Acute Hyponatraemia Protocol

A correction rate that will not cause osmotic demyelination, gated by severity · v1.1

Enter the sodium with the age, sex and weight, the potassium, glucose and osmolality where you have them, then the symptoms, volume status and chronicity.
You get the severity classified first, and then a decision on whether active intravenous correction is indicated at all.
The output is gated on that decision: mild hyponatraemia does not receive an infusion protocol.
Re-check the sodium on the schedule it prints. The commonest way this goes wrong is not a miscalculation but a sodium nobody repeated at hour four.

Children, and hyponatraemia in pregnancy. The age field starts at 18.
The cause of the low sodium. The SIADH, the cirrhosis, the hypothyroidism or the thiazide that produced the number is left entirely to you.
Exercise-associated hyponatraemia, beer potomania and psychogenic polydipsia as distinct entities.
Who needs tolvaptan, and for how long.
The monitoring itself. Every number it prints assumes the schedule is actually followed.

1. Patient Baseline

Age (yrs)

Biological Sex

Weight (kg)

Current Serum Na⁺ (mEq/L)

Serum K⁺ (mEq/L, optional)

Blood Glucose (mg/dL, for pseudo-hypoNa correction)

Serum Osmolality (mOsm/kg, optional)

Neurological Symptoms

2. Aetiology, Acuity & Risk Modifiers

Clinical Volume Status

Chronicity of Hyponatraemia

High Risk for ODS present? Check if any: severe malnutrition, alcoholism, Advanced Liver Disease, hypokalaemia, or Na⁺ below 105. The 24h ceiling then falls to 6 mEq/L. The tool ticks the box itself below Na⁺ 105, or K⁺ 3.0.

3. Infusate Selection

This selection applies only if active IV correction is clinically indicated. The engine will gate this decision.

Target IV Fluid

Kinetic Profile

Severity

Total Body Water

Litres

Total Na⁺ Deficit

mEq

(Theoretical deficit to 140. This is not the 24h correction target.)

Management Plan

Patient/Family Explanation

1. Osmotic Demyelination Syndrome: The Risk That Sets Every Limit

Osmotic demyelination syndrome, formerly central pontine myelinolysis, follows correction of chronic hyponatraemia that is too rapid. 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. Symptoms appear 2 to 6 days later: dysarthria, dysphagia, quadriparesis, locked-in syndrome, death. It is irreversible, so prevention is the only strategy.

Golden Rule: In chronic hyponatraemia, do not raise the sodium by more than 8 mEq/L in 24 hours (or 6 mEq/L in high-risk patients). If overcorrection occurs, actively re-lower sodium with D5W infusion or desmopressin (DDAVP 2 mcg IV q8h).

2. Severity Bands, and What Each One Gets

Not every patient with a sodium below 135 needs intravenous correction. The tool gates its output on severity and clinical context.

Na⁺ Range	Severity	Default Management
130 to 134	Mild	No IV correction. Fluid restriction (eu/hyper) or NS volume resuscitation (hypo). Investigate cause.
125 to 129	Moderate	Fluid restriction primary (eu/hyper). Active IV correction only if severely symptomatic or trending down.
120 to 124	Severe	Active correction indicated. ICU/HDU admission. Calculated infusion.
110 to 119	Profound	Urgent active correction. ICU mandatory. Consider DDAVP clamping.
< 110	Critical	Life-threatening emergency. ICU, bolus protocol if symptomatic, strict monitoring.

Practice Advisory: The Empirical 3% Drip
An empirical drip of 3% Hypertonic Saline, started without the Total Body Water calculated and the volume status defined, is one of the commoner routes to ODS. 3% saline is a drug, not a fluid. Continuous infusions belong in an ICU or HDU, with ABG or VBG electrolytes every 2 to 4 hours.

3. Acute Versus Chronic: The 48-Hour Rule

Chronicity decides the ceiling, because it decides whether the brain has adapted.

Chronicity	ODS Risk	Correction Approach
Acute (<48h)	Very Low	Faster correction is permitted, up to 10 mEq/L in 24 hours. The brain has not adapted.
Chronic (>48h)	HIGH	Strict slow correction (8 mEq/L/24h max, 6 for high-risk). Brain has adapted by expelling osmolytes.
Unknown Duration	Treat as Chronic	If you cannot prove onset was <48h with prior normal labs, assume chronic.

