy. Q J Med 2003; 96:601–610.
2. 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. Br Med J 2001; 322:780–2.
3. Durward A, Tibby SM, Murdoch IA. Hyponatraemia can be caused by standard fluid regimens. Br Med J 2000; 320:943.
4. Lane N, Allen K. Hyponatraemia after orthopaedic surgery. Br Med J 1999; 318:1363–4.
5. Mange K, Matsuura D, Cizman B, Soto H, Ziyadeh FN, Goldfarb S, Neilson EG. Language guiding therapy: the case of dehydration versus volume depletion. Ann Intern Med 1997; 127:848–53.
6. Sterns RH. Hypernatremia in the intensive care unit: instant quality–just add water. Crit Care Med 1999; 27:1041–2.
7. Adrogue HJ, Madias NE. Hyponatremia. N Engl J Med 2000; 342:1581–9.
8. Sterns RH, Riggs JE, Schochet SS Jr. Osmotic demyelination syndrome following correction of hyponatremia. N Engl J Med 1986; 314:1535–42.[Abstract]
9. Lin SH, Chau T, Wu CC, Yang SS. Osmotic demyelination syndrome after correction of chronic hyponatremia with normal saline. Am J Med Sci 2002; 323:259–62.[CrossRef][ISI][Medline]
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  D. Bohn, E. Hoorn, and M. L Halperin Hospital-Acquired Hyponatremia Is Associated With Excessive Administration of Intravenous Maintenance Fluid: In Reply Pediatrics, December 1, 2004; 114(6): 1744 - 1745. [Full Text] [PDF]
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