Acute Hyponatraemia: The Evidence Behind the Protocol

A 68-year-old woman from Udupi is brought to casualty after two weeks of vomiting and eating little. She weighs 50 kg. She is drowsy, her tongue is dry and her neck veins are flat. Her sodium is 116 mEq/L and her potassium 2.9. While the intern is reading the report, she has a seizure. This is an illustrative case, not a real patient.

Two opposite dangers now sit in the same bed. Left alone, a sodium of 116 with seizures can kill her today. Corrected too fast, it can leave her locked in next week. By the end of this article you will know where the speed limit comes from, how fast is fast enough, and what to do if the sodium overshoots.

1. Why there is a speed limit at all

Osmotic demyelination syndrome, once called central pontine myelinolysis, follows correction of a chronic hyponatraemia that is too rapid. Over days of low sodium, the brain cells protect themselves from swelling by pushing out small dissolved molecules called organic osmolytes. That adaptation is what makes chronic hyponatraemia so much better tolerated than you would expect from the number.

“Then why is correcting it dangerous?” Because the adaptation cannot be undone quickly. The adapted brain has expelled organic osmolytes, so when extracellular sodium rises faster than they can be replaced, water is pulled out of the neurons and they demyelinate. The symptoms come 2 to 6 days later: dysarthria, dysphagia, quadriparesis, a locked-in state, death. It is irreversible, so prevention is the only treatment.

2. Acute or chronic: the 48-hour rule

The speed limit depends on whether the brain has had time to adapt, and that takes about 48 hours. A hyponatraemia documented to be less than 48 hours old, with a normal sodium on record before it, may be corrected faster, up to 10 mEq/L in 24 hours. Everything else, including every hyponatraemia whose onset you cannot prove, is treated as chronic.

Our patient has been vomiting for two weeks and has no earlier sodium. She is chronic.

3. The limit, and who gets the lower one

In chronic hyponatraemia the tool holds to no more than 8 mEq/L in 24 hours, and 6 mEq/L in a patient at high risk. The high-risk group is remembered as SHAM: severe baseline hyponatraemia below 105, hypokalaemia, alcoholism or advanced liver disease, and severe malnutrition.

Our patient has a potassium of 2.9. That is the H of SHAM, so her limit is 6 mEq/L in 24 hours.

“Where do 8 and 6 come from?” They are the conservative end of the published range. The tool is candid about its sources. On 28 August 2026 it withdrew an attribution to a consensus statement it could not find, rather than leave an unverifiable citation in place. It names the papers on its list that bear on the rate: Sterns 1986, Adrogue and Madias 2000, Verbalis 2013 and Sterns 2015.

4. How fast is fast enough when she is seizing

The limit is a ceiling over 24 hours, not a reason to go slowly in the first hour. Severe symptoms such as seizures or coma call for 3% saline to raise the sodium by 1 to 2 mEq/L per hour for the first 2 to 3 hours. The tool prefers a fixed bolus in an emergency: 150 mL over 20 minutes, the sodium rechecked after 20 minutes, repeated up to twice more if the symptoms persist, three boluses at most. In a 70 kg patient each bolus raises the sodium by about 1.5 to 2 mEq/L.

Our patient weighs 50 kg, not 70, so each bolus will raise her sodium a little more than that. It is one reason the sodium is rechecked after every bolus: the 6 mEq/L she is allowed for the whole day can be used up in the first hour.

5. 3% saline is a drug, not a fluid

The Adrogue-Madias formula predicts the change in sodium from one litre of a fluid: the fluid’s sodium minus the patient’s, divided by the total body water plus one. For a woman of 65 or more the tool takes total body water as 0.45 times her weight, so for our patient 0.45 times 50, or 22.5 litres.

A litre of 3% saline would take her almost three times past her 24-hour limit. That is why the tool warns against an empirical 3% drip, started before the body water is calculated and the volume status defined. It is one of the commoner routes to osmotic demyelination. Continuous infusions belong in an intensive care or high dependency unit, with electrolytes every 2 to 4 hours.

