Acute Hypernatraemia: The Evidence Behind the Protocol

An 84-year-old woman is brought in from home, drowsy and dry. She has dementia and has been bed-bound since a fall last year. For three days she has had a fever, and she has hardly drunk anything. Nobody is sure when she last had a proper glass of water. She weighs 45 kg. Her sodium is 162 mEq/L, and her urine is scanty and concentrated. This is an illustrative case, not a real patient.

By the end of this article you will know how much water she has lost, how fast you may give it back, and how firm the evidence behind that speed limit really is.

1. How Much Water Has She Lost?

A high sodium in a patient like her is almost always a shortage of water, not an excess of salt. So the first question is how much water. The tool uses the free water deficit:

Free Water Deficit (L) = TBW x ((Serum Na / 140) - 1)

TBW is total body water. It is body weight times a factor: 0.6 for young men, 0.5 for young women and for elderly men, 0.45 for elderly women. For her, that is 0.45 x 45 = 20.25 L. Her sodium over 140 is 162 / 140 = 1.157. Take away 1 and you have 0.157. Multiply: 20.25 x 0.157 = about 3.2 L.

“So she needs 3.2 litres?” At least that. The figure is what she has already lost. It says nothing about what is still going out through her urine, her skin and her fever. The tool tells you to add 30 to 50% for those ongoing losses, and its own printed total adds 30%: about 4.1 L for her. Then recalculate every 12 to 24 hours. A deficit worked out once is out of date by the time the bag is up.

2. How Fast?

Here is the point residents most often miss. The size of the deficit does not set the rate. The tool says so in a warning box: the formula gives a static snapshot, and the rate is decided by how long the sodium has been high, and by the risk of cerebral oedema.

Why cerebral oedema? When the sodium rises slowly, the brain cells protect themselves. They make small molecules of their own, called idiogenic osmoles, which hold water inside the cell so that it does not shrink. If you now lower the sodium quickly, water rushes into those adapted cells and the brain swells. It is the mirror image of osmotic demyelination in hyponatraemia, where the danger is a sodium raised too fast.

So the tool asks one question first: is this acute, under 48 hours and documented, or chronic? If the onset is not known, it is treated as chronic. In chronic hypernatraemia the safe rate is 10 to 12 mEq/L per 24 hours, and the tool plans at 10. In acute hypernatraemia, under 48 hours, correction can be faster, up to 1 mEq/L/hour, because the idiogenic osmoles have not yet built up. Nobody knows when our patient stopped drinking, so hers is chronic. Her sodium should fall from 162 to about 152 in the first 24 hours, not to 140.

3. How Firm Is That Speed Limit?

“Is the 0.5 per hour limit proven, then?” Less than its reputation suggests. The tool still says that the evidence behind the 0.5 mmol/L/hour limit is thinner than its standing suggests. It used to set out the study behind that sentence:

Chauhan and colleagues, 2019, studied 449 critically ill adults and found no excess harm from correction faster than 0.5 mmol/L per hour: no rise in mortality, seizures or altered consciousness, and on chart review not one cerebral oedema attributable to the rate. That is a retrospective cohort, not a trial.

A retrospective cohort looks back at patients who were treated in whatever way their doctors chose. It cannot tell us why some were corrected faster: perhaps they were the patients who could tolerate it. A trial would allot the rate by chance, and none has been done. So the finding is reassuring, but it is not proof that faster is safe.

That is why the tool still holds to the slower limit in chronic hypernatraemia. The limit rests on physiology and case reports rather than on outcome data. This is expert practice, not strong evidence, and it is honest to say so. The study does give us one useful thing: a correction that has run slightly fast in an ICU patient is not, on its own, a reason to alarm the team. Slow down, recheck, and carry on.

4. Which Fluid?

The safest and most physiological water is plain water, by mouth or through a nasogastric tube. When that is not possible, the tool sets out the intravenous choices by their free water content. 5% dextrose (D5W) is 100% free water. Half-normal saline, 0.45% NaCl, is 50% free water, and it suits a patient who is short of volume as well as water. Quarter-normal saline, 0.225% NaCl, is 75% free water. On D5W, check the blood glucose every 6 hours, and switch to 0.45% NaCl if it rises above 200 mg/dL.