4. The Absolute Limits of Correction, and Who Is High Risk

Scenario	Max 24h Rise	Notes
Standard Risk, Chronic/Unknown	8 mEq/L	What this tool applies. See the note below the table
High Risk (SHAM), Chronic/Unknown	6 mEq/L	Sterns 2015
Documented Acute, Standard Risk	10 mEq/L	ODS risk very low
Documented Acute, High Risk	8 mEq/L	Still apply caution despite the acuity

Where these figures come from, and a correction made on 28 August 2026. The 8 mEq/L standard-risk limit carried the note "European (2014) and API (2019) consensus" until that date. That attribution has been withdrawn rather than repaired. The API expert consensus of 2019 could not be found on 28 August 2026, searched in PubMed with the JAPI journal filter, on the JAPI site and on the open web. The treatment section of the 2014 European guideline could not be opened to confirm what limit it gives, so nothing has been put in its place. The 8 and 6 mEq/L figures are the conservative end of the published range and are what this tool holds to. The sources on the reference list that bear on the rate are Sterns 1986, Adrogué and Madias 2000, Verbalis 2013 and Sterns 2015.

The high-risk group that takes the 6 mEq/L limit is SHAM:

S, severe baseline hyponatraemia, below 105 mEq/L
H, hypokalaemia, concurrent
A, alcoholism or advanced liver disease
M, malnutrition, severe

5. Volume Status: The Branching Point

Volume Status	Clinical Script & Cautions	Primary Action
Hypovolaemic	Dry mucosa, flat JVP, tachycardia. Caution: Once volume is restored with NS, ADH switches off, the kidneys dump free water, and the Na⁺ runs past the safe limit before anyone has re-checked it.	NS to restore volume. Monitor closely for auto-correction. Consider prophylactic DDAVP clamping.
Euvolaemic	Normal exam. Think SIADH, hypothyroidism, adrenal insufficiency. Caution: NS can paradoxically worsen SIADH. Always check TSH and morning cortisol first.	Fluid restriction (800-1000 mL/day). HTS only if severely symptomatic.
Hypervolaemic	Oedema, raised JVP, ascites. Total body Na⁺ is high, and the water excess is larger still.	Fluid restriction and a loop diuretic. Never give continuous saline.

6. 3% Hypertonic Saline in Practice

3% sodium chloride contains 513 mEq/L of sodium. It is for symptomatic hyponatraemia, seizures or coma, to raise the sodium by 1 to 2 mEq/L per hour for the first 2 to 3 hours.

Fixed bolus, preferred in an emergency: 150 mL over 20 minutes, recheck the sodium after 20 minutes, repeat up to twice more if symptoms persist, three boluses maximum. Each bolus raises the sodium by about 1.5 to 2 mEq/L in a 70 kg patient.

Where to get 3% saline in India. It is a stock item and not a special order: 3% sodium chloride is supplied here in 100 mL and 500 mL, so a 150 mL bolus is one and a half of the small bottles. Ask the pharmacy before improvising anything. Run it through an infusion pump, label the bag, and check the sodium every 2 hours.

Correction, 28 August 2026. This box previously read "Prepare by adding 30 mL of NaCl 23.4% to 470 mL NS". That mixture is 2.25% saline, not 3%. Thirty millilitres of 23.4% carries 120 mEq of sodium, and 470 mL of normal saline carries 72 mEq, so the 500 mL holds 192 mEq. That is 385 mEq/L against the 513 mEq/L of true 3% saline. Every rate and every bolus on this page is calculated on 513 mEq/L, so that mixture would have delivered a quarter less sodium than the plan assumed, in the one situation on this page where the timing matters most. Do not compound hypertonic saline on the ward. Where it has to be compounded, the pharmacy does it and a second person checks the calculation.

7. Four Cautions That Move the Sodium on Their Own

The potassium effect. Correcting hypokalaemia raises the serum sodium: potassium enters cells and displaces sodium outward, and every 1 mEq of potassium replaced has the same osmotic effect as 1 mEq of sodium infused. Count it against the 24 hour sodium limit.
Normal saline in SIADH. The kidneys are already maximally concentrating. A litre of 0.9% saline delivers 154 mEq of sodium, which may be excreted in 500 mL of concentrated urine, leaving 500 mL of electrolyte-free water behind. The net effect is a worse hyponatraemia despite having given sodium.
Proactive DDAVP clamping. DDAVP 1 to 2 mcg intravenously at the start of therapy rather than held in reserve, with hypertonic saline then run at a calculated rate. The patient becomes a closed system, which is the assumption the Adrogue-Madias formula was built on and the only state in which its prediction holds. The evidence for it is observational, not randomised. It matters most in the hypovolaemic patient, at highest risk of overshoot once the volume is restored.
Sodium that is not really low. Hypertonic hyponatraemia: hyperglycaemia pulls water out of cells and dilutes the sodium, which falls 1.6 mEq/L for every 100 mg/dL of glucose above 100. Corrected Na = measured Na + 1.6 × ((glucose − 100) / 100); if that is normal, treat the hyperglycaemia and not the sodium. Isotonic hyponatraemia: severe hyperlipidaemia or hyperproteinaemia such as myeloma, with a normal serum osmolality. Neither is true hyponatraemia.