A common mistake, and an understandable one, is to make 3% saline on the ward when the pharmacy seems far away. The mixture once printed on this tool, 30 mL of 23.4% saline in 470 mL of normal saline, works out to 385 mEq/L, which is 2.25% and not 3%. 3% saline is a stock item in India, in 100 mL and 500 mL bottles. Ask the pharmacy before improvising.

6. Volume status decides the fluid, and the trap

Our patient is hypovolaemic: dry mucosa, flat neck veins. Her own antidiuretic hormone is switched on by the low volume, so her kidneys are holding water. She needs 0.9% saline to restore the volume.

“So the saline is safe?” The saline is right, and that is the trap. Once her volume is restored, the antidiuretic hormone switches off, her kidneys pour out free water, and the sodium can run past the limit before anyone has rechecked it. The formula assumes the kidneys do nothing with water, so it underestimates the rise in exactly this patient. The tool advises close monitoring, and considering DDAVP given at the start to clamp the urine, so that the formula’s assumption holds. The evidence for that is observational, not randomised.

Her potassium matters here too. Every 1 mEq of potassium replaced has the same effect on the sodium as 1 mEq of sodium infused, so the potassium you give her counts against her limit of 6.

7. The morning after: the overshoot

Suppose that 18 hours later her sodium is 125. She has risen 9 mEq/L against a limit of 6. The tool’s rescue protocol is to act, not to wait:

• Stop all sodium-containing fluids and potassium replacement.
• Give 5% dextrose at 6 mL/kg over 1 to 2 hours: for her, 300 mL.
• Give DDAVP 2 mcg intravenously every 8 hours.
• Recheck the sodium every 1 to 2 hours until it is stable, and bring it back within the intended limit.

Residents often hesitate here, because lowering a sodium you have just worked to raise feels like undoing your own treatment. The tool is clear that the risk of the overshoot is far greater than the risk of putting the sodium transiently back down.

Try this

A 55-year-old man with uncontrolled diabetes has a sodium of 128 mEq/L and a glucose of 600 mg/dL. Does he need treatment for hyponatraemia? Illustrative case.

Answer. Correct the sodium for the glucose first. The tool uses a fall of 1.6 mEq/L for every 100 mg/dL of glucose above 100. His glucose is 500 above 100, so add 1.6 times 5, which is 8: a corrected sodium of 136. That is normal. Treat the hyperglycaemia, not the sodium.

Take-home points

• Treat every hyponatraemia whose onset you cannot prove as chronic.
• In chronic hyponatraemia raise the sodium by no more than 8 mEq/L in 24 hours, or 6 in a SHAM patient.
• Seizures or coma: 150 mL of 3% saline over 20 minutes, recheck, up to three boluses.
• In the hypovolaemic patient, expect the sodium to run once the volume is back, and count potassium against the limit.
• If the sodium overshoots, re-lower it at once with 5% dextrose and DDAVP.

For the patient who drinks far more water than the body needs, see the author’s article The Hydration Myth: Why Drinking “More” Is Not Always Better.

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 are worked by hand from the tool’s rules; check the tool’s result for a real patient.

References

1. Verma A, et al. API Expert Consensus on Management of Hyponatraemia. JAPI. 2019. [Could not be verified on 28 August 2026.
2. Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med. 2000;342(21):1581-1589.
3. Spasovski G, et al. Clinical practice guideline on hyponatraemia. Eur J Endocrinol. 2014;170(3):G1-47.
4. Sterns RH. Disorders of Plasma Sodium. N Engl J Med. 2015;372(1):55-65.
5. Perianayagam A, Sterns RH, Silver SM, et al. DDAVP is effective in preventing and reversing inadvertent overcorrection of hyponatremia. Clin J Am Soc Nephrol. 2008;3(2):331-336.
6. Sterns RH, Riggs JE, Schochet SS. Osmotic demyelination syndrome following correction of hyponatremia. N Engl J Med. 1986;314(24):1535-1542.
7. Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med. 2013;126(10 Suppl 1):S1-S42.