5. When the Urine Is Dilute

Our patient’s urine is concentrated: her kidneys are doing their best to hold water. If instead a hypernatraemic patient is passing large volumes of dilute urine, the kidney is losing water it should be keeping. A urine osmolality below 300 mOsm/kg against a high sodium is diabetes insipidus (DI) or an osmotic diuresis until proved otherwise. In central DI the pituitary makes too little antidiuretic hormone (ADH): after neurosurgery, head trauma or a pituitary tumour. In nephrogenic DI the kidney ignores it: lithium, hypercalcaemia, CKD, sickle cell. Desmopressin (DDAVP) separates the two. In central DI the urine concentrates, by more than 50% in urine osmolality; in nephrogenic DI nothing happens. As the tool says, in diabetes insipidus the diagnosis is the treatment.

6. The Common Mistake

The common mistake is to treat the number and forget the patient. It is easy to see why: the deficit is a satisfying calculation, and once the drip is running the problem feels solved. But the deficit is a floor, the losses go on, and the reason she became dry is still there. The tool asks a plain question at the bedside: can the patient reach a glass? For a bed-bound woman with dementia, the answer is often no, and that is the whole problem.

Back to Our Patient

Her deficit is about 3.2 L, about 4.1 L with the 30% for ongoing losses. Her hypernatraemia is chronic, so her sodium is brought down by about 10 mEq/L in the first 24 hours, with sodium checks every 4 to 6 hours. She is too drowsy to drink safely, so she gets D5W intravenously, with her glucose watched, and water by nasogastric tube once she can protect her airway. Her fever is treated. Before she goes home, her family is shown how to offer her water through the day.

Try This

A 30-year-old man is on the ward the day after pituitary surgery. Over 12 documented hours his sodium has risen from 141 to 151 mEq/L, and he is passing large volumes of pale urine. How fast may you correct it, and what else must you do? Illustrative case.

Answer. The rise is documented and under 48 hours, so it is acute: correction can be faster, up to 1 mEq/L/hour. Polyuria with dilute urine after neurosurgery points to central diabetes insipidus. Send a paired urine and serum osmolality, chart the urine hourly, and replace the ongoing losses as well as the deficit. If the DDAVP challenge confirms central DI, desmopressin is the treatment.

Take-Home Points

• Free water deficit = TBW x ((Na / 140) - 1); it is a floor, so add 30 to 50% for ongoing losses and recalculate every 12 to 24 hours.
• The deficit does not set the rate; chronicity and the risk of cerebral oedema do.
• Chronic, or onset not known: 10 to 12 mEq/L per 24 hours. Documented acute, under 48 hours: up to 1 mEq/L/hour.
• The slower limit rests on physiology and case reports; a slightly fast correction is not on its own a reason to alarm the team.
• Plain water by mouth or tube is the safest fluid; dilute urine against a high sodium means think of diabetes insipidus.

The opposite problem, and its own speed limit, is in Acute Hyponatraemia: The Evidence Behind the Protocol. For the daily water and salt a patient needs, see Maintenance IV Fluids and Calories.

Declaration: the author built and maintains the tool. It is free to use. The figures in this article are those the tool carried in its Evidence tab on 5 November 2026, each from the source the tool names. The illustrative cases follow the tool’s rules; check the tool’s result for a real patient.

References

1. Adrogué HJ, Madias NE. Hypernatremia. N Engl J Med. 2000;342(20):1493-1499.
2. Sterns RH. Disorders of plasma sodium. N Engl J Med. 2015;372(1):55-65.
3. Muhsin SA, Mount DB. Diagnosis and treatment of hypernatremia. Best Pract Res Clin Endocrinol Metab. 2016;30(2):189-203.
4. Chauhan K, Pattharanitima P, Gnanasekaran I, et al. Rate of Correction of Hypernatremia and Health Outcomes in Critically Ill Patients. Clin J Am Soc Nephrol. 2019;14(5):656-663.