8. SIADH: Diagnosis and Management

Six diagnostic criteria: serum sodium below 135, serum osmolality below 275, urine osmolality above 100, urine sodium above 40, euvolaemia, and normal thyroid and adrenal function.
Common causes in India: central nervous system infection including tuberculous meningitis and encephalitis, lung disease including tuberculosis, pneumonia and lung cancer, and drugs including SSRIs, carbamazepine and cyclophosphamide.
Management: fluid restriction to 800 to 1000 mL a day, and salt tablets, sodium chloride 3 g three times a day with meals. Tolvaptan 15 mg orally daily if that fails, started in hospital with the sodium every 6 hours (Indian brands Natrise, Tolvat). And treat the cause.

9. The Adrogue-Madias Formula and Infusate Sodium

ΔNa⁺ = (infusate Na⁺ − serum Na⁺) / (total body water + 1). It assumes zero renal water handling, so it systematically underestimates the correction in hypovolaemic patients and may overestimate it in SIADH.

IV Fluid	Na⁺ (mEq/L)	Typical Use
3% HTS	513	ICU bolus and infusion for symptomatic hyponatraemia
1.6% HTS	274	Peripheral line option
0.9% NS	154	Volume resuscitation in hypovolaemic hyponatraemia
Ringer's Lactate	130	Mild hypovolaemia

10. Overcorrection Rescue Protocol

Stop all sodium-containing intravenous fluids and potassium replacement immediately.
Give D5W at 6 mL/kg intravenously over 1 to 2 hours.
Give DDAVP 2 mcg intravenously every 8 hours.
Recheck the serum sodium every 1 to 2 hours until it has stabilised.
Goal: re-lower the sodium to within the originally intended limit, and do it without hesitating. The risk from overcorrection is far greater than the risk of putting the sodium transiently back down.

Abbreviations: ABG (Arterial Blood Gas) · ADH (Antidiuretic Hormone) · API (Association of Physicians of India) · CNS (Central Nervous System) · D5W (5% Dextrose in Water) · DDAVP (Desmopressin) · ER (Emergency Room) · HDU (High Dependency Unit) · HTS (Hypertonic Saline) · ICU (Intensive Care Unit) · IV (Intravenous) · JVP (Jugular Venous Pressure) · K⁺ (Potassium) · Na⁺ (Sodium) · NaCl (Sodium Chloride) · NS (Normal Saline) · ODS (Osmotic Demyelination Syndrome) · PO (Per Os) · SBAR (Situation, Background, Assessment, Recommendation) · SHAM (Severe Hyponatraemia, Hypokalaemia, Alcoholism or Advanced Liver Disease, Malnutrition) · SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion) · SPEP (Serum Protein Electrophoresis) · SSRI (Selective Serotonin Reuptake Inhibitor) · TB (Tuberculosis) · TBW (Total Body Water) · TDS (Three Times Daily) · TSH (Thyroid Stimulating Hormone) · VBG (Venous Blood Gas)

References

Verma A, et al. API Expert Consensus on Management of Hyponatraemia. JAPI. 2019. [Could not be verified on 28 August 2026.
Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med. 2000;342(21):1581-1589.
Spasovski G, et al. Clinical practice guideline on hyponatraemia. Eur J Endocrinol. 2014;170(3):G1-47.
Sterns RH. Disorders of Plasma Sodium. N Engl J Med. 2015;372(1):55-65.
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.
Sterns RH, Riggs JE, Schochet SS. Osmotic demyelination syndrome following correction of hyponatremia. N Engl J Med. 1986;314(24):1535-1542.
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.

How to Cite This Tool

DOIhttps://doi.org/10.5281/zenodo.22401536

AMA Style:Umakanth S. Acute Hyponatraemia Protocol. Version 1.1. MEDiscuss Clinical Decision Support System. Published 2026. Accessed . https://mediscuss.org/cdss/acute-hyponatraemia. doi:10.5281/zenodo.22401536

Vancouver Style:Umakanth S. Acute Hyponatraemia Protocol [Internet]. Version 1.1. MEDiscuss.org; 2026 [cited ]. Available from: https://mediscuss.org/cdss/acute-hyponatraemia. doi:10.5281/zenodo.22401536

Category Acute ResuscitationProtocol

Specialties Internal Medicine, Nephrology, Critical Care

Written and maintained by

Dr Shashikiran Umakanth

Last revised 24 August 2026

How these tools are written and reviewed